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ILLINOIS COLLEGE OF EMERGENCY PHYSICIANS 3000 Woodcreek Drive, Suite 200 Downers Grove, IL 60515 phone 630.495.6400 toll-free 888.495.ICEP fax 630.495.6404 web www.icep.org Disclaimer:
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This product is not sponsored by or affiliated with the American Board of Emergency Medicine, or the American Board of Osteopathic Emergency Medicine.
© 2017 – Illinois College of Emergency Physicians All rights reserved. This material may not be reproduced in any form or by any means without the written permission of the Illinois College of Emergency Physicians (The Illinois Chapter of the American College of Emergency Physicians), 3000 Woodcreek Drive, Suite 200 Downers Grove, IL 60515 USA Toll Free Phone (888) 495-4237 Phone (630) 495-6400 Fax (630) 495-6404 www.icep.org
TABLE OF CONTENTS – VOLUME 2
Pages Trauma Topics
Ultrasound Review 3-36 Robert P. Rifenburg, DO, RDMS, FACEP
Head Injury/C-spine/Spinal Cord Trauma 37-70 Scott Heinrich, MD, FACEP
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma 71-114 Michael Schindlbeck, MD, FACEP
Upper and Lower Extremity Trauma 115-160 Wesley Eilbert, MD, FACEP
Urology/GU Trauma 161-180 Wesley Eilbert, MD, FACEP
Stroke and Seizures 181-194 Daniel W. Robinson, MD
Psychiatric Emergencies 195-208 Leslie S. Zun, MD, MBA, FACEP
Miscellaneous Topics
Pulmonary Emergencies 211-236 Victor Chan, DO
Environmental Emergencies 237-288 Jay Sharp, MD, FACEP, FAWM
Gynecological and Obstetrical Emergencies 289-386 Bophal Sarha Hang, MD
EENT/Ophthalmologic Emergencies 387-418 Marc Dorfman, MD, FACEP, MACP
GI Emergencies 419-478 Brian Donahue, MD, FACEP
Infectious Disease 479-500 Paul E. Casey, MD, FACEP
Course Faculty and Planners
James Ahn, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Clinical Medicine, Section of Emergency Medicine, University of Chicago
Christine Babcock, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Clinical Medicine, Residency Program Director, Section of Emergency Medicine, University of Chicago
Kate Blackwelder Communications Manager, Illinois College of Emergency Physicians, Downers Grove
Paul E. Casey, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Medical Director, Process Improvement & Patient Experience, Director of Resident Education, Associate Chief Medical Informatics Officer, Department of Emergency Medicine, Rush University Medical Center, Chicago
Victor Chan, DO Assistant Director of Medical Student Education, Department of Emergency Medicine, OSF Saint Francis Medical Center; Clinical Assistant Professor, University of Illinois College of Medicine, Peoria
Christopher M. Colbert, DO, FACOEP Emergency Medicine Board Review Intensive Course Committee; Assistant Residency Director, Assistant Professor of Emergency Medicine, University of Illinois at Chicago, Department of Emergency Medicine; ACOEP Vice-Chair of Continuing Medical Education, Chicago
Joseph Colla, MD, RDMS Clinical Associate Professor and Ultrasound Fellowship Director, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago
Brian Donahue, MD, FACEP Clinical Assistant Professor, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, Presence Resurrection Medical Center, Chicago
Richard J. Doyle, MD, PhD Emergency Medicine Board Review Intensive Course Committee; Attending Physician, Section of Emergency Medicine, Jesse Brown VA Medical Center, Chicago
Marc Dorfman, MD, FACEP, MACP Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center, Chicago; Assistant Clinical Professor, University of Illinois at Chicago
Wesley Eilbert, MD, FACEP Professor of Clinical Emergency Medicine, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago
Carl Ferraro, MD, FACEP Education Director, Department of Emergency Medicine, Mercy Hospital and Medical Center, Chicago; Clinical Associate Professor, University of Illinois at Chicago
Lora Finucane Educational Programs and Meetings Manager, Illinois College of Emergency Physicians, Downers Grove
Shannon Finucane CME and Marketing Coordinator, Illinois College of Emergency Physicians, Downers Grove
Bophal Sarha Hang, MD Assistant Professor of Emergency Medicine, Director of Web-based Education & Assistant Simulation Director, Beaumont Health & Oakland University William Beaumont School of Medicine, Royal Oak, Michigan
Benjamin Reis Heilbrunn, MD Assistant Professor of Pediatrics, Section of Pediatric Emergency Medicine, The University of Chicago Medicine Comer Children’s Hospital, Chicago
Scott Heinrich, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Assistant Professor, Department of Emergency Medicine, Rush University Medical Center, Chicago; Assistant Residency Program Director, Department of Emergency Medicine, Rush University Medical Center
Lindsay Jin, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician, St. Francis Hospital, Evanston; Teaching Faculty, Presence Resurrection Medical Center, Chicago
Abhishek Katiyar, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician and Medical Toxicologist, Department of Emergency Medicine, Advocate Christ Medical Center, Oak Lawn
Matthew Kuhns, MD Emergency Medicine Board Review Intensive Course Committee; Instructor, Department of Emergency Medicine, Rush Medical College, Rush University, Chicago
Sara M. Krzyzaniak, MD, FACEP Assistant Program Director, Core Faculty Physician, Department of Emergency Medicine, OSF Saint Francis Medical Center; Clinical Assistant Professor of Emergency Medicine, University of Illinois College of Medicine, Peoria
John Martini, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Clinical Assistant Professor, University of Illinois at Chicago; Associate Medical Director, Presence Our Lady of the Resurrection Medical Center, Chicago
Alisa A. McQueen, MD, FAAP, FACEP Associate Professor of Pediatrics, Program Director, Fellowship in Pediatric Emergency Medicine, The University of Chicago
Timothy J. Meehan, MD, MPH, FACEP Clinical Assistant Professor, Department of Emergency Medicine, Division of Medical Toxicology, University of Illinois Hospital and Health Sciences System, Chicago; Attending Physician, Jesse Brown VA Medical Center, Chicago
Theresa Nguyen, MD Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Emergency Medicine, Loyola University Medical Center, Maywood
Henry Pitzele, MD, FACEP Chair, Emergency Medicine Board Review Intensive Course Committee; Director, Section of Emergency Medicine, Jesse Brown VA Medical Center; Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago
Robert P. Rifenburg, DO, RDMS, FACEP Associate Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago; Fellowship Director, Emergency Ultrasonography, Presence Resurrection Medical Center, Chicago
T.J. Rittenberry, MD, FACEP Emergency Medicine Board Review Intensive Course Committee Consultant; Associate Professor of Emergency Medicine, University of Illinois at Chicago (Ret.)
Daniel W. Robinson, MD Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Medicine, Section of Emergency Medicine, The University of Chicago Medicine & Biological Sciences, Chicago
Adam Rodos, MD Assistant Program Director, University of Illinois at Chicago Internal Medicine/ Emergency Medicine Residency; Clinical Assistant Professor of Emergency Medicine and Internal Medicine, University of Illinois at Chicago
Michael Schindlbeck, MD, FACEP Assistant Professor of Emergency Medicine, Rush Medical College; Assistant Program Director, Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago
Meeta Shah, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician and Assistant Professor, Department of Emergency Medicine, Rush University Medical Center, Chicago
Jay Sharp, MD, FACEP, FAWM Emergency Medicine Board Review Intensive Course Committee; Core Faculty, Emergency Medicine Residency, and Attending Physician, Presence Resurrection Medical Center, Chicago
Scott C. Sherman, MD Assistant Residency Director, Associate Professor of Emergency Medicine, Rush Medical College, Chicago; Attending Physician, Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago
David Snow, MD, MS Emergency Medicine Board Review Intensive Course Committee; Assistant Professor and Assistant Residency Director, Department of Emergency Medicine, University of Illinois at Chicago
William Sullivan, DO, JD, FACEP Attending Physician, St. Margaret's Hospital, Spring Valley; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago; Clinical Instructor, Department of Emergency Medicine, Midwestern University, Downers Grove; Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago
Henry Swoboda, MD Emergency Medicine Board Review Intensive Course Committee; Medical Toxicology Fellow, Toxikon Consortium; Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois Chicago; Instructor, Department of Emergency Medicine, Rush Medical College, Chicago
Midori Takeyasu Par, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Associate Clinical Professor of Emergency Medicine, University of Illinois College of Medicine, Chicago; Attending Physician, Presence Resurrection Medical Center and Presence Our Lady of the Resurrection Medical Center; Director, Emergency Medical Services, Presence Our Lady of the Resurrection Medical Center; Residency Coordinator, Presence Resurrection Medical Center and John H. Stroger Jr. Hospital of Cook County, Chicago
Trevonne M. Thompson, MD, FACEP, FACMT Attending Physician, Department of Emergency Medicine, and Associate Director, Division of Medical Toxicology, Department of Emergency Medicine, University of Illinois at Chicago; Consultant, Illinois Poison Center, Chicago
Carissa Tyo, MD Assistant Professor, Department of Emergency Medicine and Internal Medicine, University of Illinois Hospital and Health Sciences System, Chicago
James R. Waymack, MD, FACEP Co-Chair, Emergency Medicine Board Review Intensive Course Committee; Assistant Program Director, Assistant Professor, Division of Emergency Medicine, Department of Surgery, Southern Illinois University School of Medicine, Springfield
Deborah E. Weber, MD, FACEP Emeritus Faculty, Department of Emergency Medicine, Advocate Lutheran General Hospital, Park Ridge; Author of “Questions for Board Preparation in Emergency Medicine (Editions I, II & Slide Review)”, Author of “EM4LIFE – Emergency Medicine LLSA Article Review and CME Program (Editions 2004-2011)”, Author of “EM4LIFE – Emergency Medicine LLSA Article Review Pearls – 2012-2016”, Co-author of “Preparing for the Oral Board Exam in Emergency (Editions IV, V, VI and VII)” and Managing Editor of “Preparing for the Written Board Exam in Emergency Medicine (Editions I, II, and III)”; consulting contributor to all chapters of “Preparing for the Written Board Exam in Emergency Medicine”, 5th Edition; consulting contributor to “Preparing for the Oral Board Exam in Emergency Medicine”, 9th Edition, Riverwoods
Leslie S. Zun, MD, MBA, FACEP President, American Association for Emergency Psychiatry, Professor and Chair, Department of Emergency Medicine, Chicago Medical School, Chair, Department of Emergency Medicine, Mount Sinai Hospital, Chicago
powerful tools to pass your Boards. 4 focused days.
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Page 1
Page 2
Ultrasound Review
Robert P. Rifenburg, DO, RDMS, FACEP
Associate Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago; Fellowship Director, Emergency Ultrasonography, Presence Resurrection Medical Center, Chicago
Page 3
Page 4 Notes
ULTRASOUND REVIEW
I. EMERGENCY ULTRASOUND BASICS
A. Scanning planes:
1. Longitudinal (sagittal):
2. Transverse (axial):
Ultrasound Review Page 5 Notes 3. Coronal:
B. Image orientation:
Ultrasound Review Page 6 Notes
C. Echogenicity:
1. Hyperechoic: a. More echogenic (brighter) than surrounding tissue.
2. Hypoechoic: a. Less echogenic (darker) than surrounding tissue.
Ultrasound Review Page 7 Notes
3. Isoechoic: a. Same echogenicity (grey) as surrounding tissue.
4. Anechoic: a. Absence of echoes (completely black).
Ultrasound Review Page 8 Notes
II. TRAUMA ULTRASOUND WITH CARDIAC WINDOW (FAST EXAM)
A. Focused Assessment with Sonography in Trauma (FAST) windows:
1. RUQ window-Morrison’s Pouch view: a. Look for anechoic (black) fluid between liver and right kidney (Morrison’s Pouch).
Ultrasound Review Page 9 Notes
2. Subcostal (Sub-Xiphoid) cardiac window: a. Look for anechoic area between heart chambers and liver.
Ultrasound Review Page 10 Notes
3. LUQ window - Splenorenal recess view: a. Look for anechoic area between the left kidney and spleen.
Ultrasound Review Page 11 Notes
4. Suprapubic window - pelvic window uses two views: a. Sagittal view:
b. Transverse view: i. Pelvis:
Ultrasound Review Page 12 Notes
B. Positive FAST scans:
1. Hemopericardium – fluid will be anechoic with sharp angles between the pericardium and heart chambers.
Ultrasound Review Page 13 Notes
2. Hemoperitoneum – fluid will be anechoic with sharp angles.
Liver
Fluid
Ultrasound Review Page 14 Notes 3. Hemothorax – “loss of mirror image artifact” - see below:
III. GALLBLADDER ULTRASOUND
A. Gallbladder windows and landmarks:
1. Key landmarks = portal vein (thick walled) + intra-lobar ligament.
Ultrasound Review Page 15 Notes
2. Longitudinal (sagittal) view:
Ultrasound Review Page 16 Notes
3. Transverse view:
Ultrasound Review Page 17 Notes B. Sonographic evidence of cholecystitis:
1. Gallstones – notice “shadowing”:
2. Wall thickening – upper limit ~3mm:
Ultrasound Review Page 18 Notes 3. Pericholecystic fluid:
4. Sonographic Murphy’s sign. 5. Distended gallbladder – width >4 cm.
IV. KIDNEY ULTRASOUND
A. Windows and landmarks:
1. Key anatomy: a. Sinus/capsule = hyperechoic. b. Parenchyma = hypoechoic. c. Urine = anechoic.
Ultrasound Review Page 19 Notes
2. Right kidney: a. Coronal:
Ultrasound Review Page 20 Notes 3. Left kidney: a. Left kidney is positioned posteroinferior to the spleen. b. Stomach and bowels lie anterior to the left kidney. c. Coronal approach:
Ultrasound Review Page 21 Notes d. Hydronephrosis:
V. AORTIC ULTRASOUND
A. Windows and landmarks:
1. Key landmark – always look for spine shadow.
Ultrasound Review Page 22 Notes 2. Transverse view:
Ultrasound Review Page 23 Notes
3. Longitudinal view:
B. Identifying AAA:
1. Diameter > 3 cm. 2. Types of aneurysms: a. Fusiform. b. Saccular. 3. Indications for operative intervention: a. > 5 cm. b. Hemodynamically unstable. c. Tender to palpation.
Ultrasound Review Page 24 Notes
4. Examples of AAA:
VI. PELVIC ULTRASOUND
A. Two approaches:
1. Transabdominal sagittal. 2. Transabdominal transverse.
Ultrasound Review Page 25 Notes B. Transabdominal windows and landmarks:
1. Sagittal view: a. Bladder: i. Triangular. b. Uterus: i. Posterior. c. Vagina i. Stripe. d. Rectum i. Hyperechoic.
2. Transverse view: a. Bladder: i. Rectangular. b. Uterus: i. Oval shaped.
Ultrasound Review Page 26 Notes c. Rectum: i. Hyperechoic. d. Ovaries: i. Pathology:
C. Endovaginal windows and landmarks:
1. Sagittal view: a. Bladder – most anterior structure: i. Sliver. b. Uterus: Ultrasound Review Page 27 Notes i. Posterior to bladder. c. Rectum: i. Hyperechoic.
2. Endovaginal coronal: a. Bladder: i. Sliver. b. Uterus: i. Oval. c. Rectum: i. Hyperechoic.
Ultrasound Review Page 28 Notes
3. Intrauterine pregnancy (IUP): a. A gestational sac measuring at least 5 mm of internal diameter, with a thick concentric echogenic ring, lying within the endometrial echo of the uterus and one of the following: i. Yolk sac. ii. Fetal pole.
Ultrasound Review Page 29 Notes
b. Gestational sac - look for double decidual sign (i.e., double ring). c. Should be located in the center of the uterian fundus. d. Yolk sac – looks like a “balloon”:
Ultrasound Review Page 30 Notes
e. Fetal pole (embryo):
f. Use of BHCG with pelvic ultrasound:
g. No definitive IUP (NDIUP): i. Uterus appears empty. If gestational sac is present, doesn’t meet criteria for IUP. ii. There are no signs of an extrauterine gestation. iii. Possible differential includes: Early IUP. Abortion. Ectopic.
h. Abnormal IUP: i. Intrauterine.
Ultrasound Review Page 31 Notes ii. Gestational sac >10 mm, no yolk sac. iii. Gestational sac >16 mm, no fetal pole. iv. Obvious fetal pole and no cardiac activity.
i. Extrauterine gestation – “Ectopic”: i. A gestational sac measuring at least 5 mm of internal diameter, with a thick concentric echogenic ring, lying outside the endometrial echo of the uterus and one of the following: Yolk sac. Obvious fetal pole.
Ultrasound Review Page 32 Notes
ULTRASOUND REVIEW
PEARLS
1. KNOW YOUR ANATOMY!
2. Exam images will be straightforward.
3. Beware of normal variants.
4. Always use clinical info given to you in the question.
5. FAST scan: Fluid will appear anechoic. Fluid = blood. Fluid will form sharp angles. Look for “mirror artifact” to exclude hemothorax. FAQ - RUQ (Morrison’s) w/ free fluid. Morrison’s represents ~ 85% positive FAST scans. On exam, if FAST+, then to OR.
6. Gallbladder ultrasound: Gallstones – look for shadowing. Gallbladder wall – measure anterior wall. Gallbladder wall >3 mm is abnormal. Look for pericholecystic fluid.
7. Kidney ultrasound: Hydronephrosis – anechoic focus of fluid in sinus.
8. Aortic ultrasound: Always look for spine shadow! Look at measurements lines on screen. Diameter > 3 cm, then AAA! FAQ - exam will usually give you AAA, transverse view
Ultrasound Review Page 33 Notes
9. Pelvic ultrasound FAQ - ectopic will most likely present as NDIUP on exam. FAQ - Free fluid + NDIUP = ectopic.
Know how to correlate BHCG with pregnancy. Gestational sac 4-5 weeks. Yolk sac 5-6 weeks. Embryo/Amnion 6 weeks. HCG discriminatory zones: EV 1600-2000, must see evidence of early gestation (i.e. gestational sac). Lack of IUP when the HCG is above the discriminatory zone = ectopic or abortion.
Ultrasound Review Page 34 Notes
REFERENCES
1. Lambert, M. Emergency Medicine Ultrasound, ICEP course, November 2006.
2. Rifenburg, R. Emergency Medicine Ultrasound, ICEP EM/More in Four Course, September 2008.
3. Rumack, C. Diagnostic Ultrasound, St. Louis: Elsiever Mosby, 2005.
4. Ma, O. and Mateer, J. Emergency Ultrasound. 1st edition. New York: McGraw-Hill, 2003.
5. Simon, B. and Snoey, E. Ultrasound in Emergency and Ambulatory Medicine. St. Louis: Mosby, 1997.
08/17
Ultrasound Review Page 35
Page 36
Head Injury/C-Spine/ Spinal Cord Trauma
Scott Heinrich, MD, FACEP
Emergency Medicine Board Review Intensive Course Committee; Assistant Professor, Department of Emergency Medicine, Rush University Medical Center, Chicago; Assistant Residency Program Director, Department of Emergency Medicine, Rush University Medical Center
Page 37
Page 38 Notes
HEAD INJURY/C-SPINE/SPINAL CORD TRAUMA
I. HEAD TRAUMA
A. Anatomy:
1. Skull - rigid brain case protecting neural structures: a. Frontal, ethmoid, sphenoid, parietal (2), temporal (2), occipital bones. b. Bones of skull have inner and outer tables with cancellous bone between. c. Irregularity of floor or cranial vault increases problems with brain contusion. 2. Scalp (five layers) - pneumonic – S-C-A-L-P: a. Skin, subCutaneous, galea Aponeurotica, Loose areolar and Periosteum. b. Vascular with vessels between the dermis and galea. c. Lacerations of scalp may cause significant or even fatal hemorrhages, especially in children. d. Hematoma of the scalp occurs between galea and periosteum (subgaleal) or beneath the periosteum (subperiosteal). e. The sharp cutoff of a subperiosteal hemorrhage at a suture line may be mistaken for a fracture on palpation. 3. Meninges (intracranial hemorrhages are named in relation to these layers): a. Dura mater - tough outer covering, adheres to bone, folds compartmentalizes the brain. i. Midline falx cerebri – separates brain into 2 cerebral hemispheres. ii. Tentorium cerebelli – separates cerebellum and brainstem from cerebrum. iii. Falx cerebelli – separates cerebellum hemispheres. iv. Dural layers also separate to form dural sinuses. b. Arachnoid - thin, filmy, veil-like membrane. c. Pia mater - thin membrane adherent to brain surface. 4. CSF: a. Production by choroid plexus in lateral, third and fourth ventricles. b. Function: i. Protection during trauma. ii. Fluid pathway for delivery of substances to the brain and spinal column. iii. pH influences respiratory drive and cerebral blood flow. c. Pressure – 5-15 mmHg in ventricles. 5. Brain: a. Weighs 1400 g. b. Occupies 80% cranial cavity. Head Injury/C-Spine/Spinal Cord Trauma Page 39 Notes c. Divisions – cerebrum, cerebellum, brainstem. 6. Blood.
B. Cerebral hemodynamics:
1. Blood brain barrier (BBB) – maintains microenvironment. 2. Cerebral blood flow (CBF): a. 15% of cardiac output. b. Maintained by altering diameter of cerebral vessels. c. HTN, alkalosis, hypocarbia – vasoconstriction. d. Hypotension, acidosis, hypercarbia, hypoxia – vasodilation. e. Injured vessels lose responsiveness. f. Constant at mean arterial pressure of 50-150 mmHg. g. CBF increases linearly as MAP increases above 150 mmHg. 3. Cerebral Perfusion Pressure (CPP) - Pressure gradient across the brain: a. Estimated by MAP – ICP (intracranial pressure) = CPP. b. CBF depends on CPP, CBF remains constant when CPP is 50-160 mmHg. c. Autoregulation is lost when CPP < 40 mmHg.
C. Pathophysiology:
1. Primary brain damage: a. Mechanical, irreversible damage occurs at time of trauma – lacerations, hemorrhages, etc. b. Produces injury at the cellular level. 2. Secondary brain damage – intracellular and extracellular: a. Pathological processes arise as a direct result of trauma. b. Damage to nerve axons is followed by chromatolysis. c. Followed by either dissolution of cell or subsequent recovery. 3. ICP closed box model - intracranial pressure (ICP) is a function of the volume of these three components and any space occupying lesion. a. Increased ICP > 15 mmHg. b. 1st compensatory mechanism – displace CSF to spinal column: i. Can accommodate 50 to 100 ml lesion – after that, small increases in volume produce large increases in ICP as can be seen by the diagram below. ii. CSF production not increased in trauma unless a space occupying lesion obstructing CSF flow; usually not a major contributing factor.
Head Injury/C-Spine/Spinal Cord Trauma Page 40 Notes Pressure-Volume Curve
c. Blood - autoregulated: i. As ICP increases, CPP decreases, autoregulation is lost. d. Brain parenchyma - types of brain swelling: i. Congestive brain swelling – caused by increased blood volume. ii. Cerebral edema – increase in brain volume: Vasogenic edema – altered permeability of blood- brain barrier. Cytotoxic edema – disables Na-ATP pump, allows sodium and water to accumulate intracellularly. iii. Increase in aldosterone and vasopressin secretion, causing overall water retention.
D. Herniation syndromes:
1. Subfalcine herniation: a. Cingulate gyrus on medial part of frontal lobe is displaced medially under free end of the falx. b. Can compromise blood flow through anterior cerebral artery complexes. c. Does not usually cause brainstem effects seen in other herniation syndromes. 2. Central transtentorial herniation: a. Increased volume or pressure in the supratentorial compartment (usually frontal or occipital areas) causing bilateral or central pressure exerted on brain above. b. Results in brainstem ischemia or hemorrhage from compression and shear of perforating arteries from basilar artery (Duret hemorrhages). c. May be the etiology of the Cushing response (i.e., arterial hypertension, bradycardia and respiratory irregularities seen with increasing ICP). d. Decreased LOC. e. Motor – bilateral weakness, increased tone, bilateral Babinski’s. f. Pupils – pinpoint, loss of light reflex. g. Respiratory – yawns and sighs sustained hyperventilation slow and irregular breaths apnea. h. Posturing – decorticate decerebrate.
Head Injury/C-Spine/Spinal Cord Trauma Page 41 Notes 3. Uncal herniation (transtentorial): a. Due to increasing volume in the temporal lobe or middle cranial fossa. b. Uncus of temporal lobe herniates across incisura of the tentorium cerebelli and impacts against midbrain. c. Ipsilateral CN III compressed by the shift resulting in ipsilateral pupillary dilatation - aniscoria, ptosis, impaired EOM, sluggish pupil, finally nonreactivity. d. Contralateral Babinski develops early. e. Weakness is usually contralateral. f. 25% have ipsilateral weakness due to compression of the contralateral cerebral peduncle against the opposite tentorium (Kernohan’s notch phenomena) – gives false localizing signs. g. Impaired consciousness is NOT a reliable early sign but continued herniation results in agitation and restlessness lethargy coma. h. As herniation continues, contralateral pupil may dilate in the preterminal stage. i. Develop decerebrate posturing. j. Respiratory – normal hyperventilation ataxic breathing apnea. k. Cardiac – large fluctuations of blood pressure and cardiac conduction hypotension, pulselessness, death. 4. Cerebellotonsillar or posterior fossa herniation: a. When supratentorial compression continues unchecked, or when an expanding mass is situated in the posterior fossa or large central vertex mass. b. Cerebellar tonsils prolapse through the foramen magnum. c. Compression of the medulla and respiratory arrest (rapidly fatal). d. Pupils – pinpoint. e. Motor – flaccid quadriplegia. 5. Upward transtentorial: a. Caused by upward expanding posterior fossa lesion. b. LOC declines rapidly. c. Pupils – pinpoint. d. Downward conjugate gaze.
E. Assessment:
1. History. 2. Mechanism of injury. 3. Loss of consciousness. 4. ETOH or drugs. 5. Complaints before the trauma. 6. Assessment and treatment on the scene. 7. Posttraumatic seizures.
Head Injury/C-Spine/Spinal Cord Trauma Page 42 Notes 8. Past medical history: a. Comorbid conditions – coagulopathy. b. Medications – anticoagulants. 9. Return to normal mental status now. 10. Vital signs: a. Cushing response - hypertension, bradycardia and respiratory irregularities. b. Hypotension from head injury occurs only as a preterminal event (brainstem regulatory collapse) or from intracranial bleeding into an expandable skull of a young child. Look for associated visceral injuries. 11. Neurologic exam: a. Assess level of consciousness - single most important factor. i. AVPU – alert, awake to verbal stimuli, responds to painful stimuli, unresponsive. ii. Glasgow Coma Scale: Proposed by Teasdale and Jennett in 1974 as a means of providing uniformity for all examiners. 3 criteria:
Eye Opening Verbal Stimuli Motor Response Spontaneously 4 Oriented, converses 5 Obeys verbal commands 6 To verbal 3 Disoriented, converses 4 Localizes pain 5 To pain 2 Inappropriate words 3 Flexion withdrawal 4 None 1 Incomprehensible 2 Abnormal flexion 3 No response 1 Extension 2 No response 1
Good for rapid serial exams – not a substitute for a careful neuro exam. Falsely lowered due to hypoxia, hypotension, intoxication, intubation, non-English speaking, etc. Risk severity: •• < 8 for at least 6 hours severe injury. •• 9 – 13 moderate head injury. •• 14 – 15 mild head injury. b. Examine pupils - note size, shape, and reactivity: i. Unilateral fixed, dilated pupil: With normal mental status, R/O drops, surgery or congenital. Abnormal mental status, R/O increasing ICP and uncal herniation. ii. Pinpoint pupils: Pontine lesion. Narcotics. iii. Pupils fixed and dilated bilaterally: Hypoxia/anoxia or hypotension. Atropine/cycloplegics. Head Injury/C-Spine/Spinal Cord Trauma Page 43 Notes Brain death. Hypothermia. Herniation syndromes. c. Check extra-ocular movements (EOM) for weakness: i. Spontaneous eye opening suggests intact reticular activating system. ii. Reflexes – test the brainstem: Oculocephalic (doll’s eyes) –(must r/o C-spine injury first): •• Turn patient’s head to stimulate vestibular apparatus - movement of eyes in opposite direction intact brainstem. •• Eyes turn same direction as head damaged. Oculovestibular (caloric response) – (safe to test w/ C- spine injury): •• Need intact tympanic membrane. •• Cold water placed in ear canal results in movement of endolymph in semicircular canals. •• Interpreted by pons as movement of head in opposite direction – eyes deviated toward the ear and nystagmus away normal. •• Comatose – no nystagmus, just turn eyes toward cold water intact brainstem. These tests assess integrity of cranial nerves III, VI. Plus nuclei in the midbrain and pons. d. Assess cranial nerves II through XII. e. Check movement and power of each extremity. Also examine sensation DTRs and Babinski sign. f. Rectal sphincter tone, voluntary contraction and sensation. g. Posturing: i. Decorticate – flexion of upper and extensions of lower ext, lesion of the midbrain. ii. Decerebrate – extension of both upper and lower extremities – lesion more caudally, worse prognosis.
F. Diagnostic evaluation:
1. Skull films have little to no use clinically. 2. CT - initial imaging modality of choice. a. Availability, speed, readily detect osseous injury, foreign body and intracranial hemorrhage. b. ACEP 2008 Guidelines for CT imaging: i. Level A – CT recommended if has loss of consciousness or posttraumatic amnesia with 1 or more of the following: Headache. Physical evidence of trauma above the clavicle. Vomiting. Age > 60 years. Head Injury/C-Spine/Spinal Cord Trauma Page 44 Notes Posttraumatic seizure. Drug or alcohol intoxication. GCS score < 15. Deficits in short-term memory. Focal neurologic deficits. Coagulopathy. ii. Level B – CT considered if no loss of consciousness or posttraumatic amnesia and 1 of more of the following is present: Focal neurologic deficit. GCS score < 15. Vomiting. Coagulapathy. Severe headache. Dangerous mechanism of injury – ejection from a motor vehicle, a fall from height of > 3 feet or 5 steps. > 65 years of age. Physical signs of a basilar skull fracture. iii. PECARN for pediatric head injuries: Age <2: GCS 14 or lower or palpable skull fracture or signs of altered mental status – CT recommended. Nonfrontal scalp hematoma, LOC >5s, severe mechanism of injury, not acting normally per parents – CT vs observe (shared decision making). Age >2: GCS 14 or lower or palpable skull fracture or signs of altered mental status – CT recommended. Vomiting, LOC, severe headache, severe mechanism of injury – CT vs observe (shared decision making). 3. MRI - when patient’s symptoms not explained by CT. a. Better at detecting nonhemorrhagic contusions, brainstem injuries and SAH.
G. Risk stratification of TBI:
1. < 8 for at least 6 hours severe injury. 2. 9 – 13 moderate head injury. 3. 14 – 15 mild head injury.
H. Lesions following head injury:
1. Concussion: a. Transient loss of neurological function resulting in loss of consciousness. b. Amnesia for events before injury (retrograde) and after injury
Head Injury/C-Spine/Spinal Cord Trauma Page 45 Notes (anterograde) may be present. c. No significant gross anatomic, microscopic or radiographic damage demonstrable. d. Adults - headache, confusion, amnesia. e. Peds – confusion, restlessness, lethargy, irritability. f. Admit if: i. Unconscious for prolonged period. ii. Unstable home environment. g. Worrisome sports injury, development of several scoring systems; none accepted as the sole system to use. i. Recommendation for return to sports: Must wait 1 week after becoming asymptomatic. Must wait 1 month if period of LOC or prolonged posttraumatic amnesia. h. Second impact syndrome - sustain second concussion before complete resolution of symptoms from first concussion; experiences rapid, usually fatal, neurologic decline. i. Postconcussive syndrome – headache, sensory sensitivity, memory or concentration difficulties, irritability, sleep disturbances, or depression which persist for days to months after a concussion. 2. Cerebral contusion: a. Bruises on surface of brain after direct local trauma or sudden acceleration/deceleration injuries. b. Coup lesions occur at the site of impact. More common contrecoup lesions occur opposite the site of impact. c. Contusions occur most frequently at the frontal and temporal polar regions, as well as over the irregular basal areas. d. Neurologic deficits reflect location of the contusion. e. Can be ischemia of underlying brain tissue due to compression by blood. f. Cerebral edema with increasing ICP likely reaching maximum at 48 to 72 hours. g. Work-up includes CT and admission for observation. h. Patient is at risk for seizures so anticonvulsant prophylaxis indicated. 3. Subdural hematoma (SDH): a. Bleeding in the potential space between the dura and brain. b. From tearing of a cortical bridging vein to sagittal sinus with sudden acceleration/deceleration injuries. c. Blood spreads paralleling both brain surface and inner table of skull characteristic crescent-shaped appearance on CT. d. Often associated with significant underlying brain injury. e. Most common in alcoholics and elderly w/ atrophy. f. Classification: i. Acute subdural hematoma - discovered within the first 24 hours of injury.
Head Injury/C-Spine/Spinal Cord Trauma Page 46 Notes Fresh clotted, high density blood on CT. Have mental status changes and/or neurologic deficit. Mortality - 25% to 60%. Good functional recovery occurs 25% to 35% of cases. Surgical treatment: > 10 mm in size or > 5 mm midline shift. ii. Subacute SDH - symptomatic between 24 hours to 14 days post injury. These have improved prognosis. Appears iso-dense on CT scan. Most require surgery. iii. Chronic SDH - symptomatic greater than 2 weeks post injury. Hypo-dense or isodense on CT. Current theory - continued small hemorrhages within the capsule lead to a gradual increase in size over time. If symptomatic – need surgery. Present with subtle symptoms: H/A, dementia, lethargy, or stroke-like symptoms of focal weakness. 4. Subdural hygroma: a. Collection of clear, xanthochromic blood-tinged fluid in the dural space. b. Pathogenesis not clear. c. Sx – headache, nausea, vomiting, decreased LOC, focal motor deficits. d. Treatment – if asymptomatic observation; symptomatic surgery. 5. Epidural hematoma: a. Bleeding between inner table of skull and dura. b. Rare in elderly and children under 2 y.o. c. Due to laceration of meningeal vessel (artery or vein) or dural sinus. d. Most common site (70%) is the lateral aspect of the cerebral hemisphere with tears of the middle meningeal artery or vein due to fracture of the temporal bone. e. Occurs in frontal pole, temporal fossa, and posterior fossa (10% each). f. Bleeding strips the tightly adherent dura from the bone, yielding a bi-convex appearance on CT. g. Classical presentation - patient is stunned or knocked unconscious by a blow to the head, recovers (lucid interval), then develops a progressive contralateral hemiparesis and lapses into unconsciousness as the clot expands. h. Incidence - 1% to 2% of head injured patients presenting to ED. i. Mortality rate - 6% to 27%. j. Treatment - surgical evacuation: Head Injury/C-Spine/Spinal Cord Trauma Page 47 Notes i. > 30 cm in volume. ii. Comatose w/ anisocoia – the sooner the better. iii. Pediatric patients. 6. Intracerebral hemorrhage: a. Bleeding into the brain parenchyma from small blood vessel injury. b. Most common frontal and temporal lobe (85%). c. Reactive brain swelling as with contusions at 48 to 72 hours. d. May require surgical evacuation for control of ICP. e. Mortality rate - 55%. f. Presentation - altered level of consciousness and focal deficits depending on size and location of hematoma. 7. Traumatic subarachnoid hemorrhage: a. Trauma is the most common cause of blood in the subarachnoid space and CSF. b. Sx - headache, neck stiffness, photophobia. c. Vasospasm occurs 48 hours to 2 weeks post injury. i. Treat calcium channel blockers (nimodipine and nicardipine). d. Consider seizure prophylaxis. e. No CT angio needed. Admit for observation. 8. Diffuse axonal injury: a. Caused by mechanical shear force. b. Damaged axons become edematous and separate from each other. c. Macroscopic appearance may be normal or show small hemorrhages usually located near third ventricle, within the white matter of the corpus callosum, internal capsule of the brainstem, better seen with MRI. d. Management is directed at controlling ICP and supportive. e. Clinically, all patients present in coma, and duration of coma indicates severity of injury. i. Mild – coma 6-24 hours, 15% mortality, recover and have mild or no disabilities. ii. Moderate – coma > 24 hours, 25% mortality, awake and have persistent moderate to severe cognitive deficits. iii. Severe – coma > 24 hours, persistent brainstem and autonomic dysfunction, mortality high, few in persistent vegetative state. 9. Penetrating head injuries: a. Nonprojectile: i. Less likely to penetrate calvarium. ii. Damage usually restricted to path of travel. b. Projectile: i. More extensive damage. ii. High pressure in immediate vicinity causes more extensive tissue damage. iii. Civilian bullets are not jacketed and cause more fragmentation and more damage. Head Injury/C-Spine/Spinal Cord Trauma Page 48 Notes iv. Military bullets are jacketed and do not fragment, so less damage.
I. Skull fractures:
1. Significance - Presence of skull fracture in a conscious patient increases risk of intracranial hemorrhage 400 times. 2. Clinically significant if: a. Result in intracranial air and pass through an air-filled space (sinus). b. Associated with an overlying scalp laceration (open). c. Depressed skull fx below the inner table. d. Overlie a major dural venous sinus or middle meningeal artery. 3. Linear fractures do not have displacement of bone edges. a. May have damaged meningeal vessels with resulting epidural hematoma. b. If no intracranial hematoma is present, no specific ED treatment is required. c. Children with linear fractures should have repeat skull X-rays in 6 months to rule out a leptomeningeal cyst or growing fracture. 4. Basilar skull fracture: a. Fracture through one or more of the bones of the skull base - sphenoid, ethmoid, temporal or occipital bones. b. Usually clinical diagnosis based on signs such as raccoon eyes (periorbital ecchymosis), Battle sign (mastoid ecchymosis), hemotympanum, otorrhea, or rhinorrhea. c. Can injure CN III, IV, and V. d. Fx of sphenoid can cause carotid pseudoaneurysms or carotid venous fistulae. e. Rarely demonstrable on plain X-ray. f. Routine CT with bone windows may or may not show fracture line – can increase yield with posterior fossa views and thin cuts < 5mm. g. All require admission until cessation of CSF leak – usually 1 week. h. Increased risk of meningitis. Use of prophylactic antibiotics is controversial – usually not given in 1st week. i. Vancomycin and ceftriaxone (good CSF penetration). 5. Depressed skull fractures - bone piece below the plane of the skull: a. Greater than the full thickness of the skull require surgical treatment whether open or closed. b. Greater incidence of underlying brain injury. 6. Open fractures violate skin, nasal sinuses, and/or middle ear. a. Requires hospital admission for observation, possible antibiotic coverage / may need debridement. b. Closed fractures do not violate dura, skin, or sinus. Head Injury/C-Spine/Spinal Cord Trauma Page 49 Notes 7. Sutural diastasis – traumatic disruption of a cranial suture – coronal or lambdoid sutures. 8. Comminuted skull fracture – multiple linear fractures radiate from impact site.
J. Management of severe head trauma:
1. AVOID HYPOTENSION - Strive to maintain systolic BP of at least 90 mmHg. a. Avoid other secondary insults such as hypoxia, hyperthermia, seizures or electrolyte imbalances. 2. Elevated intracranial pressure: a. Normal ICP in adults is < 15-20 mmHg. b. CT cannot estimate or predict ICP. c. Fatal if uncontrolled > 25-30 mmHg. 3. Hyperventilation: a. Fastest means of decreasing ICP. b. PCO2 should be reduced to 30-35 torr. c. Onset of action <30 sec, peak effect 8 min. d. Should not be continued over 24 hours. e. Hyperventilation causes cerebral vasoconstriction decreasing intracranial blood volume. May cause focal areas of ischemia. 4. Osmotic agents: a. Mannitol 20% solution: i. 0.25 - 1 gm/kg IVPB. ii. Results in decrease in brain volume – draws out tissue water. iii. Onset- minutes, peak 60 minutes, duration 6-8 hours. iv. Side effects – renal failure in large amt, paradoxical intracranial hemorrhage, hypotension. v. Neuroprotective properties – blood volume expander reduces blood viscosity, free radical scavenger. vi. No evidence that fluid restriction is beneficial. Patients should be kept normovolemic. Avoid over-hydration. b. Hypertonic saline: i. Originally encouraging data; largest study done in Washington was discontinued. ii. Side effects – renal failure, central pontine myelinolysis, rebound ICP elevation. 5. Barbituate coma – Pentobarbital is drug of choice: a. Reduce cerebral metabolic demands. b. Affects vascular tone. c. Inhibits free radical-mediated cell membrane lipid peroxidation. d. Used when other methods to reduce ICP unsuccessful. e. Causes hypotension in up to ¼ of patients that receive it. 6. Steroids of no benefit – high dose methylprednisolone detrimental. 7. Decompression: Head Injury/C-Spine/Spinal Cord Trauma Page 50 Notes a. Burr holes – for herniation not responding to other methods. b. Surgical decompression – no focal lesion, but massive edema. c. External ventricular drain EVD (ventriculostomy): i. In rare circumstances, a neurosurgeon may place a bedside or emergency department EVD for drainage of CSF. ii. Controversial, but works immediately. iii. It is recommended by the Brain Trauma Foundation. 8. Seizure prophylaxis – indications: a. Depressed skull fracture. b. Paralyzed and intubated patient. c. Seizure at time of injury or ED presentation. d. GCS < 8. e. Acute subdural or epidural hematoma. f. Acute ICH. g. Prior history of seizures. h. Penetrating brain injury. 9. Antibiotics: a. Indicated – open skull fx, penetrating head injury, openly contaminated head injuries. b. Not indicated – presence of otorrhea or rhinorrhea. 10. Factor VII: a. Indicated for bleeding in the face of coagulopathy. b. Faster and cheaper than giving multiple drug products. c. Increased incidence of DVT. 11. Prothrombin Comblex Concentrates (PCC): a. Inactivated concentrates of factors II, IX, X with variable amounts of VII. b. May be considered for life-threatening bleeds. 12. Classification of patients with MINOR head injury (GSC 14-15): a. Low risk, don’t necessarily need a CT scan, possibly just a 4- hour period of observation. b. Disposition – consider admission if: i. Possible abuse. ii. Persistent or progressive symptoms. iii. Inadequate home situation. iv. Intoxication or ingestion. v. Anticoagulation – recent articles state may be ok to discharge with close phone follow-up. 13. Moderate traumatic brain injury: a. GCS of 9-14. b. All should receive CT scan. c. All should be admitted for observation regardless of CT scan. 14. Severe traumatic brain injury: a. GCS of < 8. b. All should receive CT scan. c. All should be admitted.
Head Injury/C-Spine/Spinal Cord Trauma Page 51 Notes K. Complications after head injury:
1. Hypotension: a. Occurs in 20-25% of severe TBI patients. b. Associated with increased morbidity and mortality. c. Level III rec to keep SpO2 > 89%. 2. Seizures: a. Common in children. b. Acute – within 24 hours following injury, transient, not repeated. c. Subacute – 24-48 hours following injury. d. Etiology: increasing cerebral edema, small hemorrhages, penetrating injuries. 3. Central nervous system infections: a. Meningitis after basilar skull fractures: i. Typical signs and sx of meningitis. ii. Organisms: Pneumococci – within 3 days of injury, treat w/ Ceftriaxone or ceftoxamine. Gram negatives - > 3 days after injury – Ceftriaxone or ceftoxamine plus naficillin and vancomycin. b. Brain abscess: i. Infrequent. ii. From penetrating injuries, depressed skull fx, fx that crosses paranasal sinuses. iii. Sx – headache, nausea, vomiting, decreased LOC, focal neurologic deficit, nuchal rigidity, seizure. iv. Organisms – S. aureus and gram negatives. c. Cranial osteomyelitis: i. Due to penetrating injury. ii. Sx – redness, swelling, warmth at site. iii. Diagnosis – 50% seen on plain skull films; others - bone scan or gallium scan. iv. Treatment – surgical debridement and antibiotics. 2. Medical: a. DIC: i. Develops within hours after injury. ii. Injured brain activates the extrinsic clotting system. iii. If stable, develops DIC, repeat the CT scan to find new hemorrhage. iv. Treatment – correct neurosurgical condition, treat with FFP and platelets as indicated. b. Neurogenic pulmonary edema: i. Develops minutes to days after injury. ii. Caused by altered hydrostatic forces and microvascular permeability. iii. Treatment – lower ICP. c. Cardiac dysfunction:
Head Injury/C-Spine/Spinal Cord Trauma Page 52 Notes i. Variety of arrhythmias – most common is SVT. ii. Theory – cause is autonomic nervous system dysfunction and/or high level of catecholamines. iii. Treatment goals: stop arrhythmia and support cardiac output. iv. Wide spread giant T wave inversions – “cerebral T waves”. 4. Transfer indications: a. Early transfer for patient with possible significant injury if without neurosurgical or diagnostic capabilities. b. Stabilize patient prior to transfer, if possible. c. R/O C-spine fracture or immobilize neck.
II. CERVICAL SPINE TRAUMA
A. Immobilization:
1. Indications: a. Abnormal mental status of uncertain cause. b. Any trauma victim, especially sports, motor vehicle collisions, falls. c. Head or facial trauma. d. Any neurologic deficit. e. Neck or back pain. f. Localized tenderness. g. Unexplained hypotension. h. Priapism or abdominal breathing. 2. Techniques: a. Initially at site - spine board and extrication collar. b. Immobilize head and body. c. Anchor torso to spine board. d. Blocks along sides of head. e. Tape/strap across forehead and collar to board. f. HARD COLLAR NOT ADEQUATE ALONE!
B. Initial management and assessment:
1. Primary survey: a. Ensure patient airway and ventilatory ability. i. Recommended method - orotracheal intubation with RSI and in-line stabilization. ii. LMA or cricothyrotomy – failed orotracheal intubation, associated massive facial trauma or RSI contraindicated. b. Circulation – check adequacy. i. Spinal shock – loss of reflexes and sensorimotor function below level of injury. Flaccid paralysis with loss of bladder tone and reflexes.
Head Injury/C-Spine/Spinal Cord Trauma Page 53 Notes Temporary physiologic response to trauma that lasts hours to days. ii. Neurogenic shock – Occurs w/ complete cord transection or injury above sympathetic plexus. Rarely due to temporary spinal cord concussion. Heart rate normal or bradycardic due to unopposed vagal tone. Bradycardia responds to atropine. No peripheral signs of vasoconstriction – patient usually warm and vasodilated. Diagnosis of exclusion – rule out blood loss. Start treatment with crystalloids. High cervical lesions, severe hypotension (<70 mmHg) – Trendelenburg position, vasopressors, cardiac pacing. Usually good urine output. Cessation marked by return of reflexes or bulbocavernosus reflex. 2. Secondary survey – assess motor and sensory functions completely. a. Assess breathing pattern - abdominal breathing indicates lower cervical injury - low tidal volume breaths. b. Look for muscle fasciculations. c. Look for Horner's Syndrome – unilateral facial ptosis, miosis and anhydrosis - from C7-T2 level. d. Look for painful dysesthesias. e. Palpate entire spine and musculature. f. Test DTRs – localizes and diagnostic. i. Paralysis with intact DTRs – upper motor neuron (spinal cord) lesion. ii. Paralysis with absent DTRs – lower motor neuron (nerve root) lesion or spinal shock. g. Baseline assessment of sensation: i. Light touch - posterior column. ii. Pain (pin prick) – anterior spinothalamic tract. iii. Proprioception – posterior column. iv. Islands of sparing means patient has 50% chance of functional motor recovery. Must find early to facilitate treatment. v. Evidence of incomplete injury - sacral sparing, normal rectal tone, flexor toe movement.
C. Spinal cord syndromes:
1. Mechanisms: a. Primary: i. Transection of the neural elements. ii. Compression between the vertebra. iii. Primary vascular damage – ischemia or compression.
Head Injury/C-Spine/Spinal Cord Trauma Page 54 Notes b. Secondary – cascade of events caused by the primary event causing ischemia to the neurons. 2. Complete spinal cord syndrome – nothing below injury. a. If persists greater than 24 hours after injury, 99% will not have functional recovery. b. Check for persistent perianal sensation, rectal sphincter tone or slight flexor toe movement - indicates partial lesion with potential for functional recovery. c. R/O spinal shock (see above). d. R/O intra-abdominal, etc., injuries as no sensation in abdomen. 3. Incomplete spinal cord lesions: a. Central cord syndrome (most common): i. Degenerative arthritis of neck w/ forceful hyperextension. ii. Hypertrophied ligamentum flavum buckles into cord, contuses central portion. iii. Affects pyramidal and spinothalamic tracts, in center of cord. iv. Upper extremities affected more than lower. v. Urinary retention invariably found. vi. Variable prognosis - 50% regain some function. b. Brown-Sequard syndrome: i. Functional hemisection of cord. ii. Penetrating injury or lateral mass fractures of C-spine. iii. Ipsilateral paralysis, loss of proprioception, touch and vibration (posterior column) and contralateral loss of pain and temperature (spinothalamic tract). iv. Prognosis fair to good. c. Anterior cord syndrome: i. Hyperflexion injuries, protrusion of bony fragments or herniated disc into anterior spinal canal OR by laceration/thrombosis of anterior spinal artery. ii. Complete motor paralysis and hypalgesias below level injury with preservation of position, touch and vibration (posterior column). iii. Requires surgery if ventral compression demonstrated. Need emergent MRI or CT to determine if cord decompression is indicated. d. Posteroinferior cerebellar artery syndrome - dysphagia, dysphonia, hiccups, nausea, vomiting, dizziness or vertigo, cerebellar ataxia. e. Horner’s syndrome: i. Damage to cervical sympathetic chain. ii. Ipsilateral ptosis, miosis, anhydrosis. iii. Due to direct cervico-medullary trauma or vertebral artery occlusion. f. Cauda equina syndrome: i. Perineal or bilateral leg pain. ii. Bowel or bladder dysfunction –retention is most specific. Head Injury/C-Spine/Spinal Cord Trauma Page 55 Notes iii. Perianal anesthesia. iv. Diminished rectal sphincter tone. v. Lower extremity weakness. g. Dejeune onion skin pattern: i. Analgesia of the face. ii. Damage to spinal trigeminal tract. h. SCIWORA: i. More common in peds. ii. Mechanism is unclear. iii. Brief episode of upper extremity weakness or paresthesias followed by neurologic deficits hours to days later. iv. No radiographic evidence.
D. Cervical diagnostic evaluation:
1. Indications: a. Nexus criteria – don’t need if: i. No midline tenderness. ii. No focal neurologic deficit. iii. Normal alertness. iv. No intoxication. v. No painful, distracting injury. vi. Sensitivity 99% and specificity 12.9%. b. Canadian C-spine Rule: i. Any high risk factors? > 65 years of age. Fall from height > 1 meter. Axial loading injury. High-speed motor vehicle crash > 100 km/h. Rollover. Ejection. Motorized recreational vehicle. Bicycle collision. Presence of paresthesias. ii. Any low-risk factors that allow safe assessment? Simple rear-end vehicle crashes. Sitting position in the ED. Ambulatory at any time. Delayed onset of neck pain. Absence of midline neck tenderness. iii. Is the patient able to actively rotate his or her neck 45 degrees to the left and right? 2. Cervical spine films: a. Cross table lateral - all 7 cervical and 1st thoracic vertebrae: i. Methodically review – ABCs. Alignment – anterior and posterior contour lines and spino-laminar line for smooth lordotic curvature. Bony changes – look for fractures. Head Injury/C-Spine/Spinal Cord Trauma Page 56 Notes Cartilage space assessment –anterior or posterior widening of the intervertebral space or interspinous space. b. A-P film: i. Views lower 5 cervical and upper thoracic vertebrae. ii. Overlapping articular pillars create wavy margin. iii. Spinous processes connected with straight line. iv. Bodies intact and uniform. v. Tracheal and laryngeal air shadows within midline. c. Soft tissue: i. Retropharyngeal – Ant border of C2 to posterior wall of pharynx - <7 mm in adults and children. ii. Predental space should not exceed 3 mm in adults and 5 mm for children. iii. At C3-C4 not greater than 5 mm, or ½ the width of the C2 body. iv. Retrotracheal space – anterior body of C6 to posterior surface of the trachea - < 22 mm in adults or < 14 mm less than 15 yo. d. Obliques: i. Demonstrate pedicles and facets better. ii. Laminae should look like overlapping roof shingles. iii. Laminar fractures seen well. iv. Assess the patency of the intervertebral foramina. e. Odontoid view (usually open mouth) – x-ray of atlas and axis. i. Check for alignment of lateral masses with odontoid. ii. Patient cannot be rotated or tilted. iii. Spinous process midline. iv. Inspect transverse processes for fx. f. Swimmer’s (transaxillary) helpful in trying to visualize lower C-spine. g. Flexion-extension views: i. Indicated if concern for ligamentous injury. ii. Must be awake, cooperative patients, no deficits. iii. Considered abnormal if > 3.5 mm of horizontal displacement between the disks, displaced apophyseal joints, widened disk spaces, loss of greater than 30% of the disk height, presence of prevertebral hematoma. iv. Replaced by CT and MRI. h. Pediatric variations: i. Pseudosubluxation of C2-C3 – less than 8 years: Immature muscles – hypermobile spine. If suspect injury, use posterior cervical line on lateral film line from anterior cortex of C1 spine to anterior cortex of C3 spine. ii. Retropharyngeal space: Less than 2 years old may normally be widened on expiration, so use inspiratory films.
Head Injury/C-Spine/Spinal Cord Trauma Page 57 Notes iii. Nonfusion of odontoid in kids mimics fracture. 3. CT scan: a. Indications: i. High-energy injury mechanism. ii. High-risk clinical parameter. iii. Plain films reveal an injury, an area of suspicion, or are inadequate. iv. High clinical suspicion of injury, despite normal plain films. b. Advantages – patient lies supine, can evaluate injuries already diagnosed by x-ray, sensitivity is better than x-ray. c. Disadvantages – cost and radiation. 4. MRI C-spine: a. Indications: i. Complete or incomplete neurologic deficits with radiographic evidence of fracture or subluxation. ii. Neurologic deficits not explained by plain films or CT – SCIWORA. iii. Deterioration of neurologic function. iv. Suspicion of ligamentous injury following inadequate or negative flex-ex films. b. Contraindications – pacemaker, cerebral aneurysm clips, metallic foreign bodies. c. CT and x-ray are still superior when evaluating bony structures.
E. Anatomy of spinal column – spine has three columns:
1. Anterior column: a. Vertebral bodies. b. Intervertebral discs. c. Anterior longitudinal ligament. 2. Middle column: a. Posterior portion of the annulus fibrosis and posterior vertebral wall. b. Posterior longitudinal ligament. c. Spinal cord. d. Laminae, pedicles and facets. e. Transverse processes. f. Nerve roots and vertebral arteries and veins. 3. Posterior column: a. Spinous processes. b. Nuchal ligament. c. Interspinous and supraspinous ligament. d. Ligamentum flavum.
F. Classification of spinal injuries (based on mechanism):
1. Atlanto-occipital dislocation: Head Injury/C-Spine/Spinal Cord Trauma Page 58 Notes a. Disruption of the stabilizing ligaments between C1 and occiput. b. More common in children due to large cranium. c. Fraquently fatal. d. Increased distance from basion to odontoid. 2. Atlanto-axial dislocation: a. Excessive movement between C1 and C2. b. From bony or ligamentous injury. c. Frequently associated with congenital conditions such as Down syndrome and osteogenesis imperfecta. 3. Flexion injuries: a. Simple wedge fractures - of anterosuperior vertebral body: i. Stable – rare nervous system damage. ii. Impaction of vertebrae against subjacent vertebra. iii. Becomes unstable if multiple or involves > ½ of height.
b. Flexion teardrop fracture: i. Wedge or chip-shaped fragment of antero-inferior vertebral body, displaced anteriorly. ii. Common cause of anterior cord syndrome. iii. Involves ligamentous injury and may have deficit. iv. Unstable.
c. Clay-shoveler’s fracture: i. Due to direct trauma to spinous processes or forced hyper-flexion. ii. Oblique fracture of spinous process base (C7, C6, T1). iii. Stable, no associated deficits. d. Anterior subluxation: i. Disruption of ligamentous complexes, starts posteriorly
Head Injury/C-Spine/Spinal Cord Trauma Page 59 Notes and proceeds anteriorly. ii. Potentially unstable. iii. Widening of interspinous or intervertebral spaces posteriorly. iv. High incidence of delayed instability.
e. Bilateral facet dislocation (locked facets): i. High incidence cord deficit. ii. All anterior and posterior ligaments disrupted. iii. Extremely unstable. iv. See anterior displacement of spine above level of injury (greater than 2 A-P diameter of lower body). v. Requires traction or even surgery. f. Odontoid fractures – three categories: i. Type I involves the distal portion of the dens (tip) – most stable of the three types.
ii. Type II involves the base of the dens – most common type, always unstable.
iii. Type III involves III involves the body of C2.
Head Injury/C-Spine/Spinal Cord Trauma Page 60 Notes
4. Flexion - rotation injuries: a. Unilateral facet dislocation (locked facet): i. Stable. ii. Symptom – torticollis (muscle spasm). iii. On lateral, see forward displacement of dislocated segment on vertebra below. iv. A-P and obliques helpful – loose “shingles on roof.” v. If unilateral facet dislocation occurs at C1-C2, is unstable. Seen as marked asymmetry between odontoid and lateral masses of C1 (rotary atlantoaxial dislocation). vi. Larger facets of lumbar region make this injury rare, but if one or both articular processes fracture, upper vertebra swings anterior. 5. Extension injuries: a. Posterior neural arch fracture of C1: i. Occiput compresses onto spinous process of axis. ii. Potentially unstable due to location.
b. Hangman’s fracture: i. Traumatic C2 spondylolysis. ii. Abrupt deceleration. iii. Unstable, yet cord damage usually minimal due to width of neural canal here. iv. Bilateral fractures of pedicles of C2 (axis) +/- subluxation of C2 on C3. v. Associated prevertebral swelling may cause airway obstruction.
c. Extension teardrop fracture: i. Large teardrop-shaped fragment off anteroinferior corner of vertebral body (ligament pulls it off). ii. Often occurs at C5-C7 in driving accidents. iii. Unstable. Head Injury/C-Spine/Spinal Cord Trauma Page 61 Notes iv. High association with central cord syndrome. 2. Vertical compression injuries: a. Burst fracture of vertebral body: i. Compressive forces from above or below force nuclear pulposus of disc into vertebral body. ii. Causes burst fracture. iii. Stable as all ligaments intact, although fracture segments can impinge into neural canal. iv. Associated with anterior cord syndrome.
b. Jefferson Fracture of Atlas (C1): i. Rare. ii. Lateral masses driven laterally. iii. See widening of predental space on lateral. iv. Odontoid view differentiates this from fracture of posterior neural arch of C1. v. Extremely unstable.
3. Stability: a. Stable: i. Simple wedge fracture. ii. Clay-shoveler’s fracture. iii. Unilateral facet dislocation. iv. Burst fracture. b. Unstable: i. Flexion teardrop. ii. Bilateral facet dislocation. iii. C1C2 dislocation. iv. Hangman’s fracture. v. Extension teardrop. vi. Jefferson fracture. c. Potentially unstable: i. Posterior neural arch fracture. ii. Anterior subluxation. Head Injury/C-Spine/Spinal Cord Trauma Page 62 Notes
G. Treatment (fracture, dislocation or deficit):
1. Strict immobilization. 2. Rapid neurosurgical consultation. 3. Surgery: a. Emergency - relieving impingement from herniated disks, foreign bodies, bony fragments, epidural hematoma. b. Delayed – to stabilize fracture. 4. Steroids: a. High dose methylprednisolone. b. Consortium of Spinal Cord Medicine – “no clinical evidence exists to definitively recommend the use of any neuroprotective pharmacologic agent including steroids”. c. Cochrane Review – high dose methylprednisolone is the only pharmacologic agent that has been shown to have efficacy. d. CONTROVERSIAL!!! CHECK WITH YOUR SPINAL CORD CENTER! 5. Transfer – regional spine center where all specialists are available.
Head Injury/C-Spine/Spinal Cord Trauma Page 63 Notes
HEAD INJURY/C-SPINE/SPINAL CORD TRAUMA
PEARLS
1. Cerebral blood flow is maintained at a constant level by autoregulation.
2. Increased intracranial pressure occurs if there is an increase in brain parenchyma, intracranial blood or CSF.
3. Increased intracranial pressure may result in the Cushing response - hypertension and bradycardia.
4. Hyperventilation to a pCO2 of 30 - 35 torr is the fastest means of decreasing ICP but only lasts a short while.
5. There is no evidence that corticosteroids decrease ICP.
6. Uncal herniation is the most common; symptoms of ipsilateral papillary dilatation, contralateral Babinski, and contralateral muscle weakness.
7. Central transtentorial herniation is the next most common; symptoms of decreased LOC, bilateral muscle weakness and Babinski reflexes, sustained hyperventilation, possibly Cushing’s.
8. Pinpoint pupils and a brain injury is a pontine lesion.
9. A normal doll’s eye is when the head is turned and the eyes turn in the opposite direction; that is an intact brainstem.
10. A Glasgow Coma Scale has 3 criteria: eye opening (4), verbal stimuli (5), and motor response (6).
11. Depressed skull fractures greater than the full thickness of the skull require surgical elevation.
12. Suspect a basilar skull fracture in a patient with raccoon eyes (periorbital ecchymosis), Battle sign (mastoid ecchymosis), hemotympanum or CSF rhinorrhea. The most common area is the temporal bone with hemotympanum.
13. Epidural hematomas appear at biconvex (lens-shaped) and subdural hematomas appear as crescent-shaped on CT scans.
14. Epidural hematomas are due to laceration of a meningeal artery (most commonly the middle meningeal) or a vein.
Head Injury/C-Spine/Spinal Cord Trauma Page 64 Notes
15. Epidurals are rare in children under 2 years and in the elderly, but subdurals occur in the very old, the very young and the very intoxicated.
16. Trauma is the most common cause of subarachnoid hemorrhage. Subarachnoid hemorrhage is the most common finding on a CT scan of a brain injured patient.
17. Intracerebral hemorrhage most commonly occurs in the frontal and temporal lobes.
18. Subacute subdural hematomas may not be seen well on a CT scan because they are isodense.
19. The treatment for most complications of increased ICP such as neurogenic pulmonary edema and DIC is to lower the ICP.
20. Spinal cord injury may result in spinal shock: hypotension and bradycardia but warm skin. It is a diagnosis of exclusion.
21. Central cord syndrome results in greater upper extremity weakness than lower extremity weakness.
22. Brown-Sequard syndrome results in contralateral loss of pain and temperature and ipsilateral loss of proprioception, light touch and vibration.
23. Anterior cord syndrome results in motor paralysis and hypalgesia below the level of the injury with preservation of position, touch and vibration.
24. The biggest difference between NEXUS criteria and the Canadian C- spine rule is the addition of patients 65 years and older as high risk for injury, and the ability to move the neck.
25. Adequately done C-spine x-rays miss significant injuries < 1 % of the time.
26. Bilateral C-spine facet dislocations (locked facets) are extremely unstable and require traction or surgery to reduce.
27. The Jefferson fracture of C1 is from a vertical compression resulting in an extremely unstable fracture.
28. Unilateral facet dislocations are stable. They are difficult to diagnose on x-ray. Be sure to look at the alignment of the transverse processes on the AP view.
Head Injury/C-Spine/Spinal Cord Trauma Page 65 Notes
29. High dose methylprednisolone is controversial.
30. Anterior subluxation is unstable due to the disruption of ligaments which begins posteriorly and moves anteriorly. High propensity of delayed stability.
Head Injury/C-Spine/Spinal Cord Trauma Page 66 Notes
REFERENCES
1. American College of Emergency Physicians, Centers for Disease Control and Prevention. Clinical Policy: Neuroimaging and Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute Setting. Ann Emerg Med 2008: 52; 714-748
2. ATLS Manual 8th edition. “Chapter 6: Head Trauma.” American College of Surgeons, Copyright 2008.
3. Baron BJ, McSherry KJ, Larson JL, and Scalea TM. Chapter 255: Spine and Spinal Cord Trauma.” ” Emergency Medicine A Comprehensive Study Guide7th edition. Editors: Tintinalli, Stapczynski, Ma, Cline, Cydulka, and Meckler. McGraw-Hill Copyright 2010, pg. 1709 - 1730.
4. Biros MH, Heegaard WG. “Chapter 41: Head Injury.” Rosen’s Emergency Medicine Concepts and Clinical Practice 8th Edition. Ed.: Marx, Hockberger, and Walls. Elsevier Copyright 2013: 339-367.
5. Bracken MB. “ Steroids for acute spinal cord injury.” Cochrane Database Systematic Review 2002; 3.
6. Brown, CV et al. “Recombinant factor VIIa for the correction of coagulopathy before emergent craniotomy in blunt trauma patients.” Journal of Trauma 2010 Feb;68(2): 348-352.
7. Bulger EM et al. “Out-of-hospital hypertonic resuscitation following severe traumatic brain injury: A randomized controlled trial.” JAMA 2010 Oct 6;304:1455.
8. Consortium for Spinal Cord Medicine: Early Acute Management in Adults with Spinal Cord Injury: A Clinical Practice Guideline for Healthcare Providers. Washington, DC, Consortium for Spinal Cord Medicine, 2008.
9. Davis RL, et al: Cranial Computed Tomography Scans in Children After Minimal Head Injury With Loss of Consciousness: Annals of Emer Med 1994; 24:640-645
10. Duus BR, et al: The Role of Neuroimaging in the Initial Management of Patients With Minor Head Injury: Annals of Emer Med 1994; 23:1279 – 1283.
11. Harnan SE, er at: Clinical Decision Rules for Adults With Minor Head Injury: A Systematic Review. J Trauma 2011, 71: 245-251.
Head Injury/C-Spine/Spinal Cord Trauma Page 67 Notes 12. Hockberger RS, Kaji AH, Newton E. “Chapter 43: Spinal Injuries.” Rosen’s Emergency Medicine Concepts and Clinical Practice 8th Edition. Ed.: Marx, Hockberger, and Walls. Elsevier Copyright 2013; 382-420.
13. Hoffman JR, et al: Low-Risk Criteria for Cervical-Spine Radiography in Blunt Trauma: A Prospective Study. Annals of Emergency Medicine 1992; 21:1454 1460.
14. Hoffman JR, et al: Selective Cervical spine Radiography in Bunt Trauma: Methodology of the National Emergency X-radiography Utilization Study (NEXUS). Annals of Emergency Medicine 1998; 32(4): 461 - 469.
15. Holmes JF and Akkinepalli R. Computed Tomography Versus Plain Radiography to Screen for Cervical Spine Injury; A Meta-Analysis. Journal of Trauma 2005 May; 58:902-905.
16. Jagoda, AS, et al. “Clinical Policy: Neuroimaging and Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute Setting.” Annals of Emergency Medicine 2008; December, 52:714-748.
17. Kuppermann N, Holmes JF, Dayan PS, Hoyle JD Jr, Atabaki SM, Holubkov R, Nadel FM, Monroe D, Stanley RM, Borgialli DA, Badawy MK, Schunk JE, Quayle KS, Mahajan P, Lichenstein R, Lillis KA, Tunik MG, Jacobs ES, Callahan JM, Gorelick MH, Glass TF, Lee LK, Bachman MC, Cooper A, Powell EC, Gerardi MJ, Melville KA, Muizelaar JP, Wisner DH, Zuspan SJ, Dean JM, Wootton-Gorges SL; Pediatric Emergency Care Applied Research Network (PECARN). Lancet 2009 Oct 3;374(9696):1160-70.
18. Looby S and Flanders A. “Spine Trauma.” Radiol Clin N Am 2011;49:129-163.
19. Melanson, SW. Lecture:64 and 128 Slice CTs: What’s Their Role in Emergency Medicine? ACEP Scientific Assembly October 2007.
20. Meyer S, et al: Evaluation and Significance of Pupillary Light Reflex in Trauma Patients: Annals of Emer Med 1993; 22:1052-1057
21. Miller EC, et al: Minor Head Trauma: Is Computed Tomography Always Necessary? Annals of Emer Med 1996; 27:290-294.
22. Morrison LJ, et al. “The Toronto prehospital hypetonic resuscitation- head injury and multi organ dysfunction trial (TOPHR HIT) methods and data collection tools.” www.ncbi.nlm.nih.gov/pubmed. Trials. 2009 November;20:10:105.
Head Injury/C-Spine/Spinal Cord Trauma Page 68 Notes
23. Pimental L and Diegelmann L. “Evaluation and Management of Acute Cervical Spine Trauma.” Emerg Med Clin N Am 2010; 28:719-738.
24. Reinus WR, Zwemer FL: Clinical Prediction of Emergency Computed Tomography Results: Annals of Emer Med 1994; 23:1271-1278.
25. Rockswold GL, et al. “Hypertonic saline and its effect on ICP, erebral perfusion pressure, and brain tissue oxygen.” Neurosurgery 2009 December;65(6):1035-1041.
26. Rosenthal M: Mild Traumatic Brain Injury Syndrome: Annals of Emer Med 1993; 22:1048-1051.
27. Schenarts PJ, et al. Prospective Comparison of Admission Computed Tomographic Scan and Plain Films of the Upper Cervical Spine in Trauma Patients with Altered Mental Status. Journal of Trauma 2001;51(4):663-669.
28. Siesjo BK: Basic Mechanism of Traumatic Brain Damage: Annals of Emer Med 1993;22:959-969.
29. Stiell IG, et al: Variation in ED Use of CT for Patients With Minor Head Injury: Annals of Emer Med 1997; 30:14-22.
30. Stiell IG, et al. The Canadian C-spine Rule versus the NEXUS Low- Risk Criteria in Patients with Trauma. NEJM 2003 December; 349(26): 2510-2518.
31. Stiell IG, et al. The Canadian C-Spine Rule for Radiography in Alert and Stable Trauma Patients. JAMA 2001;286(15):1841-1848.
32. Wright DW and Merck LH. “Chapter 254: Head Trauma In Adults and Children.” Emergency Medicine A Comprehensive Study Guide 7th edition. Editors: Tintinalli, Stapczynski, Ma, Cline, Cydulka, and Meckler. McGraw-Hill 2010: 1692-1709.
33. “Hypertonic Resuscitation Following Severe Traumatic Brain Injury.” University of Washington. http://www.clinicaltrials.gov/ct2/show/NCT00316004?term=Hypertonic +Resuscitation+Following+Traumatic+Brain+Injury&rank=1
34. Yuan, ZH, et al. “A meta-analysis of the efficacy and safety of recombinant activated factor VII for patients with acute intracerebral hemorrhage without hemophilia.” Journal of Clinical Neurology 2010 Jun;17(6):685-693.
08/17
Head Injury/C-Spine/Spinal Cord Trauma Page 69
Page 70
Airway/Maxillofacial/ Penetrating Neck/Thoracic/ Abdominal Trauma
Michael Schindlbeck, MD, FACEP
Assistant Professor of Emergency Medicine, Rush Medical College; Assistant Program Director, Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago
Page 71
Page 72 Notes
AIRWAY/MAXILLOFACIAL/PENETRATING NECK/ THORACIC/ABDOMINAL TRAUMA
AIRWAY MANAGEMENT IN TRAUMA
I. INITIAL MANAGEMENT
A. Assess the airway: Common indications for advanced airway management in trauma:
1. Cardiopulmonary arrest. 2. Advanced hemorrhagic shock. 3. Severe head injury (GCS ≤ 8 = intubate). 4. Significant airway burns. 5. Penetrating face or neck wounds. 6. Flail chest. 7. Pulmonary contusion.
B. Open the airway:
1. Head tilt and chin lift vs. jaw thrust (always suspect potential C- spine injury).
II. MAINTAINING THE AIRWAY
A. Oral adjunct:
1. Indications: Unconscious patient. 2. Contraindications: Awake patient, intact gag reflex. 3. Size: Central incisors to the angle of mandible. 4. Technique of insertion: 180°, then rotate (adults only) or use tongue depressor.
B. Nasal adjunct:
1. Indications: Awake patient, intact gag reflex. 2. Contraindications: Coagulopathy, significant midface trauma. 3. Size: Tip of nose to the ear lobe, same diameter as opening of nares. 4. Technique of insertion: Adequate lubrication, guide posteriorly along the floor of the nasal cavity into nasopharynx.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 73 Notes
III. NASOTRACHEAL INTUBATION
A. Advantages:
1. Can be inserted into an awake patient. 2. Can be placed blindly or with laryngoscopic guidance. 3. Patient cannot bite/occlude the ETT. 4. Requires no/minimal neck movement. 5. Not dependant on ability to adequately open the mouth.
B. Disadvantages:
1. Requires spontaneously breathing patient. 2. Blind insertion is heavily operator dependant.
C. Contraindications:
1. Apneic patient. 2. Pediatric patient. 3. Significant midface trauma. 4. Basilar skull fracture. 5. Coagulopathy (relative).
D. Technique:
1. Local anesthesia (e.g., benzocaine spray, lidocaine neb). 2. Topical vasoconstriction (e.g., phenylephrine, oxymetazoline). 3. Adequate lubrication (e.g., lidocaine jelly, Surgilube). 4. Gently insert size 7-7.5 ETT posteriorly into nasopharynx. 5. Listen carefully for exhalation/ check for tube condensation. 6. Advance tube during inhalation (vocal cords maximally open). 7. Confirm placement (optimal depth 26-28 cm): a. Inability to vocalize. b. Air movement through tube. c. Bilateral thoracic breath sounds. d. End tidal CO2. e. Chest X-ray.
E. Complications:
1. Airway trauma. 2. Epistaxis with secondary vomiting and aspiration. 3. Malposition. 4. Sinusitis.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 74 Notes
IV. OROTRACHEAL INTUBATION: TECHNIQUE OF CHOICE
A. Advantages:
1. Can be inserted in apneic patient. 2. Direct visualization precludes malpositioning. 3. Fewer infectious complications.
B. Disadvantages:
1. Increased patient discomfort. 2. Requires patient capacity to widely open mouth. 3. Increased potential for inadvertent C-spine movement.
C. Contraindications:
1. No absolute contraindications.
D. Technique:
1. Laryngoscope selection (essentially a matter of preference): a. Miller blade: i. Directly lifts epiglottis. ii. More difficult to move tongue. b. Macintosh blade: i. Indirectly lifts epiglottis. ii. Designed to sweep tongue. 2. Patient positioning: a. “Sniffing” if possible (if absolutely no concern for C-spine injury). b. C-spine immobilization, not traction. 3. Sellick’s maneuver (cricoid pressure): a. Attempt to minimize aspiration. b. Start when induction agent given. c. Release only after cuff inflated and endotracheal placement confirmed. 4. Confirm placement: a. Visualize tube pass through cords. b. End-tidal CO2 after 6 bag breaths. c. Bilateral thoracic breath sounds upon auscultation. d. Tube condensation. e. Chest X-ray.
E. Complications:
1. Airway trauma. 2. Malposition (esophagus, right mainstem bronchus). 3. Cervical cord injury secondary to movement of an unstable Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 75 Notes fracture.
V. RAPID SEQUENCE INTUBATION IN TRAUMA
A. Induction agents:
1. Etomidate (0.3 mg/kg): a. Minimal effect on hemodynamics. b. May lowers seizure threshold in patients with focal seizures. c. Transiently suppresses cortisol production. 2. Thiopental (3 mg/kg): a. Marked cardiovascular depressant. b. Transiently suppresses seizure potential. c. May lower ICP via decreasing cerebral perfusion. 3. Ketamine (2 mg/kg): a. Minimal cardiovascular effect. b. Increases ICP and IOP. c. Give with atropine to minimize secretions. d. Give with midazolam in adults to block emergence reactions.
B. Paralytic:
1. Succinylcholine (1.0-1.5 mg/kg adults, 1.5-2.0 mg/kg peds): a. Rapid onset and short duration. b. Depolarizing agent; contraindicated in acute crush injuries, subacute burns and spinal cord injury. c. Coadminister atropine in children to block excessive bradycardia. 2. Rocuronium (0.6-1.2 mg/kg): a. Non-depolarizing agent. b. Rapid onset - duration of onset roughly 30-45 minutes. c. Reversing agents in development.
C. Increased ICP/ head trauma precautions:
1. Lidocaine (1.5 mg/kg). 2. Defasciculating agent (non-depolarizing agent at 1/10th the RSI dose). 3. Fentanyl (3 mcg/kg).
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 76 Notes
Special Situations Low BP Head Injury Peds Drugs Etomidate 20 mg Lido 100 mg Give atropine with Sux 100 mg Pavulon 1 mg Sux Thiopental 200 mg Fentanyl 200 mcg Sux 100 mg Other Works for Watch the BP, lowers Age/4 + 4 = ET tube everyone seizure potential size
VI. SURGICAL CRICOTHYROTOMY
A. Indications:
1. Inability to intubate orally (can’t intubate, can’t ventilate): a. Glottic edema. b. Laryngospasm. c. Severe oropharyngeal hemorrhage/secretions. d. Foreign body obstruction. e. Masseter spasm/ clenched teeth.
B. Contraindications:
1. Laryngeal pathology. 2. Pediatric patient (<8 years old). 3. Tracheal transaction w/ retraction.
C. Technique:
1. Identify anatomic landmarks (cricothyroid membrane between thyroid and cricoid cartilages). 2. Antiseptic skin preparation. 3. 1-2 cm transverse skin incision via #11 blade (longitudinal ONLY if laryngeal pathology or significant edema precludes anatomical landmarking). 4. Tracheal hook to stabilize thyroid cartilage. 5. Dilation with hemostat or trousseau dilator. 6. Insert tube (#4 or smaller Shiley/ 6.0 or smaller ETT). 7. Secure tube. 8. Connect to ventilator/Ambu bag. 9. Confirm placement.
D. Complications:
1. Malposition: a. Subcutaneous cervical soft tissues.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 77 Notes b. Esophagus. 2. Significant hemorrhage (usually secondary to lateral incision): a. Anterior jugular veins. b. Thyroid vessels. 3. Wound infection. 4. Laryngeal injury: a. Fracture from oversized tube. b. Delayed subglottic stenosis. c. Vocal cord palsy.
VII. NEEDLE CRICOTHYROTOMY
A. Indications:
1. Same as outlined for surgical cricothyrotomy. 2. Pediatric patient (<8 years old).
B. Contraindications:
1. Same as outlined for surgical cricothyrotomy. 2. Adult patient.
C. Technique:
1. Identify anatomic landmarks (cricothyroid membrane between thyroid and cricoid cartilages). 2. Antiseptic skin preparation. 3. 14 gauge over-needle catheter attached to 5 ml syringe. 4. Advance at 45° angle caudally until air is aspirated. 5. Advance catheter and remove needle. 6. Connect to oxygen source: a. 3.0 ETT adapter and Ambu bag/ventilator. b. Direct connection of high-flow oxygen tubing with Y connector or in-line side port. c. Cycle ventilation (inspiration 1 second: expiration 4 seconds). 7. Confirm placement. 8. Carefully secure catheter without kinking. 9. Convert to formal tracheostomy ASAP.
D. Complications:
1. Subcutaneous emphysema. 2. Pulmonary barotrauma (pneumomediastinum, pneumothorax).
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 78 Notes
VIII. ALTERNATIVE AIRWAY TECHNIQUES
A. Laryngeal mask airway:
1. Indications: a. Failed intubation and inadequate BVM ventilation. 2. Pros: a. Easy/blind insertion. b. Temporizing measure. c. May facilitate secondary ETT placement. 3. Cons: a. Does not secure/protect airway.
B. Fiberoptic intubation:
1. Indications: a. Patients with significant maxillofacial and penetrating neck trauma. b. Patients with severely limited neck mobility or mouth opening. c. Patients with prior history of difficult intubation. 2. Pros: a. Allows direct visualization of airway and possible airway injury. b. Facilitates guided placement of ET tube. c. Provides a definitive/secure airway. 3. Cons: a. Requires time to call anesthesia/obtain bronchoscope. b. Adequate visualization depends upon suctioning all blood/secretions.
C. Combitube:
1. Indications: a. Failed intubation and inadequate BVM ventilation. 2. Pros: a. Easy/blind insertion. b. Temporizing measure. c. May permit OG tube placement and gastric decompression. 3. Cons: a. Does not secure/protect the airway. b. Secondary vomiting may cause esophageal rupture. c. Contraindicated in patients with caustic ingestions.
D. Wire-guided retrograde intubation:
1. Indications: a. Severe orofacial trauma with significant airway distortion. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 79 Notes 2. Pros: a. Doesn’t require neck movement. b. Provides a definitive/secure airway. 3. Cons: a. Requires ability to externally landmark significant neck anatomy. b. Requires the right kit and operator experience.
IX. INHALATION INJURIES
A. Types of inhalation injury:
1. Supraglottic injuries: a. Thermal mediated tissue destruction. b. Significant upper airway edema (minutes). c. Rapid onset post exposure. 2. Infraglottic injury: a. Chemical mediated tissue injury. b. Tracheobronchiolitis +/- secondary ARDS. c. Delayed presentation (hours-days). 3. Toxic gas poisoning: a. Impaired tissue oxygenation. b. Inhibited cellular respiration.
B. Indication for airway management:
1. Historical: a. Closed space. b. Respiratory distress/arrest. 2. Clinical: a. Facial burns/singing. b. Soot in/around nose and/or mouth. c. Carbonaceous sputum. d. Oropharyngeal edema. e. Voice changes. f. Stridor. g. Rales/wheezing.
C. Additional considerations:
1. Carbon monoxide: a. Incomplete combustion of fossil fuels. b. 280-fold higher affinity for hemoglobin than O2. c. Pulse oximetry not helpful (misreads carboxyhemoglobin as oxyhemoglobin). d. “Cherry red” blood on sampling. e. Carboxyhemoglobin levels on ABG or VBG: i. 0-15% - asymptomatic. ii. 15-50% - progressive neurologic dysfunction. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 80 Notes iii. >50% - lethal. 2. Cyanide toxicity: a. Combustion of plastics and solvents. b. Metabolic acidosis with high lactate with normal PaO2. c. “Poor man’s test” - increased venous O2 saturation. d. If concurrent CO poisoning suspected, then avoid oxidizing agents from CN- antidote kit. Treat with only IV sodium thiosulfate or IV hydroxycobalamin.
D. Management:
1. Supplemental 100% oxygen. 2. Early intubation (permissive hypercapnia/low airway pressures). 3. Ensure adequate chest wall mechanics (escharotomy). 4. Early bronchoscopy to determine severity of injury. 5. Specific antidotes as indicated.
MAXILLOFACIAL TRAUMA
I. GENERAL PRINCIPLES
A. Rarely the direct cause of death; other injuries take precedence.
1. Exceptions: a. Airway occlusion. b. Distal carotid artery injury.
B. Definitive treatment can be delayed for several days.
1. Initial tetanus and antibiotic prophylaxis as appropriate. 2. Allow time for soft tissue swelling to resolve. 3. Conclusive CT imaging completed. 4. Goal is to restore normal function and then address cosmetics.
II. INITIAL MANAGEMENT
A. Airway management:
1. Alleviate obstruction: a. Aspiration (blood, saliva, teeth, vomit, etc.). b. Inability to control tongue (pull tongue forward with towel clip or suture). c. Extensive edema of the soft palate. 2. Indications for ETT same as previously described. 3. Follow standard C-spine precautions.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 81 Notes
B. Hemorrhage control:
1. Local direct pressure. 2. Sterile packing. 3. Avoid blind clamping.
III. DIAGNOSIS
A. History and physical:
1. Mechanism (always consider abuse). 2. Dental malocclusion. 3. Facial paresthesias. 4. Visual symptoms: a. Monocular diploplia – lens dislocation. b. Binocular diploplia – extraocular muscle or nerve dysfunction. 5. Soft tissue crepitus (sinus fracture). 6. Abnormal bony mobility.
B. Imaging:
1. Radiographs: a. Water’s view useful screen in low risk patients. b. Limited utility for additional films (i.e., facial series). 2. CT imaging: a. Definitive diagnosis and surgical planning.
IV. MIDFACE FRACTURES
A. Nasal:
1. General principles: a. Most common facial fracture. b. Most displaced laterally or posteriorly. c. Clinical diagnosis, radiographs are unnecessary. 2. Signs and symptoms: a. Nasal bridge deformity. b. Epistaxis. c. Hypermobility with crepitus. d. Periorbital ecchymosis. 3. ED treatment: a. Control epistaxis. b. Identify and alleviate septal hematoma: i. Benzocaine/oxymetazoline or cocaine. ii. I&D at inferior border. iii. Pack to prevent reaccumulation. c. Ice and analgesia. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 82 Notes 4. Disposition: a. Reevaluation within 1 week by PMD or plastic surgeon.
B. Zygomatic arch:
1. General principles: a. Isolated fractures fairly uncommon. 2. Signs and symptoms: a. Facial dimpling/depression. b. Point tenderness. c. Inability to open mouth (mandibular condyle impingement).
C. Tripod (trimalar) fractures:
1. General principles: a. Fractures occur at articulations with frontal, temporal, and maxillary bones. b. Often displaced; if untreated, result in “sunken” facial asymmetry. 2. Signs and symptoms: a. Step deformity and point tenderness. b. Facial flattening. c. Cheek and/or periorbital edema. d. Circumorbital ecchymosis. e. Subconjunctival hemorrhage. f. Anesthesia of cheek and upper lip (infraorbital nerve), teeth and gums (dentoalveolar nerves). g. Enophthalmos/diplopia. h. Limited mandibular excursion. i. Overlying subcutaneous emphysema. j. Intraoral ecchymosis at upper buccal sulcus.
D. Orbit:
1. General principles: a. Blowout fractures secondary to rapid increase in intraorbital pressure. b. Classic location is inferomedial orbital border (weakest point). c. Orbital soft tissue may be herniated into the maxillary sinus. i. True entrapment of the inferior rectus is rare, ophthalmoplegia commonly resolves when swelling abates. ii. Classic radiographic findings include “teardrop sign” and maxillary sinus air-fluid level. 2. Signs and symptoms: a. Inferior globe displacement. b. Vertical diplopia. c. Infraorbital nerve hypoaesthesia. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 83 Notes 3. Associated ophthalmological injuries: a. Lens dislocation: i. Pathognomically presents with monocular diplopia. ii. Increased incidence with underlying connective tissue disorder (e.g., Marfan’s syndrome). b. Iridodialysis: i. Shearing of the peripheral iris from the ciliary body forming a secondary pupil. c. Perforation of the anterior chamber: i. “Tear-drop pupil” secondary to prolapse of the iris. ii. Positive Seidel test. d. Retrobulbar hematoma: i. Intraorbital bleeding with secondary compartment syndrome. ii. Exam findings include proptosis, increased IOP, a loss of acuity, and an afferent pupillary defect. iii. An emergent lateral canthotomy can be vision saving.
E. Maxillary:
1. LeFort I = Transverse maxillary fracture: a. General principles: i. Fracture lines extend above palate and below zygomatic process. ii. Majority are not displaced. iii. Exceptionally difficult to detect on plain film imaging. b. Signs and symptoms: i. Motion of hard palate but not nose. ii. Dental malocclusion. iii. Subcutaneous air (sinus fracture). 2. LeFort II = Pyramidal fracture: a. General principles: i. Bilateral vertical fractures extend through maxillary sinuses and infra-orbital rims joining across the nasal bridge. b. Signs and symptoms: i. Motion of hard palate and nose but not orbits. ii. Extensive swelling of the entire midface. iii. Bilateral subconjunctival hemorrhage. 3. LeFort III = Craniofacial dysjunction: a. General principles: i. Fractures extend through frontozygomatic sutures, across the orbits and through the base of the nose and ethmoidal region. b. Signs and symptoms: i. Disjointed lateral orbit rims. ii. Classic “dishface” deformity. iii. Motion of entire face relative to skull. iv. CSF rhinorrhea secondary to sphenoethmoidal Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 84 Notes involvement.
Zygomaxillary Complex Fractures with Red Lines Indicating LeFort I, II and III Patterns
V. MANDIBLE FRACTURES
A. General principles:
1. Commonly two fractures sites (similar to the pelvic ring). 2. Anatomic locations: a. Condyle: 30%. b. Angle/Ramus: 30%. c. Body: 30%
B. Signs and symptoms:
1. Significant swelling and ecchymosis. 2. Dental malocclusion. 3. Mandible deviation on opening. 4. Trismus. 5. Intraoral laceration (open fracture). 6. Sublingual hematoma. 7. Mental nerve anesthesia.
C. Imaging studies:
1. Radiographs: a. Panorex: Still the BEST, not readily available. b. Mandible series: Inadequate, classically miss condylar fractures. 2. CT mandible: preferred today by many oral surgeons
D. Specific fractures:
1. Condyle fractures: a. Jaw deviates toward fracture on maximum opening. b. Bilateral fractures result in inability to occlude the incisors (+
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 85 Notes tongue-blade test). 2. Angle/body fractures: a. Bilateral angle fractures can result in loss of tongue support and secondary airway obstruction. 3. Symphysis fractures: a. Unusual because of overall bone thickness. b. Evaluate for potential blunt carotid injury. 4. Alveolar fractures: a. Anterior or incisor areas most common. b. Focus on maintaining tooth viability. c. Most require stabilization with wires or arch bars.
E. Treatment:
1. Remove nonviable teeth. 2. Tetanus prophylaxis. 3. Prophylactic antibiotics for open fractures. 4. Reduced by wiring upper and lower teeth in occlusion. 5. Open fixation for edentulous or posterior segments.
VI. AURICULAR INJURIES
A. Auricular hematomas:
1. General principles: a. Blood accumulates between perichondrium (blood supply) and cartilage (avascular). b. May occur after blunt or shear force without laceration. c. Failure to treat results in “cauliflower ear”. 2. Treatment: a. Aspiration alone often leads to recurrence. b. Incise along curvature of pinna no greater than 1 cm, evacuate hematoma, and irrigate cavity. c. Hold direct pressure for minimum of 5 minutes span. d. Dress with antibiotic ointment and apply pressure dressing for 48-hour span to prevent reaccumulation. e. DC with PO antibiotics and recheck in 24 hours.
B. Auricular lacerations:
1. General principles: a. Cartilage involvement is very common. b. General approach should focus on prevention of skin and cartilage loss. c. All cartilage needs to be covered by skin to prevent secondary chondritis and tissue loss. 2. Treatment: a. For simple skin lacerations, meticulous closure with 6.0 nylon is usually sufficient. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 86 Notes b. For large wounds with lacerated cartilage, re-approximate cartilage with 6.0 nylon and very small knots and then close the skin as above. c. Hold direct pressure for minimum of 5 minutes. d. Dress with antibiotic ointment and apply pressure dressing for 48-hour span to prevent reaccumulation. e. DC with PO antibiotics and recheck in 24 hours. f. Refer patients with significant amount of avulsed skin to plastic surgeons for a flap closure.
PENETRATING NECK TRAUMA
I. GENERAL PRINCIPLES
A. Multiple injuries the norm (several vital tracts in close proximity):
1. Vascular. 2. Respiratory. 3. Neurologic. 4. Aerodigestive (esophagus and oropharynx). 5. Skeletal.
B. External anatomic landmarks:
1. Anterior triangle: a. Anterior to the SCM and lateral to the midline, extends from the sternal notch to the base of the skull. b. Divided into 3 zones based on craniocaudal position. c. Zone 1: i. Between sternal notch and cricoid cartilage. ii. Key structures: subclavian and carotid vessels, trachea, esophagus. d. Zone II: i. Between cricoid cartilage and mandibular angle. ii. Amenable to readily secure proximal and distal vascular control. iii. Key structures: carotid arteries, larynx, esophagus. e. Zone III: i. Between mandibular angle and base of the skull. ii. Key structures: distal carotids, oropharynx.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 87 Notes
2. Posterior triangle: a. Posterior to the SCM and anterior to the lateral border of the trapezius, extends from the clavicle to the base of the skull. b. Key structures: vertebral arteries, spinal cord, vertebrae.
C. Fascial planes:
1. Superficial fascia: a. Overlies the platysma. b. Minimal clinical significance. 2. Platysma: a. Thin superficial muscle spanning across SCM muscles. b. Traumatic violation necessitates aggressive evaluation. 3. Deep cervical fascia: a. 3 key subdivisions (investing, pretracheal, prevertebral). b. Limits external bleeding despite significant injury. c. Hematoma formation may lead to extrinsic compression of nearby structures. d. May facilitate the spread of infection into the mediastinum.
II. INITIAL MANAGEMENT
A. Primary survey:
1. Airway: Indications for definitive airway: a. Acute respiratory distress. b. Airway compromise from blood or secretions. c. Expanding hematoma. d. Massive subcutaneous emphysema (can be exacerbated by continuous BVM). e. Tracheal deviation. f. Altered mental status. 2. Breathing: a. Rule out associated pulmonary trauma (Zone I injuries). 3. Circulation: Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 88 Notes a. Hemorrhage can be external, contained, or internal. b. Control with direct pressure or packing. c. Avoid disruption of formed clot. d. Avoid blind clamping (risk for neurological injury). e. Consider mild Trendelenburg (limit potential for venous air embolism).
B. Secondary survey:
1. Physical examination: a. Check for platysma violation. b. Check for “hard and soft” signs of significant cervical injury. Hard and Soft Signs for Operative Intervention Tract Hard Signs Soft Signs Vascular Hypotension in ED. Hypotension in field. Active arterial History of arterial bleeding. bleeding. Absent carotid pulse. Tracheal deviation. Expanding Large hematoma. hematoma. Apical capping on CXR. Carotid thrill or bruit. Laryngotracheal Air/bubbling in Subcutaneous wounds. emphysema. Hemoptysis. Stridor. Dysphonia. Esophageal None. Hematemesis. Odynophagia. Neurologic Lateralizing signs. Vocal cord paralysis. CN VII palsy. Unexplained bradycardia (sympathetic chain).
2. Imaging studies: a. Plain radiographs: i. Retained foreign body. ii. Retropharyngeal/subcutaneous air. iii. Bony/cartilaginous injury. iv. Intrathoracic injury. b. CT imaging: i. Permits the workup of multiple tracts with one study. ii. Delineates path of bullet/knife and proximity to underlying structures. iii. Clinical sensitivity approaching more accepted modalities. c. Conventional angiography: i. Classically the study of choice to rule out arterial injury. ii. May assist in operative planning. iii. May be replaced by CT angiography with improving Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 89 Notes technology. 3. Endoscopic studies: a. Esophagoscopy: i. Combined with contrast esophagram is currently the gold standard to evaluate for significant esophageal injury. b. Laryngoscopy: i. Standard of care for patients with symptoms of LT tract injury. ii. Evolving role for CT imaging with improving technology.
III. MANDATORY VS. SELECTIVE EXPLORATION OF ZONE II NECK INJURIES
A. Mandatory exploration:
1. History: a. Previous to World War II: i. Expectant management with high mortality (18-35%). b. World War II onward: i. Mandatory exploration with decreased mortality (6%). ii. Increase in negative neck explorations (40-63%). 2. Current indications for emergent operative exploration: a. Hard signs of vascular injury. b. Obvious aerodigestive injury.
B. Selective management:
1. Rationale: a. High rate of negative explorations with mandatory approach. b. Low energy mechanisms with non-combat civilian wounds. 2. Indications for selective management: a. Absence of above findings mandating exploration. b. Stable patient. 3. Pros: a. Similar overall mortality rates. b. Fewer negative explorations. c. Shorter hospital stays. 4. Cons: a. Potential for undiagnosed injuries vs. mandatory exploration. b. May delay definitive operation. c. Requires 24 hour institutional support.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 90 Notes
Summary of Work Up by Zone Zone I Zone II Zone III Posterior Triangle Angiogram of Angiography of Angiography Angiography aortic arch and carotids. of carotids. of vertebral great vessels. arteries. Esophogram and Oropharyngeal Esophogram and esophagoscopy. exam. esophagoscopy. Bronchoscopy Bronchoscopy with signs and with signs and symptoms of symptoms of laryngotracheal laryngotracheal injury. injury.
THORACIC TRAUMA
I. GENERAL PRINICPLES
A. Morbidity/mortality:
1. Second leading cause of traumatic death following traumatic brain injury. 2. Immediate death on the scene: a. Cardiac and great vessel rupture. 3. Death within the “Golden Hour” (target of primary survey): a. Acute airway obstruction. b. Tension pneumothorax. c. Massive hemothorax. d. Open pneumothorax. e. Flail chest. f. Pericardial tamponade.
Emergent Life Threats Diagnosis Key Finding Treatment Airway obstruction Can’t talk, can’t breathe. Endotracheal intubation. Tension PTX Hypotension. Needle thoracostomy. JVD. Tracheal deviation. Absent breath sounds. Hyperresonance. Massive HTX Diminished breath sounds. Chest tube. Dullness to percussion. OR thoracotomy.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 91 Notes
Open PTX Sucking chest wound. Three-sided occlusive dressing. Chest tube. Flail chest Paradoxical chest wall Positive-pressure motion. ventilation. Cardiac tamponade Hypotension. IV fluid resuscitation. JVD. ED pericardiocentesis. Muffled heart sounds. OR thoracotomy.
B. Initial resuscitation:
1. Airway management: a. Indications for ETT similar as previously described. 2. Venous access: a. If central access is necessary above the waist (e.g., pelvic fracture), then place the line on the side of injury to avoid trauma to contralateral uninjured lung. b. With potential injury to the supradiaphragmatic vasculature (especially the SVC), place IV or central line below the chest (i.e., femoral line).
II. CHEST WALL INJURIES
A. Rib fractures:
1. General principles: a. Significance of this injury is not fracture itself but associated injuries (e.g., PTX, HTX): i. 1st - 2nd requires significant force and often associated with additional injuries. ii. 4th - 9th most commonly involved. iii. 6th - 12th associated with intra-abdominal injury. b. Typically break at point of trauma or posterior angle (weakest point structurally). 2. Workup: a. Upright CXR: i. Misses fractures in up to 50% of cases. ii. Useful for evaluating potential intrathoracic injury. b. Rib film indications: i. Suspected fracture of 1st - 3rd or 9th - 12th. ii. Multiple fractures. iii. Elderly patient. iv. Underlying pulmonary disease. v. Suspected pathologic fracture. 3. Management: a. Simple fractures: i. Oral analgesics.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 92 Notes ii. Pulmonary toilet. iii. Avoid binders/belts or any other restricting agents. b. Complicated fractures (elderly patients, multiple rib involvement, underlying cardiopulmonary disease): i. IV pain control. ii. Admit for aggressive pulmonary toilet.
B. Sternal fractures:
1. General principles: a. Usually secondary to blunt anterior chest trauma (3-point seat belt most likely culprit). b. Most fractures are transverse in orientation. c. Isolated sternal fractures typically benign (mortality <1%). d. Concurrent mediastinal hematoma can be life-threatening (regardless of etiology). e. Associated complications: i. Cardiac contusions (1.5 - 6%). ii. Spinal fractures (< 10%). iii. Rib fractures (21%). 2. Workup: a. CXR: i. Lateral views best for making diagnosis. b. CT chest: i. Best for evaluating for suspected secondary mediastinal injuries. c. Electrocardiogram: i. At 0 and 6 hours to evaluate for blunt cardiac injury. 3. Management: a. Adequate pain control. b. Pulmonary toilet. c. Admit complicated cases: i. Elderly patients. ii. Underlying cardiopulmonary disease. iii. Mediastinal hematoma. iv. Signs of myocardial contusion.
C. Flail chest:
1. General principles: a. Fracture of three or more adjacent ribs at 2 or more sites. b. Clinically apparent via paradoxical motion of the free chest wall segment during respiration. c. Mortality rates of 8-35%. d. Pre-hospital intubation and positive-pressure ventilation internally splints the chest wall and masks the diagnosis. e. Underlying pulmonary contusion is the true problem and the major source of respiratory compromise. f. 30% of cases missed within the first 6 hours of evaluation. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 93 Notes 2. Workup: a. CXR: i. Multiple rib fractures usually identified. ii. Evaluate for associated PTX/HTX. b. CT chest: i. More difficult to appreciate flail segment compared to CXR. ii. Better delineates presence and severity of underlying pulmonary contusions. 3. Management: a. Judicious IV fluid resuscitation. b. Supplemental 100% O2. c. Adequate analgesia. d. Pulmonary toilet. e. Selective use of endotracheal intubation (increased risk for secondary pneumonias): i. Respiratory failure. ii. Severe shock. iii. Additional injuries necessitating OR.
III. PULMONARY INJURIES
A. Pulmonary contusion:
1. General principles: a. Found in more than 30-75% of patients with major blunt thoracic trauma. b. Most common significant chest injury in children. c. Pathophysiology is secondary to direct bruising of lung parenchyma with secondary alveolar edema and hemorrhage. d. Overzealous fluid resuscitation worsens underlying alveolar injury with progressive respiratory compromise. 2. Workup: a. CXR: i. Areas of patchy consolidation beneath the site of chest wall injury. ii. May take several hours of development for accurate detection. b. CT imaging: i. Increased sensitivity to detect early evolving contusions. c. Arterial blood gasses: i. Monitor for declining PaO2 or climbing A-a gradient. ii. May be prognostic and guide decision to intubate. 3. Management: a. Essentially the same as previously outlined for flail chest. b. With unilateral lung involvement, consider double lumen intubation and differential ventilation.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 94 Notes
B. Pneumothorax:
1. General principles: a. Most common injury following penetrating chest trauma. b. Typically accompanied by concurrent hemothorax. 2. Classification: a. Simple: i. No persistent communication with the atmosphere. ii. Hemodynamically stable. iii. No mediastinal shift. b. Open pneumothorax: i. More common with high energy combat wounds. ii. Persistent communication between the intrathoracic cavity and the atmosphere. iii. Chest wall defect greater than 2/3 tracheal diameter produces “sucking chest wound” and severe respiratory compromise. c. Tension pneumothorax: i. Persistent air leak or chest wall defect with progressive accumulation of air within the pleural space. ii. Secondary elevation in intrathoracic pressure leads to mediastinal shift to the contralateral side, impaired cardiac preload and outflow, and imminent cardiovascular collapse. iii. Clinically evident in patients with severe dyspnea, marked hypotension, pronounced JVD, and tracheal deviation. d. Occult pneumothorax: i. Clinically asymptomatic PTX detected on CT imaging only. 3. Workup: a. CXR: i. Upright full inspiratory film the initial study of choice. ii. Follow-up expiratory film with high suspicion and negative initial CXR. iii. 3 hour repeat CXR in patients with negative initial study and penetrating trauma. b. US/FAST: i. Increased sensitivity compared to standard upright AP CXR (86-98% vs. 28-75%). ii. Positive findings include the presence of a “lung point sign” and/or “A-lines” and the absence of the normally visualized lung sliding and/or “B-lines” (aka comet tail artifact). c. CT imaging: i. May detect small “occult” PTX missed on initial CXR. 4. Management: a. Tension pneumothorax: i. Emergent needle thoracostomy (14G angiocatheter at 2nd Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 95 Notes intercostal space, midclavicular line). ii. Converts tension to open pneumothorax. Follow with tube thoracostomy. b. Simple pneumothorax: Indications for chest tube placement: (*some experts advocate tube thoracostomy for all pneumothoraces with traumatic etiologies): i. Moderate-to-large sized pneumothorax. ii. Respiratory symptoms regardless of the size. iii. Increasing size on serial imaging. iv. Patients on ventilator support. v. Patient requiring general anesthesia. vi. Associated hemothorax. vii. Bilateral pneumothorax regardless of size. c. Occult PTX: i. Serial observation for development of symptoms. ii. Chest tube placement for patients requiring general anesthesia.
C. Hemothorax:
1. General principles: a. Accumulation of blood in the pleural space following blunt or penetrating thoracic trauma. b. Accompanied by pneumothorax in 25% of cases. c. Sources of bleeding in order of frequency (highest to lowest) and clinical severity (lowest to highest): i. Lung parenchyma. ii. Intercostal artery. iii. Great vessel injury. d. Massive hemothorax is defined as 1500 ml of blood in adult patients. 2. Workup: a. CXR: i. 200 to 300 ml of accumulated blood will result in blunting of the costophrenic angles on upright CXR. ii. Supine films may demonstrate only a subtle diffuse hazy appearance despite up to 1000 ml of fluid. b. US/FAST: i. Can detect intrapleural fluid volumes as low as 50 ml. ii. May also demonstrate subtle findings of PTX (absent lung sliding/comet tails). 3. Management: a. Large bore (36-40F) tube thoracostomy. b. Strongly consider autotransfusion setup in unstable patients. c. Indications for OR thoracostomy: i. Initial thoracostomy tube drainage is > 20 ml/kg of blood or 1500 ml. ii. Persistent heavy bleeding at >7mL/kg/hr. iii. Worsening hemothorax on CXR despite tube Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 96 Notes thoracostomy. iv. Patient remains hypotensive despite adequate blood product replacement and additional sources of hemorrhage have been ruled out. v. Patient decompensates after initial response to resuscitation.
D. Tracheobronchial injury:
1. General principles: a. Can occur via both blunt and penetrating trauma; MVCs are the most common etiology. b. Deceleration injuries with shearing of mobile distal segments (intrapulmonary) from fixed proximal (trachea) segments vs. sudden compression of thoracic cage with closed glottis and secondary blowout. c. Most (>80%) occur within 2 cm of carina. d. Symptoms include hemoptysis, dyspnea, subcutaneous emphysema, and Hamman’s crunch. e. Up to 10% of cases are asymptomatic; some will present with an unexplained atelectasis or pneumonia several weeks post- injury. 2. Workup: a. CXR: i. Suspicious findings include large PTX, pneumomediastinum, deep cervical emphysema, or a disrupted/obstructed bronchus. b. Bronchoscopy: i. Diagnostic procedure of choice. ii. Perform when injury suspected clinically or radiographically. 3. Management: a. Gentle intubation over a bronchoscope (to limit injury progression). b. Operative repair.
IV. CARDIOVASCULAR INJURIES
A. Blunt cardiac injury: Spectrum of disease from myocardial concussion to myocardial contusion to outright ventricular rupture.
B. Myocardial concussion (commotio cordis):
1. Sudden blow to thoracic cage chest during ventricular repolarization resulting in life-threatening dysrhythmia. 2. Postmortem analysis shows no obvious histopathologic changes. Classic case is young baseball player hit in chest by pitch.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 97 Notes C. Myocardial contusion:
1. General principles: a. Most common and least serious condition. b. Typical pathophysiology is a direct blow to the anterior chest or compression between the sternum and vertebrae. c. Most commonly affects anterior right ventricle, anterior interventricular septum, and anterior-apical left ventricle. d. Clinical findings may not be present; suspect in any patient with moderate to severe upper abdomen or chest trauma. e. Gold standards for diagnosis, significance, and management do not exist. 2. Workup: a. EKG: i. Tachycardia out of proportion to blood loss. ii. Dysrhythmias/ectopy (especially PVCs). iii. Conduction blocks (especially RBBB). b. Cardiac enzymes: i. Repeatedly proven to be ineffective and costly. ii. Utility limited to patients with suspected cardiac ischemia antecedent to trauma. c. Echocardiography: i. Contused myocardium mimics ischemic tissue. ii. Use in patients with either significant dysrhythmias and/or cardiac dysfunction. 3. Management: a. Admit patients with new suspicious EKG abnormalities for 24 hour telemetry monitoring. b. In unstable patients with echocardiographic evidence of myocardial contusion, follow standard ACLS protocols minus the anticoagulation. Urgent Life Threats: consider during the secondary survey Dx Key Tx Rib/sternum fractures CXR. Respiratory therapy. CT for lower ribs. Pain control. EKG. Hospitalize elderly and sick. PTX Expiratory CXR. Chest tube. Observe if occult. Pulmonary contusion CXR findings often Careful IVFs. delayed. Ventilation. Blunt cardiac injury Mechanism. Observe. EKG. Supportive (ACLS). Traumatic aortic Mechanism. CTA screen. injury Angio if equivocal. Diaphragm injury CXR often subtle in Repair now or have penetrating trauma problems later… DPL.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 98 Notes
D. Myocardial rupture:
1. Nearly always immediately fatal. 2. Ventricles most commonly involved; concurrent aortic rupture common. 3. Survivors reach the ED secondary to intact pericardium with secondary tamponade.
E. Acute pericardial tamponade:
1. General principles: a. Less than 25% of penetrating cardiac injuries survive to reach the hospital. b. Most commonly seen with isolated stab wound to the RV (low pressure leak into the pericardial sac). c. Requires less than 100 ml of pericardial blood/clot. d. Exceptionally rare with blunt thoracic trauma. e. Common clinical findings include hypotension/tachycardia and JVD. f. Beck’s triad of hypotension, distended neck veins, and muffled heart tones is unreliable and typically occurs immediately before death. 2. Workup: a. CXR: i. Cardiomegaly/ “water bottle” silhouette not expected. ii. Traumatic pneumocardium may suggest external violation of the pericardial sac. b. EKG: i. Sinus tachycardia the most common finding. ii. Electrical alternans not expected (low volumes required for acute tamponade). c. Ultrasound: i. Subxiphoid view of pericardial sac is standard image for bedside FAST exam. ii. Sensitive (>98%) for the detection of pericardial fluid and tamponade physiology (diastolic collapse of the right ventricle). iii. A dilated IVC in a hypotensive patient is a further suggestive finding. d. CVP: i. Levels > 15 cm H2O in the setting of an unstable trauma patient is the most reliable finding. 3. Management: a. Aggressive IVF resuscitation to increase filling pressures in right atrium. b. Pericardiocentesis (samples as low as 10 ml can be a temporizing measure for unstable patients when immediate OR is not an option; high incidence of false positives and Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 99 Notes negatives). c. ED thoracotomy for patients in extremis despite aggressive IV resuscitation and suspected cardiac injury.
F. Blunt aortic injury (BAI):
1. General principles: a. Majority of patients (80%) will die at the scene. b. Suspect in patients with sudden deceleration (MVCs, falls) or high-speed side impact injuries. c. 90% of injuries occur at the isthmus of the descending aorta just distal to the takeoff of the left subclavian artery (traction between the mobile aortic arch and immobile ligamentum arteriosum). d. One-third to one-half of patients will have no external signs of thoracic trauma. e. Risk increases with age (declining elasticity of vessel wall). 2. Workup: a. CXR: i. A widened mediastinum is the most sensitive sign (50- 92%). ii. Obscured aortic knob. iii. Downwardly displaced left mainstem bronchus. iv. Displaced nasogastric tube. v. Widened paratracheal stripe. vi. Widened right paraspinal interface. vii. Left pleural apical cap. b. CT arch angiogram: i. Screening exam in patients with clinical concern (mechanism + either abnormal CXR or chest pain). ii. Modern helical CT ~ 100% sensitive for detecting BAI. iii. Evaluates for additional thoracic injuries. c. Transesophageal echocardiography: i. Alternative to CT in unstable patient. ii. Can identify intimal flaps and periaortic hematomas. iii. Can aid in operative planning. iv. Operator dependent; may not be sensitive enough to rule out BAI. d. Aortography: i. Historically the gold standard; gradually losing favor to CTA. ii. Invasive, time consuming, and not readily available at most institutions. 3. Management: a. Aggressive BP and HR control (goal systolic 100-120 mmHg, HR < 60). b. Expedient operative repair.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 100 Notes
V. ESOPHAGEAL INJURIES
A. General principles:
1. Lack of a serosal lining grants contents of perforated esophagus direct access into the mediastinum. 2. High mortality secondary to evolving suppurative mediastinitis (mortality of 5-25% if repaired within 12 hours; 25-66% if treatment delayed for more than 24 hours). 3. Most common etiologies: a. Iatrogenic (rigid endoscope most common offender). b. Ingested foreign bodies. c. Caustic ingestions. d. Blunt (exceptionally rare) or penetrating trauma. e. Spontaneous/ post-emetic rupture (Boerhaave’s syndrome). 4. Common clinical findings include pleuritic chest pain that is exacerbated by swallowing and/or neck flexion, odynophagia/ dysphagia, and hematemesis. 5. Hamman’s sign (systolic crunching sound with cardiac auscultation) can be heard secondary to pneumomediastinum.
B. Workup:
1. CXR: a. Pneumomediastinum. b. Subcutaneous emphysema. c. Left-side pleural effusion. d. Pneumothorax. e. Widened mediastinum. 2. Esophogram/esophagoscopy: a. Combination required to reach 100% sensitivity to rule out esophageal rupture.
C. Management:
1. NPO. 2. Broad-spectrum antibiotic therapy (targeted at oral flora). 3. Aggressive IV volume replacement. 4. Emergency surgical consultation.
VI. DIAPHRAGMATIC INJURIES
A. General principles:
1. More common with penetrating trauma; more obvious with blunt mechanisms. 2. Right sided and small penetrating injuries can be very difficult to diagnose. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 101 Notes 3. Suspect in any patient with intra-thoracic injury and penetrating abdominal trauma.
B. Workup:
1. CXR: a. Initial screening exam. b. Possible findings: i. Indistinct left hemidiaphragm. ii. Focal atelectasis in the left lower lobe. iii. Hollow viscera/ nasogastric tube located superior to the diaphragm in the left hemithorax. 2. CT imaging: a. Inadequate to definitively rule out subtle injuries. 3. DPL: a. With penetrating thoracoabdominal trauma, RBC counts > 10K/mL necessitate operative evaluation.
C. Management:
1. Operative repair of any detected injuries is the current standard of care. 2. Delayed clinical presentation (months to years post injury) is very common: a. Intrathoracic viscus incarceration. b. Bowel obstruction. c. Bowel ischemia.
ABDOMINAL TRAUMA
I. GENERAL PRINCIPLES
A. Blunt injuries:
1. High mortality due to difficulty in diagnosis. 2. Direct transmission of energy to abdominal viscera results in diffuse patterns of injury. 3. Sudden compression injuries (e.g., lap belts) produce rapid elevations in intraperitoneal pressures and hollow viscus rupture. a. Direct compression between the forces applied to the anterior abdominal wall and the posterior thorax/spinal column leads to contusion and rupture of solid organs (liver, spleen). 4. Sudden deceleration (significant falls) produce both solid and hollow viscus injuries secondary to traction forces as the more mobile organs shift relative to their more fixed attachments (mesentery, vascular pedicles, ligament of Treitze, duodenum and cecum). 5. Retroperitoneal injury commonly results from falls with vertical Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 102 Notes force transmitted up the axial skeleton or from high-speed horizontal deceleration injury.
B. Penetrating injuries:
1. Gunshot wounds: a. Direct injuries occur to any structure lying in the actual path of the missile. b. Indirect injuries occur from bone and/or bullet fragmentation as well as concussive injury along the secondary blast cavity. 2. Stab wounds: a. Approximately 70% of anterior abdominal stab wounds violate the peritoneum; only half of these produce visceral injury. b. Injury is confined to path of object; depth and angle often impossible to predict from history and physical exam. c. If local wound exploration demonstrates no peritoneal violation, treat like any similar soft tissue wound.
C. Explosion-related injuries:
1. Both blunt trauma (blast concussion, patient thrown into objects) and penetrating trauma (shrapnel) patterns are common.
II. INJURY PATTERNS
A. Solid organ injury:
1. Morbidity/mortality secondary to degree of blood loss. 2. The spleen is most commonly involved in blunt trauma, the liver with penetrating mechanisms. 3. Most common presenting signs are hemodynamic instability and initial abdominal tenderness progressing to frank rigidity. 4. Kehr’s sign (pain referred to the shoulder due to diaphragmatic irritation by free intraperitoneal blood) can be a useful early physical exam finding. 5. Suspect in any patient with injury to the lower ribs, abdomen or pelvis. 6. Younger patients, pregnant or intoxicated patients, and those with distracting injury/head trauma may present with minimal initial symptoms.
B. Hollow viscus injuries:
1. Morbidity/mortality secondary to both blood loss (intraperitoneal or intraluminal) and septicemia from spilled intestinal contents. 2. Penetrating injury to small bowel most common but may occur with deceleration injuries. 3. Frequently may have minimal initial symptoms. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 103 Notes 4. Peritonitis can take up to 8 hours to develop.
C. Retroperitoneal injury:
1. Duodenal injuries: a. Hematoma or rupture can occur secondary to crush injuries (hematoma formation in children is commonly associated with “handlebar” injuries). b. Very slow to develop, as hemorrhage or perforation is initially contained within the retroperitoneum. c. Symptoms are usually vague and include abdominal pain, nausea/vomiting, and fever. d. Complications arise from delayed diagnosis and include obstruction, septicemia, and hemorrhagic shock. 2. Pancreatic injuries: a. Classic mechanism is secondary to blunt forces from a handlebar or steering wheel. b. Organ disruption causes leakage of proteolytic enzymes resulting in secondary autodigestion, superinfection, and abscess formation.
III. WORK UP
A. Laboratory studies:
1. Hemoglobin/hematocrit: a. Initial hematocrit reflects baseline. Serial determinations more helpful. 2. Base deficit/lactate: a. Useful to determine initial degree of hemodynamic insult and physiologic response to resuscitative efforts. 3. Amylase/lipase: a. Neither is useful when obtained in a routing fashion. b. Normal levels do not exclude a major pancreatic injury in adult patients. c. Frequently utilized in pediatric patients due to limited reliability of physical exam and reluctance for CT imaging. 4. Liver function tests: a. Elevated transaminases can result from hepatic trauma but degree of elevation cannot estimate severity of liver injury. b. May have more established role in evaluating pediatric trauma for similar reasons outlined for pancreatic testing.
B. Radiographs:
1. CXR: a. Intraperitoneal free air indicates peritoneal violation (penetrating trauma) or hollow viscus rupture (blunt trauma). 2. AP pelvis: Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 104 Notes a. Significant pelvic fractures are frequently associated with abdominal injury. 3. KUB: a. Blunt trauma: Routine use not cost-effective. b. Penetrating trauma: Can help estimate the path of the projectile via marking the wounds and connecting the dots.
DPL FAST CT Pros Most sensitive. Sensitive. Sensitive and Unstable Noninvasive. SPECIFIC. patients. Evaluates both chest Evaluates retro- Relatively easy and peritoneum. peritoneum. to perform. Rapid. Identifies non- Repeatable. operative injury. Cons Too sensitive. Operator and patient Radiation dose. dependent. IV contrast. Time to perform.
C. CT abdomen/pelvis:
1. Advantages: a. Readily available. b. Greater specificity than alternative techniques. c. Localizes injury/source of hemorrhage. d. Can help quantify the amount of hemorrhage and determine the presence of ongoing bleeding. e. Evaluates retroperitoneum, vertebral column, and lower thorax. f. Identifies non-operative injuries. 2. Disadvantages: a. Decreased sensitivity for certain injuries (diaphragm, small bowel, mesentery). b. Exposure to ionizing radiation and IV contrast. c. Time consuming, requires patient to leave resuscitation arena.
D. DPL:
1. Has been replaced by FAST and CT per ACEP Clinical Policy noted in references. 2. Advantages: a. High sensitivity. b. Relatively fast/technically easy. c. Low complication rate. d. No need for patient to leave resuscitation arena. 3. Disadvantages: a. Lower specificity (negative laparotomy rate approaching 30%). b. Inability to localize source of hemorrhage.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 105 Notes c. Potential for iatrogenic injury. d. Examination limited to evaluation of intraperitoneal injury. e. Inability for serial evaluation. 4. Indications: a. Blunt trauma indications: i. Patient too unstable for CT imaging. ii. Unexplained hypotension with equivocal physical exam. b. Penetrating trauma indications: i. Evaluation for peritoneal violation with stab wounds. ii. Detection of diaphragmatic trauma in patients with thoracoabdominal trauma. 5. Contraindications: a. Absolute: i. Criteria necessitating operative laparotomy already met. b. Relative: i. Prior abdominal surgeries. ii. Coagulopathies. iii. 2nd/3rd trimester pregnancies. iv. Marked obesity. 6. Results: a. Regardless of etiology, aspiration of 10 ml of gross blood indicates positive test (should really make you wonder why you thought you had to tap him anyway). b. Blunt abdominal trauma and anterior abdominal stab wounds: i. RBC count > 100K/ml is >90% sensitive for positive laparotomy. c. Tangential GSW and penetrating thoracoabdominal trauma: i. RBC count > 10K/ml indicates need for operative laparotomy. d. Less helpful studies include WBC counts, bile and/or Gram staining, or vegetable matter analysis.
E. FAST exam:
1. Recommended in place of DPL by ACEP Clinical Policy. 2. Accurate bedside screening tool; highly sensitive but poorly specific. 3. Advantages: a. Easy, rapid, and repeatable. b. Non-invasive, free from iatrogenic complications. c. Does not expose patient to ionizing radiation or IV contrast. d. Very helpful in patients with relative contraindications to DPL. e. Screens for intra-abdominal, pleural and pericardial fluid. f. Bedside performance allows patient to remain in resuscitation arena. 4. Disadvantages: a. Nonspecific study. b. Inability to localize source of hemorrhage. Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 106 Notes c. Operator dependent; difficult in obese patients or those with extensive bowel gas. d. No definitive evaluation of retroperitoneum. e. Inability to detect diaphragmatic injury. f. Cannot distinguish blood from other sources of intraperitoneal free fluid (e.g., ascites).
NORMAL RUQ VIEW RUQ VIEW WITH FREE FLUID IN MORRISON’S POUCH
NORMAL SUBXIPHOID SUBXIPHOID VIEW WITH VIEW FREE FLUID
IV. MANAGEMENT
A. Hemodynamically stable:
1. Absolute indications for operative laparotomy exist: a. Time permitting, work up additional life-threatening injuries prior to OR. 2. Absolute indications for operative laparotomy do not exist: a. Follow workup for potential injury as outlined in figures below. b. Address specific injuries as encountered. c. Observe patient for serial physical exams.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 107 Notes
B. Hemodynamically unstable:
1. Aggressive IV resuscitation. 2. Determine source of hemorrhagic shock: a. Intraperitoneal (+ FAST or DPL). i. Emergent OR laparotomy. b. Retroperitoneal (+ CT scan). i. Consider angiogram with embolization based on specific injury. 3. Antibiotic prophylaxis (GI flora) with hollow viscus perforation.
Work Up by Zones in Penetrating Trauma Zone Definition Workup Anterior box Inferior to sternal CXR. notch and superior to costal margin. Bedside echocardiogram. Medial to bilateral nipples.
Gunshot wound: Posterior cardiac box CXR Arch Angiogram Between medial Esophagus w/up border of scapulae. +/- Bronchoscopy
Superior to costal Stab wound: margins. CXR Aortogram* Esophagus w/up* * If mediastinum abnormal on CXR. Thoracoabdominal Anterior: Inferior to CXR. nipples, superior to costal margins. DPL (diaphragm injury).
Posterior: CT abdomen/pelvis. Inferior to tips of scapulae, superior to costal margins.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 108 Notes
Anterior Abdomen Gunshot wound: Inferior to costal All GSW that violate margins, superior to peritoneum go to OR. inguinal ligaments. Stab wounds: CT abdomen/pelvis. Anterior to bilateral DPL.* midaxillary lines. * Diminished utility in most trauma centers. Back and Flank Inferior to the tips of 3° Contrast CT the scapulae, superior abdomen/pelvis (PO, to the iliac crests. PR, IV).
Posterior to bilateral DPL.* midaxillary lines. * Diminished utility in most trauma centers.
V. PELVIC TRAUMA WORKUP BY MECHANISM
Mechanism Workup Blunt (significant Retrograde urethrogram (especially with blood at fractures) meatus, scrotal hematoma or high riding prostate). Voiding cystogram. Penetrating Examine the outlet tracts: GI: Proctoscopy. GU: Cystogram. Gyne: Vaginal speculum exam. Vascular: Consider iliac angiography.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 109 Notes
VI. INDICATIONS FOR LAPAROTOMY
Blunt Penetrating Definitely Anterior abdominal injury Hemodynamic instability. with hypotension. Frank peritonitis. Abdominal wall disruption. Evisceration. Frank peritonitis. Retained implement in situ. Intraperitoneal free air Diaphragmatic injury (+DPL). (CXR). GI bleeding (gross blood per Diaphragmatic injury (CXR, NG or rectal). DPL). Intraperitoneal free air (CXR). Significant GI bleeding Intraperitoneal bullet. (gross blood per NG or Transperitoneal missile path. rectal). CT demonstration of vascular CT demonstration of or viscus injury. vascular or viscus injury. Maybe Positive DPL or FAST in Stab wound with positive stable patient. local wound exploration. Solid organ injury in stable patient. Hemoperitoneum without clear source.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 110 Notes
AIRWAY/MAXILLOFACIAL/PENETRATING NECK/ THORACIC/ABDOMINAL TRAUMA
PEARLS
Airway Management in Trauma
1. Trauma airway management = ACBCs. Always assume cervical spine injury.
2. Nasal trumpets in awake patients; oral airways only in unconscious patients with absent gag reflexes.
3. Nasotracheal intubation only if patient is breathing spontaneously and has no significant midface trauma.
4. 20 mg of etomidate and 100 mg of sux will intubate anyone. But 100 mg of lidocaine, 1 mg of pancuronium, 200 mcg of fentanyl, 200 mg of thiopental and 100 mg of sux are better in head injury patients.
5. Horizontal surgical cricothyrotomy if you can externally landmark the cricothyroid membrane. Vertical incision if landmarks are grossly distorted. Needle cricothyrotomy if patient < 8 years old.
6. Needle cricothyrotomy, LMA, and Combitube do not protect/secure the airway. These are only temporizing measures until help arrives.
7. Singed face/hair or soot in the airway equals supraglottic injury. Intubate expediently.
8. Infraglottic burns are typically more subtle but can be just as deadly!
Maxillofacial Trauma
1. Similar to other ring structures (e.g., pelvis), always look for more than one fracture site when dealing with the mandible.
2. Rule out concurrent globe injury with any orbital fracture.
3. Significant facial fractures (i.e., Lefort II/III) may result in retropharyngeal hematoma and secondary airway obstruction.
4. Sublingual or buccal ecchymosis is pathognomonic for a mandibular fracture.
5. Recognize and drain both septal and auricular hematomas on presentation to avoid significant long-term deformity.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 111 Notes
Penetrating Neck Trauma
1. Early intubation always leads to easier intubation, especially in cases of expanding hematomas.
2. Always consider injury to all applicable tracts: airway, vascular, gastrointestinal and neurologic.
3. Selective management is indicated in stable Zone II injuries when no hard signs of injury are present and both diagnostic modalities and surgical expertise are readily available.
4. Both esophagram and esophagoscopy are necessary to reliably exclude esophageal injury and prevent life-threatening mediastinitis.
Thoracic Trauma
1. Emergent life threats to recognize and treat during the primary survey include: airway obstruction, tension pneumothorax, massive hemothrorax, open pneumothorax, flail chest, and cardiac tamponade.
2. Tension pneumothorax is a clinical diagnosis: JVD, ipsilateral absent breath sounds and contralateral tracheal deviation.
3. Cardiac tamponade: JVD, diminished heart sounds, and hypotension (Beck’s triad).
4. Underlying pulmonary contusions are the real problem in patients with flail chest. Intubate early and avoid overaggressive IV resuscitation!
5. With any of the following – labored breathing, hemoptysis, subcutaneous emphysema, tension PTX, and persistent air leak from chest tube – consider tracheobronchial injury. Confirm with bronchoscopy.
6. Pneumomediastinum can result from esophageal perforation, tracheobronchial injury, and interstitial pulmonary emphysema tracking into the mediastinum.
7. Troponins are typically not helpful in evaluating blunt cardiac injury. Admit people with abnormal EKGs. Emergent bedside echo in unstable patients.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 112 Notes
8. Traumatic aortic injuries surviving to ED presentation are typically contained by the overlying adventitia but can rupture within 24 hours if not properly diagnosed. Get the screening CTA and control the BP!
9. Blunt diaphragmatic injury is obvious. Penetrating cases are often occult. Suspect such injuries in patients who persistently return with vague upper GI complaints following a thoracoabdominal injury.
10. Rare and generally fatal venous air embolisms occur with combined pulmonary and vascular injury, especially with concurrent positive pressure ventilation. Displace air from right ventricle outflow tract by placing head and left side down (Durant’s maneuver). Use echo for diagnosis and guidance for removal
Abdominal Trauma
1. Most common solid organ injuries: Blunt trauma – spleen. Penetrating trauma – bowel and liver.
2. In pediatric patients presenting with handlebar injuries to the epigastrium, consider pancreatic or duodenal injury.
3. Although less common in clinical practice, be familiar with DPLs: Absolute contraindications: Need for emergent laparotomy. Relative contraindications: Prior surgery, pelvic fracture, and pregnancy. Criteria for + DPL: Anterior abdominal SW: > 100,000 RBC/ml Thoracoabdominal wound: > 10,000 RBC/ml
4. FAST exam gradually replacing DPL. Advantages include repeatability, non-invasiveness, and quicker time to completion
5. CT imaging: Greater specificity than DPL or FAST. Sensitivity approaching DPL without high negative lap rate. Evaluates solid organs, retroperitoneum and pelvis.
Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 113 Notes
REFERENCES
1. Tintinalli: Emergency Medicine: A Comprehensive Study Guide, 6th edition, McGraw, 2004.
2. Marx: Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th edition, Mosby, 2006.
3. ACEP Clinical Policies Committee: Clinical Policies Subcommittee: Acute Blunt Abdominal Trauma. The Ann Emerg Med 2004: 43(2): 278 – 90. 2006 LLSA Required Reading.
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Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma Page 114
Upper and Lower Extremity Trauma
Wesley Eilbert, MD, FACEP
Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago
Page 115
Page 116 Notes
UPPER EXTREMITY TRAUMA
I. EMERGENT COMPLICATIONS OF FRACTURES
A. Hemorrhage:
1. Primarily a concern with displaced pelvic fractures. 2. Also significant with femoral shaft fractures.
B. Open fractures:
1. Open fractures are classified based on the size of the overlying laceration, the amount of soft tissue damage, and the extent of contamination. 2. Most will require debridement and irrigation in the OR. Some small, open fractures (i.e., the phalanges) may be treated in the ED. 3. Wound cultures are not necessary before antibiotics. 4. An IV first generation cephalosporin (cefazolin), with the addition of an aminoglycoside for more severe/contaminated cases is recommended.
C. Neurovascular deficits:
1. The longer a deficit goes untreated, the longer it is likely to persist and the greater the possibility that it will be irreversible. Emergent reduction of the offending fracture or dislocation is indicated.
D. Fat Embolism Syndrome:
1. Caused by the presence of fat globules in the peripheral circulation after long bone fractures - usually of the lower extremity. 2. Respiratory distress and hypoxemia are the most common manifestations, usually appearing 1-2 days after the injury. 3. ARDS, mental status changes, thrombocytopenia and a petechial rash may occur. 4. Diagnosis is clinical. 50% will have fat globules in the urine. 5. Treatment is supportive, with no specific therapy of proven benefit.
E. Fracture blisters:
1. Occurs as a result of high energy injuries in areas of little skin coverage over a fracture. The ankle, elbow, foot and knee are the most common sites. 2. Are believed to be due to increased underlying tissue pressure, Upper Extremity Trauma Page 117 Notes and may be a marker of compartment syndrome. 3. Treat the same as thermal burn blisters.
F. Compartment syndromes:
1. Occur when tissue pressures in a fascia-enclosed compartment rise to the point of compromising perfusion. Nerves and muscles are most susceptible to the resultant ischemia.
2. The clinical features of compartment syndromes can be remembered as the six Ps: a. Pain out of proportion to the injury is the earliest and most significant finding.
Upper Extremity Trauma Page 118 Notes b. Pain with passive stretch of the involved muscle group. c. Paresis (or weakness) of the involved muscle group. d. Paresthesias in the distribution of the nerve in the involved compartment. e. Pulses intact, unlike arterial injuries where pulses are absent. f. Pressure (increased) in the involved compartment. 3. Diagnosis is made by measuring the compartment pressure. Several commercial devices are available for this purpose. a. Normal compartmental pressure is 0. b. Compartmental pressures <15 mmHg are generally safe. Pressures of 20-30 mmHg may cause damage if they persist for several hours. Pressures of 30-40 mmHg are considered grounds for fasciotomy. c. Treatment is emergent fasciotomy of the involved muscle group. d. Complications include rhabdomyolysis and hyperkalemia (especially with large muscle groups). If improperly treated, loss of nerve and muscle function resulting in ischemic contracture can occur.
II. SEPTIC ARTHRITIS
A. More common in children under 3 years, the elderly, patients with HIV and chronic debilitating illnesses and those taking immunosuppressive medications, IV drug abusers and patients with prosthetic joints, and after arthrocentesis.
B. Bacterial pathogens reach joint spaces by hematogenous spread (most common), direct inoculation, and by direct spread from bony or soft tissue infection.
C. Staph aureus is the most common pathogen across all age groups.
D. Neisseria gonorrhea is a common cause in young adults, and usually causes a polyarthritis.
E. Diagnosis:
1. Patients usually complain of a painful joint, made acutely worse with movement. The joint is typically swollen and hot. 2. Fever, usually low grade, is present in the majority of cases. 3. Approximately 50% of patients have a serum WBC over 15,000. An elevated ESR, while nonspecific, is present 90% of the time, with mean values ranging from 68 to 82 mm/h. 4. Definite diagnosis is by arthrocentesis: a. WBC is usually elevated - over 50,000/mm3 in 50%-70% of patients. The percentage of PMNs is usually higher than 85%. Upper Extremity Trauma Page 119 Notes b. Gram stain will show bacteria 50%-70% of the time. c. Synovial fluid glucose is typically less than 50. d. Synovial fluid culture will grow the responsible pathogen approximately two-thirds of the time. Blood cultures are positive in less than half of all cases.
F. Treatment:
1. Hospitalization for arthrotomy and irrigation of the joint and IV antibiotics. 2. Empiric antibiotics: a. Under 3 months: Nafcillin or oxacillin plus a 3rd generation cephalosporin. b. 3 months to 14 years: Vancomycin plus a 3rd generation cephalosporin. c. 15 years to 39 years: Ceftriaxone plus Vancomycin. d. Over 40 years: Nafcillin or Vancomycin. 3. Delay in diagnosis and treatment results in destruction of the articular cartilage.
III. COMPLEX REGIONAL PAIN SYNDROMES
A. Type I (Reflex Sympathetic Dystrophy):
1. Occurs after prolonged immobilization or disuse (e.g., stroke).
B. Type II (Causalgia):
1. Occurs after peripheral nerve injury – frequently related to a fracture or gunshot wound.
C. Both types present with allodynia (pain from non-noxious stimuli) and a persistent burning or shooting pain.
D. Early signs include edema, warmth, and abnormal localized sweating.
E. Later signs include periods of edema and warmth alternating with cold, pale cyanotic skin.
F. Atrophy eventually occurs.
G. Treatment is highly controversial and may include regional sympathetic blockade.
IV. DISLOCATIONS
A. Sternoclavicular:
Upper Extremity Trauma Page 120 Notes 1. Relatively rare. 2. Anterior dislocation is more common than posterior. 3. Posterior dislocations can be associated with life-threatening injuries in the mediastinum. 4. Pain with movement of the arm or lateral compression of the shoulders. 5. Plain X-rays may be difficult to interpret; CT is the study of choice. 6. Treat with closed reduction: a. Posterior dislocations should ideally be reduced in the OR.
B. Acromioclavicular:
1. Most occur in young males. 2. Usually caused by a direct blow to the point of the shoulder while the arm is adducted. 3. Non-displaced sprains and those with minimal displacement (<5 mm) can be treated with a sling. 4. Displaced injuries may require surgical repair, often for cosmetic reasons.
Upper Extremity Trauma Page 121 Notes
C. Shoulder (the most commonly dislocated major joint):
1. Anterior dislocations (95% of all shoulder locations): a. The most common mechanism is a posterior-to-anterior force applied to an abducted, extended arm. b. Axillary nerve injury may occur (5-54%) with resultant anesthesia over the lateral aspect of the shoulder and deltoid weakness. Rotator cuff tears occur in 10-15%. c. 11-50% will have a Hill-Sachs deformity of the humeral head, 5% have a fracture of the anterior glenoid rim, and 10- 15% have an avulsion fracture of the greater tuberosity. d. After reduction, immobilize with a sling and swathe. e. Recurrence is very common (79-100%).
2. Posterior dislocations (2% of all shoulder dislocations): a. Classically caused by seizures or electrocution. Also, a fall on an outstretched, adducted arm. b. 50% are missed on initial evaluation. c. Arm is held adducted and internally rotated. d. Findings on AP X-rays can be subtle. Transscapular (“Y view”) and axillary views confirm the diagnosis. e. Fractures of the glenoid rim, greater and lesser tuberosity and humeral may occur. Neurovascular injury is rare.
Upper Extremity Trauma Page 122 Notes 3. Luxatio erecta (rare): a. Arm is locked over head. b. Almost always associated with tears of the rotator cuff. c. Injury to the axillary artery and brachial plexus may occur.
D. Elbow:
1. Posterior dislocations (most common). 2. Cause by a fall on an outstretched hand. 3. Injuries of the brachial artery occur in up to 8% of cases. 4. Median nerve injury may also occur. 5. Most can be reduced in the ED, then discharged with a posterior splint and sling. 6. Medial and lateral dislocations occur by the same mechanism as posterior dislocations and have similar complications and treatment. 7. Anterior dislocations (rare): a. Frequently open. b. Have a high incidence of vascular injury.
V. FRACTURES
A. Clavicle:
1. The most commonly fractured bone during childhood. 2. 80% occur in the middle 1/3 of the bone. 3. Caused by a direct force applied to the lateral aspect of the shoulder. 4. Most can be treated with a sling. a. Associated neurovascular injury is rare. Upper Extremity Trauma Page 123 Notes b. Fractures of the distal clavicle with displacement may require operative intervention.
B. Scapula:
1. Relatively rare. 2. Usually due to MVCs or falls. 3. 80% have associated injury to the lung, chest wall or shoulder girdle. 4. Most are treated with a sling. 5. Surgical intervention may be necessary with displaced fractures of the glenoid, acromion or coracoid.
Upper Extremity Trauma Page 124 Notes
C. Humerus:
1. Proximal humerus: a. Typically occur in elderly, osteoporotic women. b. Often due to a fall on an outstretched arm and hand. c. Most (85%) are minimally displaced. d. Fracture lines tend to occur across old epiphyseal lines (i.e., the anatomic neck, the greater and lesser tuberosities and the surgical neck). e. Injury to the brachial plexus (most commonly the axillary nerve) and axillary artery can occur, especially with displaced fractures of the surgical neck. f. Minimally displaced fractures (85%) can be treated with sling and swathe. g. Significantly displaced (>1 cm) or angulated (>45º) fractures, as well as fractures involving multiple parts of the proximal humerus may require surgical repair. h. Adhesive capsulitis (“frozen shoulder”) is the most common complication. Avascular necrosis of the humeral head may occur with displaced fractures of the anatomic neck.
Upper Extremity Trauma Page 125 Notes
2. Humeral shaft: a. Typical occur in young, active men and elderly, osteoporotic women. b. Often due to a direct blow or a fall on an outstretched hand with a torsional force. c. The most common site of fracture is the middle third. d. Concomitant injury to the axillary artery or vein, or the radial, ulnar or median nerves (most often the radial nerve) may occur. e. The vast majority are treated nonoperatively. f. Most can be treated in the ED with a sling and swathe. Other options include a “sugar-tong” splint or a hanging cast for grossly displaced fractures.
Upper Extremity Trauma Page 126 Notes
D. Elbow:
1. Since many elbow fractures may be subtle, close inspection of the lateral elbow film for abnormal fat pads (signifying intraarticular hemorrhage) is very important. The presence of any posterior fat pad or an abnormally large anterior fat pad (i.e., the “sail sign”) usually indicates the presence of intraarticular skeletal injury. 2. Several important neurovascular structures lie in close proximity to the elbow joint (i.e., the brachial artery and the median, radial and ulnar nerves). Evaluation of their function is important after any elbow injury. 3. Intercondylar T or Y fractures: a. Caused by direct trauma to the elbow that drives the olecranon against the humeral articular surface, splitting the Upper Extremity Trauma Page 127 Notes distal end. b. Usually associated with severe soft tissue injury, and notoriously difficult to treat. c. Most require ORIF to reestablish articular surface congruity. d. Patients with severe edema or displaced fractures should be admitted.
4. Epicondyle fractures: a. Lateral epicondyle fractures are extremely rare. b. Medial epicondyle fractures in adults are usually caused by a direct blow. c. Use of forearm flexors causes pain. d. Concomitant ulnar nerve injury can occur. e. Minimally displaced fractures can be treated with a posterior mold; displaced fractures may require operative repair; intraarticular fragments are an indication for surgery. 5. Trochlea fractures usually occur in the setting of posterior elbow dislocations. Displaced fractures should be treated with internal fixation. 6. Capitellum fractures also occur primarily with posterior elbow dislocations and frequently are associated with a radial head fracture. As with the trochlea, displaced fractures should be treated with internal fixation. 7. Radial head fractures are the most common fracture of the elbow. a. Usually from a fall on an outstretched hand. b. Often associated with other elbow injuries, like capitellum fractures and elbow dislocations. c. May be difficult to see on standard X-rays. May only be seen as an abnormal radiocapitellar line or an abnormal fat pad.
Upper Extremity Trauma Page 128 Notes
8. Olecranon fractures are most commonly the result of a direct blow. They can also occur by a fall on an outstretched hand with the elbow in flexion and the triceps contracting.
a. A significant percentage of these are open fractures. b. Triceps function, as tested by elbow extension, is usually impaired. c. Associated ulnar nerve injury is common. d. Best seen on lateral view elbow X-rays. e. ED management involves immobilization with the elbow in flexion. f. Displaced fractures usually require ORIF.
E. Forearm:
1. The radius and ulna are joined together along their entire length by a tough interosseus membrane. Because of this close Upper Extremity Trauma Page 129 Notes relationship, injury to one bone usually has a direct effect on the other (i.e., a displaced or angulated fracture of one bone causes a dislocation at the proximal or distal radioulnar joint). a. Nerve injuries are uncommon with most closed fractures. b. Due to collateral circulation, vascular compromise is unlikely if either the ulnar or radial artery remains intact. c. Forearm fractures are at relatively high risk for compartment syndrome. d. Most displaced forearm fractures will require operative reduction and internal or external fixation. 2. Ulnar shaft fractures (“nightstick fractures”): a. Due to a direct blow. b. Non displaced fractures can be treated with a long arm posterior splint. Displaced fractures require ORIF. i. X-rays of displaced fractures should be scrutinized for any evidence of fracture or dislocation of the radius.
3. Monteggia fracture – dislocation: a. Fracture of the ulnar shaft with a radial head dislocation. The majority of the time, it’s a fracture of the proximal third of the ulna with an anterior dislocation of the radial head. b. Typically due to a forced pronation of the forearm during a fall on an outstretched hand. c. The radial head dislocation may be subtle and noted only as a disruption of the radiocapitellar line. d. Treatment is with ORIF.
Upper Extremity Trauma Page 130 Notes
4. Galeazzi fracture: a. Fracture of the distal third of the radial shaft with a dislocation of the distal radioulnar joint. b. Usually due to a fall on an outstretched hand with the forearm pronated. c. The ulna is displaced dorsally on the lateral view X-ray. The majority will also have an ulnar styloid fracture. i. Treatment is with ORIF.
VI. SOFT TISSUE INJURIES
A. Tendonitis:
1. An overuse injury typically due to repetitive movements of the involved tendon. 2. Occurs most commonly in the hand (flexor and extensor tendons), the knee (patellar tendonitis), and the foot (flexor hallucis longus, posterior tibialis and Achilles). 3. There is pain with active or passive movement of the tendon, and pain with palpation of the tendon. 4. Treatment includes rest (including possible splinting), NSAIDs and heat.
B. Calcific tendonitis:
1. A self limiting disorder characterized by calcium crystal deposition within the tendons of the rotator cuff. Most common in middle age. 2. Presents with pain or a “catching” sensation with shoulder abduction. Symptoms typically last for 1-2 weeks. 3. Treatment includes NSAIDs, brief sling immobilization and gentle range-of-motion activities to avoid adhesive capsulitis.
Upper Extremity Trauma Page 131 Notes
C. Impingement syndrome (includes subacromial bursitis, rotator cuff tendonitis, supraspinatous tendonitis and painful arc syndrome):
1. Caused by repetitive overhead use of the arm resulting in encroachment of the subacromial space by the humeral head. 2. Causes a dull pain over the anterolateral acromion that is aggravated with overhead arm use. 3. Initial treatment includes avoidance of aggravating activities (i.e., overhead arm use), NSAIDs and gentle range-of-motion activities to avoid adhesive capsulitis.
D. Rotator cuff tears:
1. May be acute (10%) or chronic (90%). 2. Acute tears are typically traumatic, usually due to forced abduction with significant resistance (i.e., catching a falling heavy object) or an anterior shoulder dislocation. 3. Chronic tears are almost always due to repeated compression of the rotator cuff in the subacromial space caused by repetitive overhead use of the arm. 4. Physical exam is the key to diagnosis. 5. Disuse atrophy may be present with chronic tears. 6. Weakness and pain are present with active abduction and external rotation of the upper arm. 7. The drop arm test is positive if the patient is unable to hold or lower a fully extended arm at 90 degrees shoulder abduction without dropping it. 8. Treatment in the ED includes support with a sling, ice and NSAIDs. 9. Complete tears (usually a MRI diagnosis) typically require surgical repair.
Upper Extremity Trauma Page 132 Notes E. Bicep tendon rupture:
1. The vast majority occur in the proximal portion of the long head. 2. Typically occurs in middle-aged patients with a history of chronic bicipital tenosynovitis. 3. Usually described as a pop or snap during contraction against resistance. 4. Presents with pain over the anterior shoulder and a “Popeye” appearance of the arm due to distal retraction of the muscle. Active flexion is still possible due to the coracobrachialis and the short head. 5. Treat with ice, sling and analgesics. 6. Surgical repair is usually indicated for young active patients.
F. Tennis elbow (epicondylitis):
1. Most involve the lateral epicondyle, though involvement of the medial epicondyle can occur. 2. Seen in patients whose occupations require repetitive rotary motion at the elbow, such as pipe fitters and carpenters. 3. Caused by tears in the aponeurosis of the involved tendons or microavulsion fractures of the epicondyle. 4. The main symptom is a dull ache of the involved epicondyle, aggravated by grasping or twisting motions. 5. Treat by splinting with the elbow flexed, heat and NSAIDs.
G. Olecranon bursitis:
1. Most commonly caused by repetitive minor trauma. May also be due to gout or infection (i.e., septic bursitis). 2. Presents with pain, tenderness and swelling over the olecranon.
Upper Extremity Trauma Page 133 Notes 3. Aspiration is diagnostic and therapeutic. 4. Management: a. Septic bursitis: i. Bursal aspirate WBC count usually > 10,000. ii. Treat with antibiotic coverage for skin flora and MRSA. b. Non infectious bursitis: i. Bursal aspirate WBC count usually < 1,000. ii. Treat with a compressive dressing, ice, NSAIDs and avoidance of the inciting activity.
Upper Extremity Trauma Page 134 Notes
UPPER EXTREMITY TRAUMA
PEARLS
1. Most open fractures require debridement and irrigation in the OR.
2. Pain out of proportion to the injury is the earliest and most significant finding with compartment syndromes.
3. Staph aureus is the most common pathogen in septic arthritis across all age groups. N. gonorrhea is a common cause in young adults.
4. Axillary nerve injury and rotator cuff tears may occur with anterior shoulder dislocations.
5. Transscapular (“Y view”) and axillary views of the shoulder are necessary to confirm the diagnosis of posterior shoulder dislocation.
6. Posterior dislocations of the elbow are the most common type, and may have an associated brachial artery or median nerve injury.
7. Clavicle fractures, the most common fracture of childhood, can usually be treated with a sling alone.
8. A high percentage (80%) of scapular fractures have an associated injury to the lung, chest wall or shoulder girdle.
9. Proximal humerus fractures typically occur in elderly women and can usually be treated with a sling and a swathe.
10. The radial nerve is the one most commonly injured with humeral shaft fractures.
11. The presence of any posterior fat pad or an abnormally large anterior fat pad on a lateral elbow X-ray indicates the presence of a fracture (radial head fracture in adult, supracondylar fracture in children).
12. Radial head fractures, while the most common fracture of the elbow, may be very difficult to detect on standard X-rays. Look for posterior fat pad or anterior fat pad “sail sign”.
13. Olecranon fractures usually present with impairment of triceps function and are frequently complicated by ulnar nerve injury.
14. Due to the interosseus membrane, a fracture of one of the paired forearm bones usually results in dislocation of a common joint. These fracture-dislocations are unstable and require ORIF.
Upper Extremity Trauma Page 135 Notes
15. The majority of rotator cuff tears are chronic and typically present with weakness and pain on active abduction.
16. Bicep tendon ruptures usually occur during contraction against resistance and present with a “Popeye” appearance (due to distal retraction of the muscle) of the upper arm.
17. Tennis elbow (epicondylitis) occurs in patients whose occupations require repetitive rotary motions of the elbow, and present with pain and tenderness of the involved epicondyle.
Upper Extremity Trauma Page 136 Notes
REFERENCES
1. Emergency Orthopedics The Extremities 5th ed. Simon RR, Sherman SC, Koenigsknecht SJ. McGraw-Hill, 2007.
2. Handbook of Orthopedic Emergencies. Hart RG, Rittenberry TJ, Uehara DT eds. Lippincott Raven Publishers, 1999.
3. Rosen’s Emergency Medicine. Concepts in Clinical Practice, 8th Edition. Elsevier Saunders, 2014.
5. Tintinalli’s Emergency Medicine. A Comprehensive Study Guide. 8th Edition. McGraw Hill, 2016.
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Upper Extremity Trauma Page 137 Notes
LOWER EXTREMITY TRAUMA
I. PELVIC FRACTURES
A. Motor vehicle collisions are the #1 cause.
B. Often a marker of serious concomitant injuries.
C. 15% have associated injuries to intrapelvic structures (i.e., urethra, bladder, rectum, and vasculature).
D. The most common cause of mortality from a pelvic fracture is hemorrhage.
E. Diagnosis:
1. Many patients present in shock due to associated retroperitoneal hemorrhage. A pelvic fracture presenting with hypotension carries a 50% mortality rate. 2. Grey Turner’s sign (ecchymosis of the abdomen or flanks) may be present with retroperitoneal hemorrhage. 3. With associated GU trauma, urine may extravasate into the scrotum, penis abdominal wall or peritoneal cavity. 4. AP view of the pelvis will identify most fractures. Inlet and outlet (tangential) views of the pelvis are helpful in diagnosing displaced fractures of the pelvic arches, as well as SI joint disruptions and sacral fractures.
Lower Extremity Trauma Page 138 Notes
F. Classifications (multiple different classification schemes exist):
1. Fractures of individual bones without a break in the continuity of the pelvic ring (Type I fractures, i.e., avulsion fractures, isolated fractures of the pubic rami, fractures of the sacrum or coccyx): a. In general are stable injuries requiring bed rest only. b. Isolated fractures of the pubic ramus are the most common type of pelvic fracture. c. Sacral fractures may be associated with significant neurologic disability (bowel, bladder and sexual dysfunction).
2. Single break in the pelvic ring (Type II fractures, i.e. fractures of both ipsilateral pubic rami, fractures near and sublux of the symphysis pubis or the SI joint): a. Are stable if nondisplaced and treated primarily with bed rest. b. The presence of significant displacement implies a 2nd disruption of the pelvic ring (an unstable fracture).
Lower Extremity Trauma Page 139 Notes 3. Double breaks in the pelvic ring (Type III fractures): a. Are unstable fractures with a high incidence of intraperitoneal and retroperitoneal injuries. b. Straddle fractures: up to one third of patients will have lower urinary tract damage. c. Malgaigne fractures: a double vertical fracture of the pelvis, anterior and posterior to the acetabulum.
4. Fractures of the acetabulum (Type IV fractures): a. These are frequently associated with hip dislocations.
G. Treatment and complications:
1. Hemorrhage (usually retroperitoneal) is of major concern. a. The sensitivity and specificity of ultrasound FAST exam is limited in pelvic fractures. Patients with a significant mechanism of injury should undergo CT even with a negative FAST exam. b. Placement of an external fixator may be helpful, especially for displaced fractures of the anterior arch. c. ATLS recommends the use of a wrapped bedsheet for pelvic stabilization and support. d. Angiography with selective embolization of pelvic vessels. 2. Genitourinary: a. Blood at the urethral meatus warrants retrograde Lower Extremity Trauma Page 140 Notes urethrogram before catheter insertion. b. Retrograde cystogram is indicated in the presence of gross hematuria to rule out bladder rupture. c. A speculum exam may be needed to differentiate menses from vaginal lacerations. 3. Rectal injuries: a. Broad-spectrum antibiotics and diverting colostomy are indicated. 4. Nerve root injuries most commonly occur with sacral fractures and SI joint disruptions. 5. Intra-abdominal injuries: a. Closed peritoneal lavage is contraindicated. CT or open lavage should be done to avoid hitting retroperitoneal hematomas.
II. HIP & LOWER EXTREMITY
A. Avascular necrosis of the femoral head:
1. Ischemic bone death of the femoral head due to a compromise of its blood supply. 2. Trauma is the #1 cause – usually after a femoral neck fracture or hip dislocation. Other causes include: chronic corticosteroid therapy, sickle cell disease, alcohol abuse, gout and lupus. Twenty percent of cases are idiopathic. 3. Most common in relatively young males (30-50 years of age is the peak incidence) and bilateral approximately 50% of the time. 4. Presents with increasing hip, thigh or knee pain with no recent history of trauma. Decreased range of motion is noted on physical exam. 5. X-ray shows decreased bone density of the femoral head initially, followed by bone collapse and loss of head sphericity in the later stages. 6. Treatment involves surgical removal of part of the core of the femoral head, or total hip arthroplasty in more advanced cases.
B. Soft tissue injuries of the hip and thigh:
1. Bursitis: a. Several bursae surround the hip and may become inflamed due to overuse or excessive pressure. Treatment is with rest, heat and NSAIDs. b. Ischiogluteal bursitis often occurs in individuals who sit for prolonged periods of time on hard surfaces. Tenderness is present over the ischial tuberosity. In addition to the usual conservative therapy, these patients should be advised to use cushioned seating in the future.
Lower Extremity Trauma Page 141 Notes
2. Muscle injuries: a. Are more common in athletes, poorly conditioned people engaging in strenuous exercise, and in cold weather. b. Partial tears present with swelling, ecchymosis, tenderness and a mild loss of strength. c. Specific muscle groups: i. Hamstring injuries are typically due to rapid acceleration while running and present with sudden, intense pain in the posterior thigh. ii. Quadriceps injuries occur when the muscles contract against the body’s weight (e.g., stumbling to avoid a fall) and present with pain or an inability to extend the knee. iii. Iliopsoas strain results from sudden hip flexion against resistance, and often presents with intraabdominal (lower quadrant) pain. d. Partial tears usually respond to conservative therapy (i.e., NSAIDs and rest). Complete tears may require surgical repair. 3. Tendon injuries of the hip (“groin pull”) result from a force to abduct the hip during contraction of the adducting muscles. a. Pain and tenderness is noted at the inferior pubic ramus and ischial tuberosity. b. Partial tears can be managed conservatively; complete tears often require surgery.
C. Hip dislocations:
1. The most common cause is motor vehicle collision. 2. Approximately 50% are associated with fractures of the acetabulum or the femoral head. 3. Need to reduce as soon as possible to decrease complications (avascular necrosis of the femoral head). 4. Anterior dislocations (10% of all hip dislocations): a. Patients present with hip flexed, abducted and externally rotated. b. May be anterosuperior (pubic) or anteroinferior (obturator). Lower Extremity Trauma Page 142 Notes c. Damage to the femoral artery, vein or nerve may occur, but is unusual. d. Treat with closed reduction, usually under general anesthesia.
5. Central dislocations (relatively rare): a. Femoral head is dislocated medially, with a badly fractured acetabulum. b. Surgical repair is required (not surprisingly). 6. Posterior dislocations (80-90% of hip dislocations): a. The classic “dashboard injury”. b. Presents with hip flexed, adducted and internally rotated. c. Sciatic nerve injury occurs in approximately 10% of cases. d. Treatment is with closed reduction, preferably under general anesthesia.
7. Dislocation of hip prosthesis: a. Most occur in the first 3 months postoperatively. b. Reduction may cause damage to the prothesis and should be attempted only after orthopedic consultation. Lower Extremity Trauma Page 143 Notes
D. Fractures of the femur:
1. Femoral head fractures:
a. Usually occur with hip dislocation (10-16% of posterior hip dislocations will have a femoral head fracture). b. Post-traumatic arthritis and aseptic necrosis of the femoral head are potential complications. 2. Femoral neck fracture: a. Most common in elderly women, usually with relatively minor trauma. b. Some nondisplaced fractures may be subtle and require MRI or bone scan for diagnosis. c. Avascular necrosis of the femoral head in 15% of nondisplaced fractures and 90% of completely displaced fractures. d. All displaced fractures will require surgery.
3. Intertrochanteric fracture: a. Fracture line is between the greater and lesser trochanter. b. Avascular necrosis is rare.
Lower Extremity Trauma Page 144 Notes c. The vast majority will require some form of internal fixation.
4. Trochanteric fractures: a. Greater trochanter: i. In the young, this is usually secondary to forceful contraction of the gluteus medius with epiphyseal separation. ii. In adults, this usually results from direct trauma to the area. iii. Usually treated conservatively with limited weight bearing. iv. Surgical fixation is indicated if displaced more than 1 cm. b. Lesser trochanter: i. Usually occurs in young athletes. ii. Caused by powerful contraction of the iliopsoas. iii. Presents with pain and tenderness in the femoral triangle. iv. Most can be treated conservatively with gradual weight bearing. v. Surgical fixation is indicated if displaced > 2 cm. c. Subtrochanteric and femoral shaft fractures: i. These may cause significant blood loss with hematoma formation. ii. Shaft fractures are primarily in young patients who have sustained high-energy trauma and have a high incidence of concomitant injuries. iii. Fat emboli syndrome is a concern with shaft fractures. iv. Treat initially with a traction splint and, ultimately, ORIF.
Lower Extremity Trauma Page 145 Notes
E. Knee injuries:
1. Dislocations: a. The knee joint: i. A true orthopedic emergency. ii. The majority are anterior or posterior. Can also be lateral, medial or rotary. iii. 30–40% have popliteal artery injury. While there is no consensus as to the diagnostic approach to detect popliteal artery injury, some type of vascular assessment must be done (i.e., arteriography, ultrasound, arterial-brachial indices, etc.). iv. 35% have peroneal nerve injury. v. Some dislocations will reduce spontaneously prior to presentation. Stress radiographs or arthrograms may aid in the diagnosis. vi. Immediate reduction is indicated. b. The patella: i. The vast majority are lateral. ii. Risk factors include a high riding patella (patella alta) and excessive genu valgum (“knock knees”). iii. The typical patient is an obese female who experiences a sudden twisting on an extended or slightly flexed knee. iv. Reduce with knee extended and hip flexed, and then immobilize the knee in full extension. v. Superior or intra-articular dislocations warrant orthopedic consultation.
Lower Extremity Trauma Page 146 Notes
c. Femoral condyle (supracondylar, intercondylar, unicondylar): i. Usually secondary to direct trauma. ii. Associated neurovascular injury is relatively uncommon. d. Tibial spine: i. Usually present with associated damage to the cruciate ligaments. ii. Incomplete or nondisplaced fractures should be immobilized in extension. Completely displaced fractures require open reduction. e. Tibial tuberosity: i. The insertion site for the quadriceps. ii. Caused by a sudden force to flex the knee while quadriceps is contracted. iii. If tubercle is incompletely avulsed, can immobilize extension. Complete avulsions require operative repair.
f. Tibial plateaus: i. Caused by direct force (most commonly to the lateral knee that compresses the femoral condyle into the articulating surface of the tibia). ii. More common in the elderly. Lower Extremity Trauma Page 147 Notes iii. 7–15% will have associated ligamentous injury. iv. Can be difficult to detect. Oblique views may be helpful. Sometimes only a fat-fluid level is present on X-ray. v. If fracture fragment is depressed 5 mm or more, surgery is indicated.
g. Patellar fractures: i. Can be caused by direct trauma or contraction of the quadriceps during violent flexion of the knee. ii. X-ray findings can be confused with a secondary patellar ossification site (usually in the superolateral aspect). These anomalies are usually present bilaterally. iii. Other than small avulsion fractures of the rim, these are considered intra-articular fractures. iv. If overlying skin is open, these require debridement and irrigation in the OR. v. Non-displaced transverse fractures can be treated conservatively with immobilization in extension. vi. Displaced fractures require open reduction and internal fixation. Severely comminuted fracture may warrant total patellectomy.
2. Ligamentous injuries: a. Most present with hemarthroses. b. First degree sprain: no instability but pain with stress testing. c. Second degree sprain: pain and mild instability. d. Third degree sprain: marked instability (complete ligament disruption). Lower Extremity Trauma Page 148 Notes
e. Medial collateral ligament (MCL): i. Caused by a valgus force to knee. ii. If laxity is felt with valgus stress with knee in 30 degree flexion, check for laxity while in full extension. If this is present, damage to other structures (i.e., cruciate ligaments) is present. iii. The “terrible triad”: rupture of ACL and MCL with tear of the medial meniscus.
f. Lateral collateral ligament (LCL): i. Isolated injuries to this are uncommon. ii. Caused by a varus stress. iii. May have associated common peroneal nerve injury. g. Anterior cruciate ligament (ACL): i. Usually a non-contact injury. Often caused by stopping abruptly or making a sharp turn while running. ii. Patients frequently hear a “pop,” then knee gives out.
Lower Extremity Trauma Page 149 Notes iii. Diagnosed by a positive anterior drawer (not very sensitive) or Lachman (more sensitive). h. Posterior cruciate ligament (PCL): i. Not a commonly torn ligament. ii. Usually caused by pretibial trauma to the hyperflexed knee (as in the “dashboard injury”). iii. Diagnosed by a positive posterior drawer sign. i. Isolated ligament injuries can be treated as follows: i. First degree: ice, compressive wrap, non weight bearing. ii. Second degree: ice, immobilization, non weight bearing. iii. Third degree: orthopedic consultation, some may not require immediate intervention. 3. Meniscal injuries: a. Can occur primarily or with associated ligamentous injuries. b. May present with locking of the joint during flexion or extension, clicking or popping during activity or effusion after activity. c. A positive McMurray or Apley test may be present. d. Arthroscopy or MRI is used for definitive diagnosis. 4. Quadriceps/patellar tendon rupture: a. Caused by forceful contraction of quadriceps or falling on a flexed knee. b. Risk factors include chronic steroid use, hyperparathyroidism, and long-term dialysis. c. Complete ruptures require surgical repair.
F. Distal leg:
1. Fractures of the tibial shaft: a. Have a high rate of open fractures and healing complications. b. All displaced fractures require hospitalization for circulatory observation due to high incidence of compartment syndromes. c. Closed fractures with minimal or no displacement (e.g., a spiral fracture secondary to excessive rotation while skiing) can initially be managed with a long leg splint with 10 to 20
Lower Extremity Trauma Page 150 Notes degrees of knee flexion. 2. Fractures of the fibular shaft: a. Isolated fractures of the fibular shaft are uncommon. b. Usual mechanism is a direct blow. c. Fracture of head or neck may injure common peroneal nerve. d. Treatment is symptomatic. A short leg walking cast may be used for comfort. e. Maisonneuve fracture: i. Rupture of deltoid ligaments of the ankle or distal tibial fracture with a proximal fibular fracture. ii. Caused by forceful external rotation of the foot. iii. Most can be treated with cast immobilization. Any ankle instability warrants operative repair. 3. Shin splints: a. Exercise-induced pain over the medial aspect of the tibia. b. Often occurs in runners, military recruits, and those with flat feet. c. May be a repetitive trauma-induced periostitis of the tibia. d. Diagnosis is made clinically. e. A bone scan may be performed to rule out stress fracture. f. Treatment is avoidance of the repetitive trauma.
G. The ankle:
1. Inversion injuries typically cause sprains, while eversion injuries characteristically cause fractures. a. 75% of all ankle injuries are sprains and 90% of these involve the lateral ligaments. The anterior talofibular ligament is the most commonly injured lateral ligament. b. Standard X-ray views include AP, lateral and mortise (15 degree of internal rotation) views. c. The ankle can be thought of as a ring consisting of the tibia,
Lower Extremity Trauma Page 151 Notes fibula and talus bound together by medial (deltoid) ligaments, lateral ligaments and tibiofibular ligaments. Any two breaks in the ring (e.g., a fracture of both malleoli, a malleolus and a ligament, or two ligaments) leaves the joint unstable.
2. Ligamentous injuries: a. Lateral collateral ligaments: i. Usually injured by internal torsion. ii. Laxity on anterior drawer testing of the ankle indicates tear of the anterior talofibular ligament. iii. Laxity noted with inversion testing indicates a tear of the anterior talofibular and caneofibular ligaments.
b. Medial collateral ligaments:
Lower Extremity Trauma Page 152 Notes
i. Usually injured by eversion stress. ii. Almost always associated with fracture of the fibula (Maisonneuve) or separation of the tibiofibular syndesmosis. c. Treatment: i. First degree sprains can be treated with rest, ice, compression dressing and elevation. ii. Second degree sprains require immobilization and non weight bearing. iii. Third degree sprains warrant immobilization and orthopedic consultation. 3. Fractures: a. Often occur with associated ligamentous injury. b. Definitive treatment (open versus closed) is variable with the primary goal being stability of the talus within the joint. 4. Dislocations (not a common injury): a. May be posterior (most common), anterior, lateral or superior. b. Most are associated with malleolar fractures and almost half are open dislocations. c. Emergent reduction is indicated. d. There is a relatively high incidence of vascular injury and avascular necrosis of the talus. 5. Achilles tendon rupture: a. Most commonly in middle-aged men engaging in athletics. b. May be due to forceful dorsiflexion of the ankle or direct blows to a taut tendon. c. Often described as being “kicked in the back of the leg”. d. Even with complete rupture, some active plantar flexion may be present. e. A Thompson’s test (calf squeeze) aids in the diagnosis. f. Complete ruptures should be repaired surgically.
Lower Extremity Trauma Page 153 Notes
H. The foot:
1. The forefoot: phalanges and metatarsals. 2. The midfoot: the cuneiforms, cuboid and navicula. 3. The hindfoot: calcaneus and talus.
4. Calcaneal fractures: a. Usually secondary to a fall from a height. b. Bilateral 10 – 20% of the time. Associated lumbar spine injuries 10% of the time and other injuries to the involved extremity 26% of the time. c. Most fractures are through the body. d. May see a decrease in Bohler’s angle on lateral film, and special calcaneal views may aid in the diagnosis. e. Notoriously difficult to treat, often with long term morbidity.
Lower Extremity Trauma Page 154 Notes
5. Talus fractures: a. Often secondary to hyperdorsiflexion of the foot. b. The lateral view of the foot is most helpful. c. At risk for avascular necrosis, especially if fracture through neck with dislocation of the body. d. Usually require early reduction if any displacement is present.
6. Midfoot fracture: a. A rare occurrence. Usually involve the navicula. b. Usually due to direct trauma (crush injuries). c. Non displaced fractures can be treated with a walking cast; displaced fractures require orthopedic consultation. 7. Tarsometatarsal (Lisfranc) fracture/dislocations: a. Can be caused by direct (car running over foot) or indirect (excessive axial load onto plantar flexed foot) trauma. b. Very often associated with fracture of the base of the second metatarsal (this is where forefoot “locks into” the mid foot). c. Most reliable radiographic finding is separation of the first and second metatarsals. d. Notoriously difficult to reduce. e. Admission for observation for circulatory compromise of the foot (a major complication) is indicated.
Lower Extremity Trauma Page 155 Notes
8. Metatarsal fractures: a. Stress fractures of the second and third metatarsals occur with frequent “pushing off” (i.e., “march fracture”) since they are subjected to the greatest stress during this activity. b. Other fractures are secondary to direct blows or twisting type injuries. c. Can usually be treated conservatively with a short leg splint and non weight bearing. 9. Fractures of the base of the fifth metatarsal: the most common type of metatarsal fracture. a. Tuberosity fracture: i. Secondary to inversion, with avulsion of the peroneus brevis insertion. ii. Can be treated conservatively with immobilization and non weight bearing. b. Jones fracture: i. Now thought not to be an avulsion fracture. ii. Fracture line is distal to the insertion of the peroneus brevis. iii. Usually treated with screw fixation.
10. Phalangeal fractures: a. Usually secondary to direct (crushing) trauma. b. If displaced, can usually be reduced after digital anesthesia. c. Fractures of the big toe may require more immobilization (i.e., walking boot cast) given its increased role in weight bearing. i. Supportive shoe to lessen the hyperextension. 11. Puncture wounds: a. 8-15% progress to cellulitis or localized abscess. b. Associated osteomyelitis is due to pseudomonas aeruginosa 93% of the time. c. Surgical debridement and parenteral antipseudomonal antibiotics are indicated if osteomyelitis is present. Lower Extremity Trauma Page 156 Notes
LOWER EXTREMITY TRAUMA
PEARLS
1. Pelvic fractures are often a marker of serious concomitant injuries, and the most common cause of mortality from a pelvic fracture is hemorrhage.
2. Pelvic fractures with 2 breaks in the pelvic ring are the most unstable type.
3. 80-90% of hip dislocations are posterior and often secondary to motor vehicle collisions. A significant percentage (10%) of these will have associated sciatic nerve injury.
4. Femoral head fractures commonly occur with hip dislocations.
5. Trauma (usually femoral neck fracture or hip dislocations) is the #1 cause of avascular necrosis of the femoral head.
6. Femoral shaft fractures can cause a large amount of blood loss and hematoma formation.
7. A high percentage of knee dislocations have an associated popliteal artery injury. Arteriography after knee dislocation is generally warranted.
8. Most patellar dislocations can be reduced with the knee extended and hip flexed.
9. Tibial plateau fractures depressed 5 mm or more require surgical repair.
10. Tears of the medial collateral ligament are frequently associated with concomitant injury to the anterior cruciate ligament and the medial meniscus.
11. Isolated injuries to the anterior cruciate ligament are often non-contact injuries.
12. Any patient unable to actively extend his/her knee after falling on it while flexed should be evaluated for possible quadriceps/patellar tendon rupture.
13. Fractures of the tibial shaft have a high incidence of compartment syndromes and healing complications.
14. A Maisonneuve fracture is a rupture of the deltoid ligaments of the ankle or a fracture of the distal tibia with a proximal fibular fracture.
Lower Extremity Trauma Page 157 Notes 15. Inversion ankle injuries typically cause ligament sprains, while eversion injuries characteristically cause fractures.
16. The majority of ankle injuries are ligament sprains, and the vast majority of these involve the lateral ligaments.
17. Ankle dislocations have a relative high incidence of vascular injury and avascular necrosis of the talus.
18. Even with complete Achilles tendon rupture, the patient may have some active plantar flexion.
19. Calcaneal fractures are often bilateral (10-20%), associated with lumbar spine injuries (10%) and other injuries to the involved extremity (26%).
20. Tarsometatarsal (Listranc) fracture/dislocations are very often associated with a fracture of the base of the second metatarsal. Frequently, a separation of the first and second metatarsals is seen on X-ray.
21. A tuberosity fracture of the base of the fifth metatarsal is due to avulsion of the peroneus brevis insertion.
22. A Jones fracture of the fifth metatarsal is distal to the peroneus brevis insertion and is not thought to be an avulsion fracture.
23. Metatarsal stress fracture (i.e., “March fractures”) usually involves the second or third metatarsals.
24. Osteomyelitis in the foot secondary to puncture wounds is caused by Pseudonomas aeruginosa the majority of the time.
Lower Extremity Trauma Page 158 Notes
REFERENCES
1. Clinical Procedures in Emergency Medicine. 5th Edition. 2010, Saunders Elsevier.
2. Emergency Medicine. The Core Curriculum. 1998, Lippincott-Raven Publishers.
3. Emergency Orthopedics. The Extremities. 5th Edition. 2007, McGraw- Hill.
4. Rosen’s Emergency Medicine. Concepts in Clinical Practice, 8th Edition 2014, Elsevier Saunders.
5. Textbook of Pediatric Emergency Medicine. 6th Edition. 2010, Lippincott, Williams, and Wilkins.
6. Tintinalli’s Emergency Medicine. A Comprehensive Study Guide. 8th Edition. 2016, McGraw Hill.
08/17
Lower Extremity Trauma Page 159
Page 160
Urology/GU Trauma
Wesley Eilbert, MD, FACEP
Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago
Page 161
Page 162 Notes
UROLOGY/GU TRAUMA
I. NON-TRAUMATIC PROBLEMS
A. Paraphimosis:
1. The inability to reduce the proximal foreskin over the glans, resulting in distal venous congestion. This can progress to arterial compromise, gangrene, and amputation from the foreskin acting as a tourniquet around the glans. 2. Most common cause is a circular scar in the prepuce from preexisting phimosis which is then retracted behind the glans cutting off blood supply. 3. This is a true urologic emergency. 4. May be iatrogenic (i.e., foreskin not reduced after placement of a urinary catheter). 5. Attempt to reduce the foreskin often requires penile nerve block with 1% lidocaine (without epinephrine) to be successful. 6. Techniques to reduce edema of the glans: a. Place glans in rubber glove filled with ice water. b. Manual compression of the glans. c. Several punctures of the glans with a small needle to drain edema fluid. 7. If all else fails, the constricting band may be released by cutting a small dorsal slit or ultimately by circumcision.
B. Phimosis:
1. A constriction of the foreskin, with the inability to retract it over the glans. 2. Usually not a true urologic emergency. 3. Often confused with: a. Balanitis. b. Balanoposthitis. c. Paraphimosis. 4. Physiologic phimosis occurs in 96% of uncircumcised newborns, and resolves itself by the age of 3. Urology/GU Trauma Page 163 Notes 5. Caused by infection, poor hygiene or trauma that results in scarring. 6. If causing urinary outlet obstruction, you can dilate the meatus with forceps. 7. Topical steroids have been proven beneficial. 8. Definitive treatment is circumcision.
C. Priapism:
1. A prolonged, often painful erection occurring without sexual stimulation. 2. CBC and coagulation studies are indicated. 3. Immediate IV fluids and analgesia are given. 4. High flow priapism (less common) is caused by increased arterial blood flow due to an arterial-cavernosal shunt usually formed as a result of a groin or straddle injury. a. This type does not cause ischemia; is usually painless and is at low risk for permanent complications. b. Can usually be treated with arterial embolization. 5. Low flow priapism is due to a decreased penile venous outflow. a. Causes include sickle cell disease (the most common cause in children), leukemic infiltration, spinal trauma, medications (usually phenothiazine, SSRI or antihypertensives) and illicit drugs (cocaine and marijuana). In adults, usually it is idiopathic. b. Corpus cavernosum is hard but the glans and corpus spongiosum is soft. (Pathophysiology usually involves sludging of RBCs in the corpus cavernosum.) c. Treatment in sickle cell patients includes oxygen, alkalinization, hydration, pain control and, ultimately, exchange transfusion. d. Other treatment options include local anesthesia through a dorsal penile nerve block, parenterally administered vasodilators such as terbutaline or hydralazine, and cavernosal aspiration and irrigation – often with phenylephrine or epinephrine added to the irrigation solution. e. If priapism recurs after aspiration of blood, surgical shunting is needed. f. If left untreated, corporal fibrosis and erectile dysfunction Urology/GU Trauma Page 164 Notes may result. g. Treatment within 4-6 hours = low morbidity. h. Treatment after 24 hours = high morbidity.
D. Hydrocele:
1. A collection of fluid in the tunica vaginalis. 2. May be communicating – open to the peritoneal cavity, or noncommunicating. 3. Many are present at birth and may worsen with crying. Congenital hydroceles often resolve spontaneously by age 18 months. 4. Reactive hydroceles may be caused by testicular tumors, torsion or epididymitis/orchitis.
E. Varicocele:
1. Due to abnormal dilatation of the spermatic cord veins. 2. Often described as a “bag of worms” palpable superior and posterior to the testicle, and more pronounced in the upright position. 3. 85% - 95% are left-sided. 4. Intraabdominal pathology causing compression of the inferior vena cava should be suspected with right-sided varicoceles. 5. Surgical resection may be performed for symptomatic relief.
F. Testicular torsion:
1. Peak incidence at 13 years; however, there is a bimodal age distribution between the teens and the first year of life. Torsion can occur at any age. 2. At-risk testes align in a horizontal rather than a vertical axis (i.e., the “bell-clapper deformity”— see Figure 3). This is caused by malformed tunica vaginalis in infants and incomplete attachment of the gubernaculum in adults. Both of these malformations leave the testicles free to rotate. 3. Classically a sudden onset of lower abdominal or testicular pain. 4. Involved testicle is firm, tender, swollen and higher in the scrotum than the other testicle. 5. Cremasteric reflex is typically absent, which is highly sensitive for testicular torsion. SURGICAL EXPLORATION SHOULD NOT BE DELAYED FOR DIAGNOSTIC STUDIES, especially if symptoms are <12 hours old. 6. Newer color Doppler ultrasound has sensitivities of 90%-100% and specificity of 100%; helpful in indeterminate cases. 7. Manual detorsion may be attempted by “dialing out” or “opening a book” (i.e., medial to lateral direction). This is done for acute pain relief and some return of blood flow; it is not a definitive treatment and surgery is still indicated even if successful. Urology/GU Trauma Page 165 Notes 8. Testicular salvage rate of >90% if de-torsed within 4 hours, 20% within 12 hours, and almost 0% if de-torsed after 24 hours.
Figure 3: “Bell-clapper” deformity
G. Torsion of the testicular appendage:
1. Torsion of the appendix testis, a remnant of the Müllerian duct. 2. Average age is 10 years. 3. Sudden onset of testicular pain, but usually more gradual than testicular torsion. A tender nodule may be palpated. 4. The blue dot sign may be seen on cranial portion of testes or epididymis. 5. Cremasteric reflex normally present, helps to differentiate from testicular torsion. 6. Doppler ultrasound, or alternatively, nuclear scintigraphy can be used to confirm the diagnosis. 7. Treatment is conservative. The appendages will autoamputate within a week.
H. Urethritis
1. Most cases are due to Neisseria gonorrhoeae or Chlamydia trachomatis. 2. Other less common causes include Herpes simplex, Ureaplasma urealyticum and Trichomonas vaginalis. 3. Characterized by a purulent urethral discharge. 4. Treatment: ceftriaxone 250 mg IM and azithromycin 1 gram PO or doxycycline 100 mg PO BID for 7 days.
I. Epididymitis (inclusion for its similarity in presentation to torsion): Urology/GU Trauma Page 166 Notes
1. Rarely occurs before puberty. Caused by retrograde spread of urethral and bladder pathogens. 2. Under age 35, chlamydia and gonorrhea are the main pathogens. Over age 35, it’s E. coli. 3. Presents with lower abdominal and testicular pain, usually with a low grade fever. Pain may be relieved with scrotal elevation (Prehn’s sign). a. Can be difficult to distinguish from torsion. Negative Prehn’s sign can help to distinguish from epididymitis but is insensitive. (see Figure 4)
Figure 4: Torsion versus epididymitis
b. Erythema and edema of the hemiscrotum may be noted. The epididymis is usually swollen and tender. A reactive hydrocele may be present. 4. UA, urine culture, and urethral STD cultures should be sent. 5. UA may not show evidence of infection. Urology/GU Trauma Page 167 Notes 6. Empiric treatment: a. If presumed sexually acquired: single dose ceftriaxone plus doxycycline for 10 days. b. If presumed not sexually acquired: Cipro/levofloxacin for 10 days OR ofloxacin for 10 days. c. Also: bed rest, scrotal elevation (athletic supporter), ice packs, NSAIDs, urologic follow-up. 7. Complications: orchitis, abscess formation and infertility.
J. Acute prostatitis
1. E. coli is the most common cause. 2. Symptoms include low back or perineal pain, urinary hesitancy, frequency and dysuria. Fever may be present. 3. Clinical findings include perineal tenderness and prostatic tenderness or bogginess on rectal exam. 4. Diagnosis is clinical since urinalysis and urine culture may both be negative. 5. Treat with a fluoroquinolone for 14 days. In younger patients and those at high risk for sexually transmitted disease, treat with ceftriaxone 250 mg IM and doxycycline 100 mg PO BID for 14 days.
K. Acute urinary retention:
1. Most common cause is prostatic hypertrophy. Other causes include: multiple sclerosis, diabetes, urethral stricture, spinal cord compression and drugs (antihistamines, anticholinergics, TCAs and sympathomimetics). 2. An intact sensory exam, anal sphincter, and bulbocavernosus reflex differentiates chronic outlet obstruction from the sensory or motor neurogenic bladder. 3. A normal-sized prostate on physical exam does not eliminate it as a cause of obstruction. 4. To decompress the bladder, start with a 16Fr or 18Fr catheter. If the obstruction is at the level of the prostate, a 16Fr Coude- catheter can be tried. Ultimately, a suprapubic cystostomy may be needed. 5. BUN/Cr and UA should be sent to check renal function and for infection respectively. 6. Complete drainage of a distended bladder can be accomplished rapidly without the need for repeated clamping of the catheter. Rapid decompression may cause transient gross hematuria or hypotension, but this is usually insignificant. 7. Postobstructive diuresis may occur. For this reason, patients should have urinary output measured for 4-6 hours after catheterization. Postobstructive diuresis warrants admission for IVF and monitoring of electrolytes.
Urology/GU Trauma Page 168 Notes L. Fournier’s gangrene:
1. A necrotizing fasciitis of the perineum, usually involving the penis and scrotum, but can also affect women. 2. Main risk factor is immunosuppression, especially diabetes. 3. Often proceeded by perineal trauma (i.e., scratches, burns, anal intercourse). 4. Perineal and genital pain and itching is followed by fever, toxic appearance and perineal swelling. Subcutaneous crepitance is often present. CT may show edema and gas in scrotal skin. 5. A polymicrobial infection, usually aerobic and anaerobic, with bacteria from the distal colon. 6. Treat with aggressive fluid resuscitation, appropriate antibiotics (ticarcillin/clavulanate or ampicillin/sulbactam or piperacillin plus gentamicin plus metronidazole), and, most importantly, immediate urologic consultation and surgical debridement. 7. Elasticity of genital skin allows for surgical closure even if 60% of skin is lost; more than 60% loss with require grafts. 8. Mortality rate of 13-22%.
M. Renal calculi (kidney stones):
1. Incidence may be as high as 10% -12%. Three times more common in males. 2. Usually occur in between the ages of 20 and 50 years. 3. Risk factors include: arid climates, family history, sedentary lifestyle, a history of hyperparathyroidism, milk-alkali syndrome, sarcoidosis, history of recurrent UTIs, and HIV medications (protease inhibitors). a. Types of stones: i. Calcium. Calcium oxalate or calcium phosphate stones comprise 75% of all kidney stones. ii. Struvite (magnesium-ammonium-phosphate) stones account for 15% of stones. These occur exclusively in patients with UTIs caused by urea-splitting organisms. iii. Uric acid stones make up 10% of renal calculi. These are radiolucent. iv. Cystine stones are rare and due to inborn errors in metabolism. b. Clinical features: i. Classically, a sudden onset of a colicky pain in the flank, radiating laterally around the abdomen and into the groin. Pain may radiate to the testicle. Nausea and vomiting are common. c. Patient unable to find a position of comfort - writhing in bed. d. Abdomen is minimally tender, if at all. 4. Diagnostic studies: a. Hematuria, gross or microscopic is present in 85% of cases. b. Urinary pH >7.6 many indicate the presence of urea-splitting Urology/GU Trauma Page 169 Notes organisms (struvite stones). c. “Unenhanced helical CT is best radiographical test for diagnosing urolithiasis in patients with acute flank pain” (Miller, 2007). Sensitivity and specificity >94%. d. Intravenous pyelogram (IVP) is not as sensitive as CT, but has the advantage of evaluating kidney function. i. The most reliable and earliest indicator of a calculus is a delay in the appearance of the contrast on the affected side. ii. Other signs of a calculus: visualization of the entire ureter (columnization), dilatation of the collecting system, extravasation of the contrast out of the collecting system. e. Ultrasound causes no radiation exposure, making it the study of choice in pregnant patients. It is only modestly sensitive and specific for kidney stones, though 98% sensitive for detecting hydronephrosis. f. Abdominal plain films can determine whether stones are radio-opaque and can be used to monitor disease activity. 5. Treatment should be with NSAIDs (which also help decrease ureteral spasm) and narcotics. a. Indications for admission include: obstruction with infection, uncontrolled pain, persistent vomiting, urinary extravasation out of the collecting system, and a solitary or transplanted kidney. b. Outpatient treatment includes increased fluid intake and straining of urine. If the stone is obtained, it should be taken to the urologist for analysis. c. The most important predictor of stone passage is its size. 90% of stones <4 mm pass spontaneously, while only 10% of those >6 mm do. Stones in the distal ureter have a greater likelihood of passage than those more proximal. d. Shock wave lithotripsy can be used to fragment stones <2 cm but is contraindicated for staghorn calculi. e. Ureteroscopy with instruments for fragmentation or removal can be used where lithotripsy fails. f. Percutaneous nephrolithotomy can be used to create an access tract into the collecting system but is invasive and used only as a last resort. g. Alpha blockers and calcium channel blockers have both been shown to increase the rate of stone expulsion. h. Irreversible renal damage begins to occur if obstruction persists beyond two weeks.
N. Urinary tract infections (UTIs):
1. Uncomplicated UTIs occur in otherwise healthy, reproductive- aged women who are not pregnant. E. coli is the pathogen in >80% of cases. 2. Complicated UTIs occur in males, and females with risk factors Urology/GU Trauma Page 170 Notes for complicated infections (i.e., premenarchal, post menopausal, pregnant, diabetic or with structural abnormalities) These patients are frequently infected with more resistant organisms. 3. The diagnostic standard is 105 CFUs/ml on culture. 4. On urinalysis, the presence of > 5 WBCs/hpf on a centrifuged specimen is abnormal. 5. Antimicrobial agents should be chosen according to local resistance patterns. In general, nitrofurantoin, quinolones and 3rd generation cephalosporins have the lowest resistance rates. 6. Uncomplicated cystitis can be treated with 3-day antibiotic therapy. A urine culture does not need to be sent. 7. Complicated cystitis and all pyelonephritis should be treated with 10-14 days of antibiotics, and a urine culture should be sent. 8. Indications for inpatient treatment of pyelonephritis include: pregnancy, excessive vomiting, immunocompromise and obstruction (e.g., kidney stone)
II. GU TRAUMA
A. Penile injuries:
1. Penile amputation should be treated with reimplantation if the distal penis is in satisfactory condition and the ischemia time is <12-24 hours. Chances or reimplantation can be increased by proper handling of amputated portion: a. Penis wrapped in saline soaked gauze and put in sterile bag. b. Immerse bag in ice slush until surgery can be performed. 2. Penile “fracture” or traumatic rupture of the tunica albuginea and underlying corpus cavernosum occurs when an erect penis impacts forcibly on a hard surface such as the pubic bone (often during vigorous intercourse). a. Often a snapping sound is heard, with localized pain, detumescence and a progressive penile hematoma. b. Most require surgical repair of the torn tunica albuginea. “Egglant deformity” (see Figure 5) on physical exam with swollen ecchymotic penis. c. About 1/3 of penis fractures also involve an underlying urethral injury so a retrograde urethrogram should be performed. d. Treatment: surgical exploration. 3. Superficial penile and scrotal lacerations may be closed with 4-0 absorbable sutures. 4. Penile skin trapped in a zipper can be treated with lidocaine infiltration followed by mineral oil application to help free the skin. Otherwise, wire cutting pliers can be used to divide the median bar of the zipper, causing it to fall apart.
Urology/GU Trauma Page 171 Notes
Figure 5: Eggplant deformity
B. Scrotal injuries:
1. The mobility of the testes combined with their tough, fibrous capsule make their rate of injury low. a. Penetrating injuries to the scrotum should be operatively explored. b. All blunt testicular injuries should undergo color Doppler ultrasound examination to evaluate the integrity of the testes. 2. “Testicular fracture” or rupture: a. Caused by a deforming force rupturing the tunica albuginea, which functions to protect the seminiferous tubules. b. Difficult to distinguish from a scrotal contusion or hematoma. c. Usually follows assault or sports injury. d. Risk can be as high as 50% following major blunt trauma to testicles. e. Ultrasonography aids in diagnosis, but definitive diagnosis is made surgically. f. Treatment is early surgical correction. Medically managed cases result in atrophy, necrosis, and infection.
C. Urethral trauma:
1. Urethral trauma is suggested by the presence of a pelvic fracture, blood at the urethral meatus, a high-riding or absent prostate on rectal exam, or a perineal, scrotal or penile hematoma. Also, these patients have acute urinary retention with a palpable bladder. a. A Foley catheter should never be placed if urethral trauma is suspected without first performing a retrograde urethrogram.
Urology/GU Trauma Page 172 Notes b. A retrograde urethrogram (see Figure 6) is performed by placing the end of a Toomey syringe into the urethral meatus for a snug fit and then injecting 60 mL of contrast into the urethra over 30-60 seconds. A radiograph of the length of the urethra is taken during the injection of the last 10 mL of contrast. Extravasation of contrast outside of the urethra with concomitant bladder filling distinguishes a partial urethral laceration from a complete disruption (where no contrast reaches the bladder).
Figure 6: Retrograde urethrogram
2. Anterior (10%) urethral injuries (those below the urogenital diaphragm) are usually secondary to direct trauma (e.g., kicks and straddle injuries). 3. Posterior (90%) urethral injuries (those above the UG diaphragm) are typically associated with pelvic fractures, which often cause prostatomembranous urethral disruption (sign: high- riding or absent prostate on DRE). Quick diagnosis and treatment of these injuries significantly lowers chances of incontinence and erectile dysfunction. 4. Partial urethral lacerations are usually managed with an indwelling urethral catheter. Attempted placement of this catheter in the ED is controversial. 5. Complete urethral disruption requires placement of a suprapubic catheter for bladder drainage pending definite surgical repair. 6. Urethral strictures, erectile dysfunction, and incontinence are the main long-term complications.
D. Bladder injuries:
1. Usually associated with blunt trauma, pelvic fractures, and deceleration with compression of the bladder (as in MVCs). There is a high incidence of associated life-threatening non- urologic injuries. 2. Evaluation of potential bladder injury should take place only after potential urethral injuries have been ruled out (i.e., do the urethrogram before the cystogram). 3. Suspicion of bladder injury should arise with the presence of gross hematuria, especially in the setting of a pelvic fracture. Urology/GU Trauma Page 173 Notes 98% of patients with bladder rupture have gross hematuria. 4. Symptoms are non-specific and include suprapubic pain and inability to void. 5. Retrograde cystogram or retrograde CT cystography are the diagnostic procedures of choice for suspected bladder injury. a. Retrograde cystogram is performed by allowing 300-400 mL of contrast to flow by gravity from a Toomey syringe through a Foley catheter into the bladder. If the bladder contracts before the instillation of 300 mL, 50 mL more of the contrast should be inserted with hand pressure. The Foley catheter is then clamped, and AP and lateral radiographs of the bladder taken. The Foley is then unclamped, the bladder drained, and a postevacuation film taken. b. Retrograde CT cystography is performed in the same fashion but using CT for imaging. c. With extraperitoneal bladder perforations, the extravasated dye is seen in the area of the pelvic outlet (see Figure 7) but does not enter the peritoneal cavity. d. With intraperitoneal perforations, the contrast enters the peritoneal space and outlines the intraperitoneal structures. e. Extraperitoneal bladder ruptures will usually heal spontaneously in 14 days with Foley catheter drainage. f. Intraperitoneal bladder ruptures require surgical repair.
Figure 7: Cystograms in bladder rupture
E. Ureteral injuries:
1. Rare and usually occur secondary to penetrating trauma. Often, several non-urologic injuries are also present.
Urology/GU Trauma Page 174 Notes 2. Much more likely to be iatrogenic from gynecological, vascular, or complex urological procedures. 3. Hematuria, flank pain and a palpable mass in the lower abdomen are the classic features. Often there is a delay in making this diagnosis. Hematuria is not sensitive for ureteral injury. 4. These are usually diagnosed by CT with contrast or retrograde pyelogram. IVP may be used though is less sensitive. 5. If the cause is penetrating trauma, a ureterocuteneous fistula may form. 6. Most are treated surgically.
F. Renal injuries:
1. The most common of all urologic injuries; usually due to blunt trauma. History is important to distinguish blunt from penetrating traumas. 2. More than 80% of those patients with kidney injuries have other concurrent injuries, often life-threatening. 3. Contusions account for over 90% of renal injuries. Kidney lacerations and pedicle injuries each make up <5% of all renal injuries. 4. The main indications for imaging the kidneys after blunt trauma are: a. Gross hematuria. b. Microscopic hematuria with multiple injuries or hemodynamic instability (shock). c. A mechanism that includes rapid deceleration. 5. Any penetrating trauma with the potential for renal injury warrants an imaging study, even in the absence of hematuria. Hematuria, often present, does not correlate with severity of injury. 6. CT with IV contrast is the imaging procedure of choice for potential renal injuries. IVP may be used if CT is not available or if the patient’s instability does not allow time for CT (i.e., a “one shot” IVP in the ED or OR). 7. Renal contusions are managed non-operatively. 8. Renal injuries are graded from I-V (see Figure 8, next page). Higher grade injuries are more likely to require surgical repair. 9. Indications for operative intervention for renal injuries include: a. Uncontrolled renal hemorrhage. b. Penetrating injuries. c. An avulsed major renal vessel. d. Extensive urine extravasation. e. Shattered kidney or lacerations extending through to the collecting system.
Urology/GU Trauma Page 175 Notes
Figure 8: Grades of Renal Trauma
Urology/GU Trauma Page 176 Notes
UROLOGY/GU TRAUMA
PEARLS
Urology
1. Definitive treatment of phimosis is circumcision.
2. Sickle cell anemia is the most common cause of priapism in children.
3. Color flow Doppler ultrasound of the scrotum is as accurate as radionuclide scanning and much faster to rule out torsion.
4. Don’t delay surgical exploration of a potential testicular torsion for diagnostic studies, since the salvage rate markedly decreases after 4 hours of ischemia.
5. Manual detorsion may be attempted, medial to lateral.
6. Epididymitis under age 35 is usually caused by gonorrhea or chlamydia. Over 35, E. coli is the main pathogen.
7. BPH is the #1 cause of acute urinary retention in men.
8. Patients catheterized for acute urinary retention should be observed for 4-6 hours for postobstructive diuresis.
9. Treatment of Fournier’s gangrene involves aggressive fluid resuscitation, antibiotics, and, most importantly, surgical debridement.
10. The majority of kidney stones contain calcium.
11. The most common site of ureteral stone impaction is the ureterovesical junction.
12. Helical CT is the preferred imaging study for kidney stones.
13. Ultrasound is good to diagnose ureteral hydronephrosis and obstruction. It is poor for imaging the stone itself.
14. 90% of kidney stones <4 mm in size will pass spontaneously, while only 10% of those >6 mm will.
GU Trauma
1. A retrograde urethrogram should be performed before inserting a Foley catheter if urethral injury is suspected.
Urology/GU Trauma Page 177 Notes
2. 95% of patients with bladder rupture will have gross hematuria.
3. Retrograde cystogram or retrograde CT cystography are the diagnostic procedures of choice for suspected bladder injury.
4. Extraperitoneal bladder ruptures usually heal spontaneously (with Foley catheter drainage), while intraperitoneal ruptures require operative repair.
5. Indications for imaging the kidneys after blunt trauma are: gross hematuria, microscopic hematuria in the presence of multiple injuries or hemodynamic instability, and a mechanism that includes rapid deceleration.
6. CT with IV contrast is the imaging procedure of choice for potential renal injuries.
7. The majority of renal injuries occur in the presence of other, usually life-threatening injuries.
Urology/GU Trauma Page 178 Notes
REFERENCES
1. Benway, Brian. "Bacterial Prostatitis". Urologic Clinics of North America 2008: 23-32.
2. Frenkl, Tara Lee. "Sexually Transmitted Infections". Urologic Clinics of North America 2008: 33-46.
3. Davis JE: Male Genital Problems, in Tintinalli JE (Ed. In Chief): Emergency Medicine: a Comprehensive Study Guide 8th ed., McGraw-Hill Inc., 2016, 608-609.
4. Ban KB, Easter JS: Selected Urologic Problems, in Marx JA, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice 8th ed., Elsevier Saunders, 2014, 1291-1354.
5. Nicolle, Lindsay. "Uncomplicated Urinary Tract Infections in Adults Including Uncomplicated Pyelonephritis". Urologic Clinics of North America 2008: 1-12.
6. Selius, Brian. "Urinary Retention in Adult: Diagnosis and Initial Management". American Family Physician March 1, 2008: 643-650.
7. Tracy, Chad. "Diagnosis and Management of Epidydimitis". Urologic Clinics of North America 2008: 101-108.
08/17
Urology/GU Trauma Page 179
Page 180
Stroke and Seizures
Daniel W. Robinson, MD
Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Medicine, Section of Emergency Medicine, The University of Chicago Medicine & Biological Sciences, Chicago
Page 181
Page 182 Notes
STROKE AND SEIZURES
Stroke
I. STROKE SYNDROMES
A. Anterior cerebral artery:
1. Paralysis of the opposite leg, worse than arm. 2. Sensory deficit paralleling paralysis. 3. Altered mental status; confusion. 4. Bowel or bladder incontinence.
B. Middle cerebral artery:
1. Paralysis opposite body, arm, face, worse than legs. 2. Sensory deficit paralleling paralysis. 3. Blindness in lateral half of visual field (hemianopsia). 4. Dysphasia. 5. Agnosia (inability to recognize objects).
C. Posterior cerebral artery:
1. Hemianopsia. 2. 3rd nerve paralysis. 3. Cortical blindness. 4. Altered mental status.
D. Vertebrobasilar artery:
1. Vertigo, nystagmus. 2. Facial numbness/paresthesias. 3. Contralateral loss of pain and temperature. 4. Bilateral spasticity. 5. Syncope, drop attacks.
E. Subarachnoid hemorrhage:
1. ¾ occur in the Circle of Willis-Berry Aneurysm. 2. Most occur before age 50. 3. Aneurysm, AVM. 4. 85% have headache. 5. 40% have nausea or vomiting. 6. Only 15% have meningeal signs. 7. CT scan in SAH: a. 95% of ICH can be seen on CT. b. Will miss the very small and those in the 5-9 day window. c. 90% of SAH can be seen on CT. Stroke and Seizures Page 183 Notes d. LP on all negative CT. i. Xanthochromia . e. Use of CT angiography. f. High density hemorrhage injury: i. Interhemospheric fissure. ii. Inferior frontal sulci. iii. Third ventricle. iv. Ambient cistern. v. Sylvian fissure.
II. TREATMENT
A. Nimodipine:
1. Ca channel blocker. 2. Inhibits contraction of vascular smooth muscle. 3. Greater effect on cerebral arteries: lipophilic. 4. Decreases neurological deficits in SAH. 5. 60 mg PO every 4 hours.
B. Intracerebral hemorrhage – treatment:
1. Head of the bed to 45 degrees. 2. Hyperventilation to a CO2 of 25-30 mmHg – only as temporizing measure. 3. Diuretic: mannitol 20% solution 0.25 g-1.0 g per kg. 4. If intubation is necessary, remember ICP. 5. Lower hypertensive blood pressure to a diastolic of 100-110. 6. Medications: a. Nitroprusside. b. Labetalol. c. Nicardipine. d. Esmolol. 7. Surgery: a. Usually not helpful in ICH. b. Used in large ICH to prevent herniation or hydrocephalus. c. Recommended in SAH: timing is controversial. d. Recommended in cerebellar hemorrhage.
III. TRANSIENT ISCHEMIC ATTACK (TIA)
A. Overview:
1. Focal symptoms: usually weakness or numbness. 2. Usually not: dizziness, syncope, or altered mental status. 3. Lasting < 24 hours. 4. Majority last 10-15 minutes. 5. Risks for stroke completion: a. 5% have a stroke within 48-72 hours. Stroke and Seizures Page 184 Notes b. 20% have a stroke within 1 month. c. 50% have a stroke within 5 years.
B. Ischemic stroke and tPA eligibility:
1. Age 18 or older. 2. Diagnosis of ischemic stroke with neurological deficits. 3. Time of symptom onset to drug administration less than 3 hours.
C. Exclusion criteria:
1. Similar to cardiac tPA: a. Head injury within 3 months. b. Surgery within 2 weeks. c. GI or GU bleeding within 3 weeks. 2. Currently on anti-coagulants, INR > 1.7. 3. Platelet count <100,000. 4. Improving symptoms. 5. Post treatment blood pressure >185/110. 6. Isolated or mild neurological deficits. 7. Glucose < 50 or > 400 mg/dl. 8. Recent myocardial infarction. 9. Seizure related to stroke, no longer exclusion. 10. Clinical presentation suggestive of SAH.
D. Clinical outcomes:
1. 14% absolute increase for the best clinical outcomes as measured by an NIHSS of 0-1. 2. Benefit = Need to treat 8 patients with tPA in order to have one additional patient with this best outcome. 3. 6% absolute increase in the number of symptomatic ICH. 4. Harm = will have one symptomatic ICH for every 16 patients treated with tPA. 5. 2 patients will have a minimal or no deficit for every one patient with a symptomatic ICH.
E. tPA protocol:
1. Administered within 3 hours from the onset of symptoms, not arrival in ED. 2. Head CT. 3. Blood pressure control. 4. 0.9 mg/Kg to a maximum of 90 mg. 5. 10% bolus over 1-2 min. 6. 90% infusion over 1 hour. 7. Time goals: a. Door to doctor: 10 minutes. b. Door to CT: 25 minutes. Stroke and Seizures Page 185 Notes c. Door to CT: 45 minutes. d. Door to tPA: 60 minutes.
Seizure and Status Epilepticus
I. SEIZURE CLASSIFICATION
A. Generalized: both cerebral hemispheres.
B. Partial: one cerebral hemisphere (localized).
C. Convulsive: tonic-clonic.
D. Non-convulsive: absence.
E. Primary generalized: starts as tonic-clonic seizure.
F. Secondarily generalized: tonic-clonic seizure develops from a non- convulsive partial seizure, i.e., aura (common).
G. Simple partial: no impaired consciousness.
H. Complex partial: impaired consciousness.
I. Specific types of seizures:
1. Absence: Petit mal. 2. Partial: Jacksonian, focal motor. 3. Complex partial: temporal lobe, psychomotor.
II. ALTERED MENTAL STATUS AND SEIZURE
A. Mental status should improve by 20-40 minutes.
B. If patient comatose, subtle SE is possible: EEG.
C. Up to 20% of patients in coma are still in SE.
III. STATUS EPILEPTICUS - SE
A. Definition:
1. Seizure > 5- 10 minutes. 2. Two seizures without a lucid interval (assumes ongoing seizure during coma).
Stroke and Seizures Page 186 Notes
B. Classification of SE:
1. GCSE: (Generalized convulsive SE) with tonic-clonic motor activity. 2. Non-GCSE: a. Non-convulsive SE: i. Absence SE. ii. Complex-partial SE. b. Subtle SE: i. Late generalized convulsive SE. ii. Coma, persistent ictal discharge. iii. Very grave prognosis. 3. SE mortality: a. SE mortality > 30% when seizure longer than 60 minutes. b. Underlying seizure etiology contributes to mortality.
IV. PHARMACOTHERAPY OF SEIZURES
A. Overview:
1. Benzodiazepines. 2. Phenytoin. 3. Barbiturates. 4. Other agents: a. Valproate. b. Propofol. c. Lidocaine.
B. Benzodiazepines:
1. Indirect GABA inhibition. 2. Diazepam: short acting, limited AMS and protection. 3. Lorazepam: prolonged AMS and protection. 4. Pediatric seizure: IV lorazepam limits respiratory compromise. 5. Rectal diazepam: a. Diazepam rectal gel pre-packaged for rapid use. b. Dose 0.5 mg/kg, less respiratory depression seen than with IV use.
C. Phenytoin:
1. Stabilize memb Na+ channels, regulate Ca+ + channels. 2. For generalized seizures, and SE. 3. Constant infusion over IVP. 4. Use pump to prevent comp. 5. Therapeutic at 10-20 µg/mL. 6. Oral Phenytoin load: a. 18 mg/kg oral load. Stroke and Seizures Page 187 Notes b. 64% reach 10 mg/mL levels by 8 hrs (therapeutic). Delayed absorption due to large loading, or drug prep.
D. Fosphenytoin:
1. Pro-drug, dose same as phenytoin. 2. Infuse at 150 mg/min in SE. 3. Can be given IM up to 20 cc. 4. Pruritis not allergic reaction. 5. Delayed level: 2 h IV, 4 h IM.
E. Phenobarbital:
1. GABA-inhib, effective SE Rx. 2. Infuse up to 50 mg/min. 3. 20-30 mg/kg, 10 mg/kg doses. 4. Therapeutic > 40 µg/mL. 5. Respiratory depression. 6. Hypotension.
F. Valproate:
1. Likely GABA mechanism. 2. Useful in peds, possibly SE. 3. Rate up to 300 mg/min. 4. 25-30 mg/kg, 3-6 mg/kg/min. 5. Therapeutic > 100 µg/mL.
G. Propofol:
1. Likely GABA mechanism. 2. Provides burst suppression. 3. 2 mg/kg loading dose. 4. Hypotension, acidosis, hypoventilation. 5. Rapid onset, easily reversed.
H. Midazolam:
1. GABA mechanism. 2. Equal to diazepam infusion. 3. Greater breakthrough seizure rates. 4. Less hypotension than propofol, pentobarbital.
I. Pentobarbital:
1. Likely GABA mechanism. 2. Provides burst suppression. 3. 5 mg/kg loading dose. 4. 25 mg/kg infusion rate. Stroke and Seizures Page 188 Notes 5. ICU monitoring required.
J. No IV access:
1. PR diazepam. 2. IM midazolam. 3. IM fosphenytoin. 4. Buccal, intranasal midazolam. 5. No IM phenytoin/phenobarbital.
Stroke and Seizures Page 189 Notes
STROKE AND SEIZURES
PEARLS
Stroke
1. 50% of TIAs go on to CVAs in five years.
2. Gaze is TOWARD the affected side in intracerebral lesions and AWAY from the affected side in brain stem abnormalities.
3. Cerebellar hematomas require immediate neurosurgical evaluation.
4. Pontine hemorrhages result in pinpoint pupils.
5. Anterior cerebral artery infarct produces weakness in the contralateral leg more than arms and face.
6. Middle cerebral artery infarct (the most common infarct) produces weakness in the contralateral arm and face more than the leg.
7. TIAs last less than 24 hours.
8. The easiest way to lower the intracranial pressure is to put the head on the bed at 45 degrees.
9. tPA must be administered within 3 hours of the ONSET of symptoms when treating an ischemic stroke.
10. The dose for tPA for ischemic stroke (0.9 mg/kg, max 90 mg) is different from that used to treat a myocardial infarction.
Seizures
1. SE mortality exceeds 30% when seizures occur for longer than 60 minutes.
2. SE occurs when there is a seizure of greater than 10 minutes duration or two seizures without a lucid interval.
3. CNS neuron injury can occur even if the systemic effects of seizures (fever, motor activity, hypertension) are controlled.
4. Mental status changes should begin to resolve within 20-30 minutes of a seizure. Failure of the mental status changes to begin to resolve within this time period suggests subtle SE.
Stroke and Seizures Page 190 Notes
5. Subtle SE is electrical SE without the associated motor activity. It is a late manifestation of prolonged SE and is associated with a high mortality.
6. Subtle SE can only be diagnosed by EEG monitoring. EEG monitoring should be considered with prolonged altered mental status, after neuromuscular paralysis, and with pentobarbital coma or general anesthesia.
7. All first-line therapies for seizures are about 80% effective when used quickly in appropriate doses (based on mg/kg dosing).
8. Seizures caused by INH overdoses must be treated with pyridoxine in order for control to be achieved by standard seizure therapies.
9. Alcohol withdrawal seizures are best controlled and prevented with lorazepam.
10. Seizures associated with eclampsia are best treated and prevented with magnesium sulfate.
11. Greater than 50% of psychogenic seizure patients will have at least one neurogenic seizure, such that therapy should only be withheld if the diagnosis of psychogenic seizures is confirmed clinically.
12. When IV access is not available, rectal diazepam, IM midazolam and IM fosphenytoin all can be used to control seizures.
Stroke and Seizures Page 191 Notes
SUGGESTED READINGS
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2. Marler JR, Winters Jones P, Emr M Eds: Proceedings of a national symposium on rapid identification and treatment of acute stroke. The National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland, August 1997.
OTHER REFERENCES
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19. Lyden, P, Thrombolytic therapy for acute stroke – not a moment to lose. NEJM 2008; 395:13:1393
20. Multicenter Acute Stroke Trial-Italy (MAST-I) Group: Randomized controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischemic stroke. Lancet 1995; 346: 1509-1515.
21. Multicenter Acute Stroke Trial-Europe study group: Thrombolytic therapy with streptokinase in acute ischemic stroke. NEJM 1996; 335:3: 145-150.
22. Nassissi D: Acute stroke. Emergency management and future interventions. Mt Sinai J Med 1997; 64:4-5: 241-248.
23. Porteous GH, Corry M, et al.: Emergency medical dispatcher identification of stroke and TIA victims. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:314.
Stroke and Seizures Page 193 Notes
24. Quality standards subcommittee of the American Academy of Neurology: Practice Advisory: Thrombolytic therapy for acute ischemic stroke- summary statement. Neurology 1996; 47: 835-839.
25. TenBroeke M, Vincent A, et al.: Lubeluzole: Molecular reversal of Nitric Oxide induced programed cell death. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:330.
26. The European Cooperative Acute Stroke Study (ECASS): Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. JAMA 1995; 274: 1017-1025.
27. The International Stroke Trial (IST): a randomized trial of aspirin, subcutaneous heparin, both or neither among 19435 patients with acute stroke. Lancet 1997; 349: 9065: 1569-1581
28. The NINDS rt-PA Stroke Study Group: Tissue plasminogen activator for acute ischemic stroke. NEJM 1995; 333:24: 1581-1587.
29. The NINDS rt-PA Stroke Study Group: Effect of rt-PA on ischemic stroke lesion size by computed tomography: preliminary results from the NINDS rt-PA stroke trial. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:287.
30. TOAST investigators: Usefulness of a low molecular weight heparinoid in improving outcomes at 7 days and 3 months after stroke. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:286.
31. von Kummer R, Meier D, et al.: Extent of ischemic lesion and hemorrhage in ECASS II. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:289.
32. Zhang R, Chopp M: Administration of anti-CD18 antibody extends the therapeutic window for thrombolysis in rats. 23rd International Joint Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:282.
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Stroke and Seizures Page 194
Psychiatric Emergencies
Leslie S. Zun, MD, MBA, FACEP
President, American Association for Emergency Psychiatry; Professor and Chair, Department of Emergency Medicine, Chicago Medical School; Chair, Department of Emergency Medicine, Mount Sinai Hospital, Chicago
Page 195
Page 196 Notes
PSYCHIATRIC EMERGENCIES
I. MEDICAL EVALUATION
A. Differentiate medical from psychiatric.
B. Clues in history:
1. Prior psychiatric history. 2. Medical problems. 3. History of substance use or withdrawal.
C. Physical exam:
1. Abnormal vital signs. 2. Abnormal exam. 3. Focal findings.
D. Laboratory testing:
1. New onset of mental illness. 2. Red flags of medical etiology.
II. PSYCHIATRIC EVALUATION
A. Make the patient feel comfortable.
B. Develop a rapport.
C. Ask open-ended questions.
D. Allow the patient time to reply.
E. Mental Status Exam:
1. Elements routinely assessed while interviewing patient: a. Appearance, behavior and attitude. b. Mood and affect. 2. Not routinely assessed while interviewing patient: a. Disorders of thought - suicidal and homicidal ideation. ? admit. b. Insight and judgment - knowledge about illness. c. Disorder of perception - hallucinations and delusions. d. Sensorium and intelligence - cognitive impairment. ? delirium. e. Diagnose changes in cognitive function.
Psychiatric Emergencies Page 197 Notes
III. MEDICAL ETIOLOGY
A. 1st psychotic event age < 12 or > 45.
B. Acute onset.
C. History of medical illness.
D. History of recent trauma.
E. Recent hospitalization.
F. Medication.
G. Visual hallucinations.
H. Drug or alcohol use.
I. History of incontinence, ataxia.
J. Vital signs.
K. Eye pathology: nystagmus, icterus.
L. Neurological disturbances.
M. Endocrine disease
IV. AGITATION
A. Verbal de-escalation:
1. Respect personal space. 2. Do not be provocative. 3. Establish verbal contact. 4. Be concise. 5. Identify wants and feelings. 6. Listen closely to what the patient is saying. 7. Agree or agree to disagree. 8. Lay done the law and set clear limitations.
B. Medications:
1. If the patient is willing to take the medication po, then give it. 2. Calm the patient, do not sedate. 3. Perform an agitation scale prior to medicating. 4. Tailor the medication to the underlying etiology. 5. Options: Psychiatric Emergencies Page 198 Notes a. Neuroleptics: First generation and second generation. b. Benzodiazapines: Ativan.
C. Seclusion: placing a patient alone in a locked room.
1. Monitoring. 2. Documentation of reason. 3. Specific room that is safe for the patient.
D. Physical restraints:
1. Team approach. 2. Six members. 3. Protective gear. 4. Start with four point restraints. a. Explain why to the patient. 5. Once decided, do not negotiate. 6. Undress the patient. 7. Document the reason. 8. Frequent monitoring.
E. Legality of restraints:
1. Ensure that restraints are not negligently performed. 2. 3 duties to protect from harm: a. The patient. b. The ED staff. c. Third parties.
V. SUICIDE
A. Overview:
1. 8th leading cause of death in the U.S. 2. 2nd leading cause in students. 3. 30,000 deaths/year. 4. Women 3x more likely to attempt suicide. 5. Men 3x more likely to complete suicide.
B. Screening tool - mnemonic: SAD PERSONS
S = sex (male) A = age (older) D = depression
P = previous attempt E = ethanol abuse R = rational thinking loss S = separated, widowed, divorce Psychiatric Emergencies Page 199 Notes O = organized plan N = no social supports S = sickness
C. Patient screens in, need to do suicide risk assessment:
1. Determine low, intermediate and high risk: a. Low risk can go home. b. Moderate risk needs psych eval. c. High risk needs admission. 2. Use static and dynamic factors. 3. Consider protective factors.
VI. DELIRIUM
A. Overview:
1. Inability to maintain attention. 2. Abnormal speech. 3. Decreased level of consciousness. 4. Hallucinations, often visual. 5. Change in psychomotor activity. 6. Memory impairment.
B. Causes of delirium:
1. Drugs of abuse, anticholinergics. 2. Withdrawal. 3. CNS: tumors, bleeds. 4. Infection: meningitis, sepsis. 5. Endocrine: hyperthyroidism. 6. Metabolic: hypoglycemia.
VII. DEMENTIA
A. Overview:
1. Impaired memory. 2. Change in personality. 3. Impaired judgment. 4. Insidious onset. 5. No clouding of consciousness.
B. Causes of dementia:
1. Drugs: sedatives, steroids. 2. Alzheimer’s disease. 3. Vascular = multi-infarct. 4. AIDS. Psychiatric Emergencies Page 200 Notes 5. Neurological: Parkinson’s disease. 6. Depression.
VIII. MANIA
A. Abnormal and persistently elevated, expansive, and irritable mood lasting at least one week.
B. Affective, psychiatric disorder.
C. Mean age at onset is early 20s.
D. Begins suddenly.
E. Rapid escalation of symptoms.
F. May appear pleasant, watch out.
G. Three or more of the following:
1. Inflated self-esteem or grandiosity. 2. Decreased need for sleep. 3. Extremely talkative. 4. Flight of ideas. 5. Distractibility. 6. Increased activity. 7. Dangerous activities.
IX. DEPRESSION:
A. Affective, functional disorder.
B. Disturbance in mood.
C. Most common psychiatric disorder.
D. Incidence twice as high in women.
E. 5 or more for at least 2 weeks:
1. Depressed mood. 2. Diminished interests. 3. Significant weight gain or loss. 4. Insomnia or hypersomnia. 5. Psychomotor agitation or retardation. 6. Fatigue. 7. Feeling of worthlessness. 8. Diminished concentration. 9. Preoccupation with death or suicide. Psychiatric Emergencies Page 201 Notes 10. Symptoms impair outside relationships.
F. Depression can have psychotic features.
G. Psychosis can lead to suicide.
H. Mnemonic: IN SAD CAGES
IN = interest decreases
S = sleep disorder A = appetite change D = dysphoric mood
C = concentration decreases A = affect blunted G = guilt E = energy diminishes S = suicide risk
X. BIPOLAR DISORDER
A. Cycles of both mania and depression.
XI. SCHIZOPHRENIA
A. Functional illness.
B. Gradual onset in adolescence.
C. Rare after age 40.
D. Symptoms present for 6 months.
E. Delusions.
F. Hallucinations: often auditory.
G. Disorganized thinking.
H. Disorganized behavior.
XII. ANXIETY DISORDERS
A. Overview:
1. Increasing frequency in the U.S. 2. Incidence same as depression.
Psychiatric Emergencies Page 202 Notes B. Panic attacks:
1. Period of intense fear. 2. Start suddenly and peak rapidly. 3. Imminent danger or doom. 4. Need to escape. 5. Palpitations. 6. Sweating. 7. Trembling. 8. Shortness of breath. 9. Feeling of choking. 10. Chest pain. 11. Nausea or abdominal pain. 12. Dizziness. 13. Fear of losing control. 14. Fear of dying. 15. Paresthesias. 16. Chills or hot flashes.
XIII. PSYCHIATRIC MEDICATIONS
A. Neuroleptic side effects:
1. Tardive dyskinesia: involuntary facial and oral muscle movement. 2. Neuroleptic Malignant Syndrome: hyperthermia, rigidity, altered mental status. Consider dantrolene. a. Acute Dystonic Reaction Dystonia – abnormal postures. b. Treat with diphenhydramine or benztropine. 3. Extrapyramidal symptoms: a. Parkinsonism. b. Akathisia: motor restlessness.
B. Combined dopamine and serotonin antagonists:
1. Clozapine (Clozaril). 2. Risperidone (Risperdal). 3. Ziprasidone (Geodon). 4. Olanzapine (Zyprexa).
C. Antidepressants:
1. Mono Amine Oxidase Inhibitors – MAOIs: a. Block the metabolism of norepinephrine, serotonin, dopamine. b. Phenelzine (Nardil), tranylcypromine (Parnate). c. Food and drug interactions. d. Serotonin Syndrome: i. Hyperthermia, hypertonicity, CNS depression. Psychiatric Emergencies Page 203 Notes ii. Consider cyproheptadine. 2. Tricyclic Antidepressants – TCAs: a. Block many different receptors. b. Many varieties out there. c. Adverse effects: arrhythmias, seizures, hypotension. 3. Selective Serotonin Reuptake Inhibitors – SSRIs: a. Fewest adverse effects. b. GI upset. c. Sexual dysfunction. d. Hyponatremia (SIADH).
Psychiatric Emergencies Page 204 Notes
PSYCHIATRIC EMERGENCIES
PEARLS
1. The first and most important part of assessing patients for psychiatric illness is to rule out a medical emergency, e.g., hypoglycemic, post-ictal state, drug-induced state, etc.
2. Assume medical etiology until proven otherwise, as they are potentially reversible.
3. Auditory hallucinations that are stable and fixed suggest psychiatric disease, such as schizophrenia.
4. Historical findings significant to determine a medical etiology from psychiatric.
5. Abnormal vital signs, neuro deficits, signs of autonomic excess, and delirium suggest medical etiology.
6. Red flags of medical etiology: onset after age 40, headache, recent trauma, incontinence, systemic illness, known alcohol or drug abuse.
7. Disorientation is more commonly found with medical illnesses, such as delirium; whereas psychiatric illnesses, such as schizophrenics, generally retain orientation.
8. In dealing with an agitated patient, use verbal de-escalation first in the treatment process.
9. Document the reasons for restraining the patient.
10. Restraints should always be the last resort to protect the patient and staff.
11. Depression is the most common psychiatric disorder.
12. Suicide screening is not the same as suicide risk assessment.
13. Suicide risk assessment including review of dynamic, static and protective risk factors.
14. Women attempt suicide more often than men; men complete suicide more often than women.
15. Those at greater risk for suicide include those who live alone with little social support. Teens and elderly are at greatest risk. Psychiatric Emergencies Page 205 Notes
16. Psychiatric illness and substance use are risk factors for suicide.
17. Look for evidence of a potentially violent patient: past history of violence, agitated state, verbal threats, pressured speech, and lability.
18. Patients with mania are potentially violent and frequently can have wild mood swings.
19. Delirium has a rapid onset with fluctuating symptoms during the day when missed has a high rate of mortality.
20. Dementia generally has a gradual onset.
21. Neuroleptics side effects include: autonomic anticholinergic properties, extrapyramidal side effects, dystonic reactions, tardive dyskinesia, neuroleptic malignant syndrome.
Psychiatric Emergencies Page 206 Notes
REFERENCES
1. Garland H Holloman, Jr, MD, PhD and Scott L Zeller, MD. Overview of Project BETA: Best Practices in Evaluation and Treatment of Agitation. West J Emerg Med. 2012 Feb; 13(1): 1–2.
2. Stowell KR, Florence P, Harman HJ, Glick RL. Psychiatric Evaluation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project Beta Psychiatric Evaluation Workgroup. West J Emerg Med. 2012 Feb;13(1):11-6.
3. Nordstrom K, Zun LS, Wilson MP, Md VS, Ng AT, Bregman B, Anderson EL. Medical Evaluation and Triage of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project Beta Medical Evaluation Workgroup. West J Emerg Med. 2012 Feb;13(1):3-10.
4. Knox DK, Holloman GH Jr. Use and Avoidance of Seclusion and Restraint: Consensus Statement of the American Association for Emergency Psychiatry Project Beta Seclusion and Restraint Workgroup. West J Emerg Med. 2012 Feb;13(1):35-40.
5. Wilson MP, Pepper D, Currier GW, Holloman GH Jr, Feifel D. The Psychopharmacology of Agitation: Consensus Statement of the American Association for Emergency Psychiatry Project Beta Psychopharmacology Workgroup. West J Emerg Med. 2012 Feb;13(1):26-34.
6. Violence Prevention in Emergency Medicine, Foresight, Issue 47, Winter 1997, ACEP.
7. DSM-V. Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Association, 2013.
8. Olshaker JS, Browne B, et al. Medical Clearance and Screening of Psychiatric Patients in the Emergency Department. Academic Emergency Medicine, 1997;4:124-128.
9. Armitage DT, Townsend GM. Emergency Medicine, Psychiatry, and the Law. Emergency Medicine Clinics of North America. 1993;11:869-887.
10. Hill HF III. Use of Restraints. In: Emergency Medicine Risk Management. A Comprehensive Review, 1991:381-385.
11. Tueth, MJ. Predicting Suicide in the Emergency Department. American Journal of Emergency Medicine. 1996;14:434.
Psychiatric Emergencies Page 207 Notes 12. Kane JM. Schizophrenia. New England Journal of Medicine. 1996;334:34-41.
13. Hutzler JC, Rund DA. Behavioral Disorders: Emergency Assessment and Stabilization. In: Emergency Medicine-A Comprehensive Study Guide. Tintinalli JE, Ruiz E, et al. 4th ed. 1996:1334-1340.
14. Kim SW. Panic Disorder: In: Emergency Medicine-A Comprehensive Study Guide. Tintinalli JE, Ruiz E, et al 4th ed. 1996:1348-1350.
15. Henneman, PL, et al. Prospective Evaluation of Emergency Department Medical Clearance. Annals of Emergency Medicine. 1994;24:672.
16. Hoffman DP, Dubovsky SL. Depression and Suicide Assessment. Emergency Med. Clinics of North America. 1991;9:107-121.
17. Weissman MM, et al. Suicidal Ideation and Suicide Attempts in Panic Disorder. New England J of Medicine. 1989;321:1209.
18. Patterson WM, Dohn Hospital, et al. Evaluation of Suicidal Patients: The SAD PERSON Scale. Psychosomatics. 1983;24:343-349.
19. Schmidt T. Suicide. In: Rosen P, Barkin R, et al. Emergency Medicine-Concepts and Clinical Practice. 3rd ed. 1992:2066-2072.
20. Geldmacher DS, Whitehouse PJ. Evaluation of Dementia. New England Journal of Medicine. 1996;335:330-336.
21. Hall RC, Gardner ER, et al. Physical Illness Manifesting as Psychiatric Disease. Archives of General Psychiatry. 1980;37:989-995.
22. Centers for Disease Control. Suicide Among Older Persons. JAMA. 1996;275:509.
23. Lessmeier TJ, et al. Unrecognized Paroxysmal Supraventricular Tachycardia: Potential for Misdiagnosis as Panic Disorder. Archives Internal Medicine. 1997;157-537.
24. Alexopoulos, G.S. Treatment of Agitation in Older Persons with Dementia. Postgraduate Medicine, April 1998.
25. Zun LS: Pitfalls in the care of the psychiatric patient in the emergency department. J Emerg Med. 2012;43(5):829-35.
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Psychiatric Emergencies Page 208 powerful tools to pass your Boards. 4 focused days.
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for ConCert & Qualifying Exam Prep Miscellaneous Topics
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Page 210
Pulmonary Emergencies
Victor Chan, DO
Assistant Director of Medical Student Education, Department of Emergency Medicine, OSF Saint Francis Medical Center; Clinical Assistant Professor, University of Illinois College of Medicine, Peoria
Page 211
Page 212 Notes
PULMONARY EMERGENCIES
I. ASTHMA
A. Definition:
1. A chronic, nonprogressive lung disorder characterized by increased airway responsiveness to a variety of stimuli. 2. Airway inflammation. 3. Reversible airway obstruction.
B. Epidemiology:
1. 22 million in U.S. 2. 1.5 million ED visits. 3. 500,000 hospitalizations. 4. 5,500 deaths. 5. D/I costs totaled 11.3 billion. 6. Prevalence: a. Children > adults. b. Females > males. c. African-Americans > Caucasians.
C. Disturbing trend:
1. Incidence and prevalence of asthma are increasing across all races, gender, and age strata. 2. Mortality increased in U.S. in 1980s to early ’90s. 3. Most substantial increase was among children. 4. Most common chronic disease of childhood. 5. Mortality rates in African-Americans are consistently higher. 6. Factors contributing to these trends include poor initial assessment; use of OTC medications which delays treatment; and consistent under-use of corticosteroids.
D. Pathophysiology:
1. Was historically felt to be a combination of IgE mediated and cholinergic effects. 2. Focus now is upon inflammatory response, both immediate and delayed. 3. Usually begins with some type of “trigger”: a. Allergens. b. Environmental antigens. c. Exercise. d. Menstruation. e. Medications (aspirin). f. Gastroesophageal reflux. Pulmonary Emergencies Page 213 Notes
E. Pathology:
1. Events above lead to: a. Recurrent bronchoconstriction. b. Congestion. c. Edema. d. Mucous production. 2. Chronic disease ultimately leads to cell damage and irreversible airway damage.
F. Risk factors for death from asthma:
1. History of severe/sudden attacks. 2. Prior intubation. 3. Prior ICU admission. 4. Two or more admissions in previous year. 5. Three or more ED visits in previous year. 6. Use of >2 MDI short acting B2 agonist per month. 7. Illicit drug use. 8. Recent withdrawal from systemic corticosteroids. 9. Serious psychiatric or psychosocial problems.
G. Presentation:
1. Clinical triad of wheezing, dyspnea, and cough. 2. Ominous signs: a. “Silent” chest. b. Agitation/lethargy. c. Paradoxical respirations. d. Cyanosis (very late finding due to left shift of oxyhemoglobin dissociation curve in respiratory alkalosis). e. Diaphoresis. 3. Possible signs of severe attack: a. Tachypnea. b. Tachycardia. c. Pulsus paradoxus >10. d. Accessory muscle use. e. Inability to speak >3-4 word sentences. f. PEFR <50% of P/SFB. g. ALL OF THE ABOVE MAY BE ABSENT EVEN IN A SEVERE ATTACK. 4. Poor initial predictors of severity: a. Patient’s perception of attack. b. Intensity of wheezing. c. Pulse ox.
Pulmonary Emergencies Page 214 Notes
H. Diagnostic evaluation:
1. Spirometry: a. Forced expiratory volume in 1 second (FEV1). b. Peak expiratory flow rate (PEFR) (L/s): i. Easy to perform at bedside/home. ii. Initial reading can predict disposition with >85% sensitivity/specificity. iii. Absolute number not useful; need to calculate percent of predicted (P) (based on height/weight) or percent of symptom free best (SFB). iv. Severity assessment can be made based on initial PEFR: Mild = >80% P/SFB. Moderate = 50 – 80% P/SFB. Severe = <50% P/SFB. 2. Arterial blood gas: a. Measures gas exchange, not pulmonary function; has not demonstrated usefulness in clinical decision making. b. Demonstrates ventilatory failure. 3. Chest radiography: a. Will be abnormal in 1/3 of all patients. b. Usually show concomitant disease (pneumonia, pneumothorax, etc.). 4. CBC, ESR, ECG, etc., rarely useful in acute exacerbations of patients with known disease.
I. Differential diagnosis:
1. “All that wheezes is not asthma”: a. CHF. b. COPD. c. Pneumonia. d. Foreign body. e. Tumor. f. Croup. g. Aspiration. h. Pulmonary embolism. 2. Be especially cautious in the elderly patient with no previous history of asthma/COPD/smoking: a. “Cardiac asthma”- in acute pulmonary edema, fluid in alveoli increases wall tension with collapse during inspiration/ exhalation which causes wheezing. b. Incidence greater than “new asthma” in patients >60 years. c. B-agonist induced tachycardia may increase myocardial oxygen demand and worsen ischemia.
Pulmonary Emergencies Page 215 Notes
J. Treatment:
1. Goals are to ensure oxygenation, reverse obstruction, relieve inflammation, reduce relapse, and treat concomitant disease. 2. Oxygen - always good/never bad - should be placed on patients at presentation. 3. β-agonist: a. Increase cyclic-AMP - causes bronchodilatation and increases mucociliary clearance. b. Can be β-selective or non-selective, injected or inhaled, nebulized or MDI, standard or long acting. c. Selective: albuterol sulfate, metaproterenol, pirbuterol, terbutaline. d. Non-selective: epinephrine. e. Long acting: salmeterol (Serevent), formoterol - no role in acute treatment at this time. f. Many studies demonstrate similar efficacy of using nebulized agent vs. MDI in acute exacerbation; however, MDIs require patient compliance/proper use. g. Standard dose of albuterol (adult) is 2.5 mg per nebulized treatment. h. Albuterol has R and S isomer: i. S isomer has no bronchodilatory activity and may induce bronchial hyperreactivity. ii. Levalbuterol (Xopenex): R isomer only now available but no strong evidence of superior clinical efficacy yet. iii. IV albuterol not used in U.S.; used extensively elsewhere. Efficacy is controversial. SQ epinephrine is less efficacious than nebulized albuterol. Epinephrine (SQ) should be used only in patients with inadequate ventilation for nebulizer therapy. Caution is advised in patients with heart disease. 4. Corticosteroids: a. Inhibit recruitment of inflammatory cells and release of proinflammatory mediators. b. May restore β-2 responsiveness (controversial). c. Standard of care in moderate to severe attack. d. Has been shown to significantly reduce relapse. e. Onset of action around 6 hours. f. No benefit to IV vs. oral. g. No benefit to “high dose” (>2 mg/kg prednisone). h. Standard dose (adult): i. Prednisone (40-60 mg). ii. Methylprednisolone (60-125 mg). 5. Anticholinergic agents: a. Reverse large airway bronchoconstriction and may have additive effect on β-2 response. b. Nebulized ipratropium bromide (Atrovent) is most studied Pulmonary Emergencies Page 216 Notes drug and only approved in U.S. c. Standard dose (adult) is 0.5 mg per nebulized treatment. d. Studies show that these agents are probably most efficacious in moderate to severe exacerbations. 6. Magnesium sulfate: a. Relaxes bronchial smooth muscle. b. Majority of studies show benefit of use in severe attacks. c. Dose: 1-3 gm slow IV infusion or push. 7. Heliox: a. Mixture of helium (60-80%) with oxygen (20-40%). b. Reduces gas density, airway resistance, and non-laminar flow. c. Reduces work of breathing. d. Studies on outcome data vary - consider in severe attack. 8. Leukotriene modifiers: a. Diminish bronchoconstriction. b. Zafirlukast (Accolate) and montelukast (Singulair) currently recommended for maintenance treatment. c. Use in acute exacerbations is evolving (not currently recommended for ED use), but multiple ongoing and completed trials show improved PFTs and decrease relapse with use. 9. Ketamine: a. Causes bronchodilation, so good choice as induction agent for intubation. 10. Methylxanthines: a. Mechanism of action is unclear. b. Have a very narrow therapeutic window. c. Not recommended for use in acute exacerbations at this time.
K. Ventilatory support:
1. Noninvasive (CPAP, BiPAP): a. Some data show benefit to use but no large randomized controlled studies have shown reduced intubation, relapse, etc. b. Currently not recommended as standard of care. 2. Intubation: a. <1% of asthmatics will require. b. Indications: i. Absolute - apnea, coma. ii. Relative - hypercarbia, depressed level of consciousness, exhaustion. c. Rapid sequence orotracheal intubation has lowest complication rate and highest success rate. i. Lidocaine (1.5 mg/kg) given 3 minutes prior to neuromuscular blocking agent may reduce bronchospasm. ii. Ketamine is preferred induction agent. Pulmonary Emergencies Page 217 Notes d. Mechanical ventilation: i. Need to reduce/eliminate auto-PEEP. Inhaled volume exceeds exhaled volume. Leads to air-trapping, pneumothorax, and decreased right heart filling. ii. Permissive hypercapnia (hypoventilation): Goal is to oxygenate and reduce airway pressure while tolerating increased pCO2. Low tidal volumes (5-7 cc/kg). Short inspiration/long expiration. Paralyze patient to rest muscles and reduce vent cycling. Allow elevated pCO2 to 60-80, pH to 7.1.
L. Disposition:
1. Multifactorial based on patient’s response to therapy. 2. Socioeconomic status, expectation of compliance, etc. 3. 10-20% of all patients will relapse to ED within two weeks. 4. Response to treatment using PEFR % is best clinical tool. a. Patients >70% P/SFB without persistent symptoms and with access to medication and follow-up care can be safely discharged home. b. Patients <50% P/SFB should be admitted regardless of symptoms. c. Patients with persistent symptoms and/or P/SFB between 50- 70% are in the gray zone - consider admission, close medical follow-up, or observation unit if available. Err on the side of admission.
M. Pregnancy and asthma:
1. Asthma complicates 4% of all pregnancies. 2. 35-45% of these women required hospitalization in one study. 3. Treatment generally does not change; β-agonist and corticosteroids are considered safe. 4. Hyperventilation of pregnancy: a. Leads to an expected elevation of pO2 and decrease of pCO2. b. This means that a pO2 <70 mmHg or pCO2 >35 mmHg is significant and may represent hypoxemia and/or respiratory failure in the pregnant patient.
Pulmonary Emergencies Page 218 Notes
II. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
A. Definition:
1. Best described as a spectrum of three diseases alone and in combination and their resultant pathologic condition: a. Chronic asthma (airway reaction). b. Chronic bronchitis (airway inflammation). c. Emphysema (airway collapse). 2. The combination of these entities ultimately leads to airway destruction.
B. Epidemiology:
1. In U.S., approximately 10% of those over age 55 are affected. 2. 4th leading cause of death. 3. ONLY one of the top five causes of death that is increasing in prevalence. 4. Mortality rate for women is increasing.
C. Predisposing factors:
1. Cigarette smoking accounts for 80-90% of all cases. a. Age of starting and total pack-years is predicative of mortality. b. Only 15% of all smokers develop clinically significant COPD. 2. Environmental and occupational causes are probably significantly under-recognized and under-reported. 3. Alpha1-antitrypsin deficiency is only proven genetic risk factor.
D. Pathophysiology:
1. Very complex and progressive mechanism but generally a cycle of recurrent bronchoconstriction and mucous plugging leading to airway obstruction, impaired elasticity and destruction.
E. Presentation:
1. Asthma - see above. 2. Emphysema - pink puffer: a. Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles. b. Very thin, secondary to chronic tachypnea. c. Alert, anxious. d. Pursed lips on expiration increases intraluminal bronchial pressure (auto-PEEP). e. Hunched forward, which increases accessory muscle Pulmonary Emergencies Page 219 Notes efficiency. f. Hyperresonant lungs and diminished breath sounds. 3. Chronic bronchitis - blue bloater: a. Productive cough on most days for three months over two years where other causes have been eliminated. b. Heavyset, no tissue wasting. c. Plethora and cyanosis secondary to polycythemia and hypoxemia. d. JVD and anasarca often present secondary to cor pulmonale. e. Cough, purulent sputum, rhonchi.
F. Diagnostic evaluation:
1. Clinical observation directs most treatment. 2. FEV1 is superior to PEFR in predicting outcome - multiple guidelines established in the pulmonary literature - usefulness in ED questioned. 3. ABG allows monitoring of hypercarbia, especially if patient is aware of baseline levels. 4. Pulse oximetry allows constant monitoring of oxygenation; however, most COPD patients expected to be below 95%. Comparison to patient’s baseline is most useful (with O2 on if that is normal for patient). 5. Chest radiography - will demonstrate some abnormality in most cases (hyper-inflated lung fields, decreased vascular markings) - most useful for diagnosing coexisting pathology. 6. ECG - used to diagnose concomitant cardiac disease - continuous cardiac monitoring probably more important.
G. Treatment:
1. Goals of treatment: a. Ensure tissue oxygenation. b. Assist gas exchange. c. Reverse bronchospasm. d. Treat concomitant disease. 2. Oxygen induced hypercapnia is very controversial (both its mechanism and its effect, deleterious or not, on treatment). pCO2 does rise in oxygen administration, but minute ventilation changes very little. All sources, however, suggest limiting O2 as tolerated with a goal of 60 mmHg pO2, or 90% oxygen saturation. Nasal canula or Venturi masking at a fixed FiO2 is recommended. 3. Pharmacotherapy is similar to that of acute asthma (see above). a. Increased efficacy of anticholinergics has been shown. b. Methylxanthines probably have expanded role here in acute exacerbations: i. Increases diaphragm strength. ii. Improves spirometry. Pulmonary Emergencies Page 220 Notes iii. However, data doesn’t demonstrate clinical efficacy. iv. Aminophylline - load 5 mg/kg over 10-15 minutes in acutely ill patients not previously taking (Rosen). 4. Empiric antibiotics: a. Controversial topic in acute bronchitis but most studies support their use in COPD (some texts suggest treatment in every exacerbation even in the absence of pneumonia symptoms). b. Those with signs/symptoms of CAP should be treated per protocols (see below).
H. Ventilatory support:
1. Noninvasive assisted ventilation: a. CPAP, BiPAP, IPAP recruit alveoli, reduce dead space - all have been shown to be efficacious. b. Little difference in efficacy of above in multiple studies. c. Patient must be cooperative, not vomiting, protecting airway. 2. Intubation: a. Indications are similar to asthma. b. Pressure support method has been used extensively and is described as being most comfortable for the patient and may accelerate weaning. c. Permissive hypercapnia has shown to cause the least amount of ventilator complications. d. Neither of the above has shown to improve outcome as compared with volume-cycled modes.
I. Disposition:
1. There is limited role for discharge of patients with acute exacerbation of COPD secondary to: a. Limited pulmonary reserve. b. High likelihood of comorbid disease. c. High incidence of relapse. 2. Patients considered for discharge home should have: a. Home O2 as needed. i. Adequate bronchodilator treatment with appropriate knowledge and use of device. b. Corticosteroid dosing. c. Close follow-up and/or home care. d. If available, and FEV1 of >50% predicted.
Pulmonary Emergencies Page 221 Notes
III. PNEUMONIA
A. Epidemiology:
1. 6th leading cause of death in U.S. 2. 1 million hospitalizations annually. 3. D/I cost of $23 billion per year. 4. Frequency of atypical, resistant, and opportunistic infections is increasing secondary to: a. Immunocompromised and immunosuppressive states. b. Improper antibiotic use. c. Increase in foreign travel. 5. Good news is that morbidity and mortality can be drastically reduced by prompt diagnosis and initiation of appropriate therapy in the ED.
B. Pathophysiology:
1. Organisms inhaled or aspirated. 2. Hematogenous seeding also possible but less common. 3. Inflammatory response in alveoli: a. Air space fills with WBC, bacteria, and exudate.
C. Clinical features (atypical agents follow this pattern less frequently and generally have vague symptoms):
1. Cough (80-90%). 2. Fatigue (90%). 3. Fever (75%). 4. Sputum production (60%). 5. Pleuritic chest pain (40%).
D. Predisposing factors:
1. Nursing home, chronic care residences. 2. Chronic lung disease - COPD, CHF, cancer. 3. Systemic disease - diabetes, valvular heart disease. 4. Immunocompromised states - HIV, SS, leukemia, chemotherapy. 5. Chest wall disorders - trauma, post-op pain, neuropathies. 6. Aspiration risks - intoxication, seizure, syncope, sedatives, debilitated. 7. Impaired mucociliary clearance - smoking, age. 8. Iatrogenic - indwelling catheters, bronchoscopy, intubation.
E. Patient history:
1. Very important to obtain a thorough history. 2. May give clues to etiologic agents that vary depending on Pulmonary Emergencies Page 222 Notes patient’s: a. Age. b. Comorbid disease. c. Travel. d. Season of illness. e. Symptoms.
F. Diagnostic evaluation:
1. WBC count: a. Usually not predictive of outcome or disposition. b. >15,000 increases the probability that the patient has a pyogenic bacterial etiology. c. Less useful at extremes of age - look for a left shift in the absence of elevation, especially in the elderly. d. May be most useful to look for immunocompromised state- absolute neutropenia necessitates IV therapy. 2. Sputum cultures: a. Theoretically, should be the most useful information; however, therapy must begin prior to results. b. Gram staining can be done, but correlation to ultimate culture results is poor (<40%). 3. Blood cultures: a. Again, most useful before antibiotics. b. Considered a Quality Indicator; however, few are positive and results rarely change the antibiotic chosen. 4. Chest radiography: a. Most useful diagnostic tool. b. May give important clues to causative agent while ruling in/out other pathology. i. Must be used along with clinical picture, and should never rule out diagnosis of pneumonia as symptoms usually precede radiographic findings. ii. Dehydration, leukopenia, immunocompromised states, and elderly status all delay appearance of infiltrate. 5. ABG/pulse oximetry: a. Used to determine oxygenation and ventilation status. b. Respiratory failure more common at extremes of age. 6. Tests specific for agent may be needed: a. Legionella DFA, urinary antigen testing. b. Mycoplasma ELISA testing. c. Strep pneumoniae IFA.
G. Specific etiologic agents:
1. Streptococcus pneumoniae: a. Gram+, lancet shaped, encapsulated. b. Most common cause of CAP. c. Winter and early spring. Pulmonary Emergencies Page 223 Notes d. Splenectomized/immunocompromised patients prone to severe, rapidly progressive illness. e. Drug resistant Strep is becoming much more common (15- 20% in Chicago area) (see below). f. Classic picture: i. Single shaking rigor. ii. Pleuritic chest pain. iii. Rust colored sputum. iv. Single lobar infiltrate - usually in the lower lobes or right middle lobe (effusions present in 10-25%). 2. Haemophilus influenzae: a. Gram-, pleomorphic rods, +/- encapsulated. b. Winter and early spring. c. Becoming most common in elderly and debilitated. d. Classic picture: i. Elderly or debilitated patient, possibly from nursing home. ii. Cough and severe SOB, green sputum. iii. Diffuse rales without consolidation. iv. Patchy, multilobar infiltrate. 3. Klebsiella pneumoniae: a. Gram-, encapsulated rods. b. Common in alcoholics, diabetics, COPD. c. Fall and winter. d. Upper lobe infiltrates. e. Classic picture: i. Alcoholic/non-domiciled. ii. Sudden cough with multiple shaking chills. iii. Severe SOB with cyanosis. iv. Sputum thick, progressing to currant jelly-like (thick, dark, caused by necrotizing nature of illness). v. Elevated WBC count. vi. RUL infiltrate +/- empyema. 4. Staphylococcal aureus: a. Gram+, in clumps. b. Less common but can be very severe in nature. c. Classic picture: i. Debilitated patient with antecedent mild URI. ii. Purulent sputum. iii. Hemoptysis. iv. Empyema, abscess formation. 5. Mycoplasma pneumoniae: a. Gram-, but doesn’t stain well (smallest free living organism). b. Seen often in older children and young adults. c. Classic picture: i. Adolescent. ii. Prolonged constitutional symptoms: arthralgias, cephalgias, ear ache, URI, bullous myringitis. iii. Diffuse rhonchi, possibly wheezing. Pulmonary Emergencies Page 224 Notes iv. Diffuse interstitial infiltrate, sometimes with bilateral lower lobe small consolidations or effusions. 6. Legionella pneumophila: a. Summer/fall. b. Smokers, diabetics, COPD, immunocompromised, those who sleep or work near incubation sites such as cooling towers, compressors. c. Probably underdiagnosed and more common cause of CAP than expected. d. Male > females. e. Gastrointestinal symptoms very common. f. Classic picture: i. Middle aged male, smoker. ii. Multiple constitutional symptoms - fever, cough, cephalgia, diaphoresis, arthralgias. iii. Severe nausea and watery diarrhea. iv. Progresses to confusion/mental status change. v. High fever with relative bradycardia. vi. Lower lobe patchy infiltrate - 30% may have effusions. 7. Chlamydia pneumoniae: a. Now called Chlamydophile pneumoniae. b. Obligate intracellular parasite - positive or negative but usually not well seen in gram stain. c. Probably accounts for 8-10% of all CAP but underdiagnosed due to difficulty in isolating. d. Classic picture: i. Similar to Mycoplasma - multiple constitutional symptoms. ii. Mucoid green sputum. iii. Focal infiltrate. 8. Viral pneumonias: a. Influenza A and B. b. Often responsible for outbreaks (especially nursing homes). c. Usually self limiting, but may cause secondary bacterial pneumonia. d. Classic picture: i. Fever, myalgias, coryza, non-productive cough. ii. Diffuse patchy infiltrates. iii. Treatment with antiviral medications is usually only indicated in patients with severe underlying illness, immunocompromised states, or with evidence of severe disease (hypoxia). Must be initiated in first days of illness to be effective. 9. Animal exposure and pneumonia: a. Bat caves = Histoplasma capsulatum. b. Turkeys, ducks, chickens = Chlamydia psittaci. c. Rabbits = Francisella tularensis. d. Cattle, sheep, goats = Coxiella burnetti 'Q fever' e. Rodent feces = hantavirus. Pulmonary Emergencies Page 225 Notes 10. Aspiration pneumonia: a. Is separate and secondary entity of ‘aspiration,’ which is the inhalation of ingested material and/or gastric contents causing a local inflammatory response. b. Classic picture: i. Debilitated patient with impaired glottic reflex or receiving tube feedings. ii. Choking or spasmodic cough productive of very foul smelling sputum. iii. RLL infiltrate is most common if patient was upright when he/she aspirated. iv. Anaerobic coverage needed (ESFQ, clindamycin, ticarcillin, piperacillin). c. Prevention is key: i. Debilitated patients should be placed upright. ii. Prokinetic agents and antacid should be used. iii. If observed, immediate bronchoscopy to remove large material. d. Antibiotic treatment prior to symptoms is controversial. e. Steroids are not indicated and have shown to be of no benefit. 11. Nursing home acquired: a. Higher incidence of Chlamydia pneumoniae. b. Influenza outbreaks leading to S. aureus, Klebsiella. 12. Nosocomial acquired: a. Higher incidence of Klebsiella and Pseudomonas species.
H. Disposition criteria:
1. Multiple guidelines have been developed to predict severity (Pneumonia Severity Index, CURB 65) but these should not supersede clinical judgment. 2. Absolute indications for admission are: a. Severe hypoxia. b. Immune compromised state. c. Failed appropriate outpatient treatment. d. Unable to tolerate p.o. antibiotics. 3. Relative criteria for admission are: a. Comorbid disease. b. Limited supportive care. c. Elderly.
I. Treatment:
1. Empiric treatment recommendations have been set forth by numerous organizations including: a. American Thoracic Society. b. Centers for Disease Control and Prevention. c. Infectious Disease Society of America. d. Antibiotic Selection for CAP 2010 Consensus Report. Pulmonary Emergencies Page 226 Notes 2. There is general but not absolute consensus in these reports. 3. Previously from 2005: recommendations all generally accept the following: a. Atypical organisms are increasing. b. Drug resistant S. pneumo considered. c. Early administration is key to reduce morbidity and mortality. d. Based on age, comorbid factors, etc. e. Now divided into 2 broad classes: i. Community Acquired (CAP). ii. Health Care Associated (HCAP). 4. CAP vs. HCAP: a. Acute care hospital > 1 days in last 90 days. b. Nursing home residence in last 90 days. c. Output chemo or abx in last 30 days. d. Home wound care in last 30 days. e. Dialysis center in last 30 days. f. Known close contact with MRD organism.
CAP Treatment Recommendations
First Alternative Outpatient Healthy <60 y.o Azithromycin Clarithromycin ESFQ, Doxycycline Erythromycin
>60 y.o. Pcn + β-lactam inhib ESFQ Comorbid disease Plus a macrolide
Inpatient Non-ICU 3rd Gen Ceph ESFQ Plus a macrolide
5. Newest update: 2016 IDSA/ATS Guideline Update, which addresses VAP/HAP: a. Coverage for MDR in VAP/HAP: i. IV Abx use in last 90 days. ii. Chronic structural lung dx. iii. Septic shock. iv. Intubated. b. Inflammatory markers such as CRP and ESR should not be used to guide initiation of therapy. c. Double coverage for pseudomonas is no longer recommended unless patient is in septic shock or has structural lung disease. d. Check local sensitivities to guide treatment. e. Did not specifically address HCAP; expected to be grouped with CAP update in 2017.
Pulmonary Emergencies Page 227 Notes
IV. TUBERCULOSIS
A. Epidemiology:
1. 6 percent of deaths worldwide. 2. Leading infectious cause of death above age 5. 3. Increase in U.S. from 1984-1992: a. HIV predominant. b. Homeless, drug abuse, immigration. c. Multi-drug resistance. d. Receiving immunosuppressive therapy (TNF inhibitors). 4. Control programs improved in 1992. 5. Yr 2000 = 16,377 cases.
B. Pathophysiology:
1. Mycobacterium tuberculosis: a. Slow-growing aerobic rod. b. Acid-fast property. c. Transmission through inhalation of droplet nuclei. 2. Host defense: a. Immune-competent: i. Rare - all organisms killed in lung. ii. Usual - transport to regional lymph nodes: Tubercles (granulomas) formed by Macrophages. Tubercles are evidence of primary infection. May necrose and calcify -> Ghon complex. b. Some organisms spread through body: i. Remain dormant in low oxygen areas. ii. Latent infection. iii. + Tuberculin test. 3. Immune-compromised: a. Latent infection may reactivate when host’s immune system can no longer contain foci of spread: i. 5% within 2 years of primary infection. ii. 5% over lifetime. iii. 7-10% in HIV +. b. At risk groups: i. Extremes of age. ii. Immune compromised disease states. iii. Cancer of solid organs. iv. Leukemia. v. Transplant patients. vi. DM. vii. Renal failure. 4. Clinical features: a. Primary infection:
Pulmonary Emergencies Page 228 Notes i. Usually asymptomatic and identified by purified protein derivative (PPD). ii. Can be a pneumonitis. iii. In immune-compromised, may be rapidly progressive and fatal. b. Reactivation: i. Systemic: Fever. Night sweats. Malaise, fatigue. Weight loss. ii. Pulmonary: Hemoptysis. Cough. Pleurisy. Dyspnea. c. Miliary TB - results from initial wide hematogenous spread during primary infection with seeding of multiple organs: i. Hepato- and splenomegaly. ii. Diffuse lymphadenopathy. iii. Pancytopenia. iv. Hyponatremia. v. CXR shows numerous small nodules. d. CNS - tubercles can form in meninges during primary infection – Rich Foci: i. Rupture of Rich Foci- tuberculous meningitis. ii. CSF may show low glucose and mononuclear cells. 5. Diagnosis: a. Tuberculin skin test (Mantoux) - subcutaneous injection of 0.1 ml of PPD: i. Delayed-type hypersensitivity reaction. ii. Read at 48-72 hours - positive if: >5 mm in immune-compromised host, suspicious CXR, or individual in close contact with TB patient. >10 mm in IV drug user, high prevalence groups, chronic lung disease, children< 4 year old. > 15 mm in general healthy population. b. Chest radiograph - use as screening tool after positive PPD or patient with signs/symptoms of disease. c. Primary infection - parenchymal infiltrates, isolated hilar or mediastinal adenopathy. d. Reactivation - cavitary and non-cavitary lesions of the upper lobe of the lung. e. Microbiology: i. Gold standard - blood or sputum for culture. ii. Acid-fastness may provide presumptive diagnosis but 40% of culture + are AF neg. 6. Treatment: Pulmonary Emergencies Page 229 Notes a. 2016 CDC recommendations: i. Four regimens are recommended: Minimum of four drug therapy for 2 months (INH, EMB, PZA, RIF). Continued 2 drug therapy for 4 months. All regimens maintain INH (Isoniazid) and Rifampin or Rifapentine throughout treatment. ii. Choice of regimens based on patient compliance, local practices. iii. All therapy is prolonged in immune-compromised patients. iv. Hepatitis is the most common side effect (INH, RIF, PZA). b. Multi-drug resistance: i. Peaked during TB resurgence and most cases were co- infected with HIV. ii. Incidence now decreasing with improved surveillance. iii. Foreign-born persons currently account for >70% of new cases. iv. Most treatment regimens involve 4-6 drugs for 18-24 months.
V. HEMOPTYSIS
A. Expectoration of blood from the respiratory tract below the level of the larynx:
1. Most cases are not life-threatening, but frightening to patients. 2. Cause is not identified in up to 25% of patients. Mild = < 20 ml in 24 hours; moderate = 20-600 ml; severe = > 600 ml.
B. Epidemiology:
1. 25% rule: a. In industrialized countries: i. 25% = infectious (non-tubercular). ii. 25% = neoplasm. iii. 25% = miscellaneous (identified cause, not a or b). iv. 25% = idiopathic (no identified cause, sometimes referred to as cryptogenic hemoptysis). 2. These percentages vary by patient demographic. a. Risk factors for neoplasm: i. Male (60/40). ii. Smoking. iii. Age >40. b. Rare in children: i. Cystic fibrosis. ii. Congenital heart disease.
Pulmonary Emergencies Page 230 Notes iii. Infection.
C. Common causes of hemoptysis:
1. Infectious - bronchitis, pneumonia, lung abscess, tuberculosis. 2. Neoplastic - lung cancer, bronchial adenoma. 3. Cardiovascular - pulmonary embolism, mitral stenosis, congestive heart failure, pulmonary hypertension. 4. Alveolar hemorrhage syndromes - Beçhet syndrome, Goodpasture syndrome, Wegener granulomatosis. 5. Hematologic - uremia, platelet dysfunction, anticoagulant therapy. 6. Traumatic - foreign body aspiration, ruptured bronchus. 7. Iatrogenic - bronchoscopy, lung biopsy. 8. Inflammatory - cystic fibrosis, bronchiectasis.
D. Diagnosis:
1. Chest radiograph: a. 70% will be abnormal in all cases. b. 80-90% abnormal in patients with neoplasm. 2. CT - limited data suggest CT is more efficient than bronchoscopy at identifying cause and has significantly lower complications. 3. Bronchoscopy - allows for biopsy, and better identifies luminal tumors.
E. Treatment:
1. Immediate airway stabilization as needed: a. 8.0 ETT or larger to allow bronchoscopy. b. If bleeding is massive, advancement of ETT into mainstem bronchus of non-bleeding lung. 2. Position patient with bleeding lung down to minimize soiling of normal lung. 3. Bronchoscopy as needed. 4. Antibiotic/antiviral/antitubercular treatment as needed. 5. FFP or platelet concentrates to correct any identified coagulopathies. 6. Cough suppression with codeine or opioids. 7. Emergency consultation with pulmonologist and/or thoracic surgeon. 8. Bronchial artery embolization.
Pulmonary Emergencies Page 231 Notes
PULMONARY EMERGENCIES
PEARLS
Asthma
1. Defined as reversible airway obstruction secondary to an inflammatory response.
2. Incidence is increasing across all strata, highest among children. Mortality rates higher in African-Americans.
3. Usually begins with some type of trigger.
4. Patient’s perception of exacerbation, intensity of wheezing, and pulse oximetry are poor predictors of severity.
5. Bedside spirometry at presentation can predict response/disposition with >85% sensitivity and specificity. Chest radiography usually shows concomitant disease.
6. ABG is usually not useful in clinical decision-making.
7. Nebulized Beta specific agonist much more efficacious than Beta non- specific given SQ.
8. R isomer of albuterol available, but no strong evidence of clinical superiority.
9. Corticosteroids and anticholinergics should always be used in moderate to severe exacerbations. Steroids should be started early secondary to lag in response time.
10. Leukotriene modifiers may develop role in acute exacerbations.
11. Magnesium and Heliox should be considered in severe exacerbations.
12. Mechanical ventilation by permissive hypercapnia should be used; goal is to reduce auto-PEEP.
13. Disposition should be based on response to therapy by spirometry measurement and compared to predicted or symptom free best.
14. Treatment does not change in the pregnant patient.
Pulmonary Emergencies Page 232 Notes
COPD
1. Is a spectrum of diseases including chronic asthma, chronic bronchitis, and emphysema.
2. Is the only one of the top five causes of death increasing in prevalence.
3. Cigarette smoking accounts for 80-90% of cases but only 15% of all smokers develop clinically significant disease.
4. The emphysema patient (pink puffer) develops increasing lung destruction, expanding chest cavity, weight loss, and sits hunched forward with pursed lips.
5. The chronic bronchitis patient (blue bloater) develops polycythemia, plethora and cyanosis, hypertension, and cor pulmonale.
6. FEV1 is best tool to predict outcome.
7. Chest radiography will be abnormal in most cases.
8. Oxygen administration should be limited to keep patient’s pO2 greater than 60 mmHg.
9. Pharmacotherapy similar to asthma.
10. Methylxanthines probably efficacious in these patients.
11. Liberal use of empiric antibiotics probably warranted.
12. Non-invasive assisted ventilation very useful to recruit alveoli and reduce dead space.
13. Limited role for discharge of patients in acute exacerbation.
Pneumonia
1. Frequency of atypical, resistant, and opportunistic infections is increasing.
2. Morbidity and mortality can be drastically reduced by early recognition and intervention.
3. History can give important clues to etiologic agent involved.
4. Sputum cultures always recommended but EP must begin empiric therapy prior to results.
Pulmonary Emergencies Page 233 Notes 5. Chest radiography may give important clues to etiology.
6. Streptococcus - single shaking rigor, rust colored sputum, pleuritic chest pain.
7. Haemophilus - debilitated, green sputum, diffuse rales.
8. Klebsiella - alcoholic, multiple chills, cyanosis, high WBC count, currant jelly sputum.
9. Staphylococcus - debilitated patient after mild URI, purulent sputum, empyema.
10. Mycoplasma - young adult, constitutional symptoms, bullous myringitis.
11. Legionella - gastrointestinal symptoms, mental status change, relative bradycardia.
12. Chlamydia - constitutional symptoms, mucoid green sputum.
13. Nosocomial and nursing home patients have higher incidence of Klebsiella, Pseudomonas, Chlamydia, and Influenza outbreaks.
14. Empiric treatment early is key; must include atypical coverage.
Tuberculosis
1. Increase in cases in 1980s due to HIV epidemic.
2. Host defense leads to formation of tubercles and dormant organism in low oxygen areas.
3. Latent infection reactivates in immune-compromised states.
4. Primary infection is usually asymptomatic and identified by PPD.
5. TB skin test is read differently for different at-risk groups. The greater the risk of disease, the smaller the induration needs to be for positive.
6. CDC suggests multiple regimens based on patient compliance; all utilize 3-4 drugs initially and INH and Rifampin/Rifapentine throughout therapy.
Pulmonary Emergencies Page 234 Notes
7. Hepatitis is the most common side effect of therapy.
8. Immune-compromised patients and those with muti-drug resistant strains require prolonged therapy.
Hemoptysis
1. Most cases are not life-threatening.
2. 25% of cases are neoplasm.
3. Chest radiograph will be abnormal in ¾ of patients.
4. Immediate airway stabilization is most important treatment in life- threatening cases.
Pulmonary Emergencies Page 235 Notes REFERENCES
1. Marx JA, Hockberger RS, Walls RM, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 7th edition.
2. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 7th edition.
3. Harwood-Nuss A, Wolfson AB, et al. The Clinical Practice of Emergency Medicine, 5th edition.
4. Emergency Medicine. The Core Curriculum. 2008.
5. Rivers CS, et al. Preparing for the Written Board Exam, 6th Edition.
08/17
Pulmonary Emergencies Page 236
Environmental Emergencies
Jay Sharp, MD, FACEP, FAWM
Emergency Medicine Board Review Intensive Course Committee; Core Faculty, Emergency Medicine Residency, and Attending Physician, Presence Resurrection Medical Center, Chicago
Page 237
Page 238 Notes
ENVIRONMENTAL EMERGENCIES
I. HIGH-ALTITUDE ILLNESS
A. General characteristics:
1. The environment at altitude: a. Decreased barometric pressure. b. Decreased partial pressure of O2. c. Hypobaric hypoxia. d. Physiologic responses: Increased ventilation, RBC production, BP/HR/CO. 2. Incidence of altitude illness is dependent on: a. Rate of ascent. b. Final altitude. c. Sleeping altitude. d. Duration at altitude. e. Individual susceptibility. 3. AMS incidence: a. Up to 67% incidence with rapid ascent (1-2 days) >14,000 ft. b. 0% incidence for skiers visiting resorts and sleeping < 9000 ft. c. 15-20% of people that ascend to 8500-9000 feet from sea level in one day. 4. HAPE (High Altitude Pulmonary Edema) incidence: a. <1-2%. b. Affects 0.01% skiers in Colorado (8-12,000 ft) each year. c. 1 in 50 climbers of Mt. McKinley (20,000 ft). d. Varies with rate of ascent. 5. HACE (High Altitude Cerebral Edema) incidence <1%.
B. Clinical manifestations:
1. Acute mountain sickness (AMS): a. Signs and symptoms: i. Generally benign and self-limited. ii. Symptoms may become debilitating. iii. Onset 4-12 hours after ascent. iv. Headache. v. Anorexia/nausea/vomiting. vi. Fatigue. vii. Weakness. viii. Dizziness. ix. Lightheadedness. x. Difficulty sleeping due to periodic breathing. xi. Presence of ataxia a useful sign of progression of AMS to HACE. b. Differential diagnosis: Environmental Emergencies Page 239 Notes i. Viral syndrome. ii. Exhaustion. iii. Alcohol hangover. iv. Carbon monoxide poisoning. c. Treatment: i. Mild cases usually self-limited. ii. Symptomatic treatment. iii. Halt ascent until symptoms resolve. iv. Oxygen – in severe cases; 2L/min by mask/NC especially at night. v. Simulated descent with Gamow Medical Tent. vi. Acetazolamide: Drug of choice for prevention and treatment. Mechanism: •• At higher elevations, arterial oxygenation decreases, resulting in hyperventilation and a pronounced respiratory alkalosis that limits the medullary respiratory center’s response to fully compensate for hypoxemia. •• Causes renal excretion of bicarbonate. •• Improves ventilatory response to the high altitude and thus arterial oxygenation. •• Combats fluid retention. 75% effective in preventing AMS at 14,000 feet. Dose – 125-250 mg BID starting 24 hrs prior to ascent. Aspirin or acetaminophen for headache. Prochlorperazine for nausea. vii. Dexamethasone: Effective in prevention/treatment. Used only for treatment due to possibilities of side effects. Dose 4-8 mg QID. d. Prevention: i. Graded ascent – climb high, sleep low. ii. Avoid increase in sleeping altitude greater than 2,000 feet when over 8,000 feet. iii. Acetazolamide for prevention. iv. Avoid alcohol and sleeping pills. 2. High-altitude cerebral edema (HACE): a. Signs and symptoms: i. Life-threatening. ii. Occurs in presence of AMS or HAPE: Seen rarely as an isolated entity. iii. Onset: May occur 12 hours after the onset of AMS. Usually requires 1-4 days for development. iv. Ataxia. Environmental Emergencies Page 240 Notes v. Severe headache. vi. Altered mental status (confusion/drowsiness/stupor/ coma). vii. Nausea/vomiting. viii. Seizure. ix. Focal neurologic deficit. b. Differential diagnosis: i. Cerebrovascular accidents/transient ischemic attacks. ii. Focal neurologic signs suggest a vascular lesion. c. Treatment: i. ABCs. ii. Immediate evacuation to lower altitude. iii. Oxygen - 2-4 L/min. iv. Dexamethasone - 4-8mg IV/IM/PO. v. Bed rest with elevation of head at 30 degrees and in severe cases, aggressive management of elevated intracranial pressure. 3. High-altitude pulmonary edema (HAPE): a. Pathophysiology: i. Noncardiogenic pulmonary edema. ii. Precise pathophysiology unknown; combination of alveolar leakage with overperfusion; impaired endothelial/epithelial barrier; intense pulmonary artery vasoconstriction causing pulmonary hypertension. b. Signs and symptoms: i. Fatigue. ii. Weakness (occurs 2-4 days after ascent). iii. Dyspnea at rest (early). iv. Cough (dry at first, then productive). v. Tachypnea. vi. Rales – first heard in right axilla. vii. Cyanosis. viii. Severe respiratory distress and death may occur. c. Radiographs: i. CXR in HAPE: Reveal fluffy (alveolar) infiltrates which are patchy in distribution, with areas of clearing between the patches; peripheral location rather than central. Unilateral or bilateral infiltrates (right midlung field being most common). X-ray findings generally correlate with severity of disease and degree of hypoxemia. Cardiomegaly, bat-wing distribution of infiltrates, and Kerley B lines (typical of cardiogenic pulmonary edema) are absent in HAPE. d. Differential diagnosis: i. Pneumonia. ii. High-altitude bronchitis and pharyngitis.
Environmental Emergencies Page 241 Notes iii. Pulmonary embolism: More rapid onset. Pleuritic chest pain. e. Treatment: i. ABCs: Endotracheal intubation for impending respiratory failure, hyperventilation or airway protection. Continuous positive airway pressure (CPAP). ii. Supplemental oxygen: Lowers pulmonary artery pressure and respiratory rate. Raises oxygen saturation. iii. Descent: Immediate descent for moderate/severe symptoms. iv. Mild cases may be managed without descent if: Lowers pulmonary artery pressure. Adequate oxygen supplies available. Serial medical examinations possible. Immediate descent for any deterioration in clinical status. v. Bed rest (to avoid exercise-induced pulmonary hypertension). vi. Medications: Sildenafil (Viagra®): •• Selective phosphodiesterase-5 inhibitor. •• Reduces pulmonary hypertension at rest and during exercise while maintaining gas exchange and systemic blood pressure. Nifedipine: •• For prevention and treatment. •• Lowers hypoxic pulmonary hypertension by reducing pulmonary vascular resistance. •• Does not quickly improve oxygenation. Lasix, morphine, acetazolamide used with varying success.
A. General characteristics:
1. Gas laws: a. Henry’s law: i. Amount of gas that will dissolve in a solution is directly proportional to the partial pressure of that gas. ii. Increases in partial pressure result in larger amount of gas dissolved in tissue. iii. Decreases in partial pressure result in gas coming out of solution. Environmental Emergencies Page 242 Notes b. Dalton’s law: i. Total pressure exerted by a mixture of gases is equal to the sum of the partial pressure of each of the component gases. c. Sequence: i. Increases in ambient pressure cause an increase in partial pressure of nitrogen inspired. ii. Nitrogen accumulates in the tissues in higher and higher concentrations the longer pressures remain elevated. iii. Decompression sickness (DCS) results when ambient pressure keeping nitrogen in solution decreases too rapidly on ascent, preventing gradual removal of the excess body burden of nitrogen. iv. As the nitrogen removal gradient is overwhelmed, tissues become supersaturated, and bubble formation occurs. 2. Etiology: a. Bubble location determines clinical effects: i. Blood flow obstruction and tissue ischemia from intravascular bubbles. ii. Tissue distention and compression from interstitial bubbles. iii. Compression of arterioles, nerves, and lymphatics. iv. Endothelial damage leading to stimulation of coagulation and clotting cascades. v. Bubbles sensed as foreign by host defenses lead to the release of chemotactic and other factors. b. Risk factors for DCS: i. Greater depth, longer bottom time, and quicker rate of ascent. ii. Use of dive tables/computers do NOT eliminate DCS. iii. Increased incidence with age and weight (body fat), hypothermia, dehydration, exercise, multiple dives in a day. c. Airplane flight can precipitate DCS due to lower cabin pressure.
B. Clinical manifestations:
1. Signs and symptoms: a. Cutaneous: i. Scarlatiniform, erysipeloid or mottled rash. ii. Peau d’orange appearance due to lymphatic obstruction. b. Musculoskeletal: i. Pain: Classic bends. Dull deep aching.
Environmental Emergencies Page 243 Notes Often in a joint (elbow and shoulder most common). Not exacerbated by movement or reproduced with palpation. No external physical signs. c. GI: i. Nausea/vomiting. ii. Abdominal pain. d. Pulmonary: i. Dyspnea. ii. Chokes (triad of substernal pressure, cough, dyspnea): Due to large bubbles in the pulmonary tree. e. CNS: i. Weakness/fatigue. ii. Numbness/paresthesia. iii. Agitation. iv. Headache. v. Dizzy. vi. Vertigo. vii. Convulsion. viii. Bowel/bladder incontinence. ix. Lethargy. x. Visual disturbance. xi. Staggers: Vestibular system and the posterior column involvement. f. Time after surfacing to presentation of DCS: i. 50% - symptoms within 1 hour. ii. 95% - symptoms within 12 hours. iii. 60% of neurologic DCS within 10 minutes. 2. Treatment: a. ABCs. b. Provide normobaric (100%) oxygen via mask or ETT: i. Increase inert gas (nitrogen) elimination from the tissues reducing gas bubble size. ii. Increase oxygen delivery to the injured tissue. c. Early recompression in hyperbaric chamber: i. For all DCS except for cutaneous. ii. Arrange transportation to nearest hyperbaric facility. iii. Aircraft capable of full pressurization of flight below 1,000 feet are best suited for transfers. iv. Prophylactic chest tube for simple pneumothorax to prevent conversion to tension pneumothorax. v. Fill endotracheal and foley catheter balloons with water or saline to avoid shrinkage/damage during recompression. d. IV rehydration with 0.9% NS: i. Diver usually dehydrated due to diuretic effect of pressure, exercise, breathing dry compressed air.
Environmental Emergencies Page 244 Notes ii. Increased fluid assists with off-gassing and dissolution of nitrogen. e. Water recompression: i. Returning injured diver/patient to a depth where symptoms are ameliorated. ii. Extremely difficult. iii. Need large amount of surface support. iv. Controversial. v. Use as a last resort only. f. Divers Alert Network (DAN): i. Based at Duke University Medical Center. ii. Provides a 24 hour emergency hotline for medical consultation on the treatment of dive related injuries and for referrals to hyperbaric chambers. www.diversalertnetwork.org 800-446-2671. 919-684-4DAN (4326).
III. BAROTRAUMA
A. General characteristics:
1. Injury to the body as a result of the expansion and contraction of gas in an enclosed space. 2. Boyle’s law states that at a constant temperature, pressure (P) is inversely related to volume (V): a. PV=K (constant) or P1V1=P2V2. b. Increase of pressure mandates a reduction of volume by same factor. 3. Gas filled cavities in the body subject to expansion/ contraction: a. Lung. b. Middle ear. c. Sinus. 4. Solid and liquid filled spaces distribute the pressure equally. 5. Volume changes experienced during ascent are greatest in the few feet nearest the surface. 6. Key points: a. For barotrauma of descent, unless an air filled cavity has ruptured, no progression of the disease expected upon return to normal atmospheric pressure. b. If patient transport requires air evacuation, maintain air cabin pressure at one atmosphere or fly below 1,000 feet to avoid aggravating barotrauma.
Environmental Emergencies Page 245 Notes
B. Clinical manifestations:
1. Middle ear (barotitis media): a. General: i. Barotrauma of descent. ii. Most common type of barotrauma. iii. Seen in 30% of inexperienced divers and 10% of experienced divers. iv. Results from inadequate equalization of pressure between the middle ear and the external ear canal. v. Eustachian tube provides the sole route of pressure equalization for the middle ear. b. Signs and symptoms: i. Begins as a clogged sensation. ii. Increasingly painful as the pressure differential across the tympanic membrane (TM) increases. iii. Progresses to rupture of the TM. iv. Tympanic membrane appearance: Teed Grading System: 0 – Symptoms without otologic findings. 1 – Erythema and mild retraction of the TM. 2 – Erythema of the TM with mild hemorrhage within the TM. 3 – Gross hemorrhage throughout the TM. 4 – Grade 3 changes plus gross hemorrhage within the middle ear (hemotympanum). 5 – Free blood in middle ear plus TM perforation. c. Treatment: i. Decongestants. ii. Antihistamines for allergic component. iii. Antibiotics for TM rupture. iv. Prevent with decongestants prior to dive. 2. Inner ear/ labyrinthine window rupture: a. General: i. Barotrauma of descent. ii. Results from forceful attempts at equalizing middle ear pressure. iii. Increased middle ear pressure can raise intracranial pressure and cause rupture of the round or labyrinth windows allowing perilymph to enter the middle ear. b. Signs and symptoms: i. Sudden, severe vertigo, disorientation during dive. ii. Tinnitus. iii. Sensorineural hearing loss in the affected ear. iv. Nystagmus. c. Treatment: i. Bed rest. ii. Avoidance of straining.
Environmental Emergencies Page 246 Notes iii. Prompt surgical repair advocated by some. 3. Mask squeeze: a. General: i. Barotrauma of descent. ii. Air volume in mask decreases with increasing ambient pressures, resulting in rupture of capillaries. iii. Easily prevented by exhaling through nose into mask to equalize pressures. b. Signs and symptoms: i. Skin ecchymosis. ii. Subconjunctival hemorrhage. iii. Lid edema. iv. Hyphema – rarely. c. Treatment: i. Most cases are asymptomatic. ii. Resolves spontaneously after days to weeks. iii. Cold compresses and analgesics if needed. 4. Paranasal sinuses: a. General: i. Barotrauma of descent. ii. Nasal ostia act as a valve to regulate sinus pressure. iii. If the ostia fail to allow pressure equalization, congestion, edema, and hemorrhage can occur. b. Signs and symptoms: i. Sinus congestion. ii. Pain. iii. Epistaxis. c. Treatment: i. Decongestants. ii. Antibiotics for severe cases. 5. External objects: a. General: i. Air pockets in dive suit/mask expand/contract. b. Signs and symptoms: i. Tight fitting dive suit – edema and erythema of the skin. c. Treatment – none; resolves with time. 6. Teeth (barodontalgia): a. General: i. Air trapped inside a filling. ii. Can occur with ascent or descent. b. Signs and symptoms: i. Severe tooth pain. 7. Gastrointestinal (aerogastralgia): a. General: i. Barotrauma of ascent. ii. Swallowed air in the GI tract expands as external pressure decreases. b. Signs and symptoms: i. Excessive belching. Environmental Emergencies Page 247 Notes ii. Flatulence. iii. Abdominal distention. 8. Pulmonary (Pulmonary Overpressurization Syndrome): a. General: i. Occurs with ascent. ii. Lungs expand against a closed glottis. iii. Cause for arterial gas embolism [see below]. iv. Divers with decreased lung compliance/increased lung volumes at increased risk (COPD, asthma). b. Signs and symptoms: i. Dyspnea. ii. Cough with frothy red sputum; subcutaneous emphysema. iii. Delayed symptoms including a bull neck appearance, dysphagia, and changes in voice character. iv. Specific clinical manifestations depend on the location and amount of air that accumulates: Pneumomediastinum. Pneumothorax. Tension pneumothorax. c. Treatment: i. Treatment varies based on clinical findings and severity of injury. ii. 100% oxygen for ill-appearing patients. iii. Intubation for patients with massive subcutaneous emphysema of the neck. iv. Immediate needle thoracostomy for evidence of tension pneumothorax.
IV. ARTERIAL GAS EMBOLISM
A. General characteristics:
1. Extreme manifestation of pulmonary barotrauma. 2. Overpressurization of lung tissue causes pleural tear with air entering the vascular circulation: a. Air bubbles tend to rise and enter the cerebral vessels where they can occlude vascular flow. b. Boyle’s law: pressure x volume = constant. c. Trapped air (in lungs with closed glottis) expands on ascent. 3. Arterial embolism can also occur via pulmonary AV shunts, or as paradoxical embolism via a patent foramen ovale (up to 18% of the adult population). 4. Etiology: a. Breath holding during ascent: i. Symptoms attributable to a shower of bubbles and multiple blood vessel involvement. b. Iatrogenically during placement of CVP lines, cardiothoracic surgery, or hemodialysis.
Environmental Emergencies Page 248 Notes c. Penetrating wounds to heart with emergent repair of cardiac wound.
B. Clinical manifestations:
1. Signs and symptoms: a. Cerebral: i. Dive-related stroke. ii. Second leading cause of dive-related death (after drowning). iii. Two main presentations: Apnea and full cardiopulmonary arrest. Any combination of neurologic deficits. iv. Presentation depends on the arterial distribution of the gas embolism. v. Change in level of consciousness/loss of consciousness (40%). vi. Sensory loss (20%). vii. Motor deficit (20%). viii. Paraplegia (10%). ix. Seizure (4%). x. Visual changes. xi. Aphasia. xii. Paresthesias. xiii. Timing of presentation: 10% during the ascent. 80% <5 min. after surfacing; must occur within 10 min. of ascent. 10% 5-10 min. after surfacing. xiv. Spontaneous improvement minutes after the initial deficits may occur: High incidence of relapse. Improvement may be transiently related to postural changes that affect the distribution of the bubbles flowing to the brain. b. Pulmonary: i. Shortness of breath. ii. Bloody, frothy sputum. iii. Subcutaneous air. c. Cardiac: i. Myocardial infarction due to air in the coronary vessels. ii. Reduced cardiac output due to air trapped in ventricle. iii. Hamman’s sign: crepitus on auscultation of the heart. d. Renal: i. Renal infarction due to air embolism. 2. Treatment: a. Initial stabilization: i. ABCs.
Environmental Emergencies Page 249 Notes ii. 100% oxygen by tight fitting mask. iii. Intubation for ventilation/protection of airway required. iv. IV access with volume augmentation. b. Recompression treatment: i. All cases of AGE must be referred for recompression treatment (hyperbaric oxygen therapy). Rapidly increasing ambient pressure to reduce intravascular bubble volume and to restore tissue perfusion. Slow decompression to avoid the reformation of bubbles. ii. Rapid transport: Arrange transportation to nearest hyperbaric facility. Aircraft capable of full pressurization or flight below 1,000 feet are best suited for transfers. iii. Prophylactic chest tube for simple pneumothorax to prevent conversion to tension pneumothorax during recompression. iv. Over 50% of victims of AGE have complete functional recovery. c. Controversies: i. Trendelenburg positioning patients with cerebral AGE is not effective. ii. Hypothesized that elevation of the legs could cause the air bubble to migrate away from the cerebral circulation and that increased hydrostatic pressure in brain will shrink bubbles. iii. Trendelenburg positioning may increase injury by increasing the intracerebral pressure and worsening cerebral edema. d. Cautions: i. Patients who experience sudden neurologic recovery can relapse quickly as bubble positions change.
V. ELECTRICAL INJURY
A. General characteristics:
1. Amperage (electron flow): a. Most directly related to injury. b. Varies directly with voltage and indirectly with resistance: Ohm’s Law I=V/R. (I=current in amp; V=voltage in volts; R=resistance in ohms). i. Decrease in resistance (with moisture) results in worse injury. Increase in voltage leads to worse injury.
Environmental Emergencies Page 250 Notes c. Narrow margin of safety:
Milliamperes at 60 Hz Effect
0.2-2 tingling sensation
1-4 pain
6-22 inability to let go/tetanic contractions
30-50 diaphragmatic/intercostal tetany
100 ventricular fibrillation
1000 ventricular standstill
2. Voltage: a. Unit of electromotive force or electric pressure that causes current to flow. b. Force or push of electrons. c. Often only parameter known in electrical injury.
Source Voltage
Automobile 12V
Telephone line 65V
Home 110V or 220V
Residential/industrial area lines 7620V
Cross country power lines >110,000V
Skin Type Resistance in Ohms
Heavily calloused 1,000,000
Average 5,000-30,000
Moist 1-2,000
3. Resistance: a. Varies depending on skin properties. b. Varies according to diagram (below). c. High voltage will cause resistant tissues (fat, tendons, bone) to heat up and coagulate.
Environmental Emergencies Page 251 Notes Tissue of least resistance
Nerve Blood Muscle Skin Fat Bone Tissue of most resistance
4. Watt: a. Unit of electrical power delivered to tissue when one ampere flows through one ohm for one second. b. Energy defined in watt-second. c. One joule = one watt-second. 5. Type of current: a. Alternating current 3x more dangerous than direct current. b. Alternating current at 60 cycles/second causes muscle tetany and grasping of source since flexors stronger than extensors and may cause respiratory muscle tetany. c. Direct current causes muscle contraction, which pushes victim away from the source. 6. Duration: a. Longer duration – worse injury. b. Skin resistance falls with continued contact with source. c. Resistance does not return to previous high level immediately after withdrawn from source. 7. Current pathway determines damage: a. Current through thorax - heart damage. b. Current through head - brain injury. c. Degree of cross section diameter inversely proportional to injury.
B. Clinical presentation:
1. Signs and symptoms: a. General: i. Crush-type trauma involving deep tissues that may be extensive relative to small skin burns. b. Cardiac: i. Dysrhythmias: PVC. Sinus tachycardia. Atrial fibrillation. Ventricular fibrillation: •• Most common cause of death. •• Induced by alternating current at levels of 50 to
Environmental Emergencies Page 252 Notes 60 Hz (household current). Asystole results from direct current. Myocardial damage: •• Occurs rarely. •• Generally epicardial, not transmural. •• Patch-like damage does not follow distribution of coronary arteries. •• ECG will not show standard injury patterns. c. Respiratory: i. Respiratory arrest may occur from: Electrical brain injury causing respiratory center inhibition. Tetanic contraction of chest wall muscles and/or diaphragm. Prolonged paralysis of respiratory muscles. Post-cardiac arrest respiratory arrest. d. Neurologic: i. Acute: Respiratory arrest, amnesia, altered mental status, seizures, coma, quadriplegia, localized paresis. ii. Delayed: Ascending paralysis, transverse myelitis, amyotrophic lateral sclerosis. e. Vascular: i. Venous thrombosis. ii. Compartment syndrome secondary to edema. f. Renal: i. Renal failure secondary to myoglobinuria. g. Musculoskeletal (forceful muscle contraction from electro- stimulation cause): i. Vertebral column fracture. ii. Posterior shoulder dislocation. iii. Fractures or dislocations secondary to falls. iv. Compartment syndrome. h. Ophthalmologic: i. Cataracts (onset 4-6 months post injury). ii. Corneal burns, intraocular hemorrhage, uveitis, retinal injuries and optic nerve atrophy. i. Dermatologic. i. Thermal burns from current arcing or clothes burning. ii. Kissing burns from flexor surface arcing as current exits and reenters the skin. iii. Entry/exit wounds. j. Pediatric considerations: i. Fetus much less resistant to electrical shock than mother. ii. All pregnant patients must undergo a period of fetal monitoring. iii. Oral commissure burn:
Environmental Emergencies Page 253 Notes Results from child biting an electrical cord. Associated with bleeding from the labial artery 7- 10 days post injury. May heal with significant contractures.
C. Diagnosis:
1. Essential work-up: a. ECG - indications: i. High voltage electrical injury. ii. Presence of risk factors: decreased skin resistance, tetany, current path across heart. iii. Large body surface burns. iv. LOC/AMS. v. Findings often non-diagnostic since injury pattern patchy rather than following coronary vessels. vi. Normal ECG associated with absence of late arrhythmias. b. Urinalysis for myoglobin. c. Cardiac monitor: i. Controversy abounds on the subject of the need for 24 hour monitoring. ii. Prolonged monitoring is not necessary in asymptomatic patients with a normal ECG with no arrhythmias, and an exposure to <240 volts. iii. Indications: Abnormal ECG. LOC. Dysrhythmia. Significant burn size. 2. Laboratory: a. Determined by the nature of the injury. b. For most exposures to household current, no testing indicated. c. Creatinine kinase (CK) indications: i. Positive urine myoglobin. ii. High voltage exposures. d. Troponin and CK MB indications: i. Abnormal ECG. ii. Dysrhythmia. e. Electrolytes, BUN, Cr: i. For high voltage exposures. ii. Provides baseline renal function. iii. Hyperkalemia occurs due to cell death. iv. Metabolic acidosis with significant injury. 3. Differential diagnosis: a. Thermal burns from electrical arcing flash injuries.
Environmental Emergencies Page 254 Notes
D. Treatment:
1. Pre-hospital: a. Caution: i. Care must be exercised in removing patients to ensure that rescuers do not contact live electrical sources. ii. Spinal precautions for transport. iii. Standard BLS/ACLS care. iv. Remove smoldering clothes. b. Initial stabilization: i. ABCs. ii. Standard ACLS measures for arrhythmias. iii. Spine immobilization when indicated. 2. ED treatment: a. IV fluid resuscitation: i. Larger fluid volumes required due to extensive third spacing in injured muscle. ii. As much as 7 ml/kg/% body burn. iii. Rapid administration to reach urine output of 1 ml/kg/hr. iv. Titrate to urine output and CVP measurement. b. Foley catheter. c. Prevent renal failure from myoglobulinuria: i. Maintain good urine output. ii. IV bicarbonate increases solubility of myoglobin in urine. iii. Furosemide/mannitol. iv. Monitor renal function. d. Immobilize/reduce fractures and dislocations. e. Local wound care for thermal burns. f. Tetanus prophylaxis. 3. Admissions criteria: a. Documented LOC. b. Dysrhythmias observed on monitor. c. Abnormal ECG. d. Suspicion of deep tissue burns. e. Myoglobinuria. f. Acidosis. g. Significant skin burns/associated injury.
VI. LIGHTNING INJURIES
A. General characteristics:
1. Voltage – several million to 2 billion. 2. Acts as direct current which causes asystole and respiratory arrest. 3. Due to the brief duration (1-100 milliseconds) of lightning: a. Current passes over the skin rather than through the body (flashover). Environmental Emergencies Page 255 Notes b. Deep tissue injuries are rare. c. Some experimental evidence that the current may enter the cranial orifices- eyes, ears, nose, mouth. i. May explain myriad of eye and ear symptoms. 4. Mechanisms of injury: a. Direct strike - strikes victim directly. b. Splash injury - moves from one object to victim of lesser resistance to current flow. c. Contact injury - holding object that is hit or splashed by lightning. d. Ground strike - current moves through ground and may injure multiple victims. e. Blunt injury due to direct explosive effect. f. Thermal burning - objects worn by victim heat up or clothes catch on fire.
B. Clinical presentation:
1. Signs and symptoms: a. Cardio-respiratory. b. Cardiac asystole: i. Due to direct current injury. ii. May resolve spontaneously as the heart’s intrinsic automaticity resumes. c. Respiratory arrest: i. Due to paralysis of medullary respiratory center. ii. May persist longer than cardiac asystole and lead to hypoxia induced Vfib. d. Acute myocardial infarction rare. e. Shock. f. Neurogenic (spinal injury). g. Hypovolemic (trauma). h. Mottled or cold extremities: i. Due to autonomic vasomotor instability. ii. Usually resolves spontaneously in a few hours. i. Neurological injuries: i. Confusion. ii. Memory defects. iii. Alteration of level of consciousness (>70% of cases). iv. Flaccid motor paralysis. v. Seizures. vi. Fixed dilated pupils due either to serious head injury or autonomic dysfunction. j. Traumatic injuries: i. Head or spine. ii. Fractures, dislocations, muscle tears and compartment syndromes. iii. Ruptured tympanic membrane with ossicular disruption (up to 50%). Environmental Emergencies Page 256 Notes iv. Burns: Discrete entrance and exit wounds uncommon. Thermal burns due to evaporation of water on skin, ignited clothing, heated metal objects (buckles or jewelry). Feathering (fern-like) burns: •• Cutaneous imprints from electron showers that track over skin. •• Pathognomonic of lightning injury. •• Resolve within 24 hours. k. Ophthalmologic injuries: i. Cataracts occur days to years post injuries. ii. Corneal lesions. iii. Intraocular hemorrhages. iv. Retinal detachment.
C. Diagnosis:
1. Confirmatory history from bystanders or rescuers of the circumstances of the injury: a. Consider lightning strike in unwitnessed falls, cardiac arrests or unexplained coma in an outdoor setting when a thunderstorm was present. 2. Laboratory: a. CBC for baseline Hct. b. Urinalysis for myoglobin. c. Electrolytes for acidosis. d. BUN, Cr for baseline renal function. e. CK and CKMb and Troponin fraction for muscle/cardiac damage. 3. Imaging/special tests: a. CXR. b. C-spine radiograph. c. CT head for altered mental status or significant head trauma. d. ECG should be performed in all cases: i. Non-specific ST changes common. ii. QT prolongation. iii. Acute myocardial infarction rare. 4. Differential diagnosis: a. Other causes of coma, cardiac dysrhythmia, or trauma: i. Hypoglycemia. ii. Intoxication. iii. Drug overdose. iv. Cardiovascular disease. v. CVA.
Environmental Emergencies Page 257 Notes
D. Treatment:
1. Pre-hospital: a. Controversies: i. Field triage should rapidly focus on providing ventilatory support to unconscious victim(s) or those in cardio- pulmonary arrest. ii. Prevents reversible asystolic cardiac arrest from degenerating into hypoxia induced Vfib. iii. Conscious victims are at lower risk of imminent demise. b. Cautions: i. Spine immobilization for: Cardiopulmonary arrest (suspected trauma). Significant mechanical trauma. Suspected loss of consciousness at any time. ii. Cover superficial burns with sterile saline dressings. iii. Immobilize injured extremities. iv. Rapid extrication prevents exposure to repeat lightning strike. c. Initial stabilization: i. ABCs. ii. Standard ACLS measures for cardiac arrest. iii. Diligent primary and secondary survey for traumatic injuries: Maintain cervical spine precautions until cleared. Treat altered mental status with glucose, naloxone, and thiamine as indicated. Hypotension requires volume expansion and pressor agent. 2. ED treatment: a. IV access for medication administration. b. Volume expansion: i. Do not follow burn treatment formulas as flashover burns are rarely the cause of fluid loss. ii. Occult deep burn injury is rare when compared to other types of electrical current injury. iii. Titrate volume administration to urine output; fluid loading may be dangerous with head injuries. c. Clean and dress burns. d. Tetanus prophylaxis. e. Treat myoglobinuria with: i. Diuretics, such as furosemide or mannitol. ii. Alkalinization of urine to a pH of greater or equal to 7.45. iii. Maintain urine output with IV fluid administration. f. Compartment syndrome: i. Must be distinguished from vasospasm, autonomic dysfunction, and paralysis, which are usually self-limited
Environmental Emergencies Page 258 Notes phenomena. ii. Delay fasciotomy if possible since it will rarely be necessary. 3. Admission criteria: a. Seriously injured and post-cardiac arrest victims. b. History of change in mental status/altered level of consciousness. c. Myoglobinuria. d. Acidosis. e. History of dysrhythmias or ECG changes: i. May not resolve spontaneously. ii. 24-48 hour observation period discriminates potentially unstable cases.
VII. NEAR DROWNING
A. General characteristics:
1. Definitions: a. Drowning: i. Death by suffocation after submersion in a liquid. ii. Death within 24 hours of the accident. b. Near drowning: i. Survival, or at least temporary survival, following a submersion accident. ii. Survival beyond 24 hours. 2. Stages of drowning: a. Stage I: i. Unexpected submersion with struggle. ii. Aspiration of small amount of water. iii. Laryngospasm. b. Stage II: i. Increased hypoxia and panic. ii. Large volume of water swallowed. c. Stage III: i. Wet drowning: (85-90% of cases). ii. Laryngospasm relaxes due to persistent hypoxia. iii. Aspiration of large volumes of water or gastric contents if victim vomits. iv. Dry drowning: (10-15% of cases): Aspiration of small amount of water. Further laryngospasm. Severe hypoxia leading to seizure or death. 3. Physiologic responses: a. Saltwater drowning: i. Protein-rich fluid pulled into the alveoli causing pulmonary edema and hypoxia. ii. Reduced circulating blood volume with elevated
Environmental Emergencies Page 259 Notes hemoglobin and sodium. b. Freshwater drowning: i. Affects surface-tension properties of surfactant making the alveoli unstable. ii. Collapse or atelectasis of alveoli. iii. Intrapulmonary shunting of alveoli. iv. Hypotonic fluid absorbed quickly into the circulation and redistributed into the body. v. Hemodilution and fluid overload. vi. Reduced hemoglobin and serum electrolytes. vii. Lysis of red cells leads to hyperkalemia. 4. Pathophysiology: a. Aspiration: i. Small volume of water usually aspirated. ii. Significant electrolyte changes uncommon. iii. Grossly contaminated water may further increase pulmonary injury/infection. b. Hypoxemia: i. Metabolic lactic acidosis. ii. Multisystem organ dysfunction. iii. Myocardial dysfunction. iv. Coagulation abnormalities (DIC). v. Renal failure. vi. CNS dysfunction.
B. Clinical presentation:
1. Signs and symptoms: a. Cardiovascular: i. Cardiopulmonary arrest – apneic and pulseless. ii. Cyanosis. b. Pulmonary: i. Dyspnea. ii. Cough. iii. Copious pulmonary secretions. c. CNS: i. Loss of consciousness. ii. Hypoxic induced cerebral injury or cerebral edema. d. Other: i. Evidence of trauma. ii. Cervical spine injury. e. Hypothermia: i. More common in young children due to larger body surface to mass ratio and less subcutaneous fat. ii. Decreases the metabolic rate. iii. Survival and full recovery possible after prolonged submersion in cold water (66 minutes-record). iv. Diving reflex: Young children may be more susceptible. Environmental Emergencies Page 260 Notes Potentiated by fear. Triggered by submersion of face in cold water. Bradycardia ensues with redistribution of blood flow to the heart and brain.
C. Treatment:
1. Prehospital: a. Cautions: i. Avoid further aspiration. ii. Apply cricoid pressure during bag-to-mask ventilation until airway is secured by intubation. iii. Strict C-spine precautions. b. Controversies: i. Abdominal thrusts to remove water: Not appropriate to remove water from the lungs. Increased risk of aspiration. Only useful if foreign body is lodged in airway. 2. Initial stabilization: a. ABCs. b. Remove wet clothing. c. Obtain accurate core temperature: i. Initiate rewarming (see Hypothermia section below). 3. ED treatment: a. Correct hypoxemia: i. Titrate to oxygen saturation. ii. Intubate and provide mechanical ventilation with positive end-expiratory pressure to maintain oxygenation. b. Evaluate and treat traumatic injuries. c. Correct acidosis: i. Administer sodium bicarbonate if pH <7.1. d. Cardiopulmonary arrest: i. Initiate ACLS measures and continue resuscitation until core temperature > 32oC, or until spontaneous pulse and respirations return. e. Importance of admission: i. Pulmonary edema may develop as long as 12 hours later. ii. Delayed neurologic abnormalities. 4. Admission criteria: a. ICU: i. Patients who required CPR or artificial ventilation. ii. Abnormal chest radiograph. iii. ABG abnormalities. b. Admit observation status: i. Submersion for >1 minute. ii. History of cyanosis or apnea. iii. Patients who required brief assisted ventilation.
Environmental Emergencies Page 261 Notes 5. Discharge criteria: a. Questionable history of submersion: i. Observe in ED for 6-8 hours. ii. No signs or symptoms of respiratory distress or change in neurologic status.
VIII. HYPOTHERMIA
A. General characteristics:
1. Description: a. Definition - body temperature <35°C. 2. Etiology: a. Decreased heat production: i. At age extremes. ii. With endocrine failure and malnutrition. b. Impaired thermoregulation: i. Central CNS conditions affecting the hypothalamus. ii. Spinal cord transection. c. Increased heat loss: i. Immersion in cold water and wet clothes. ii. Burns. iii. Alcohol – increased vasodilation/altered behavior. d. Medications/toxins decrease the body’s ability to respond to cold stress.
B. Clinical presentations:
1. Signs and symptoms:
Temp C Signs/Symptoms
35 (95°F) maximum shivering
34 amnesia/dysarthria
33 ataxia/apathy
32 stuporous
31 (88°F) shivering ceases
30 Afib
28 (82°F) Vfib
27 reflexes/voluntary motion cease
24 significant hypotension
19 EEG flat Environmental Emergencies Page 262 Notes
18 (64°F) asystole
15.2 lowest accidental hypothermia survival
a. Cardiovascular: i. Early tachycardia followed by bradycardia: Caused by decreased spontaneous depolarization of pacemaker cells. Refractory to atropine. ii. Cardiac cycle lengthens resulting in increased intervals. iii. Osborn J Wave = Hypothermic Hump: Repolarization abnormality seen at the junction of the QRS and ST segments at temperatures less than 32C. iv. Dysrhythmia: All atrial/ventricular dysrhythmia encountered below 32C. v. Core temperature after drop: Decline in a temperature after removal from the cold. Most common during active external rewarming where peripheral vasoconstriction and A-V shunting are reversed. b. CNS system: i. Linear decrease in cerebral metabolism of 6-7% per degree C from 35-25C. c. Respiratory system: i. Progressive respiratory depression with CO2 retention. d. Renal system: i. Paradoxical large initial diuresis due to: Relative central hypovolemia. Cold induced defects in distal tubular reabsorption of sodium and water. ii. Renal blood flow depressed 50% at 27-30C. e. Pediatric considerations: i. Infants have a large body surface to mass ratio and are at greater risk for hypothermia.
C. Responses to hypothermia:
1. 32.2-35°C: a. Thermogenesis preserved via shivering/endocrine mechanisms. 2. 24-32.2°C: a. Vasoconstriction preserved. b. Shivering/endocrine mechanisms fail. 3. <24°C: a. All heat conservations mechanisms fail.
Environmental Emergencies Page 263 Notes D. Diagnosis:
1. Essential work-up: a. Accurate core temperature confirms diagnosis. 2. Laboratory: a. ABG: i. Temperature correction not needed. b. CBC: i. Hematocrit rises due to decreased plasma volume. ii. Leukopenia does not imply absence of infection. c. Electrolytes, BUN/Cr: i. Vary during rewarming – recheck frequently. d. PT, PTT, and platelets: i. Prolonged clotting times with thrombocytopenia common. e. Toxicology screen: i. Alcohol/drug ingestions – common risk factors. 3. Imaging/special tests: a. CXR – pneumonia common complication.
E. Treatment:
1. “No one is dead until warm and dead”: a. Near normal recovery of Norwegian hypothermic man who was successfully resuscitated using warmed IV fluids and heated peritoneal lavage after 6 hours of CPR. 2. Prehospital: a. Cautions: i. Prolonged palpation/auscultation for cardiac activity. ii. Apparent cardiovascular collapse may be depressed cardiac output often sufficient to meet metabolic demands. iii. Do not want to induce Vfib with unwarranted chest compressions. b. Controversies: i. CPR not recommended if: Electrical rhythm present without palpable pulse or blood pressure with short transport time. 3. Initial stabilization: a. ABCs: i. Supplemental oxygen. ii. Oral and nasotracheal intubation are safe. iii. Cardiac monitor. iv. Warmed D5.9NS preferred over lactated ringers. b. Remove wet clothing and begin passive external rewarming. c. Administer Narcan, D50W (or Accu-Cheks), and thiamine with an altered mental status. d. Obtain accurate core temperatures using rectal temperature. 4. ED treatment: a. Cardiac arrest resuscitation: Environmental Emergencies Page 264 Notes i. Vfib induction occurs with rough handling, chest compressions, hypoxia, and acid/base changes. ii. CPR is less effective due to decreased chest wall elasticity. b. Defibrillation: i. Defibrillation is rarely successful at temperatures <30°C. ii. Defibrillate 1 to 3 times and then again post rewarming. iii. Direct current results in myocardial damage. c. Arrhythmia management: i. Atrial fibrillation: Common below 32°C. Usually converts spontaneously with rewarming. ii. Malignant ventricular arrhythmias: Bretylium drug of choice if available. Medication most effective > 30C. Avoid lidocaine and procainamide B (may incr. Vfib). 4. Rewarming techniques: a. Faster rewarming rates (1-2C/hr) generally have better prognosis than slower rewarming rates (<0.5C/hr). b. Active rewarming is necessary at core temperatures below 32C: i. Internal thermogenesis (shivering extinguished) insufficient to increase the body temperature. c. Passive external rewarming: i. Ideal technique for the majority of healthy patients with mild hypothermia. ii. Cover the patient with dry insulating material. iii. Endogenous thermogenesis must generate an acceptable rate of rewarming. d. Active external rewarming: i. Delivers heat directly to the skin. ii. Associated with core temperature afterdrop. iii. Safe in previously healthy young acutely hypothermic victims. e. Active core rewarming techniques: i. Airway rewarming (complete humidification at 40- 45C): Administer to all patients. ii. Heated IVF (40-42C): High flow rates to deliver warmed fluid. Heat one liter of crystalloid in a microwave set at high for two minutes. iii. Heated gastric irrigation via NG or OG tubes: Not recommended. Low amount of surface area. Aspiration risk if the airway has not been secured.
Environmental Emergencies Page 265 Notes iv. Pleural irrigation (0.9% NS at 40-42C): Use in severe hypothermia without cardiac activity. One or two chest tubes. Contraindicated in patients with a cardiac rhythm since the chest tube may induce Vfib. v. Heated peritoneal lavage (0.9% NS at 40-45C): Use in unstable hypothermic patients or stable patients with severe hypothermia whose rewarming rates are <1C/hr. One or two catheters. Advantageous in patients with an overdose or rhabdomyolysis. vi. Hemodialysis: Initiate for patients with drug overdoses or severe electrolyte disturbances. vii. Cardiopulmonary bypass: Treatment of choice in severe hypothermia especially for those patients in cardiac arrest. Complications include: •• Hemolysis. •• Vascular injury. •• Air embolism. •• Coagulopathies. 5. Admission criteria: a. Moderate to severe hypothermia (<32C). b. Young healthy patients with no co-morbid illness who have mild accidental hypothermia (32-35C) that responds well to warming: i. Admit to an observation area. ii. Discharge if asymptomatic after 8-12 hours. 6. Discharge criteria: a. Young healthy patients with no co-morbid illness. b. Very mild accidental hypothermia (>35C) that responds well to warming. c. Safe, warm environment to go to after discharge.
IX. FROSTBITE
A. General characteristics:
1. Definitions: a. Frostnip: i. Mildest form of cold injury. ii. Transient numbness and paresthesias resolve after rewarming. iii. Due to superficial and reversible ice crystal formation with intense vasoconstriction without tissue destruction. iv. Warming results in freedom from epidermal/dermal Environmental Emergencies Page 266 Notes damage. b. Chilblain: i. Usually located on face, anterior tibia, dorsum of hands/feet. ii. Chronic vasculitis of dermis provoked by repeated exposures to cold temperature above freezing. iii. Secondary to sympathetic instability and vascular hypersensitivity to cold with microvascular stasis/thrombosis. iv. Localized erythema, cyanosis, plaques and vesicles. c. Trenchfoot: i. Feet exposed to wet conditions and temperatures between 0-20°C. ii. Neurovascular damage occurs without ice crystal formation. iii. Hyperemia may be present for up to 6 weeks. iv. Pallor, mottling, paresthesias, pulselessness, paralysis, numbness and cramps. d. Frostbite: i. Freezing of skin/subcutaneous tissues. 2. Frostbite injury: a. Inability to physiologically compensate for cold that produces injury. b. Factors include: i. Duration of contact, humidity, wind, altitude, clothing, medical conditions, behavior, and individual variability. c. Prefreeze state: i. Tissue cooling, increased viscosity, capillary constriction- dilation cycle. d. Frozen state: i. Extracellular ice crystal formation, intracellular dehydration and hyperosmolarity, fluid crossing cell membrane. e. Ischemic and vascular complications: i. Reperfusion injury, leaky endothelium, coagulation from stasis, leakage of prostaglandins and free radicals, vasoconstricting and AV shunting, necrosis/gangrene. f. Three zones of injury: i. Zone of coagulation: Most severe, distal region of damage; irreversible. ii. Zone of hyperemia: More superficial, proximal region; least cellular damage; recovers in < 10 days. iii. Zone of stasis: Middle ground; severe, possibly reversible cell damage.
Environmental Emergencies Page 267 Notes
B. Clinical presentation:
1. Signs and symptoms: a. Penis, fingers, toes, ears and nose most commonly affected. b. Initial appearance of an injury often fails to predict eventual depth or outcome. i. Devitalized tissue demarcates as the injury evolves over weeks to months. 2. 1st degree frostbite: a. Partial skin freezing. b. Erythema, edema, hyperemia. c. Lack of blisters or necrosis. d. Stinging/burning/throbbing. e. Prognosis – excellent. 3. 2nd degree frostbite: a. Full thickness skin freezing. b. Substantial edema over 3-4 hrs. c. Erythema. d. Formation of clear blisters (6-24hrs) that desquamate and form eschar. e. Numbness/aching/throbbing. f. Prognosis – good. 4. 3rd degree frostbite: a. Damage extends into subdermal plexus. b. Hemorrhagic blisters form. c. Skin necrosis, blue-gray discoloration. d. “Block of wood”. e. Burning/throbbing/shooting pains. f. Prognosis – poor. 5. 4th degree frostbite: a. Extension into subQ, muscle, bone, and tendon. b. Little edema. c. Mottled, nonblanching cyanosis. d. Forms deep, dry, black eschar. e. Deep aching joint pain. f. Prognosis – extremely poor. 6. Post-rewarming appearance: a. Post-rewarming edema begins within 3 hours, lasting 5 days. b. Large, clear blebs form within 6-24 hours. c. Small, hemorrhagic blebs form after 24 hours: i. Associated with deeper injury. d. Eschar forms in 9-15 days. e. Mummification in 3-6 weeks. f. Persistent mottling and anesthesia despite edema after rewarming are unfavorable prognostic indicators.
Environmental Emergencies Page 268 Notes
C. Treatment:
1. Pre-hospital: a. Protect and immobilize frostbitten area during transport. b. Remove restrictive or wet garments. c. Avoid dry rewarming of the frostbitten limb if there is a likelihood of refreezing of the injury: i. If the evacuation will be delayed, and suitable facilities are available, field rewarming in warm (40-42°C) water can be attempted. d. Rubbing, manipulating the limb or applying snow while it is still frozen is contraindicated. e. Hypothermia: i. Common in frostbite victims. ii. Avoid rough handling to minimize possibility of cardiac dysrhythmias in the seriously hypothermic patient. f. Look for evidence of intoxication, head injury, trauma, hypoglycemia, cardiac, or neurologic problems as underlying etiologies and treat them appropriately. 2. Initial stabilization: a. ABCs. b. Identify and correct hypothermia. c. IV fluid volume expansion with 0.9% NS for severe frostbite. d. Protect frostbitten areas from excessive handling or dry warming during resuscitation. 3. ED treatment: a. If the injury is less than 24 hours old and has not yet been rewarmed: i. Initiate rapid thawing of the injured extremity for 10- 30 minutes in 40-42°C water. ii. Stop treatment when the limb is warm, red, and pliable. iii. Monitor water temperature closely to prevent thermal injury. b. Analgesia. c. NSAID (ibuprofen): i. Combat the effects of prostaglandins on skin necrosis. d. Aloe vera topical cream: i. Combats the arachidonic cascade. ii. Recommended for all intact blisters. e. Blister debridement or aspiration: i. Indicated for clear blebs (removes thromboxane and prostaglandins). ii. Contraindicated for hemorrhagic blebs (exposes deeper structures to dehydration and infection). f. Tetanus prophylaxis. g. Antibacterial prophylaxis: i. Consider during the hyperemic recovery phase (at least 2- 3 days) in severely frostbitten areas. Environmental Emergencies Page 269 Notes ii. Against streptococci, staphylococci and Pseudomonas species (cephalosporin, penicillinase-resistant penicillin, quinolone). iii. Topical antibacterial agents interfere with the use of aloe vera cream and should be considered a second line approach. h. Elevation and splinting of frostbitten area. i. Two to four times daily dressing change. j. Avoid vasoconstrictive agents (including tobacco). k. Amputation after 3-4 weeks. l. Admit all but the most isolated and superficial cases. m. Investigational treatments: i. Dextran, heparin, calcium channel blockers, hyperbaric oxygen therapy not effective consistently. ii. Alpha blockers such as phenoxybenzamine – under study. iii. Medical or surgical sympathectomy –beyond the scope of the emergency department. iv. Topical methylprednisolone 1% cream – not as effective as aloe vera.
X. HEAT-RELATED ILLNESS
A. General characteristics:
1. Mechanism: a. Continuum of increasingly severe illnesses secondary to overwhelming heat stress. b. Begins with dehydration and electrolyte abnormalities and progresses to thermoregulatory dysfunction and multi-system organ failure. c. Heat dissipation: i. Body temp: heat production vs. heat loss (or gain). ii. Conduction: heat exchange b/t two surfaces in contact. iii. Convection: heat exchange b/t a surface and a gas or liquid. iv. Radiation: transfer of heat b/t body and environment through electromagnetic waves. v. Evaporation: one-way heat flow from body to environment. d. Heat regulation: i. 3 distinct systems of control: Thermosensors: temperature sensitive structures found in skin, spinal cord, limb muscles, and preoptic area of anterior hypothalamus. Central integrative area: interprets data from thermosensors; probably located in hypothalamus or spinal cord. Thermoregulatory effectors: structures that respond to
Environmental Emergencies Page 270 Notes physiologic changes to decrease temperature (peripheral vasodilatation and sweating - most important). 2. Heat stroke: a. Loss of thermoregulatory function, severe CNS dysfunction, and multi-system organ failure. b. Classic heat stroke: i. Occurs in those with compromised homeostatic mechanisms (elderly, debilitated). ii. Develops over days to weeks. iii. Severe dehydration. c. Exertional heat stroke: i. Occurs in younger, athletic individuals with a combined environmental and exertional heat stress. ii. Develops over hours. iii. Internal heat production overwhelms dissipating mechanisms. iv. May be sweating. 3. Heat exhaustion: a. Fluid and electrolyte depletion. b. Thermoregulatory function is maintained. 4. Heat cramps: a. Secondary to excessive sweating and sodium loss.
B. Etiology:
1. Circulatory insufficiency: a. Age extremes. b. Dehydration. c. CHF. d. Obesity. e. Diuretics. f. Laxatives. 2. Pharmacologic causes: a. Sympathomimetics. b. LSD. c. MAO inhibitors. d. PCP. e. Anticholinergics. f. Antihistamines. g. Drug or alcohol withdrawal. 3. Excessive head load: a. Environmental. b. Fever. c. Exertional. d. Lack of acclimatization. 4. Decreased cardiovascular function: a. Beta-blockers. b. Sympatholytics. Environmental Emergencies Page 271 Notes 5. Pediatric: a. Children are at increased risk of heat illness due to increased body surface area to mass ratio.
C. Clinical presentation:
1. Signs and symptoms: a. Heat edema: i. Swelling of dependent areas of body. ii. Resolves after acclimatization. b. Heat syncope: i. Consequence of a reduced “effective” blood volume. ii. Brief and responds to horizontal positioning and improved venous return. c. Heat cramps: i. Cramps in heavily exercised muscles. ii. During or after exercise. iii. Primarily in lower extremities. d. Heat tetany: i. Carpal-pedal spasm (secondary to hyperventilation). e. Heat exhaustion: i. Core temp: <104°F. ii. CNS: headache, fatigue, malaise, agitation. iii. CV: mild tachycardia, dehydration. iv. Pulmonary: tachypnea. v. Renal: elevated BUN/Cr due to dehydration. vi. GI: nausea, vomiting. f. Heat stroke: i. Core temp: >105°F. ii. CNS: severe confusion/lethargy, coma, seizure, ataxia or focal deficits. iii. CV: tachycardia, hypotension. iv. Pulmonary: tachypnea. v. GI: nausea, vomiting, diarrhea. vi. Skin: dry and hot in classic heat stroke; moist/sweating with exertion/ heat stroke. vii. Renal: acute oliguric renal failure due to rhabdomyolysis/ dehydration. viii. Liver: hepatic failure.
D. Diagnosis:
1. Essential work-up: a. Accurate core temperature. b. Obtain history of heat exposure. c. Heat exhaustion – diagnosis by exclusion of other causes. 2. Laboratory (for heat stroke and heat exhaustion): a. CBC: i. Leukocytosis might point toward infection. Environmental Emergencies Page 272 Notes b. BMP: i. Hypernatremia with severe dehydration. ii. Acute renal failure. iii. Hyperkalemia with severe heat stroke. c. UA: i. Myoglobin present in rhabdomyolysis. ii. Bacteria/WBC. d. LFTs: i. Hepatic necrosis. e. PT/PTT/DIC panel: i. Clotting abnormalities. 3. Imaging/special tests: a. ECG indicated in elderly or those at cardiac risk. b. CT head for altered mental status. c. CXR for ARDS, aspiration pneumonia. 4. Differential diagnosis: a. Febrile illness/sepsis. b. Thyroid storm. c. Pheochromocytoma. d. Malignant hyperthermia. e. Cocaine. f. PCP. g. Anticholinergics. h. MAO inhibitors. i. Meningitis. j. Encephalitis. k. Cerebral falciparum malaria. l. Delirium tremens.
E. Treatment:
1. Pre-hospital: a. Institute cooling measures for severe heat illness: i. Remove from heat stress. ii. Disrobe patient. iii. Ice packs to axilla, groin, and neck. iv. Cover body with wet sheet. b. IV 0.9% NS at TKO - 500 cc fluid bolus if hypotensive. c. If altered mental status – glucose (or accucheck), thiamine, naloxone. 2. Initial stabilization: a. ABCs. b. Immediate/rapid cooling if temperature >40C. 3. ED management: a. Cooling measures: initiate for body temperature >40C. i. Evaporative: Extremely effective (0.05-0.3C/min). Spray disrobed patient with fine mist of warm
Environmental Emergencies Page 273 Notes water (prevents shivering). Airflow with fans blow over patient. ii. Conductive: Ice packs to groin/axilla combine with evaporative adjunctive treatment above. Iced or cold water immersion very effective (0.13C/min) but impractical. Iced peritoneal lavage and cardiopulmonary bypass for refractory cases. iii. To avoid hypothermia, stop cooling therapy at 39C. b. Supportive measures: i. Rehydration for heat stroke: Initial rehydration with 0.5-1.0 L 0.9% NS. Avoid overhydration may contribute to development of ARDS. Peds: 20 cc/kg bolus. ii. Glucose/naloxone/thiamine for altered mental status. iii. Chlorpromazine to stop shivering. iv. Benzodiazepine for seizure. v. Analgesics and oral or IV hydration with electrolyte containing fluid for heat cramps. vi. Reassurance/calming measures/rebreathing in closed system (bag or non-rebreather without oxygen) for hyperventilation heat tetany. vii. Lower extremity elevation/removal from heat stress for heat edema. 4. Admission criteria: a. Heat stroke to the ICU. b. Heat exhaustion: i. Severe electrolyte abnormalities. ii. Renal failure/evidence of rhabdomyolysis. iii. Elderly.
XI. RADIATION INJURY
A. General characteristics:
1. Description: a. Acute radiation syndrome results after a major portion of the body is irradiated by deeply penetrating radiation with a dose usually >1 Gy. b. Measuring radiation: i. Rad (radiation absorbed dose) is a measure of energy imparted to matter. 2. 1 rad = 100ergs/g. a. 1 Gray (Gy), the SI (International System of Units) Measure = 100 rad. 3. Types of exposure: Environmental Emergencies Page 274 Notes a. External contamination: i. Follows irradiation from an external source (e.g., radiation therapy). ii. Radioactive material in contact with a patient’s clothing or skin. iii. Must remove radioactive material. iv. Contain radioactive material to prevent further contamination. v. No contamination hazard. b. Internal contamination: i. Inhalation or ingestion of radioactive material. ii. Treat as heavy metal ingestion. 4. Etiology: a. Alpha, beta, X- and gamma rays emitted during the decay of unstable isotopes: i. Responsible for acute radiation syndrome. b. Alpha particles: i. Equivalent to a helium nucleus and derived from the decay of certain nuclides of heavy elements. ii. Penetration limited to the epidermis. iii. Contamination treated by skin cleaning. c. Beta particles: i. Electrons or positrons ejected at high velocity from a nucleus undergoing beta decay. ii. Skin penetration of 8 mm causes thermal-like burns. iii. Clothing blocks penetration. iv. Measured by radiation meters. v. Removed by skin cleaning. d. Gamma rays: i. Primary cause of radiation injury. ii. Deeply penetrating high energy wave similar to X-rays.
B. Clinical presentation:
1. Signs and symptoms: a. Tissues with greater rates of cellular division more radiosensitive. b. GI and heme systems most vulnerable. 2. Skin: a. With increasing radiation exposure develop: i. Epilation. ii. Erythema. iii. Dry desquamation. iv. Wet desquamation. b. Erythema that develops within 48 hours usually progresses to ulceration or chronic radiodermatitis. c. Treat as thermal burn. 3. Gastrointestinal: a. Anorexia/nausea/vomiting/diarrhea. Environmental Emergencies Page 275 Notes b. Dehydration due to transudation of plasma into the GI tract. c. Major source of septicemia when combined with bone marrow suppression. d. Higher doses result in an earlier onset and more protracted course: i. <0.5 Gy - onset >6 hrs. ii. <2 Gy - onset 2-6 hrs. iii. >4 Gy - onset <2 hrs. iv. >10 Gy - onset <30 min. 4. Hematopoietic: a. Pancytopenia due to bone marrow suppression: i. Anemia. ii. Thrombocytopenia with doses exceeding 2-4 Gy after about 4 weeks. iii. Lymphopenia/neutropenia causing fever and increased risk of infection. b. Bone marrow depression develops after a latent phase. 5. Central nervous system: a. Headache. b. Altered mental status. c. Vertigo. d. Occurs after massive exposure – associated with near 100% mortality within 48 hours; survivable if exposure is limited to the head.
C. Diagnosis:
1. Essential work-up: a. Radiation monitoring to insure decontamination. 2. Laboratory: a. CBC/platelet count: i. Baseline important. ii. Absolute lymphocyte count (ALC) at 48 hours correlates with prognosis: >1200/mm3 -good prognosis. 300-1200/mm3 -fair prognosis. <300 mm3 -poor/critical prognosis.
Environmental Emergencies Page 276 Notes
3. Illness categorization:
Degree Gy Clinical Scenario Treatment/ Disposition mild <2 mild GI for 24 hours discharge if ALC(48h)2,000 asymptomatic; follow daily CBC and platelets moderate 2-4 moderate GI for 4 days admit for supportive care ALC(48h)1,200 and observation severe 4-10 severe GI for 7 days admit for reverse ALC(48h)<1,200 isolation, antibiotics, symptomatic anemia transfusions; consider infections common bone marrow transplant; about 50% mortality fatal >10 GI and CNS within admit for palliative 30 mins measures; death ALC(48h)<300 expected within 1 week
D. Treatment:
1. Pre-hospital: a. Activate plan when predefined criteria met. b. Early notification of type of incident to receiving hospital. c. Transport after decontamination if medically stable. d. Site decontamination. 2. Remove/bag clothing and leave at scene for disposal. 3. Clean with soap and water: a. Protective clothing includes respirators, rubber gloves and shoe covers for rescue personnel. 4. Initial stabilization: a. Field decontamination except for patients in extremis. b. ABCs: i. 0.9% NS IV fluid bolus for extensive thermal burns/hypotension. c. General principles: i. Irradiated, non-contaminated victim is not radioactive and poses no risk to health care workers. ii. Contaminated victims are unlikely to represent a significant risk of radiation exposure to health care workers and the treatment of serious medical problems take priority over radiation concerns. 5. ED management: a. Protect all hospital personnel: i. Cover skin with gown. Environmental Emergencies Page 277 Notes ii. Use radiation survey monitors to prevent contamination. iii. Set up containment and decontamination areas with running water and drainage. b. Irrigate open wounds with saline followed by 3% hydrogen peroxide if contamination persists. c. Irrigate contaminated eyes and ears. d. Gently scrub skin with soap and water 3 minutes (do not abrade). e. GI decontamination for ingestions: i. Whole-bowel irrigation and activated charcoal within 2 hours of exposure. f. Pulmonary decontamination: i. Consider bronchoalveolar lavage. g. Supportive treatment: i. IV fluids to replace GI losses. ii. Antiemetics and analgesics. iii. Monitor for need of reverse isolation. iv. Cover severe burns with sterile dressing. v. Early and broad spectrum antibiotics for fevers or other signs of infection. vi. Early surgery for associated trauma to reduce risk of infection and bleeding. h. Potassium iodine to prevent thyroid uptake of radioactive iodine-131 ingestion: i. Indications: >100 rad for adult/ >50 rad for child. ii. Blocks 90% I-131 if given within 1 hr; 50% if given within 5 hr. i. Chelating agents for radioactive heavy metals: i. Aluminum reduces absorption of strontium. ii. Barium reduces and precipitates radium. iii. EDTA precipitates lead. iv. Penicillamine for lead, copper, cobalt. v. Prussian blue for thallium, cesium, rubidium. vi. DTPA for transuranics, heavy metals. vii. Deferoxamine for plutonium, iron. viii. Water diuresis for tritium, Na+ ,K+. ix. Dimercaprol for mercury, arsenic, bismuth, chromium, nickel, lead. j. For expert assistance contact Radiation Emergency Assistance Center in Tennessee: 615-481-1000 (24 hr/day). 6. Admission criteria: a. Exposure to a dose of radiation >1Gy. 7. Discharge criteria: a. Asymptomatic patients with dose of radiation less than 1 Gy with close laboratory follow-up.
Environmental Emergencies Page 278 Notes
XII. BURNS
A. Degree of injury:
1. 1st degree: a. Red skin, no blisters, painful. b. Heal over several days with no scarring. 2. 2nd degree: a. Superficial partial thickness: i. Epidermis and superficial dermis. ii. Pink, moist, tender, thin blisters, heal in 2 weeks. iii. Very painful to the touch. iv. Scarring is minimal and usually full return of function. b. Deep partial thickness. c. Extends into dermis (damage to hair follicles and sweat and sebaceous glands). d. Red, blanched white, decreased 2pt discrimination. e. Thick walled blisters, usually ruptured, heal in 4 weeks. f. Scarring is common; surgical debridement and skin grafting may be necessary. 3. 3rd degree: a. Full thickness, destroyed epidermis/dermis. b. White leathery appearance, clotted vessels, numb. c. < 1cm heal by contraction. d. Skin grafting for larger lesions. 4. 4th degree: a. Full thickness with destruction of all deep structures. b. Extensive debridement and reconstructive surgery.
B. Burn size - % body surface area:
1. The Rule of Nines: a. Front and back of torso – 18% BSA each. b. Each leg – 18% BSA each. c. Each arm – 9% BSA each. d. Head – 9% BSA. e. Perineum – 1% BSA. 2. Back of patient’s hand is ~1% BSA.
C. Burn categories:
1. Major: a. Full thickness: >10% TBSA. b. Partial thickness: >25% TBSA adults; >20% TBSA >50 yr or <10 yr. c. Miscellaneous: face, hands, feet, perineum, chemicals, electrical, complicated by inhalational injury, increased co- Environmental Emergencies Page 279 Notes morbidities. d. Disposition: i. Transfer to a burn unit. 2. Moderate: a. Full thickness: 2-10% TBSA. b. Partial thickness: 15-25% TBSA adults; 10-20% TBSA >50 yr or <10 yr. c. Disposition: i. Admit to the hospital. ii. Burn unit unnecessary. 3. Minor: a. Full thickness: <2% TBSA. b. Partial thickness: 15% TBSA adults; <10% TBSA >50 yr or <10 yr. c. Disposition: i. Outpatient management.
D. Treatment:
1. Keep burns clean. 2. Wash/dress area with cool water: a. No ice. 3. Pain meds: a. Morphine. 4. IV fluids if >20% TBSA 2nd or 3rd degree burns: a. IV through unburned skin. b. Parkland formula: i. LR @ 4 cc/kg / %TBSA burn IV 1st 24 hrs. ii. ½ in first 8 hrs. iii. ½ in next 16 hrs. iv. Maintain UO @ 0.5 – 1.0 cc/kg/hr. 5. Special situations: a. If suspect inhalational injury: i. Check CN level. ii. Check COHb level. Half-life of carbon monoxide is: •• 4-5 hours at room air. •• 80-90 minutes with 100% oxygen supplementation. •• 20-30 minutes with hyperbaric oxygen treatment. Indications for hyperbaric oxygen treatment include: •• Persistent symptoms after 4 hours of oxygen treatment. •• CO level greater than 15-40. •• Any history of syncope. •• Any neurovascular or cardiovascular impairment. •• Pregnant women who are symptomatic or with a level exceeding 15.
Environmental Emergencies Page 280 Notes b. Pediatric “Parkland formula”: i. Galveston formula. ii. D5/LR 5000cc / m2 TBSA burned + 2000 cc / m2 IV in 24 hrs. iii. ½ in first 8 hrs. iv. ½ over next 16 hrs. c. FT circumferential burns: i. Perform escharotomy. 6. Wound care: a. Shur-Clens or sterile saline for cleaning. b. Debride blisters: not on palms or soles. c. Apply silver sulfadiazine: not on face. d. dPT > 10y and < 64y.o., Td. e. Cover with sterile gauze or specialized burn dressings.
Environmental Emergencies Page 281 Notes
ENVIRONMENTAL EMERGENCIES
PEARLS
1. The range of illness due to high altitude includes acute mountain sickness, pulmonary edema, cerebral edema, and retinal hemorrhage. The most serious of these is high altitude cerebral edema.
2. Acute mountain sickness is manifested by headache, nausea, vomiting, exertional dyspnea, and difficulty sleeping. It lacks specific physical findings. It can be avoided by gradual ascent, and is usually self- limited. Acetazolamide and dexamethasone are useful for prevention and treatment.
3. High altitude pulmonary edema is a noncardiogenic permeability edema that may be life-threatening. In contrast to acute mountain sickness, victims have physical signs and symptoms of pulmonary edema. Immediate descent is important.
4. High altitude cerebral edema is the least common but most serious form of altitude illness, manifested by ataxia and mental status changes and sometimes focal deficits. Immediate descent is mandatory. Steroids, oxygen, and elevation of head may be beneficial.
5. Three gas laws should be understood to explain the pathophysiology of dysbarism:
Dalton’s Law: The total pressure of a mixture of gases is equal to the sum of the partial pressures of each gas.
Henry’s Law: The amount of gas which is dissolved in any solution is proportional to the pressure of the gas with which it is in equilibrium (i.e., in descent, with an increase in pressure, a greater amount of gas dissolves in solution. In ascent, with a decrease in pressure, gas dissipates from the solution.)
Boyle’s Law: At constant temperature, the volume of a gas varies inversely with pressure. (PV=nRT).
6. Barotrauma which occurs in descent is frequently the result of a pressure imbalance of a gas contained in a closed space, such as sinuses or ear. The result may be ear squeeze with rupture of the TM, round or oval window, or hemorrhage into a closed space such as the sinuses.
7. Barotrauma from ascent is the most serious dysbaric illness. It results from gas coming out of solution as the pressure decreases (“the bends”) or air emboli. Decompression sickness occurs when ascent is too rapid and gas bubbles form. It is a multisystem disorder which may include Environmental Emergencies Page 282 Notes skin rashes, edema, periarticular joint pain, spinal cord ischemia, pulmonary venous embolism, cerebral embolism (as discussed above.)
Treatment requires immediate 100% oxygen and recompression in a hyperbaric chamber.
The onset of decompression illness may be delayed for up to 12-24 hours after surfacing.
8. Risk factors for decompression illness include too rapid ascent, obesity, fatigue, alcohol use, dehydration, heavy exertion, and respiratory tract infections.
9. Skin is a good resistor of electrical flow, although moisture decreases its resistance. Nerve and blood tissue are least resistant to electrical flow. Bone is most resistant.
10. Alternating current is more dangerous than direct current, causing tetany, sometimes preventing the patient from letting go of the electrical source.
11. The amount of tissue injury sustained from an electrical injury is usually much greater than would be expected from any visible burn. Muscle necrosis, hyperkalemia, hyperphosphatemia, metabolic acidosis, and renal failure should be anticipated. Treatment involves volume loading to achieve a urine output of 1 cc/kg/hr, urinary alkalinization to facilitate excretion of myoglobin.
Cardiac arrhythmias, fractured bones, and neurological complications should be searched for and anticipated.
12. Electrical cord bite injuries may be complicated by late bleeding from the labial artery when the eschar separates 7-10 days post injury.
13. In contrast to electrical injury, lightning injuries are usually flash-over with superficial skin burns. Many injuries may be mild; however, a massive countershock can cause cardiac asystole, and paralysis of the medullary respiratory center can cause apnea. If the victim is thrown from the force of the shock, multiple blunt trauma may result in any number of injuries. Other common injuries include cataract formation and TM rupture.
14. 10-20% of drowning deaths are “dry drownings,” which occur from laryngospasm without aspiration of fluid.
15. Fresh water aspiration may differ from salt water drowning but usually only when more than 22 cc/kg of water are aspirated. Fresh water drownings with significant aspiration may be complicated by surfactant washout with atelectasis, an increase in total plasma volume with a Environmental Emergencies Page 283 Notes decrease in serum lytes, hemolysis with hyperkalemia. Salt water drowning with significant aspiration will cause a decrease in plasma volume and an increase in serum lyte concentrations.
16. Post-immersion syndrome or secondary drowning refers to the development of ARDS preceded by a relatively asymptomatic period of hours to days. It usually occurs in significant drowning events with transient hypoxia or aspiration that are effectively resuscitated. All patients should have ABGs and CXRs done to determine anyone at risk.
17. Hypothermia may be due to decreased heat production (hypothyroidism, adrenal insufficiency), increased heat loss (burns, ETOH), or impaired thermoregulation (CVA, drug overdoses).
18. Osborn J waves are one sign of hypothermia, occurring at temperatures less than 32oC.
19. Mild hypothermia can be managed by passive external rewarming techniques (remove wet clothes, apply warm covers).
20. Active core rewarming techniques should be employed for temperature less than 32oC including warmed humidified oxygen, heated IVFs (40- 42oC), and possibly heated peritoneal dialysis and cardiopulmonary bypass.
21. Rapid rewarming in a water bath at 40-42oC is the treatment of choice for frostbite.
22. Early debridement is contraindicated in frostbite.
23. Heat exhaustion is a clinical syndrome of headache, nausea, malaise, tachycardia, orthostasis, and muscle cramps but normal mental status. Treatment is rest in a cool environment with rehydration.
24. Heat stroke is characterized by altered mental status, confusion, possibly progressing to seizures and coma. Classical “dry” heat stroke occurs in the elderly or very young; exertional “wet” heat stroke occurs in the young, fit individuals, usually overzealous athletes.
25. Treatment of heat stroke is supportive with rapid cooling best accomplished by spraying the body with a fine mist and placing near fans to increase evaporative loss.
26. Ionizing radiation includes: Alpha particles: penetrate only the epidermis. Beta particles: penetrate skin to about 8 mm. May decay to more dangerous gamma rays. Gamma rays: deep penetration with deep tissue injury.
Environmental Emergencies Page 284 Notes
27. Tissues that are most radiosensitive are those with the fastest rate of cellular division, especially G1 and hematopoietic cells.
28. The mean lethal dose of acute radiation exposure is 350 rads.
29. A 48 hour lymphocyte count is prognostic in acute radiation illness: a value less than 300 is critical with predictable bone marrow failure.
30. The half-life of carbon monoxide is: 4-5 hours at room air. 80-90 minutes with 100% oxygen supplementation. 20-30 minutes with hyperbaric oxygen treatment.
31. Indications for hyperbaric oxygen treatment include: Persistent symptoms after 4 hours of oxygen treatment. CO level greater than 15-40. Any history of syncope. Any neurovascular or cardiovascular impairment. Pregnant women who are symptomatic or with a level exceeding 15.
Environmental Emergencies Page 285 Notes
REFERENCES
1. Auerbach, PJ. Wilderness Medicine 5th Ed. Philadelphia. Mosby Elsevier 2007.
2. Bailey B, Gaudreault P, Thivierge R. Turgeon, J. Cardiac Monitoring of Children with Household Electrical Injuries. Ann Emerg Med 1995;25:5:612-617.
3. Bartlett RB. Diving Emergencies in Critical Decisions in Emergency Medicine. Vol 10. Num 10. Lesson 20. Published by ACEP.
4. Bortsch P, Maggiorini M, Ritter M, Noti C, Vock P, Oelz O. Prevention of high-altitude pulmonary edema by nifedipine. N Engl J Med. 1991:325:1284-1289.
5. Bradley ME. Pulmonary Barotrauma. In Bove AA, Davis JC. Diving Medicine. 2nd Ed. Philadelphia. WB Saunders. 1990; 188-91.
6. Britt LD, Dascombe WH, Rodriguez A: New horizons in management of hypothermia and frostbit injury. Surg Clinics of NA. 1991; 71(2) 345-70.
7. Browne, B.J.and Gaasch, W.R., Emergency Medicine Clinics of North America, 10:2:211-30, 1992.
8. Cooper MA, Andrew CJ, Holle RL: Lightening Injuries, Auerbach PS (ed): Wilderness Medicine 5th Ed., Mosby Elsevier, 2007, pp.67-108.
9. Danzl DF et al: Accidental hypothermia. NEJM. 1994;331(26), 1756- 60.
10. DeNicola LK, Falk JL, Swanson ME, Gayle MO, Kissoon N: Submersion injuries in children and adults. Crit Care Clinics. 1997;13:477-502.
11. Edmonds C, Lowry C, Pennefather J. Diving and Subaquatic Medicine. Butterworth-Heinemann. Oxford 1992.
12. Fields AI: Near-drowning in the Pediatric Population. Crit Care Clinics 1992;8:113-129.
13. Fish, R., Electric Shock, Part II: Nature and Mechanisms of Injury, Journal of Emergency Medicine, Vol. 11, pp.457-462, 1993.
14. Fontanarosa, P., Electrical Shock and Lightning Strike, Annals of Emergency Medicine, 22:2 Part 2 February 1993, pp 378-386.
Environmental Emergencies Page 286 Notes
15. Garcia, C. Smith, G., Cohen, D., Fernandez, K., Electrical Injuries in a Pediatric Emergency Department, Annals of Emergency Medicine, 26:5, November 1995, pp.604-608.
16. Ghofrani HA, et al: Sildenafil Increased Exercise Capacity during Hypoxia and Low Altitudes and at Mount Everest Base Camp. Annals of Internal Medicine 141:3; Aug, 2004, pp169-177.
17. Grissom CK, Roach RC, Sarnquist FH, Hackett PH. Acetazolamide in the treatment of acute mountain sickness: Clinical efficiacy and effect on gas exchange. Ann Int Med. 1992: 116:6:461-465.
18. Heifetz In. Radiation Accidents. In Harwood-Nuss, A et al: The Clinical Practice of Emergency Medicine, Philadelphia, 1996, J.B. Lippincott Company.
19. Honigman B, Theis MK, McLain J, Roach RC, Yip R, Houston C et al. Acute mountain sickness in a general tourist population at moderate altitudes. Ann Int Med. 1993: 118:8:587-592.
20. Jerrard DA. Diving Medicine. In Emergency Medicine Clinics of North America. Vol 10. Num 10 May 1992.
21. Jerrard DA. Diving Medicine. In Emergency Medicine Clinics of North America. Vol 10. Num 2 May 1992.
22. Jolly BT, Ghezzi KT: Accidental hypothermia. Emerg Med Clinics NA. 1994; 10, (2); 311-327.
23. Kizer KW, Van Hoesen KB. Diving Medicine. Auerbach PA (ed.) Wilderness Medicine. 5th Ed. Philadelphia. Mosby Elsevier; 2007. 1599-1638.
24. Lavelle JM, Shaw KN, Seidl T, Ludwig S: Ten-year Review of Pediatric Bathtub Near-drownings: Evaluation for Child Abuse and Neglect. Annal Emerg Med, 1995;25:344-348.
25. Lee-Chiong TL, Stitt JT: Heat Stroke and Other Heat-Related Illnesses. Postgraduate Medicine 1995 Jul;26-36.
26. Lichtenberg R, et al, Cardiovascular Effects of Lightning Strikes, Journal of the American College of Cardiology, 21:2:531-6, 1993.
27. Madsen J, Hink J, Hyldegaard O. Diving Physiology and Pathophysiology. Clinical Physiology (1994) 14, 597-626.
Environmental Emergencies Page 287 Notes
28. Markovchick, V, Radiation Injuries. Marx JA, Hockenberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th ed, Philadelphia, Mosby Elsevier, 2006. pp. 2316-2325.
29. Moon RE, Vann RD, Bennett PB. The Physiology of Decompression Illness. Scientific American. August 1995.
30. Olshaker JS: Near Drowning. Emrg Med Clin NA, 1992; 10:339-349.
31. Price TG, Cooper MA: Electrical and Lightning Injuries, Marx JA, Hockenberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th ed, Philadelphia, Mosby Elsevier, 2006, pp. 2267-2278.
32. Primavesi, R. Electrical Injuries: Current Issues, Canadian Journal of CME June 1996, pp. 85-96.
33. Quan L, Wentz KR, Gore EJ, Copass MK: Outcome and Predictors of Outcome in Pediatric Submersion Victims Receiving Prehospital Care in King County Washington. Peds, 1990;86:586-593.
34. Raymond LW. Pulmonary Barotrauma and Related Events in Divers. Chest. 1995; 107;1648-52.
35. Simon HB: Hyperthermia. New England Journal of Medicine. 1993 Aug 12;329 (7) 483-7.
36. Smith RM, Neuman TS. Elevation of Serum Creatine Kinase in Divers with Arterial Gas Embolism. NEJM. 1994;330:19-24.
37. Tek D, Olshaker J: Heat Illness, Emergency Medical Clinics of North America. 1992 May; 10(2) 299-310.
08/17
Environmental Emergencies Page 288
Gynecological and Obstetrical Emergencies
Bophal Sarha Hang, MD
Assistant Professor of Emergency Medicine, Director of Web-based Education & Assistant Simulation Director, Beaumont Health & Oakland University William Beaumont School of Medicine, Royal Oak, Michigan
Page 289
Page 290 Notes
GYNECOLOGICAL EMERGENCIES
Vaginitis
I. TRICHOMONIASIS
A. Epidemiology:
1. Trichomonas vaginalis is an anaerobic flagellate protozoan. 2. Does NOT normally inhabit the GU tract. 3. High prevalence among black women compared to whites (13% versus 1.8%). 4. It is transmitted sexually. a. Incidence increases with number of sexual partners. b. Low socioeconomic class is a risk factor. c. Men and women are usually asymptomatic.
B. Pathophysiology:
1. Infection may cause vaginitis, urethritis, cervicitis and cystitis. a. Vaginitis is the primary infection in women. b. Cervicitis: i. Occurs in 13%. ii. Associated with “strawberry cervix.” c. Urethra infected in up to 90%. 2. Coexisting infections: a. Gonorrhea in up to 50%. b. Bacterial vaginosis. 3. Complications: a. Polymicrobial PID. b. During pregnancy: i. Premature rupture of membranes. ii. Preterm labor. iii. Post-partum endometritis.
C. Presentation:
1. Profuse vaginal discharge, pruritus and irritation. 2. May complain of dysuria and dyspareunia.
D. Diagnosis:
1. Speculum exam reveals vaginal discharge: a. Often not the classic yellow-green frothy discharge. b. Usually discharge is grey in color and profuse. c. Frothy discharge only present in 10%. 2. Strawberry cervix:
Gynecological Emergencies Page 291 Notes a. “Flea-bitten” appearance due to punctate submucosal hemorrhage. b. Only present in 2%, but denotes cervicitis. 3. Definitive diagnosis: a. Culture - prolonged incubation time, not used much. b. Wet-mount slide: i. Rapid and practical. ii. Positive for trichomonads in 60-80%. iii. See motile trichomonads microscopically. iv. Trichomonads are about the same size as leukocytes, which are usually also present. c. Nucleic acid amplification (NAAT) tests are highly sensitive. d. KOH “whiff” test - will emit a fishy odor if trichomonads are present. e. Gonorrhea and chlamydia testing should also be sent. 4. Bimanual examination will reveal no cervical motion tenderness or adnexal or uterine tenderness in a patient with isolated vaginitis.
E. Treatment:
1. Metronidazole: a. Anti-protozoan drug. b. Dosage: i. 2 grams orally as a single dose. ii. 500 mg twice a day for 7 days. iii. Single dose therapy usually initial course of choice. c. Produces a disulfiram-type reaction if taken with alcohol. d. Patients should refrain from drinking alcohol for at least 24 hours after taking Metronidazole. e. Reoccurrence rates are low. f. Class B in pregnancy. 2. Tinidazole: a. 2 gm orally as a single dose. b. Class C in pregnancy. c. Avoid alcohol for 72 hours. 3. All sexual partners need to be seen and treated prior to further sexual activity, as the organism is found in 70% of partners of an infected patient. 4. During pregnancy: a. Symptomatic patients need to be tested and treated. b. Adverse pregnancy outcomes: i. PPROM. ii. Preterm delivery. iii. Low infant birth weight. c. Metronidazole 2 g PO x 1.
Gynecological Emergencies Page 292 Notes
II. BACTERIAL VAGINOSIS
A. Epidemiology:
1. Previously referred to as nonspecific vaginitis, Haemophilus vaginalis, Gardnerella vaginalis or corynebacterium vaginale. 2. Preferred term now is bacterial vaginosis. 3. Microbial etiology is controversial: a. Polymicrobial. b. Overgrowth of normal flora. 4. Not inherently transmitted sexually.
B. Complications:
1. Polymicrobial PID. 2. During pregnancy: a. PROM. b. Preterm labor. c. Postpartum endometritis.
C. Presentation:
1. Patient will complain of a profuse watery and malodorous vaginal discharge. 2. Usually not a purulent discharge (unlike Trichomonosis). 3. Dysuria, dyspareunia and abdominal pain are rare.
D. Diagnosis:
1. Speculum exam often reveals profuse, watery, grayish malodorous vaginal discharge. 2. There is usually little or no inflammation (unlike Trichomonas or Candida). 3. Gonorrhea and Chlamydia testing should also be sent. 4. Wet prep will reveal many small bacteria with absence of white blood cells (unlike Trichomonas). 5. May see “clue cells” - epithelial cells studded with these tiny bacteria. 6. Gram stain may reveal gram negative coccobacilli instead of normal Lactobacillus which are gram positive. 7. Amine (fishy) odor released when vaginal discharge is mixed with KOH. 8. pH of vaginal fluid greater than 4.5.
E. Treatment:
1. Antibiotics effective against anaerobic bacteria. a. Metronidazole: Gynecological Emergencies Page 293 Notes i. 500 mg two times per day for 7 days. ii. Metronidazole gel 0.75% (5g) intravaginally daily for 5 days. b. Clindamycin: i. 2% vaginal cream 5 g intravaginally qHS for 7 days. ii. 300 mg po bid for 7 days. iii. 100g ovules intravaginally qHS x 3 days. 2. In pregnancy: a. Metronidazole 250 mg po tid for 7 days. b. Metronidazole 500 mg po bid for 7 days. c. Clindamycin 300 mg po bid for 7 days. d. It has been shown that treatment during pregnancy lowers the complication rate for BV in symptomatic women and in asymptomatic women at high risk for preterm labor. 3. Reoccurrence rates are high no matter which therapy chosen. 4. Treatment of sexual partners is currently not indicated.
III. VULVOVAGINAL CANDIDIASIS
A. Epidemiology:
1. Usually a fungal infection caused Candida albicans. 2. Although Candida species normally inhabits the gastrointestinal tract, it is usually NOT found in the vulva or vagina. 3. 75% of women have at least one episode of vulvovaginitis. 4. Under certain conditions, Candida may proliferate and invade the epithelium of the vagina or vulva. 5. Predisposing conditions to Candida vulvovaginitis include: a. Pregnancy. b. Immunosuppression. c. Medication: i. Oral contraceptives. ii. Antibiotics. iii. Corticosteroids. d. Diabetes mellitus. e. Hormonal - luteal phase of menstrual cycle. 6. Isolated Candida infection is not usually sexually transmitted.
B. Presentation:
1. Whitish vaginal discharge, pruritus and vulvar irritation. 2. Not odoriferous (unlike bacterial vaginosis or Trichomonas). 3. Patient may complain of dysuria, dyspareunia and vulvovaginal burning. 4. Complicated infections may cause edema, fissures and excoriations.
Gynecological Emergencies Page 294 Notes C. Diagnosis:
1. Speculum examination reveals a white curdy discharge. 2. Vulvar erythema is the most common sign. 3. Abdominal and bimanual examination should be unremarkable. 4. Cultures - impractical because of time constraints. 5. Wet mount reveals white blood cells without clue cells. 6. KOH prep: a. Of the discharge or scrapings of the border of the vulvar irritation. b. Classically demonstrates pseudohyphae or branching dendritic chains.
D. Treatment:
1. Clotrimazole: a. 100 mg vaginal tablet x 7 days. b. Two 100 mg vaginal tablets x 3 days. c. 1% cream - 5g intravaginally x 7 - 14 days. d. Cream applied locally to the vulva may lessen symptoms. 2. Miconazole nitrate: a. 200 mg suppository intravaginally q HS x 3. b. 100 mg vaginal suppository x 7 days. c. 2% cream - 5g intravaginally x 7 days. d. 1,200 mg vaginal suppository x 1 dose. 3. Butoconazole intravaginal agent: a. 2% cream – 5 g intravaginally x 3 days. b. 2% cream sustained release – 5 g intravaginally x 1 dose. 4. Nystatin intravaginal agent 100,000 unit vaginal tablet daily x 14 days. 5. Tioconazole intravaginal agent – 6.5% ointment 5 g intravaginally x 1 dose. 6. Terconazole intravaginal agent: a. 0.4% cream 5 g intravaginally x 7 days. b. 0.8% cream 5 g intravaginally x 3 days. c. 80 mg vaginal suppositories – 1 daily x 3 days. 7. Fluconazole (Diflucan) - 150 mg PO x 1 dose. 8. Partners should be referred for diagnosis and treatment only if symptomatic. 9. Diabetes and immunocompromised consider prolonged (i.e. 7- 14 days) treatment regimens. 10. Pregnancy: a. Incidence increases 10-20 times in the pregnant patient. b. Treat with topical azoles for 7 days. c. Fluconazole is pregnancy category D.
Gynecological Emergencies Page 295 Notes
Genital Ulcers
I. HERPES SIMPLEX TYPE 2
A. Epidemiology:
1. The prevalence of HSV 1 and 2 in the U.S. remains very high. 2. Overall, 16% of Americans between the ages of 14 and 49 (or 1 in 6) are infected with HSV, while black women have a prevalence rate of 48% (CDC, 2010). 3. Spread primarily through sexual contact. 4. Increasing prevalence of anogenital herpetic infections due to HSV-1 among young women and MSM.
B. Pathophysiology:
1. Following the initial attack, the virus harbors in dorsal nerve root ganglia of the affected site. 2. The viral disease is then reactivated in up to 50% of cases by emotional or physical stress.
C. Presentation:
1. Primary herpetic infection: a. Begins 3-7 days after contact with the virus. b. Vulvovaginal pain, dysuria, fever, malaise and myalgias. c. Tender nonfluctuant, bilateral inguinal lymphadenopathy. d. 2-4 mm clear fluid vesicles with erythematous bases. e. These vesicles then rupture and form small ulceration. f. Usually lasts from 2-6 weeks. 2. Reoccurrence: a. Occur in up to 50% of cases. b. Heralded by a tingling sensation in the genitals. c. Usually less painful and there is no systemic illness or tender lymphadenopathy after the primary infection. d. Duration is much shorter than with the primary infection.
D. Diagnosis:
1. Classic lesions: painful, multiple vesicular or ulcerative lesions in the anogenital region. 2. Tzanck smear: a. Multinucleated giant cells with intranuclear inclusion bodies. b. Only 40-50% as sensitive as viral cultures. 3. Viral cultures specific for Herpes Simplex Type 1 or 2. Gynecological Emergencies Page 296 Notes 4. PCR assay for HSV DNA is the most sensitive method. 5. Type-specific serologic testing (80-98% sensitive) may be useful in these clinical settings: a. Recurrent or atypical symptoms with negative PCR or viral culture. b. Clinical diagnosis without lab confirmation. c. Exposure to a partner diagnosed with HSV.
E. Treatment:
1. Symptomatic treatment: a. Burow’s solution. b. Sitz baths. c. Analgesics. 2. Specific treatment: a. Primary Herpes Simplex: i. Acyclovir (Zovirax): 200 mg po 5 times daily or 400 mg tid for 7-10 days. Shortens the duration of pain. Decreases the viral shedding. Shortens the systemic symptoms. ii. Famciclovir: 250 mg po tid for 7-10 days. iii. Valacyclovir: 1 g po bid for 7-10 day. . b. Recurrent Herpes Simplex - episodic therapy: i. Acyclovir: 400 mg po tid for 5 days. 800 mg po bid for 5 days. 800 mg po tid for 2 days. ii. Famciclovir: 125 mg po bid for 5 days. 500 mg po x 1, then 250 mg bid for 2 days. 1000 mg orally twice daily for 1 day. iii. Valacyclovir: 500 mg po bid for 3 days. 1 g po once daily for 5 days. c. Topical acyclovir - not therapeutic. d. Severe disease – acyclovir 5-10 mg/kg IV tid until clinical resolution. e. Pregnancy: i. High rate of transmission during primary infection (30-50%). ii. Requires suppressive therapy. iii. Acyclovir 400 mg tid or valcyclovir 500 mg bid.
Gynecological Emergencies Page 297 Notes
II. CHANCRE
A. Epidemiology:
1. Between 2014 and 2015, incidence of primary and secondary syphilis increased 19%. 2. High risks groups are men who have sex with men (MSM) or HIV positive.
B. Smooth, painless ulcer.
C. Forms at the site of initial inoculation in primary syphilis.
D. Syphilis review:
1. Primary syphilis: a. 21-day incubation period (can range 10-90 days). b. Chancre forms at the site of initial inoculation and usually heals in 3-6 weeks. c. Smooth, painless ulcer. 2. Secondary syphilis: a. 4-10 weeks after the primary chancre. b. Macular pink or reddish-brown rash on trunk, extremities including palms and soles, sparing the face. c. Condyloma lata on moist intertriginous areas. d. Fever, malaise, generalized lymphadenopathy, mucous patches. 3. Latent syphilis: a. Tests are positive, but patient is asymptomatic. 4. Tertiary syphilis: a. 10 years after initial chancre. b. Neurosyphilis, cardiovascular, auditory, ophthalmologic or gummatous syphilis.
E. Diagnosis:
1. Wear gloves, as all primary and secondary syphilitic lesions are highly infectious. 2. Dark-field examination for spirochetes from exudate aspirated from chancres, condyloma lata or mucous patches. 3. Nontreponemal (NT) serologic tests: a. VDRL or RPR. b. Good screening tool. c. Many false positives. d. Useful in following treatment as test reverts back to negative when syphilis infection is eradicated.
Gynecological Emergencies Page 298 Notes e. For high risk patients with negative VDRL or RPR, repeat NT test is recommended in 2-4 weeks to evaluate for early infection. 4. Treponemal serologic tests: a. FTA-ABS – Fluorescent Treponemal Antibody Absorption. b. TP-PA – Treponema Pallidum Particle Agglutination. c. EIA – Enzyme immunoassays. d. CIA – Chemiluminescent immunoassays. e. Very specific used to detect Treponema antibodies and confirm the diagnosis if NT test +. f. Once the test has turned positive, usually remains positive for life. g. Therefore not useful in following management.
F. Treatment:
1. Primary, secondary and latent (less than 1 year) syphilis: a. Benzathine pen G 2.4 million U I.M. for one dose therapy. b. Penicillin allergic: i. Tetracycline 500 mg orally QID x 14 days. ii. Or Doxycycline 100 mg orally BID x 14 days. 2. Tertiary or latent (greater than 1 year) syphilis: a. Benzathine pen G 2.4 million U IM per week x 3 weeks. b. Penicillin allergic: Tetracycline or Doxycycline for 28 days if latent; Infectious Disease consult if tertiary. 3. Pregnancy - Penicillin (desensitize if allergic). 4. Neurosyphilis – Penicillin G 3-4 million units IV every 4 hours for 10-14 days. 5. Children: a. Benzathine pen G 50,000 units/kg IM, up to the adult dose of 2.4 million units in a single dose for primary, secondary and early latent syphilis. b. Benzathine pen G 50,000 units/kg IM per week x 3 weeks, up to the adult dose of 7.2 million units for late latent and tertiary syphilis.
III. CHANCROID
A. Painful genital ulcers.
B. Declining prevalence but might still occur in some regions of Africa and the Caribbean.
C. Hemophilus ducreyi.
D. Clinical diagnosis with inguinal lymphadenopathy and painful ulcers.
Gynecological Emergencies Page 299 Notes E. Rule out herpes simplex and syphilis.
F. Treatment:
1. Azithromycin 1 gram PO x 1. 2. Ceftriaxone 250 mg IM. 3. Erythromycin base 500 mg tid x 7 days. 4. Ciprofloxacin 500 mg bid x 3 days.
Genital Warts
I. CONDYLOMA ACUMINATA
A. Caused by the human papillomavirus.
B. Painless, nonpruritic, pedunculated or sessile warts.
C. Sexually transmitted:
1. 25% of sexual partners of the index case will get the lesions. 2. Risk increased even further in immunocompromised patients. 3. 12-34% of patients with genital warts also have gonorrhea, chlamydia or syphilis infections. 4. Associated with cervical neoplasia.
D. Diagnosis - by site, biopsy all tissue removed.
E. Treatment:
1. Provider - Podophyllin, cryotherapy, laser therapy, trichloroacetic acid or bichloracetic acid 80-90%. 2. Patient - Podofilox 0.5% solution or gel, Imiquimod 5% cream, Sinecatechins 15% ointment.
II. CONDYLOMA LATA
A. Warty lesions caused by syphilis.
B. Wart is smoother and moister than Condyloma acuminatum.
Bartholin Abscess
I. CHARACTERISTICS
A. Very painful.
B. Contains mixed bacterial pathogens from the vagina. Gynecological Emergencies Page 300 Notes
C. Gonorrhea implicated in @ 10% of cases.
II. TREATMENT
A. Incision and drainage of the cyst or abscess in the emergency department.
B. Placement of a Word catheter after the I & D.
C. A CO2 laser may be used alternatively to recreate a duct orifice.
Cervicitis
I. NEISSERIA GONORRHEA
A. Pathophysiology:
1. Gram negative intracellular diplococci. 2. Causes 5 different patterns of disease in women: a. Asymptomatic carriers. b. Cervicitis. c. Pelvic Inflammatory Disease (PID): i. Up to 20% of patients with GC develop PID. ii. 33-80% of patients with PID have GC. d. Disseminated gonorrhea - hematogenous spread: i. Migratory septic arthritis. ii. Arthritis-Dermatitis syndrome: Fever, chills. Polyarticular arthritis or arthralgias. Rash. Tenosynovitis of extensor tendons of hands, wrists and ankles. iii. Meningitis – rare. iv. Endocarditis – rare. v. Perihepatitis. vi. 80% of disseminated GC occurs in women. vii. ≈ 66% develop within the first week following the last menses. e. Ophthalmitis.
B. Presentation:
1. Purulent endocervical discharge. 2. Usually symptomatic soon after menses begins. 3. Lower abdominal pain.
Gynecological Emergencies Page 301 Notes C. Diagnosis:
1. Gram negative intracellular diplococci on gram stain: a. 95% specific. b. Less than 60% sensitive. So do not rule out GC if gram stain inconclusive. 2. Culture on Thayer-Martin plate with 3-5% CO2. 3. Finding other pathogens on microscopy also does not rule out GC: a. 35% of patients with GC also had Trichomoniasis. b. 19% of patients with GC also had Candida vaginalis. 4. Nucleic acid amplification and hybridization testing (NAAT) more sensitive than culture.
D. Treatment:
1. Urethral, cervical, rectal or pharyngeal gonorrhea: a. Ceftriaxone 250 mg IM - 1 dose. b. Cefixime 400 mg PO - no longer recommended by CDC. c. Fluoroquinolone no longer recommended due to high resistance rates. 2. Ophthalmologic: a. Ceftriaxone 1 gram IM - 1 dose. b. Saline irrigation. 3. All patients with GC should be tested for Chlamydia if reliable for follow up, or treated with doxycycline (100 mg bid for 7 days) or Azithromycin (1 gram orally x 1 dose). 4. Cephalosporin allergy: a. Azithromycin 2 grams orally as a single dose, but high level of resistance developing. b. Fluoroquinolone if antimicrobial susceptibility is documented by culture.
II. CHLAMYDIA TRACHOMATIS
A. Pathophysiology:
1. Most common of all the STIs. 2. Highest prevalence in < 25 years of age. 3. Obligate intracellular parasite. 4. Causes 5 patterns of disease in women: a. Asymptomatic. b. Acute urethral syndrome - pyuria without bacteria. c. Cervicitis. d. PID. e. Lymphogranuloma venereum (LGV): i. Small painless vesicle which then ulcerates. ii. Tender, ulcerated unilateral inguinal lymphadenopathy. Gynecological Emergencies Page 302 Notes iii. May mimic protocolitis in MSM and anorectal exposure in women.
B. Presentation:
1. Mucopurulent cervical discharge; may be watery and non- purulent. 2. Cervical erythema. 3. Usually less symptomatic than with gonorrhea.
C. Diagnosis:
1. Gram stain that shows > 10 PMN leukocytes without bacteria. 2. Direct fluorescent monoclonal antibody test of cervical exudate. 3. Chlamydia culture. 4. Nucleic acid amplification and hybridization testing (NAAT) more sensitive than culture.
D. Treatment:
1. Urethritis or cervicitis: a. Doxycycline 100 mg PO bid for 7 days. b. OR Azithromycin 1 gram PO - 1 dose. c. OR Erythromycin 500 mg PO qid for 7 days. d. OR Ofloxacin 300 mg PO bid for 7 days. e. OR Levofloxacin 500 mg daily for 7 days. f. In pregnancy: i. Azithromycin 1 gram PO for 1 dose. ii. OR Amoxicillin 500 mg tid for 7 days. 2. LGV: a. Doxycycline 100 mg PO bid for 21 days. b. OR Erythromycin 500 mg PO qid for 21 days.
Pelvic Inflammatory Disease
I. EPIDEMIOLOGY
A. Most common serious infection in reproductive-aged women in the U.S.
B. 2.5 million patient visits annually for PID.
C. 250,000 hospitalizations annually.
D. 150,000 surgical procedures for complications of PID annually.
E. Estimated annual cost: $3.5 billion/year. Gynecological Emergencies Page 303 Notes
II. PATHOPHYSIOLOGY
A. PID can be acute (< 30 days), subclinical or chronic (>30 days).
B. Hallmark is pelvic tenderness with evidence of lower genital tract inflammation (e.g., cervical mucopurulent discharge, friability or positive swab test).
C. Infection-induced inflammation of the upper reproductive:
1. Endometrium – endometritis. 2. Fallopian tubes – salpingitis. 3. Ovaries – oophoritis.
D. May progress to tuboovarian abscess or pelvic peritonitis.
E. PID usually begins as a cervical infection with Neisseria gonorrhea and/or Chlamydia trachomatis (85%).
F. The resulting cervicitis alters the vaginal-cervical microenvironment, leading to overgrowth of endogenous and anaerobic flora.
G. Thus PID is a polymicrobial disease. Common pathogens:
1. Neisseria gonorrhea. 2. Chlamydia trachomatis. 3. Anaerobes (e.g., bacteroides, peptostreptococcus). 4. Haemophilus influenza. 5. Escherichia coli. 6. Group B strep.
III. PRESENTATION
A. Risk factors:
1. Previous history of PID. 2. Multiple sexual partners. 3. Intrauterine conception device (IUD) usage. 4. Adolescence: a. Inverse proportion of incidence to age. b. 75% of cases occur between the ages of 15-25. 5. Instrumentation of the uterine cavity: a. Dilation and curettage. b. Endometrial biopsy. c. Hysterosalpingography. d. Cervix cautery or cryotherapy.
Gynecological Emergencies Page 304 Notes B. Symptoms:
1. Classic presentation is acute onset of lower abdominal pain - usually bilateral during or shortly after menses. 2. Clinical symptoms may vary. 3. Purulent vaginal discharge - present in over 50% of patients. 4. Abnormal vaginal bleeding - from endometritis. 5. Dyspareunia. 6. Fever and general malaise. 7. Nausea and anorexia. 8. Dysuria without frequency or urgency.
C. Physical findings:
1. Lower abdominal tenderness. 2. Cervical motion tenderness (Chandelier sign). 3. Adnexal tenderness bilaterally. 4. Adnexal mass may be present if patient has a tuboovarian abscess. 5. Purulent cervical discharge - if absent, this does not preclude the diagnosis of PID. 6. Fever is not a prominent feature of PID (< 1/3 patients).
IV. DIAGNOSIS
A. Criteria for empiric treatment of PID:
1. CDC minimum criteria: a. Cervical motion tenderness. b. OR adnexal/uterine tenderness. c. In a patient with lower abdominal or pelvic pain, at risk for STDs and no other cause for the illness is identified. 2. Other supporting evidence for PID: a. Abnormal cervical mucopurulent discharge or friability. b. Leukocytosis in vaginal secretions. c. Temperature greater than 38.3 degrees C (101 F). d. Laparoscopy. e. Inflammatory mass detected by bimanual examination or sonography. f. Erythrocyte sedimentation rate over 15 mm/h. g. Elevated C-reactive protein.
B. Testing for N. gonorrhea or Chlamydia trachomatis:
1. Gram stain of cervical secretions: a. Gram-negative intracellular diplococci – N. gonorrhea. b. Vaginal flora. 2. Culture and sensitivity of cervical secretions: a. Chocolate agar or Thayer Martin plate – N. gonorrhea. Gynecological Emergencies Page 305 Notes b. Chlamydia trachomatis. 3. Nucleic acid amplification and hybridization testing (NAAT): a. More sensitive than culture. b. Can be run on cervical secretions or urine.
C. HCG determination:
1. To rule out pregnancy. 2. Very unusual (i.e., reportable) to have PID and pregnancy because after implantation, a mucous plug forms that prevents spread of infection from the lower to the higher genital tract.
D. Leukocytosis – not always present.
E. Pelvic ultrasound - to rule out tuboovarian abscess or other pelvic abscess if patient unresponsive to antibiotic therapy after 48-72 hours or if unilateral symptoms in a toxic-appearing patient.
V. COMPLICATIONS OF PID
A. Chronic pelvic pain.
B. Dyspareunia.
C. Infertility.
D. Ectopic pregnancy.
E. Tuboovarian abscess:
1. Walled off abscess originating in the infected fallopian tube, which may then extend to involve the fimbriae and the ovary as well. 2. Patients appear septic, have exquisite unilateral adnexal tenderness and usually have a mass or fullness appreciated on bimanual examination. 3. This is primarily an anaerobic infection and generally needs to be drained surgically and treated with parenteral antibiotics.
F. Fitz-Hugh-Curtis Syndrome:
1. Perihepatitis secondary to PID. 2. Occurs in 8-10% of patients with PID. 3. It is most commonly associated with Chlamydia trachomatis (but also associated with N. gonorrhea). 4. Purulent discharge from the fallopian tube ascends to the tissue adjacent to the liver, in the right colic gutter. 5. Causes adhesion formation between the liver capsule and the Gynecological Emergencies Page 306 Notes abdominal wall. 6. Patients usually complain only of sudden, severe, sharp RUQ pain; this may be pleuritic and may be referred to the right shoulder. 7. The RUQ pain may be so severe that patients do not complain of vaginal discharge or bilateral lower pain. 8. Thus the presence of RUQ pain in a woman of childbearing age mandates a pelvic exam to rule out perihepatitis. 9. Physical exam will reveal vaginal purulent discharge, bilateral lower quadrant AND right upper quadrant abdominal tenderness. 10. The patient with Fitz-Hugh-Curtis usually has systemic illness, including fever, chills, nausea, vomiting and generalized malaise. 11. Elevated liver enzymes.
VI. TREATMENT
A. 25-50% of patients with culture-proven N. Gonorrhea are co- infected with Chlamydia, so treat for both.
B. Indication for admission include any of the following criteria:
1. Suspected tuboovarian abscess. 2. Temperature greater than 101 F (38.3 C). 3. Pregnancy. 4. Patient unable to hold down fluids (and thus oral antibiotics). 5. Evidence of Fitz-Hugh-Curtis: a. RUQ tenderness. b. Elevated liver function studies. 6. Peritonitis. 7. Patient unreliable for oral antibiotic therapy and follow-up. 8. Patient who fails outpatient management. 9. Uncertain diagnosis and in whom surgical emergencies such as appendicitis, ovarian torsion, etc., cannot be excluded. 10. Patient who appears septic. 11. Prepubertal children (rule out sexual abuse). 12. Patients with IUD in place. 13. Consider admission for the nulliparous patient.
C. In-patient management:
1. Gonorrhea is notoriously penicillin and fluoroquinolone resistant. 2. Chlamydia is rarely resistant to current therapy. 3. Cefoxitin 2 grams IV q 6 hours or Cefotetan 2 grams IV q 12 hours. 4. WITH: Doxycycline 100 mg PO or IV q 12 hours. 5. Treat with IV antibiotics for approximately 24 hours after the Gynecological Emergencies Page 307 Notes patient improves, then continue oral Doxycycline (100 mg bid) to complete a 14 day course. 6. Alternatives regimens: a. Clindamycin 900 mg IV q 8 hours AND Gentamicin 2 mg/kg load followed by 1.5 mg/kg q 8 hours. b. OR Ampicillin/Sulbactam 3 g IV qid PLUS Doxycycline 100 mg bid PO/IV for 14 days.
D. Outpatient management:
1. Ceftriaxone 250 mg IM once PLUS Doxycycline 100 mg bid for 14 days with/without Metronidazole 500 mg PO bid x for 14 days. 2. OR Cefoxitin 2 gm IM with Probenecid 1 gm PO PLUS Doxycycline 100 mg bid for 14 days with/without Metronidazole 500 mg bid for 14 days. 3. Discharge instructions to include: a. No sexual activity (intercourse, oral, etc.) until all sexual partners have also been seen and treated and the patient and partners have had a negative culture after antibiotic therapy is complete. b. Referral numbers for follow-up for both the patient and their partners with specific instructions that their partners need to be evaluated also. c. 72 hour follow-up or sooner if patient develops any signs or symptoms that would necessitate admission (see 6-B above).
Pelvic Pain
I. GENERAL
A. Pelvic pain must be differentiated from pain of gastroenteric or urologic origin.
B. Pelvic pain is the second most common gynecologic presenting complaint (abnormal vaginal bleeding is the first).
C. It is important that a pregnancy test be done on all women of reproductive age presenting with abdominal pain or abnormal vaginal bleeding.
D. If the patient is pregnant, ectopic pregnancy must then be ruled out.
E. If the patient is not pregnant, the following differential diagnosis of pelvic pain should be entertained: PID, ovarian mass complications, fibroids, mittelschmerz, and endometriosis.
Gynecological Emergencies Page 308 Notes
II. PID
A. PID is the most common cause of pelvic pain.
B. See above section on PID.
III. OVARIAN CYST OR MASS
A. Pathophysiology:
1. Types of ovarian masses: a. Functional cysts - most common: i. Follicular cysts occur the first two weeks of the menstrual cycle. ii. Corpus luteal cysts occur the last two weeks of the menstrual cycle. b. Benign and malignant cystic and solid ovarian masses. 2. Ovarian enlargement due to cystic and solid ovarian masses are usually asymptomatic unless one of five things occur: a. Cyst rupture. b. Torsion of the ovary. c. Intratumor hemorrhage. d. The mass pushes on contiguous structures. e. The bulk of the mass is so large that the patient experiences abdominal pain, ascites and abdominal enlargement.
B. Ruptured ovarian cyst:
1. Presentation: a. Patient develops sudden, sharp, severe unilateral pain. b. Often rupture occurs during intercourse, exercise or an aggressive pelvic examination. c. Signs of peritonitis may be evident: i. Hemorrhagic corpus luteum cyst rupture - will develop peritonitis from hemoperitoneum. ii. Ruptured dermoid cyst may produce a chemical peritonitis - with fever, ileus and distention. d. Signs and symptoms may quickly abate after rupture of a simple follicular cyst. e. Unilateral adnexal tenderness and possible fullness will be elicited on bimanual pelvic examination. 2. Diagnosis: a. hCG testing - to rule out ectopic pregnancy rupture. b. Hg/Hct may be lowered in patients with ruptured hemorrhagic corpus luteal cyst.
Gynecological Emergencies Page 309 Notes c. Pelvic ultrasound may demonstrate free fluid in the posterior cul-de-sac. The type of fluid, however, may not be differentiated by sonographic examination. d. Laparoscopy may be necessary for diagnosis in a patient with peritoneal findings. 3. Treatment: a. Observation - ruptured follicular cyst. b. Gynecology consult and possible surgery: i. Ruptured hemorrhagic corpus luteal cyst. ii. Ruptured dermoid cyst.
C. Ovarian torsion:
1. Pathophysiology: a. Occurs if limited enlargement of an ovarian mass occurs. i. Stretching of the mesovarium from the enlarging mass, to the point that it effectively acts as a pedicle. ii. The “pedunculated” mass then may twist on its pedicle. iii. Ovarian blood supply then becomes compromised. iv. Leading to painful ischemic degeneration of the ovary. v. Eventual gangrenous necrosis of the ovary. b. Torsion is more likely to occur if there is a solid tumor or a dense cystic tumor of the ovary. c. Ovarian torsion can occur at any age. d. 15% of cases occur in premenarchal girls. e. Complications: i. Scarred fallopian tube. ii. Thrombosis of infundibulopelvic vessels with possible resultant pulmonary embolization. iii. Ovarian abscess and/or necrosis. iv. Peritonitis and shock. 2. Presentation: a. Torsion may produce intermittent, recurrent attacks of colicky pain, nausea, vomiting and low grade fever. b. Or, torsion can present with signs and symptoms of an acute abdominal process (rebound tenderness with rigidity, etc.). c. Pain is often described as sudden, sharp and severe. d. Unilateral lower quadrant tenderness is most common, but may progress to diffuse abdominal tenderness. e. Adnexal fullness and tenderness is usually evident on pelvic exam. f. Associated nausea and vomiting are frequently present. 3. Diagnosis: a. hCG testing - to rule out ectopic pregnancy. b. Pelvic sonography – color flow Doppler is diagnostic.
Gynecological Emergencies Page 310 Notes c. Laparoscopy - may be necessary since it may be impossible to differentiate appendicitis, ovarian torsion, and ovarian cyst rupture or intratumor hemorrhage with peritonitis pre-operatively. 4. Management: a. Urgent gynecologic consultation. b. Laparotomy: i. Important that the ovarian mass not be de torsed until clamping of the more proximal vascular pedicle occurs; to prevent thrombi dislodgement and pulmonary embolization. ii. Salvage rate for the torsed ovary is low.
IV. MITTELSCHMERZ
A. Pathophysiology:
1. Unilateral adnexal pain at the time of ovulation. 2. Secondary to rupture of a follicle with ovum extrusion or from bleeding from the follicle site itself, resulting in a limited hemoperitoneum and thus local irritation. 3. Occurs in up to 25% of ovulating women. 4. Less common after the third decade of life.
B. Presentation:
1. Unilateral pain, usually lasting a few hours, but may last for 3 days. 2. Sharp, well localized abdominal tenderness without peritoneal findings. 3. Withdrawal spotting may be present. 4. Malaise and nausea may be present.
C. Diagnosis:
1. hCG testing. 2. Observation - symptoms should abate.
D. Treatment:
1. Nonsteroidal anti-inflammatory agents. 2. Reassurance. 3. Ovulation suppression therapy if symptoms are severe.
V. UTERINE FIBROIDS
A. Incidence:
1. Most common tumor of the uterus. Gynecological Emergencies Page 311 Notes 2. Occur in ≈ 20% of women over age 35. 3. More common in black women. 4. Tend to occur at an earlier age in black women. 5. New tumors rarely develop after menopause. 6. There may be some regression in size after menopause.
B. Complications:
1. Sarcomatous transformation to cancerous leiomyosarcoma occurs in less than 1% of patients. 2. Red degeneration or carneous degeneration: a. Hemorrhagic necrosis of fibroid may occur during pregnancy because the tumor outgrows its blood supply. b. May mimic other obstetrical emergencies such as abruptio placenta. c. May produce pain, fever, leukocytosis. d. Treatment is symptomatic: bed rest and analgesics.
C. Presentation:
1. Patients may complain of heaviness or fullness of the abdomen. 2. Rarely cause pain, unless complication such as torsion, ischemia, necrosis or hemorrhage occurs. 3. May cause pressure effects: a. Difficulty voiding. b. Stress urinary incontinence. c. Urinary retention. d. Constipation. e. Neuropathy if impinge on nerve roots. 4. Most common symptom is increasingly heavy and longer lasting menstrual bleeding. 5. Physical examination may reveal a palpable mass or an enlarged and irregular uterus.
D. Diagnosis:
1. hCG testing. 2. Pelvic ultrasound will reveal a uterine mass. 3. Hg/Hct - patients with hypermenorrhea secondary to fibroids will often be anemic.
E. Treatment:
1. Gynecology referral. 2. Possible elective leiomyectomy or hysterectomy.
Gynecological Emergencies Page 312 Notes VI. ENDOMETRIOSIS
A. Epidemiology:
1. Occurs in 8-15% of all menstruating women. 2. 75% of patients are diagnosed between the ages of 25-45. 3. More common among women in whom pregnancy has been delayed. 4. More common in upper socioeconomic groups. 5. Relatively common cause of pelvic pain and infertility.
B. Pathophysiology:
1. Growth of endometrial tissue in extra-uterine locations - endometrium normally lines the uterine cavity. 2. Sites of ectopic endometrial tissue: a. Ovaries = most common. b. Uterine ligaments, rectovaginal septum, pelvic peritoneum, umbilicus, laparotomy scars, hernia sacs, vagina, vulva, cervix, pleura of lung, lymphatics (rare). 3. Advanced disease may involve all peritoneal organs. 4. Tissue responds to hormonal stimulation at the ectopic sites, just as normal endometrium does. a. Why patients classically get symptoms at the time of menstruation. b. Useful in therapy. 5. Complications: a. Distortion of pelvic structures. b. Adhesion formation. c. Infertility - from peritubal adhesions.
C. Presentation:
1. Causes secondary dysmenorrhea in older women. 2. Patients present with chronic abdominal pain, dyspareunia, abnormal vaginal bleeding or infertility. 3. History of repeated attacks. 4. Although there are no absolute classic symptoms, dysmenorrhea is common. 5. Dyspareunia occurs when there is involvement of the uterosacral ligaments. 6. Infertility is common, which is unfortunate since one of the best treatments of endometriosis is pregnancy. 7. Severity of symptoms correlates poorly with extent of endometriosis. 8. Physical exam findings: a. No abnormal findings may be present. b. Fixed retroverted uterus. c. Ovarian masses (chocolate cysts). Gynecological Emergencies Page 313 Notes d. Uterosacral nodularity. e. Recto vaginal nodularity.
D. Diagnosis:
1. Diagnosis can be suspected on the basis of history and physical. 2. Definitive diagnosis is made by visualization with laparoscopy or by biopsy.
E. Treatment:
1. Analgesics. 2. Gynecology referral. 3. For patients who want to preserve reproductive function: a. Danazol (Danocrine): i. Methyl sterone derivative. ii. Medically produces a “menopausal” state. b. High dose estrogen. c. Progesterone. d. Combined oral contraceptives: i. Continuous usage. ii. Produces a “pseudopregnancy” state. e. Pregnancy - will stop the cyclic endometrial changes and lead to regression of endometriosis. 4. For symptomatic patients whose families are complete: a. TAH-BSO may be considered. b. Bilateral oophorectomy will stop the hormonal cycling.
Vaginal Bleeding
I. DEFINITIONS
A. Amenorrhea – Bleeding absent for 6 months or more in a non- menopausal woman.
B. Dysmenorrhea – Painful menstruation.
C. Dysfunctional uterine bleeding – Ovulatory or anovulatory bleeding, diagnosed after the exclusion of pregnancy, medications, iatrogenic causes, genital tract pathology, and systemic disease.
D. Menorrhagia – Bleeding occurring at regular intervals, but with heavy flow (≥80 ml) or duration (≥7 days).
E. Metrorrhagia – Bleeding among premenopausal women at irregular intervals.
F. Postmenopausal bleeding – Recurrence of bleeding in a menopausal Gynecological Emergencies Page 314 Notes woman at least 1 year after cessation of cycles.
II. DIFFERENTIAL DIAGNOSIS
A. Newborn:
1. Maternal estrogen withdrawal (lasts 3-4 days). 2. Bleeding disorders.
B. Children:
1. Foreign bodies. 2. Trauma (red flag). 3. Precocious puberty (ovarian, adrenal or CNS tumors). 4. Zebra: sarcoma botryoides.
C. Menarche:
1. Anovulatory DUB. 2. Blood dyscrasias (ITP).
D. Postmenopausal:
1. Endometrial cancer. 2. Estrogen therapy. 3. Atrophic vaginitis. 4. Anatrophic endometrium. 5. Polyps.
E. Reproductive years:
1. Disturbances of pregnancy. 2. Fibroids (menorrhagia; fullness or pressure but no pain). 3. Cervicitis/PID. 4. IUD/foreign body. 5. Breakthrough bleeding from BCP usage - need reassurance only. 6. Post-partum hemorrhage (>500 ml): a. Retained products. b. Uterine atony. 7. Endometritis (post Ab or perinatal). 8. Trauma. 9. Metabolic: a. Hyperthyroid. b. Hypothyroid. c. Cushing’s. 10. Nutritional extremes. 11. Cancer: a. Endometrial. Gynecological Emergencies Page 315 Notes b. Cervical. c. Vaginal. d. Ovarian. 12. Polyps: a. Cervical. b. Endometrial. 13. Blood dyscrasia: a. Thrombocytopenia. b. Coumadin prescription. c. Hypermenorrhea. d. Polymenorrhea. 14. Endometriosis or adenomyosis (with pain). 15. Psychogenic factors (stress). 16. Dysfunction uterine bleeding - DUB (85% anovulatory).
III. WORK-UP
A. Laboratories:
1. Hg/Hct. 2. Rh if pregnant. 3. HCG. 4. Quantitative B-HCG for follow up if pregnant. 5. T&C. 6. Consider PT/PTT/platelets.
B. Pelvic ultrasound.
IV. TREATMENT
A. ABCs - unusual to have severe hemorrhage in the non-pregnant patient, but can occur with:
1. Cervical cancer. 2. Post-operative hemorrhage. 3. Dysfunctional uterine bleeding in adolescents.
B. Gynecology referral or urgent consult if severe bleeding.
C. All patients over the age of 35 with dysfunctional bleeding and all post-menopausal women with bleeding other than withdrawal bleeding from estrogen therapy, should have timely gynecologic follow-up for endometrial sampling (endometrial biopsy or dilatation and curettage sampling).
V. DISPOSITION - ADMIT
A. Hemodynamic instability.
Gynecological Emergencies Page 316 Notes B. Suspect child abuse.
C. Children needing GA for PE or repair.
D. All significant third trimester bleeds.
E. Cancer work-up in patient likely to be lost to follow-up.
Sexual Assault by History
I. INTRODUCTION
A. Definition:
1. Varies from state to state. 2. Most statutes define rape as the “penetration, no matter how slight, of the vagina or anus with any body part or object, or oral penetration by sex organ of another person, without the consent of the victim.” 3. Evidence must support the allegations that: a. Force or threat of force was involved. b. The action was against the will of the accuser. c. A sexual act actually occurred.
B. Revised laws:
1. Most states have expanded the traditional rape statutes: a. Marital rape. b. Date rape. c. Shield laws - prevent past sexual practices of the victim from being introduced as evidence. 2. Because of changing law and also inter- and intra-state variability, it is important for each emergency department to have access to applicable statutes for their jurisdiction.
C. Violent crime.
D. Legal aspects:
1. Burden of proof is on the accuser. 2. Defendants charged with rape are four times less likely to be convicted than defendants charged with other crime. 3. Rape is a legal term, not a medical diagnosis.
II. INCIDENCE
A. In the United States, it is estimated that one out of every 6 women is raped in her lifetime.
Gynecological Emergencies Page 317 Notes B. In the United States, a rape is reported every 2-5 minutes.
C. It is estimated that only one in five rapes of adult women are actually reported.
D. Sexual assault is the fastest growing violent crime in the United States.
E. Over 300,000 women and 92,000 men are raped each year in the United States; more than 1/3 of all lifetime rapes occur before the age of 12, while more than half occur before the age 18.
F. 5-6% of sexual assault victims are male.
III. ROLE OF THE EMERGENCY PHYSICIAN
A. Evaluate for any life-threatening injury.
B. Assessment and treatment of physical injuries.
C. Prevention of venereal disease and pregnancy.
D. Collection of evidence.
E. Recognition and management of emotional trauma.
IV. HISTORY
A. History of the assault:
1. Should not be exhaustive. a. Patient may not remember details accurately while she is so emotionally distraught. b. May later prove confusing in court. 2. Important information to gather: a. Date and time of the assault. b. Areas of the body affected: i. Physical trauma. ii. Sexual contact. c. Location in which the attack occurred. d. Perpetrator: i. Known to victim in up to 80% of cases. ii. Number of assailants. iii. Description - will be done by police. e. Threats of violence should be noted. f. Use of weapons, restraints, foreign bodies, etc. should be documented. g. Type of sexual acts: i. Vaginal, oral or anal penetration or attempt at Gynecological Emergencies Page 318 Notes penetration. ii. Did perpetrator wear condom? iii. Did ejaculation occur?
B. Historical data surrounding the incident:
1. Post assault clean-up: a. Douching. b. Bathing/showering. c. Defecation. d. Urination. e. Change of clothes. f. Brush teeth. 2. Pre-assault factors: a. Gravidity, parity, LMP. b. Contraceptive usage. c. Date of last consensual intercourse. 3. Past medical history: a. Allergies. b. Medications. c. Past medical or surgical diseases.
V. PHYSICAL EXAMINATION
A. Clothing should be placed in a paper bag and transferred to the police as evidence when they arrive.
B. Modesty of the patient should be respected.
C. Skin:
1. Carefully examine for scratches, bruises, teeth marks, rope marks, burns, etc. 2. Special attention to neck, oral mucosa, face, lips, perineum, medial thighs, breasts and wrists.
D. Cervical spine tenderness:
1. Strangulation. 2. Battering/falls.
E. Wood’s lamp for identification of seminal fluid in areas where ejaculation may have occurred, but fluorescence is not pathognomonic of semen (urine and other stains also fluoresce).
F. Photograph physical findings with the patient’s permission.
G. Pelvic examination:
Gynecological Emergencies Page 319 Notes 1. External genitalia: a. Trauma. b. Semen? c. Hymen - intact, absent, traumatized. 2. Speculum exam: a. Gentle exam using a narrow speculum (when possible) moistened with warm tap water. b. No lubricant jelly for speculum exam - interferes with studies. c. Search for vaginal or cervical lacerations. d. Posterior fornix secretions: i. Aspirate. e. Place in sterile receptacle. f. Wet mount of cervix and vagina for sperm and Trichomonas. g. GC and chlamydia cultures. 3. Bimanual examination.
H. Rectal examination - as indicated.
I. Penis and testicle examination in male victims.
VI. EVIDENCE COLLECTION
A. Sexual assault kit.
B. Non pelvic collections:
1. May be done by nursing staff. 2. Combings of victim’s scalp and pubic hair. 3. Victim’s plucked scalp and pubic hair samples. 4. Buccal swabs - saliva sample. 5. Foreign matter: a. Hair, fibers, soil or vegetation. b. Found on victim's body or clothing. 6. Fingernail scrapings.
C. Collections to be obtained during pelvic examination:
1. Vagina and cervix secretions: a. Smears. b. Swabs. 2. Wet mount of cervix and vagina for sperm: a. Sperm present. b. Motile or not. 3. Cervical cultures or FDA-approved nucleic acid amplification tests for GC and Chlamydia. 4. Smears and swabs of other affected areas: a. Oropharynx. Gynecological Emergencies Page 320 Notes b. Anus. 5. Chain of evidence must be maintained: a. Proper labeling. b. Proper documentation.
VII. LABORATORY ANALYSIS IN THE EMERGENCY DEPARTMENT
A. ABO analysis.
B. Syphilis and hepatitis serology.
C. hCG:
1. Unless assault occurred in remote past, +hCG denotes previous pregnancy prior to the assault. 2. + hCG will alter management.
D. Nucleic acid amplification tests should be sent with results forwarded to the patient’s gynecologist or referral physician.
E. Wet mount:
1. Check for trichomonads, hyphae or clue cells. 2. Check for sperm - note motility on record.
F. HIV testing may be discussed:
1. Referral for testing and reporting of results. 2. If drawn in emergency department, a plan for reporting results and possible counseling should be determined in consultation with the patient’s private or referral physician.
VIII. TREATMENT
A. Pregnancy prophylaxis:
1. Establish a current negative hCG. 2. Low probability of pregnancy from rape – about 1%. 3. The 1% risk of pregnancy and the available choices of pregnancy prevention and risks of each should be told to patient. 4. Victim’s options: a. Do nothing. b. Therapeutic abortion if hCG negative now, but becomes positive in 1-2 weeks. c. Hormonal therapy: i. Needs to be started within 72 hours of the assault: Ovral 2 tabs q 12 hours x 2 doses.
Gynecological Emergencies Page 321 Notes Most common ED management. Feminization of male fetus - theoretical risk. ii. Plan B: 0.75 mg q 12 hr x 2 – OTC progesterone only. iii. Premarin 50 mg IV qd x 2 doses. d. Reluctance of physician to prescribe above: i. Gynecology consultation.
B. Sexually transmitted disease prophylaxis:
1. Gonorrhea: a. 2-13% incidence after sexual assault. b. Ceftriaxone 250 mg IM x 1 dose (**2010 change). c. Cefixime 400 mg orally x 1 dose – no longer recommended. d. Penicillin allergic: Azithromycin 2 gm orally as a single dose. e. Pregnant patient: Ceftriaxone 250 mg IM. 2. Chlamydia: a. Post rape incidence @ 5-10%. b. Azithromycin 1 gm orally as a single dose. c. Doxycycline 100 mg bid x 7 days. d. Pregnant patient: i. Azithromycin 1 gram orally as a single dose. ii. Amoxicillin 500 mg tid for 7 days. iii. Erythromycin base 500 mg qid for 7 days. 3. Trichomonas: a. Metronidazole 2 grams orally x 1 dose. b. No treatment in asymptomatic first trimester pregnant patient but ensure timely follow-up. 4. Syphilis: a. 0.1% incidence after sexual assault. b. Draw baseline VDRL, with referral for repeat testing at 6, 12 and 24 weeks. c. Prophylaxis probably not routinely indicated. 5. HIV: a. .0001 risk per episode receptive vaginal penetration. b. .008 - 0.032 risk per episode receptive anal penetration. c. CDC now recommends prophylaxis. d. 3 dose prophylaxis. i. Truvada: Tenofovir 300 mg & Emtricitabine 200 mg) daily for 28 days with Raltegravir 400 mg po bid OR Dolutegravir 50 mg PO daily. ii. Initiate within 72 hours post assault. iii. If victim is HIV negative, re-test 6 weeks, 3 months and 6 months later. iv. Do not wait to begin prophylaxis if baseline HIV results are unavailable. 6. Hepatitis B:
Gynecological Emergencies Page 322 Notes a. Hepatitis B vaccine if unvaccinated. b. Repeat doses at 1-2 and 4-6 months. c. Hepatitis B immunoglobulin not necessary for prophylaxis unless offender is known to have acute Hepatitis B and victim is not vaccinated.
IX. EMOTIONAL SUPPORT
A. Important to treat the patient with respect and provide a safe and calming environment.
B. Expedite care when possible, and allow the victim to have support persons present at her request.
C. Rape crisis counselors are very helpful.
D. Follow-up counseling for victim and her family should be provided.
Gynecological Emergencies Page 323 Notes
GYNECOLOGICAL EMERGENCIES
PEARLS
1. Ovarian torsion and ruptured ovarian cyst should be considered in a patient with sudden onset of severe lower abdominal pain, a tender adnexal mass, and a negative pregnancy test. The ruptured cyst will have fluid in the cul de sac and both are diagnosed by laparoscopy.
2. Follicular cysts occur during the first 2 weeks of the menstrual cycle while corpus luteum cysts occur during the last 2 weeks of the cycle.
3. Mittlesmertz is midcycle pain due to the ovum extruding from the ovary.
4. Endometriosis most commonly involves the ovaries.
5. Risk factors for ectopic pregnancy include previous tubal infection, IUD use, tubal surgery, congenital abnormality of the tube, and prior ectopic.
6. Pregnant females with trichomonas vaginalis in should be treated. Treatment of asymptomatic cases of bacterial vaginosis is thought to lower the complication rate in pregnancy. In either disease, when treatment is warranted in pregnant patients, only oral forms of antibiotics should be used.
7. Clue cells are seen with bacterial vaginitis whereas multinucleated giant cells on Tzanck smear are seen with herpes simplex.
8. Chlamydia is the most common sexually transmitted disease.
9. Fitz-Hugh-Curtis syndrome is bacterial perihepatitis with RUQ tenderness associated with PID.
10. Indications for admission for PID include uncertain diagnosis particularly if surgical diagnoses (e.g., appendicitis) cannot be ruled out, suspected pelvic abscess, pregnancy, severe illness, lack of response to outpatient therapy, inability to tolerate oral medicine, prepubertal age, lack of follow-up or IUD presence.
Gynecological Emergencies Page 324 Notes
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6. Chomvarin C, Chantarsuk Y, Thongkrajai P, et al. An assessment and evaluation of methods for diagnosis of chlamydia and gonococcal infections. Southeast Asian J Trop Med Public Health 1997 Dec; 28 (4):791-800.
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8. Dicker LW, Mosure DJ, Steece R, Stone KM. Testing for sexually transmitted diseases in U.S. public health laboratories in 2004. Sex Transm Dis 2007;34:41-6.
9. Brunhum RC, Gottlieb MD, Paavonen J. Pelvic Inflammatory Disease. NEJM. 2015 May:371:2039-48.
10. Hurd WW. Criteria that indicate endometriosis is the cause of chronic pelvic pain. Obstet Gynecol, 1998 Dec: 92(6):1029-32.
11. Jackson SL, Soper DE. Sexually transmitted diseases in pregnancy. Obstet Gynecol Clin North Am 1997 Sep:24(3):631-44.
12. Kaplan B, Rabinerson D, Gibor Y. Single-dose systemic oral fluconazole for the treatment of vaginal candidiasis. Int J Gynaecol Obstet 1997 Jun:57(3):281-6.
Gynecological Emergencies Page 325 Notes
13. Livengood CH, Soper DE, Sheehan KL, et al. Comparison of once-daily and twice-daily dosing of 0.75% metronidazole gel in the treatment of bacterial vaginosis. Sex Transm Dis 1999 Mar:26(3):137-42.
14. Nadel E, Talbot-Stern J. Obstetric and gynecologic emergencies. Emerg Med Clin North Am 1997 May:15(2):137-42.
15. Newman L, Moran JS, Workowski KA. Update on the management of gonorrhea in adults in the United States. Clin Infect Dis 2007; 44:S84-S101.
16. Seamens C, Slovis C. Abnormal vaginal bleeding in the nonpregnant patient. Emergency Medicine Reports 1996:17(22):219-228.
17. Tjaden P, Thoennes N. 2006. Extent, nature, and consequences of rape victimization. Findings from the National Violence Against Women Survey. Washington: US Department of Justice; Publication No NCJ210346.
18. US Department of Justice Archives (2016): An updated definition of rape. https://www.justice.gov/archives/opa/blog/updated-definition-rape. Accessed Jun 16, 2017.
08/17
Gynecological Emergencies Page 326 Notes
OBSTETRICAL EMERGENCIES
Diagnosis of Pregnancy
I. DATING PARAMETERS
A. Gestational age:
1. Estimates pregnancy duration from the first day of the LMP. 2. @ two weeks before ovulation and fertilization. 3. @ three weeks before implantation.
B. Fetal heart tones:
1. Doppler: a. Detectable as early as 10 weeks gestational age (GA). b. Consistently heard by 12 weeks GA. 2. Normal range: 120-160 beats per minute.
C. Uterine enlargement:
1. 12-13 weeks (3rd month) GA. a. Fundus palpable abdominally just above the symphysis. b. Uterus changes from pelvic to abdominal organ. 2. 16 weeks GA - fundus midway between umbilicus and symphysis. 3. 20 weeks GA - fundus at the level of the umbilicus. 4. 28 weeks GA - fundus @ 28 cm above the symphysis pubis.
II. LABORATORY DIAGNOSIS
A. Pregnancy tests:
1. Human chorionic gonadotropin (hCG): a. First detectable in the serum within 24 hours of implantation. b. The concentration of hCG doubles every 1.4 to 2.1 days. c. Plateaus at a peak concentration of approximately 100,000 mIU/mL at 8-11 weeks GA. d. Remains at this level and is detectable until approximately two weeks after pregnancy termination. 2. Radioimmunoassay (RIA): a. Specific for the beta subunit of hCG. b. Most specific and sensitive test for the past 30 years. c. False-negative rates <1% (5 mIU/mL hCG 2nd IS). d. False-positive rates are also infrequent. 3. Urine two site ELISA tests: a. Sensitive to 10 mIU/mL to 75 mIU/mL. Obstetrical Emergencies Page 327 Notes b. 99+% specific for the B-hCG molecule. c. Detect pregnancy at 2-3 weeks GA. d. Simple, inexpensive and timely. e. Cannot be quantified. 4. Serum two site ELISA test: a. Sensitive to 5 mIU/mL hCG (IRP). b. Can be quantified. c. False negative rates <1% with ELISA or RIA. d. Sensitivity of 20 mIU/mL (IRP). e. Causes of false negativity: i. Dilute urine samples. ii. “Chronic” ectopic gestations. 5. Quantitative B-hCG: a. RIA or 2-site ELISA. b. Both single and serial levels are useful. c. Single levels: i. Tend to be lower in ectopic pg, but not diagnostic. ii. In combination with ultrasound - very helpful. d. Serial levels: i. In normal early IUP, B-hCG increases ~ 53% every 2 days (*slower than previously reported). ii. Failure to double q 48 hrs suggests abnormal pregnancy. iii. <20% rise or a fall in the level is 100% predictive of nonviable IUP, aborted IUP, or ectopic pregnancy. iv. Need consistency in measuring serial levels - same laboratory and international standard.
Hypertension Disorders in Pregnancy
I. GENERAL
A. Classification:
1. Pregnancy-induced hypertension (acute hypertension of pregnancy): a. Hypertension develops after 20 weeks GA (earlier if trophoblastic disease) or within 24 hours postpartum. b. AND hypertension resolves within 10 days postpartum. c. 3 entities (pathophysiologic continuum): i. Without proteinuria - gestational HTN. ii. With proteinuria – preeclampsia. iii. With seizures in nonepileptic woman – eclampsia. 2. Chronic (coincidental) hypertension: a. Persistent hypertension antedating pregnancy or prior to 20 weeks GA (without trophoblastic disease). b. Or persistent hypertension beyond 6 weeks postpartum. 3. Pregnancy-aggravated hypertension: a. Superimposed preeclampsia or eclampsia in a patient with Obstetrical Emergencies Page 328 Notes chronic hypertension.
B. Hypertension defined as any one of the following:
1. DBP of 90 mmHg or greater. 2. Rise in DBP of 15 mmHg. 3. SBP of 140 mmHg or greater. 4. Rise in SBP of 30 mmHg. 5. This rise must be present on two or more readings that are at least six hours apart. 6. Diastolic pressure is more prognostic.
II. PREECLAMPSIA
A. Clinical presentation:
1. Except in molar pregnancies, signs and symptoms develop after the 20th week of pregnancy. 2. Hypertension - see Section I.B. above (although definitions changing – see ACOG). 3. Proteinuria: a. + screen - urine dipstick reading of 1+ or greater protein. b. Diagnostic criteria: i. Greater than 0.3 gm/L in a 24-hour urine collection. ii. 1 gm/L or greater protein concentration of 2 separate urine collections 6 hours apart. c. Proteinuria is a late sign. d. Degree of proteinuria in a 24-hour specimen correlates with disease severity and maternal morbidity. 4. Edema - can be seen with preeclampsia, but no longer part of the definition: a. >1+ pitting edema after 12 hours of bed rest. b. Pedal edema accompanied by edema of hands and face. c. Rapid weight gain may be an early sign: > 6 lbs/month. 5. Severe preeclampsia: a. DBP > 110 mmHg. b. Marked proteinuria: i. >2+ on several occasions or >5 gm/24 hours. c. Clinical indications of severe disease: i. Visual disturbances: Secondary to retinal arteriolar spasm. Blurred vision, “floaters or spots.” Funduscopic exam: •• Segmental arteriolar spasm. •• No hemorrhage or exudates. ii. Severe, unrelenting headache. iii. Hyperreflexia. iv. Right upper quadrant pain:
Obstetrical Emergencies Page 329 Notes Secondary to stretching of the liver capsule. Suggestive of impending seizure. v. Thrombocytopenia. vi. Liver or renal dysfunction.
B. Work-up:
1. Hgb, Hct, WBC, urinalysis, electrolytes, BUN, uric acid, creatinine, plasma estriol. 2. Consider type and cross for 2-3 units packed red blood cells. 3. 12 or 24 hr urine for quantitative protein and Cr clearance.
C. Management:
1. General: a. Safety of the mother is the first priority. b. Hospitalization is indicated in the majority of patients. c. Definitive treatment of toxemia is delivery of the infant: i. Removal of inciting trophoblastic tissue. ii. Indications for urgent delivery: Immature infant and severe preeclampsia. Mature infant and any degree of preeclampsia. d. Expectant therapy: i. Hospitalization with frequent evaluations. ii. Enforced bed rest. iii. Salt restriction. iv. Seizure precautions. e. Outpatient management, while infrequent, may be tried if: i. SBP < 135 mmHg, DBP < 85 and no proteinuria. ii. Patient reliable for follow-up and strict bed rest. f. Goals of preeclamptic management: i. Prevention of seizures. ii. Blood pressure control. iii. Stabilize and deliver if greater than 34 wks GA. iv. If less than 34 wks, stabilize and carry to 34 weeks IF THE MOTHER REMAINS STABLE. Otherwise deliver. 2. Prevention of seizures: a. Magnesium sulfate (MgSO4): i. Drug of choice. ii. Controls and prevents seizures due to toxemia. iii. Dosage: Loading dose - 4-6 grams in 10% solution IV over 5-10 minutes. Maintenance dose: •• 1-2 grams IV/hour. •• Hold maintenance doses if: ••• Patellar reflex absent.
Obstetrical Emergencies Page 330 Notes ••• Depressed respirations. ••• Urine output < 100 mL/4 hr. iv. Toxicity: Dose dependent. < 7 mEq/L - negligible toxicity. 7-10 mEq/L - loss of patellar reflexes. > 10 mEq/L - respiratory depression. 10-15 mEq/L - prolonged cardiac conduction. •• Prolonged P-R and QRS intervals. >15 mEq/L - cardiac arrest in diastole. Antidote: •• Calcium gluconate 10% solution-10-20 mL over 3 min. •• Calcium chloride for cardiac arrest. b. Anti-convulsants other than MgSO4: i. Benzodiazepines: Examples: Diazepam, lorazepam. Indicated if high dose magnesium ineffective. Side effects: •• Maternal respiratory depression. •• Maternal hypotension. •• Crosses placenta: ••• Neonatal apnea. ••• Low Apgar scores. ii. Phenytoin (Dilantin) or barbiturates. iii. Second line therapy. 3. Antihypertensive therapy: a. General: i. All antihypertensive agents have a risk of lowering placental perfusion. ii. Antihypertensive agent indicated if DBP > 110 mmHg. iii. Attempt to maintain DBP of 90-100 mmHg. b. Hydralazine (Apresoline): i. Drug of choice in pregnancy. ii. Thought to lower placental perfusion the least. iii. Dosage: Initial dose: 5 mg IV. Repeat 5-10 mg IV every 10-20 minutes prn. c. Labetalol: i. Alpha and beta adrenergic blockade (ratio = 1:5). ii. Also considered as a safe, first line drug in pregnancy. iii. 20 mg IV bolus followed by 40 mg IV if not effective in 10 minutes to max total dose of 220 mg. d. Nitroprusside (Nipride): i. Arterial and venous vasodilator. ii. Benefit: most rapid onset and shortest half-life. iii. Risk: Placental transfer may lead to neonatal cyanide Obstetrical Emergencies Page 331 Notes toxicity. iv. Reserved for hypertension refractory to hydralazine or labetalol. e. Diazoxide: i. Arteriolar vasodilator. ii. 2nd or even 3rd line drug. f. Nimodipine: i. Relatively safe. g. Nifedipine immediate oral release may be given as first line treatment
D. Prognosis:
1. Maternal: a. Better prognosis in preeclampsia than eclampsia: i. Mortality – negligible. ii. Morbidity - higher; secondary to complications: DIC. Abruptio placenta. Renal failure. Intracerebral hemorrhage. Pulmonary edema. b. Signs and symptoms resolve swiftly following delivery. 2. Neonatal: a. Prognosis is guarded in both preeclampsia and eclampsia. b. Prognosis dependent on onset of disease process. c. Mortality: i. 15% perinatal mortality. ii. Primarily due to prematurity. d. Morbidity: i. Fetal growth retardation. ii. Prematurity. 3. Prognosis is worse when toxemia is superimposed on chronic hypertensive disease.
III. ECLAMPSIA
A. Pathophysiology and clinical presentation:
1. Same as with preeclampsia. 2. Eclampsia is said to occur when patient develops seizures: a. Generalized tonic-clonic seizure activity. b. Seizures are more frequent the closer to term. i. ≈ 50% develop seizures prior to labor. ii. ≈ 25% develop seizures prior to delivery. iii. ≈ 25% develop seizures within 48 hours postpartum. 3. If seizure develops after 48 hours postpartum: a. Potentially could be eclampsia (up to 1 week postpartum).
Obstetrical Emergencies Page 332 Notes b. Must rule out CNS lesion, however. 4. RUQ tenderness (stretching of liver capsule) in the setting of preeclampsia - may warn of impending seizure activity.
B. Treatment:
1. Delivery is curative: a. Must deliver even in face of known fetal prematurity. b. Mother’s health is physician’s first priority. 2. Treat seizures and prevent further seizure activity: a. High dose magnesium sulfate. b. Benzodiazepines, Phenytoin, barbiturates: i. All second line drugs in eclampsia. ii. All may lead to neonatal apnea and low Apgar scores. c. Supportive care - including seizure precautions. 3. Treat hypertension - same therapy as used for preeclampsia.
C. Prognosis:
1. Maternal: a. Mortality approaches 5%. b. Morbidity also increased from that seen in preeclampsia. c. Complications (same as with preeclampsia): i. DIC. ii. Abruptio placenta. iii. Renal failure. iv. Intracerebral hemorrhage. v. Pulmonary edema. d. Complications (secondary to seizure activity): i. Apnea. ii. Aspiration. iii. Trauma. iv. Acidosis. v. Rhabdomyolysis with resultant renal failure. 2. Neonatal: a. Mortality primarily related to infant prematurity as delivery is mandatory regardless of degree of prematurity. b. Maternal and neonatal morbidity and mortality increased when eclampsia is superimposed on chronic hypertension.
IV. HELLP SYNDROME
A. Pathophysiology:
1. Hemolysis, elevated liver enzymes, low platelet count: a. First described in 1954. b. Occurs on its own or in association with preeclampsia. c. Multi-system disease with abnormal vascular tone, vasospasm and coagulation defects. Obstetrical Emergencies Page 333 Notes d. Causes microvascular endothelial damage and intravascular platelet activation, which releases thromboxane A and serotonin, leading to a cascade of platelet aggregation and further endothelial damage. e. Occurs in ≈ 0.4% of pregnancies (less common than preeclampsia). f. Superimposed HELLP syndrome develops in 4-12% of patients with preeclamptic symptoms. g. Unlike preeclampsia, it occurs more often in multiparous women. 2. Develops antepartum in 70% and postpartum in 30%: a. Most commonly develops in the third trimester. b. Postpartum presentation of HELLP usually develops within 48 hours of delivery but may develop up to one week later.
B. Clinical presentation:
1. Patients may present with a variety of symptoms: a. General malaise - 90%. b. Right upper quadrant pain - 65%. c. Headache - 31%. d. Nausea and vomiting - 30%. e. Blurred vision and jaundice. 2. Hypertension may be absent or mild; thus this disorder is often initially misdiagnosed. 3. Proteinuria may also be absent or mild. 4. RUQ tenderness is present in ≈ 90%. 5. Often initially misdiagnosed as cholecystitis, gastritis, hepatitis, ITP, TTP, hemolytic uremic syndrome, and acute fatty liver of pregnancy.
C. Work-up:
1. CBC: a. Hematocrit may be low; however, this is often preceded by laboratory evidence of thrombocytopenia and liver enzyme abnormalities. b. Decreased serum haptoglobin level is a more sensitive indicator of hemolysis. c. Elevated liver enzyme levels (AST, ALT, LDH, bilirubin). 2. Thrombocytopenia: a. Most reliable indicator of HELLP syndrome. b. Used to classify risk of maternal morbidity and mortality: i. Class I <50,000 platelets B highest risk for complications. ii. Class II 50,000-100,000 platelets. iii. Class III 100,000-150,000 platelets – no longer meets criteria for HELLP syndrome. Obstetrical Emergencies Page 334 Notes c. PT, PTT and fibrinogen levels are normal, unless DIC is also present. d. Patients with preeclampsia who have a positive D-dimer are thought to be at increased risk of also developing HELLP. e. Best lab markers to guide therapy are the maternal platelets count and LDH. 3. Subscapular hematoma or rupture can occur and are not always reflected by laboratory abnormalities, so any woman with HELLP syndrome who complains of right upper quadrant, neck or shoulder pain should undergo hepatic imaging. 4. Lab abnormalities usually worsen after delivery, peak at 24-48 hours, and begin resolving 3-4 days postpartum.
D. Management:
1. Delivery of the infant if the mother is unstable or infant is 34 wks GA: a. IV fluids - judiciously to avoid fluid overload. b. Strict bed rest. c. IV corticosteroids (Dexamethasone 10mg IV q 12 h). d. Magnesium sulfate prophylaxis (prevent seizures or coma) 4-6g IV bolus over 1 hour, followed by 2 g/hr infusion. e. Treat hypertension if BP > 160/110. f. Maintain diastolic pressure 90-100. g. Reduces the risk of maternal cerebral hemorrhage and seizure and possible placental abruption. h. Hydralazine 5mg IV, then 2.5-5 mg IV q 15-20 minutes. i. Labetalol. j. Blood products: i. Platelet transfusion. ii. For platelet counts <20,000. iii. Or <50,000 who undergo cesarean section. iv. Fresh frozen plasma and PRBC in those who develop DIC. v. Consider plasmapheresis in severe cases. 2. Prognosis: a. 1% maternal mortality rate . b. Higher morbidity secondary to complications - DIC, placenta abruption, ARDS, hepatorenal failure, pulmonary edema, subscapular hematoma and hepatic rupture. c. Infant mortality range from 10-60% depending on fetal GA at delivery and severity of maternal disease. d. High reoccurrence rate of developing HELLP syndrome (19-27%) or preeclampsia (43%) in subsequent pregnancies.
Obstetrical Emergencies Page 335 Notes Ectopic Pregnancy
I. DEFINITION
A. Pregnancy that implants and develops outside of the intrauterine cavity.
II. SITE
A. Tubal - 95%:
1. Ampulla: a. 80%. b. Rupture at 8-10 weeks gestational age. c. Tubal abortion is common. 2. Isthmus: a. 15%. b. Rupture at 6-8 weeks gestational age. c. Rupture is common. 3. Interstitial or cornual: a. 2.5%. b. Can rupture late (2nd - 4th month). c. Physical exam may reveal asymmetry of uterus with no adnexal mass. d. Often produces fatal hemorrhage due to involvement of both ovarian and uterine vessels. 4. Fimbrial.
III. COURSE
A. Death of ovum in tube and resorption:
1. 10-50%. 2. Under diagnosed. 3. Few days of lower abdominal pain, then asymptomatic.
B. Tubal abortion (NONRUPTURED ECTOPIC PREGNANCY):
1. Extrusion of the products of conception (POC) through the fimbriae. 2. More frequent than rupture. 3. Especially frequent in ampullary pregnancies. 4. Less dramatic and with a more prolonged clinical course. 5. Symptoms increase as the mass increases. 6. Incomplete extrusion - leakage of blood from the fimbriae cause gradual intraperitoneal hemorrhage. 7. In complete extrusion, early tubal abortion symptoms are similar to late painful menses.
Obstetrical Emergencies Page 336 Notes C. Abortion into the uterine cavity.
D. Rupture through the tubal wall (RUPTURED ECTOPIC PREGNANCY):
1. Sudden, intense pain. 2. Often preceded by vigorous exam, intercourse or trauma.
IV. PATHOPHYSIOLOGY
A. Implantation:
1. Tubal implantation is very similar to intrauterine implantation. 2. Exception: no decidua is formed. 3. Trophoblastic cells erode through the mucosa and muscularis as they proliferate. 4. This destroys tissues and opens blood vessels, producing an intratubal hemorrhage. 5. Increasing size of the tubal mass is due to this hemorrhage. 6. Slow leakage of blood may occur through the fimbriated ends of the fallopian tube. a. This may result in accumulation of blood in the posterior cul-de-sac in the absence of tubal rupture. b. This occurs in 65% of unruptured ectopic pregnancies.
B. Uterine changes:
1. Also very similar to normal pregnancy. 2. The uterine endometrium is converted to decidua in response to maternal hormones. 3. Unlike normal pregnancy, there are no chorionic villi present. 4. When the fetus dies, gestational hormones are no longer produced, and decidual growth ceases. 5. This endometrial decidua then degenerates and is shed: a. Producing external bleeding when shed in pieces. b. Less commonly, it is shed in one piece: i. Decidual cast. ii. 5% of ectopic pregnancies. iii. May be mistaken for a complete abortion. 6. Pathologic analysis of “fetal tissue” to search for chorionic villi or fetal parts.
V. INCIDENCE
A. 2% of all pregnancies.
B. Incidence of ectopic pregnancy increased between 1970 and 1992 but has since remained stable.
Obstetrical Emergencies Page 337 Notes 1. Proposed etiology of this increase: a. Increased usage of intrauterine device (IUD) contraception. b. Increased incidence of pelvic inflammatory disease (PID). c. Antibiotic usage to treat PID. d. Increased diagnosis of resorbed and tubal abortion.
C. Incidence of maternal mortality is decreasing:
1. 0.5 deaths per 1000 pregnancies. 2. 4/100,000 live births. 3. Increased awareness leading to earlier diagnosis. 4. Sensitive hCG determinations and sonography.
D. Still remains the leading cause of first trimester maternal death.
E. Is the largest single cause of maternal death in non-Caucasians.
F. Ectopic pregnancy is responsible for 6% of maternal deaths.
VI. HISTORY
A. Risk factors:
1. Anything that impedes ovum transport. 2. PID (endosalpingitis): a. Largely responsible for increasing incidence. b. 30% of patients with ectopic give history of PID in past. c. Up to 50% with histopathologic evidence of PID. 3. Exosalpingitis or peritubal adhesions: a. Prior history of appendicitis, diverticulitis or abortions. b. Prior generalized peritonitis. c. 30% give history of previous abdominal surgery. 4. Current adjacent tumors - ovarian cysts, fibroids, endometriosis. 5. Failed tubal ligation or prior tubal surgery: a. 16% risk. b. 0.4% chance of pregnancy, but 50% of these are ectopic. 6. Failed intrauterine device: a. 14% risk. b. Increased risk of PID. c. Decreased receptivity of uterus. d. Patient still ovulates, but has difficulty with intrauterine implantation. 7. Previous ectopic pregnancy: a. 10% risk with one prior ectopic and 25% with two or more ectopic pregnancies. b. Especially if prior salpingotomy. c. 8 times the risk. Obstetrical Emergencies Page 338 Notes 8. Infertility: a. In vitro fertilization increases risk of ectopic. b. Also increases the risk of heterotopic pregnancy from 1/4000 to 1/100 with in vitro fertilization. 9. Increased maternal age. 10. Repeat visits, not responding to therapy for presumed diagnosis.
B. Symptoms:
1. Signs and symptoms dependent on: a. Extent of intraperitoneal hemorrhage: i. Slow leakage. ii. Actual rupture. b. Site of implantation. c. Duration of the pregnancy. 2. Symptoms of unruptured ectopic pregnancy: a. Usually vague. b. Less frequently diagnosed (15%) vs ruptured (85%). 3. Classic triad: a. Abdominal pain, vaginal bleeding, amenorrhea. b. 15% sensitive; 14% specific. 4. Abdominal pain: a. Occurs in 95% of patients with ectopic pregnancy. b. Poorly localized to the lower abdomen. c. Dull and aching secondary to tubal distension. d. Sudden sharp pain often occurs at the time of rupture. e. After rupture, pain becomes generalized (peritonitis). f. Pain typically unilateral, but not always. g. Pain may radiate to the back, shoulder (10%) or rectum. 5. Vaginal bleeding: a. Incidence is 50-84%. b. Rarely profuse: i. May occur with cornual pregnancy. ii. More often seen with spontaneous abortion. c. Slight spotting is much more typical. d. Abdominal pain without abnormal vaginal bleeding occurs in up to 1/3 of patients with ectopic pregnancy. 6. Amenorrhea: a. Incidence is 50-80%. b. Inquire if LMP was normal. 7. Miscellaneous symptoms: a. Symptoms of pregnancy (23%). b. Tenesmus. c. Three S's for ruptured ectopic pregnancy: i. Less frequent but quite significant: Shock 8-18%. Syncope 15%.
Obstetrical Emergencies Page 339 Notes Shoulder pain 10%. •• Danforth’s sign. •• Hemoperitoneal diaphragm irritation.
VII. PHYSICAL EXAMINATION
A. Orthostatic vital signs:
1. Initial presentation of shock is rare; usually occurs after cornual rupture. 2. Shock: a. Incidence is 8-18%. b. Out of proportion to the amount of vaginal bleeding. 3. Lack of tachycardic response in face of hypotension: a. Reported in 55% of patients in one study. b. Parasympathetic response to hemoperitoneum. c. All patients tested had significant orthostatic changes.
B. Abdominal exam:
1. Abdominal tenderness present in 70%. 2. Unilateral tenderness in 37-72%. 3. Rebound tenderness in 25-50%. 4. Signs dependent on status of tube integrity: a. Ruptured - peritoneal findings expected. b. Unruptured - abdominal exam may be unremarkable.
C. Pelvic examination:
1. Chadwick’s sign - bluish cervix. 2. Less cervical softening than a normal pregnancy. 3. Uterus is enlarged, but small for dates in 25%. 4. Cervical motion tenderness present in 50%. 5. Unilateral adnexal tenderness (but may be bilateral) in 95%. 6. Adnexal mass is absent in 70% of patients with ectopic. 7. Bulging, tender cul-de-sac suggests hemoperitoneum.
D. High index of suspicion for ectopic pregnancy necessary:
1. In any patient with lower abdominal pain or vaginal bleeding with a positive pregnancy test in the first trimester. 2. Any female of reproductive age presenting in shock without history or evidence of trauma.
VIII. DIFFERENTIAL DIAGNOSIS
A. Positive B-hCG:
1. Intrauterine pregnancy: Obstetrical Emergencies Page 340 Notes a. Round ligament pain. b. Persistent or ruptured corpus luteum cyst. 2. Spontaneous abortion: a. Threatened, complete or incomplete abortion. b. Usually cause more bleeding, less pain. c. Pain usually described as midline cramping. d. Adnexal mass could be corpus luteum cyst. e. “Tissue” could be decidual cast: i. Decidual cast shed intact in 5% of ectopic pregnancy. ii. Send all tissue to pathology lab to assure presence of chorionic villi or fetal tissue. 3. Normal intrauterine pregnancy with any surgical emergency: a. Appendicitis. b. Ovarian torsion. c. All need operative intervention. 4. Molar pregnancy: a. More vaginal bleeding. b. Uterus large for dates. c. Ultrasound diagnostic.
IX. DIAGNOSTIC MODALITIES
A. High index of suspicion for ectopic pregnancy is critical.
1. Difficult to diagnose: a. History and physical exam alone correctly establish the diagnosis in 50% of patients. b. 50% of patients with ectopic pregnancy have been previously seen by a least one physician prior to diagnosis. 2. Recognizing the pregnant patient is the most important step.
B. Quantitative B-hCG:
1. Single levels: a. Serum B-hCG levels tend to be lower in patients with ectopic pregnancy but this is variable. b. Discriminatory zone (DZ) (see Table 1 below): i. Minimum hCG level at which a uterine gestational sac is seen by ultrasound in every viable IUP. ii. Typically between 1500 and 3000 mIU/mL. iii. DZ vary at different institutions. iv. DZ value dependent upon: Type of probe - vaginal vs. abdominal. Resolution of sonography. Sonographer’s experience level. Specificity, sensitivity and reference standard of the hCG determination used. c. The combination of ultrasound with B-hCG level within
Obstetrical Emergencies Page 341 Notes the DZ has a predictive value of 93% to 99%. 2. Serial quantitative hCG levels: a. Useful if the quantitative hCG level is unavailable or below the DZ at the time of presentation. b. May be performed on an outpatient basis if: i. < 5 weeks gestational age by dates. ii. Vital signs are stable. iii. There is no evidence of peritoneal irritation on exam. c. Failure of hCG to double every 48 hours suggests an abnormal pregnancy. d. Ectopic rupture can occur despite low or declining levels. e. Lack of chorionic villi or fetal tissue following a D & C for a nonviable pregnancy strongly suggests ectopic pregnancy. f. 10% of patients with ectopic pregnancy have normal doubling times initially.
C. Pelvic ultrasound:
1. Ultrasound results consistent with definitive ectopic pregnancy: a. Detection of extrauterine fetal cardiac activity. b. Uncommon with either TAS or TVS approach: i. Occurs in 10%-24% of patients with ectopic gestation. ii. More often seen with TVS than with TAS. c. Late finding: i. Cardiac activity detected at 6-7 weeks GA with TVS. ii. Cardiac activity detected at 7-8 weeks GA with TAS. 2. Ultrasound results consistent with definitive intrauterine pregnancy: a. Visualization of cardiac activity, a fetal pole or a yolk sac within the uterine cavity. b. Seen approximately 1 week earlier with TVS versus TAS. c. False negative rate of ectopic when IUP is identified is rare: i. Simultaneous ectopic and intrauterine gestation: 1/30,000 - calculated in 1948. Current figure is 1/4,000. Incidence may be as high as 1/100 in fertility patients on ovulation stimulation therapy. Check for cul-de-sac fluid or complex adnexal mass. ii. Cornual (interstitial) ectopic pregnancy: May be misidentified as IUP with TAS. Potentially fatal hemorrhage if ruptures. 3. Ultrasound results suggestive of intrauterine pregnancy: a. Intrauterine gestational sac noted. b. True gestational sac - present in IUP:
Obstetrical Emergencies Page 342 Notes i. Located eccentric to the endometrial stripe. ii. Double decidual sac sign (DDSS): Decidua vera - present in IUP and ectopic. Decidua capsularis - present in IUP only. IUP has double ring surrounding the sac. Ectopic has one ring surrounding the intrauterine pseudogestational sac. c. Pseudogestational sac - present in ectopic pregnancy: i. Located centrally along the endometrial stripe. ii. Surrounded by a single echogenic ring. iii. Present in 10-20% of patients with ectopic pregnancy. 4. Ultrasound findings suggestive of ectopic pregnancy: a. “Empty uterus” in patients with hCG above the DZ: i. DZ = minimum hCG value at which an intrauterine gestational sac is seen sonographically in all IUPs. ii. The DZ is lower for TVS versus TAS. iii. Diagnose 1 week earlier with TVS vs TAS (Table 1). iv. Only 10-40% of women with ectopic have B-hCG > 6500 at the time of presentation - so TVS preferred. v. Differential of empty uterus at an hCG value > DZ: Ectopic pregnancy. Blighted ovum. Spontaneous abortion. b. Complex adnexal mass. c. Adnexal gestational sac may be visualized. d. Internal echoes within this adnexal ring strongly suggests ectopic gestation. e. Moderate to large amount of posterior cul-de-sac fluid. 5. Inconclusive ultrasound findings: a. 2-3 week window where ultrasound is nondiagnostic: i. hCG detectable at ≈ 3 weeks GA. ii. TVS detects IUP at ≈ 5 weeks GA. iii. TAS detects IUP at ≈ 6 weeks GA. b. In some emergency departments, quantitative B-hCG levels are unavailable at the time of presentation. c. Consider alternative diagnostic modalities: i. Repeat quantitative B-hCG level in 48 hours. ii. Culdocentesis. iii. Admit for observation. iv. Laparoscopy. d. If pelvic pain/bleeding and low B-hCG (<1000), still do ultrasound, checking for free cul-de-sac fluid or complex adnexal mass.
Obstetrical Emergencies Page 343 Notes
TABLE 1 Discriminatory hCG Levels
Finding TAS TVS Gestational sac 5-6 weeks* 4-5 weeks 1800 IRP 1300 IRP
Fetal pole 7-8 weeks 6-7 weeks 6500 IRP 1800 IRP
Fetal heart beat 7-8 weeks 6-7 weeks 21,000 IRP 12,000 IRP
*Gestational age (weeks from onset of LMP) from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan- Wiggins, L(ed): Emerg Med Clin N Amer, WB Saunders, 1994:12(1):9-43.
D. Laparoscopy:
1. A definitive test in equivocal cases. 2. Unlike other diagnostic modalities, it permits definitive treatment.
X. TREATMENT
A. Hemodynamically unstable patient – to OR.
B. Hemodynamically stable pregnant patient – urgent Obstetrics & Gynecology consult.
C. Removal of the ectopic gestation:
1. The earlier the diagnosis: a. The more conservative approach may be attempted. b. The greater the chance of subsequent fertility. 2. Methotrexate: a. Halts thymine and purine, and thus DNA, production. b. Inclusion criteria: i. Ectopic mass < 3.5 cm (3 cm) diameter. ii. B-hCG < 3500 mIU/mL. iii. No significant hemoperitoneum exists. iv. The tubal serosa must be intact (nonruptured). v. No intratubal cardiac activity noted. c. Multidose regimen shown to have higher success rates than single dose (93% versus 88%). Given in four doses of 1 mg/kg of methotrexate IM or IV on alternating days,
Obstetrical Emergencies Page 344 Notes with 0.1 mg/kg of leucovorin given on the intervening days. d. Alternative dosing is a single dose regimen (50 mg/m2) for patients with hCG < 5000 mIU/mL. e. Using proper inclusion criteria, early studies show a 93- 95% success rate; side effects have been minimal and minor. 3. Operative management - salpingostomy, salpingectomy. 4. Observation: a. Avoids surgery in patients in whom spontaneous tubal abortion or reabsorption may occur, hCG < 1000 mIU per mL. b. Natural course of an ectopic, however, is difficult to predict. c. Confers no advantage to conservative surgery in terms of subsequent fertility or repeat ectopic pregnancy rate. d. Reasonable option in an asymptomatic patient with low, declining levels of serum hCG. e. Patients who present to the ED are rarely asymptomatic. 5. Persistent ectopic pregnancy: a. 5% risk in patients treated by conservative methods. b. Patient may present with recurring symptoms, and tubal rupture is also possible. c. Patients undergoing conservative surgical or chemical therapy need to be monitored for this complication.
XI. PROGNOSIS
A. Mortality - up to 60% in undiagnosed, ruptured ectopic pregnancies.
B. Morbidity:
1. Increased risk of subsequent ectopic pregnancies. 2. Subsequent fertility and pregnancy difficulties: a. 40% will be infertile. b. Of the 60% who do become pregnant: i. 10% have repeat ectopic pregnancies. ii. 15-20% will have a spontaneous abortion. c. 60% of a particular subset eventually have a term pregnancy: i. This is the most optimistic scenario. ii. These women have no underlying tubal pathology. iii. They were treated conservatively for their prior ectopic.
Obstetrical Emergencies Page 345 Notes
Hemorrhage in Early Pregnancy
I. ABORTION
A. Terminology:
Table 2. Clinical Classification of Spontaneous Abortion
Type of Abortion Internal Cervical Os Products of Conception
Threatened Closed Not Passed Inevitable Open Not Passed Imminent Open Within Dilated Cervix Incomplete Usually Open Partially Passed Complete Closed Completely Passed from: Wyte CD: Hemorrhage in early pregnancy. In: Harwood-Nuss et al (eds):The Clinical Practice of Emergency Medicine, 2nd ed. In press.
B. Epidemiology:
1. Up to 25% of first trimester pregnancies complicated by bleeding. 2. ≈ Half of all women with first trimester bleeding go on to abort. 3. Abortion rate markedly decreased if positive fetal heart tones at time of presentation to 10%, and < 5% if normal fetal heart tones. 4. History of prior spontaneous abortion is best predictor of subsequent abortion. a. Probability increases with the number of previous losses: i. @15% - no prior spontaneous abortions. ii. 19% to 24% - following one spontaneous abortion. iii. 25% - following two spontaneous abortions. iv. 30-40% - in women with habitual abortion (3 or more consecutive spontaneous abortions).
C. Natural history:
1. First trimester intrauterine bleeding outcome: a. Half proceed to actual abortion. b. 40% have a viable intrauterine pregnancy. c. ≈ 10% have an ectopic pregnancy. d. Rarely, have a molar pregnancy.
Obstetrical Emergencies Page 346 Notes D. Clinical presentation:
1. Threatened abortion: a. Spotting or brownish vaginal discharge. b. Mild, crampy suprapubic pain (may radiate to lower back). c. Less bleeding and pain than seen with incomplete abortion. d. No passage of fetal tissue; however, clots may be mistaken for fetal tissue. e. Internal cervical os will be closed. 2. Complete abortion: a. History of severe bleeding and cramping that rapidly subsided after passing fetal tissue or “clots.” b. Cervical os closed. c. Minimal vaginal bleeding and abdominal pain. 3. Incomplete, inevitable or imminent abortion: a. Moderate to severe crampy lower midline abdominal pain. b. Significant vaginal bleeding: i. May be quite severe. ii. Continues until all POC are expelled. c. Continued dilatation of the internal cervical os. d. With only a slight amount of retained tissue, it may be difficult to differentiate complete from incomplete abortion on clinical grounds alone - ultrasound may be helpful. e. Distinction between incomplete, imminent and inevitable abortion not clinically necessary - management is the same. 4. Emergent problems: a. Major complications are hemorrhage and infection. b. Other less common but potentially fatal complications: i. DIC. ii. Septic shock. iii. Pelvic thrombophlebitis with possible embolization. iv. Endotoxic shock. v. Peritonitis. vi. Uterine rupture. c. All complications more common in late first trimester incomplete or missed abortion.
E. Differential diagnosis:
1. Non-gynecologic: a. Urethral hemorrhage. b. Rectal hemorrhage. 2. Careful history and pelvic and rectal examination. 3. Gynecologic - non pregnancy-related: a. Cervicitis or vaginitis. Obstetrical Emergencies Page 347 Notes b. Lacerations or abrasions - cervical or vaginal trauma. c. Cervical polyps. d. Cervical carcinoma. e. Careful history and speculum examination. 4. Gynecologic – pregnancy-related: a. Ectopic pregnancy: i. Most important to rule out - see ECTOPIC section. ii. Usually less bleeding and more pain than abortion. iii. Difficult to differentiate by physical exam alone. iv. Sonography may be diagnostic. b. Ruptured hemorrhagic corpus luteal cyst: i. If peritoneal signs or hypovolemia - diagnose in OR. ii. In the stable patient, ultrasound may be useful. c. Trophoblastic disease - see below.
F. Emergency department evaluation:
1. Physical examination: a. Assessment and resuscitation of hemodynamic instability. b. Frank shock: i. Ruptured ectopic pregnancy. ii. Ruptured hemorrhagic corpus luteal cyst. iii. Incomplete abortion. c. Narrowed pulse pressure or orthostatic changes. d. Lower abdominal tenderness - NO peritoneal signs. e. Speculum examination: i. Briskness of external hemorrhage. ii. Evidence of vaginitis, cervicitis, lacerations or polyps. iii. Patency of the internal os. iv. POC within the dilated cervix - imminent abortion. f. Clots disintegrate easily when pulled apart - tissue does not. g. Bimanual exam: i. Patency of the internal cervical os: Multiparous with normal laxity of external os. Incomplete abortion - internal os patent. ii. Uterine tenderness, consistency, shape and size: Size larger than expected for dates- mole. Size smaller than dates: •• Missed abortion. •• Ectopic pregnancy. iii. Posterior cul-de-sac fullness – hemoperitoneum. iv. Unilateral adnexal tenderness and enlargement: Nonspecific. Ectopic pregnancy. Hemorrhagic corpus luteal cysts. Multiple cysts seen with molar gestation. Corpus luteal cyst in normal pregnancy. Obstetrical Emergencies Page 348 Notes v. Fetal heart tones: Hand-held Doppler. Worrisome if absent after 12 weeks GA. 2. Pregnancy testing: a. Should be done in all women of child-bearing age who present with abnormal vaginal bleeding or abdominal pain. b. Patient interview alone is often unreliable. c. Quantitative serum B-hCG level: i. Used with ultrasound to exclude ectopic pregnancy. ii. Marked elevation: Molar pregnancy. Multiple gestation. d. Serial quantitative B-hCG levels: i. B-hCG increases 53% every 2 days in early viable IUP. ii. Failure of B-hCG to increase: Ectopic pregnancy. Nonviable IUP. Recent spontaneous abortion. 3. Other laboratory studies: a. CBC if bleeding is either severe or prolonged. b. Rho(D) blood typing. c. Type and cross-match if potential hemorrhagic shock. 4. Ultrasound: a. Use in first trimester hemorrhage: i. Exclusion of ectopic pregnancy. ii. Assessment of fetal viability. iii. Identification of retained products of conception. iv. Diagnose molar pregnancy. b. Not needed if clinical evidence of incomplete or septic Ab. c. Use in predicting outcome of pregnancy: i. Risk of eventual abortion decreased to 5% when normal fetal cardiac activity present. ii. Fetal bradycardia predicts a high risk of fetal demise. d. Subchorionic fluid and hemorrhage: i. Both very common - occur in half of all pregnancies. ii. Unrelated to fetal death in the absence of bleeding. iii. Minimal increased risk if present with overt bleeding: 16% - 22% risk. Expectant management indicated. e. Blighted ovum: i. Sac size > 2 cm TAS or 0.9 cm TVS without yolk sac. ii. Sac 0.9 cm (TVS) or greater without cardiac activity. f. Missed abortion - 5 mm fetal pole (TVS) without heartbeat. g. Hydatidiform mole - classic snowstorm pattern. h. Retained POC: i. Ultrasound not indicated if presumptive diagnosis of Obstetrical Emergencies Page 349 Notes incomplete or septic abortion is made clinically (i.e., severe abdominal pain, hemorrhage, dilated os). ii. 15% of patients thought to have a complete abortion had retained POC on curettage analysis. iii. Sonography had a 98% negative predictive value. iv. Sonography had a 69% positive predictive value. v. If unclear diagnosis, sonography is indicated. vi. If results of Rubin’s study are confirmed, sonography may be indicated in presumed complete abortion. 5. Send all tissue to pathology lab for analysis: a. Chorionic villi or fetal parts should be present if abortion. b. If absent, must rethink diagnosis (ectopic, ectopic, ectopic). c. Molar “pregnancy” with classic pathology findings.
G. Emergency department management:
1. Definitive care: a. Threatened abortion: i. Expectant management. ii. Quantitative hCG. iii. Rho(D) testing. iv. Anti-D immunoglobulin (RhoGAM) indicated if: Rho(D) negative. AND a negative indirect Coomb’s test. v. Discharge to home with 48 hr. gynecology follow-up: Re-evaluation. Repeat quantitative hCG testing. vi. Avoid strenuous activity, intercourse, tampon usage. vii. Intercourse may resume when bleeding has ceased. viii. Return to ED promptly if increased bleeding or pain, develop fever or pass tissue. ix. Expelled tissue should be brought in for analysis. b. Complete abortion: i. Administer RhoGAM if indicated. ii. Send specimens to path lab for analysis. iii. If any doubt as to retained POC, further evaluation with ultrasound or dilation and curettage is indicated. iv. Discharge instructions - return to ED promptly if fever, increased pain or bleeding or if pass further tissue. c. Incomplete abortion: i. Requires urgent D & C by gynecologist. ii. Oxytocin (Pitocin) or the ergot alkaloids: May be used to temporize hemorrhage while awaiting curettage. 10 to 20 IU Oxytocin added to 1L isotonic IVF. Administer at a rate of 200 to 500 mL/hour.
Obstetrical Emergencies Page 350 Notes 0.2 mg methylergonovine (Methergine) IM. iii. RhoGAM if indicated. 2. Indications for admission: a. Hemodynamic instability. b. Coagulopathy. c. Trophoblastic disease. d. Severe anemia. e. Ectopic pregnancy. f. Septic abortion.
II. TROPHOBLASTIC DISEASE (MOLAR PREGNANCY)
A. Pathophysiology:
1. Rare cause of late first trimester hemorrhage. 2. Chorionic villi of normal pregnancy are converted to a mass of clear vesicles which hang from pedicles in a cluster, like grapes. 3. Both the fetus and amnion fail to develop. 4. Etiology is fertilization which results in a pair of paternal chromosomes (absent maternal genetic material): a. Fertilization by two sperm of a chromosome-devoid ovum. b. Fertilization of an ovum by a haploid sperm with duplication of the paternal chromosomes after meiosis. 5. Infrequently, the trophoblast of a molar “pregnancy” will progress: a. Invasive mole which invades the myometrium. b. Malignant transformation to choriocarcinoma (rare). 6. Incidence of hydatidiform mole: a. One in 1,500 to 2,000 pregnancies. b. Higher in Mexico and in native Alaskans. c. Highest incidence (1 in 150 to 200) in Asian race. d. Also very high incidence in women 45 years and older.
B. Clinical presentation:
1. Typically develop symptoms in the second trimester. 2. Problems may arise in late first trimester. 3. Abdominal cramping. 4. Vaginal bleeding - scant spotting or profuse hemorrhage. 5. Often with persistent vaginal bleeding and resultant anemia. 6. Uterine size is large for dates in half of the cases. 7. Fetal heart tones and quickening are absent. 8. Severe and prolonged hyperemesis. 9. Grape-like clusters of tissue may be passed. 10. Preeclampsia prior to 24 weeks GA is almost pathognomonic.
Obstetrical Emergencies Page 351 Notes
C. Diagnosis:
1. Marked elevation in quantitative B-hCG levels. 2. Ultrasound typically reveals a classic “snowstorm” appearance.
D. Treatment:
1. IV Oxytocin to control hemorrhage temporarily. 2. Dilation and curettage. 3. Must be carefully followed by a gynecologist.
Third Trimester Hemorrhage
I. INCIDENCE
A. Occurs in 4% of pregnancies.
B. Approximately 50% are significant.
II. DIFFERENTIAL DIAGNOSIS
A. Abruptio placenta – 1% incidence - see Section V.
B. Placenta previa – 0.5% incidence - see Section VI.
C. Vasa previa:
1. Abnormal velamentous insertion of the fetal umbilical vessels into the amniotic membranes. 2. Membrane rupture or fetal descent may thus cause fetal blood loss. 3. Patient presents with painless vaginal bleeding. 4. Fetal distress is common. 5. Diagnosis possible with APT test: a. Mix 1 part vaginal blood to 1 part 25% NaOH. b. With fetal hemorrhage, no color reaction forms. c. With maternal hemorrhage, light brown color forms.
D. Uterine rupture:
1. Incidence is 0.07%. 2. Significant, however, since responsible for 5% of maternal deaths. 3. Possible in any trimester. 4. Patient presents with massive painful hemorrhage, shock, easily palpable fetal parts and regressive cervical dilation and station. Obstetrical Emergencies Page 352 Notes 5. Predisposing factors: a. Uterine scars. b. Cephalic-pelvic disproportion. c. Oxytocin usage. d. Grand multiparity. e. Trauma.
E. Miscellaneous - @ 50% of third trimester hemorrhage:
1. Cervical effacement: a. “Bloody show”: i. Small amount of blood-tinged mucous. ii. Cervical canal mucous plug expulsion. iii. Precedes labor by up to 72 hours. 2. Cervicitis or vaginitis - minimal blood. 3. Erosions or tumors or trauma to the birth canal.
III. INITIAL MANAGEMENT
A. ABCs:
1. Supplemental oxygen. 2. 2 or more large bore intravenous lines: a. Consider blood transfusion for maternal shock. b. Consider fresh frozen plasma if DIC exists. c. Ensure early volume resuscitation: i. Maternal blood volume increased up to 50% at term. ii. Clinical evidence of hypovolemia may not be evident until 30% of maternal blood volume is lost. iii. Maternal physiology is maintained at the expense of fetal circulation. iv. Thus fetal distress (i.e., bradycardia) is often the first detectable sign of impending maternal shock. 3. Place patient in the left lateral decubitus position: a. Relieves venal caval compression. b. May increase maternal cardiac output up to 30%. 4. Continuous cardiac monitoring of the mother. 5. Monitor fetal heart tones: a. Normal range 120-160. b. Fetal bradycardia is evidence of impending maternal shock. 6. Consider pneumatic antishock garment: a. Leg compartments inflated . b. Contraindicated to inflate abdominal portion. 7. Obtain rapid obstetrical consultation: a. All patients with third trimester hemorrhage need admission to an obstetrical unit for further evaluation and monitoring. b. Maternal instability and fetal distress may necessitate Obstetrical Emergencies Page 353 Notes emergency caesarean section.
IV. DIAGNOSIS
A. History:
1. Estimated date of confinement (EDC). 2. Gestational history: a. Multiparous women with increased incidence of: i. Placenta previa. ii. Placenta abruption. iii. Uterine rupture. b. History of C-section? Increases risk of: i. Uterine rupture. ii. Placenta previa. 3. Previous history of placenta abruptio is a major risk factor for recurrent placenta abruption. 4. Past medical history - hypertension, diabetes, renal failure, etc. 5. Complications during this pregnancy: a. Preeclampsia. b. Abdominal trauma. c. Hypertension. d. Prior bleeding episodes. 6. Amount and duration of bleeding. 7. Is the patient experiencing abdominal pain? a. Placenta previa is a painless hemorrhage. b. Placenta abruptio is usually painful hemorrhage. c. Uterine rupture can be painful or relatively painless.
B. Physical examination:
1. Vital signs: a. Narrowed pulse pressure. b. Tilt test. 2. Fetal heart tones. 3. Abdominal examination: a. Assess for tenderness: i. Nontender - consider placenta previa. ii. Tenderness noted: Placenta abruptio. Uterine rupture. b. Assess fundal height. c. Assess for uterine firmness and tenderness. d. Assess for uterine contraction. 4. Pelvic or rectal examination: a. May dislodge the placenta, resulting in catastrophic hemorrhage. b. Thus a vaginal or rectal examination should NOT be
Obstetrical Emergencies Page 354 Notes done on any patient with third trimester hemorrhage unless: i. Placenta previa has been definitively ruled out. ii. The exam is performed by an obstetrician in an operating suite with “double setup,” in the event that immediate caesarean delivery becomes necessary.
C. Diagnostic studies:
1. CBC. 2. DIC panel - PT, PTT, platelets, fibrinogen, fibrin split products (FSP). 3. Baseline renal function studies. 4. Type and cross-match: a. Consider transfusion if evidence of maternal shock. b. Consider fresh frozen plasma transfusion if DIC ensues. c. Rh status. 5. Pelvic ultrasound: a. Only perform if mother is hemodynamically stable. i. In the unstable patient, diagnosis should be made in the operating suite with “double setup” by an obstetrician. b. Transabdominal approach only. c. Useful to diagnose placenta previa: i. TAS can reliably diagnose placenta previa in 93% to 98% of cases. ii. False positive results: Urinary bladder over distension. Migrating placenta: •• 5-30% incidence in second trimester. •• Decreases drastically by term. d. In placenta abruption: i. Ultrasound able to definitively diagnose placenta abruptio in less than 1% of cases. ii. Retroplacental hemorrhage is difficult to distinguish by current sonographic evaluation. iii. Ultrasound’s only role in abruption is in excluding placenta previa.
V. ABRUPTIO PLACENTA
A. Premature separation of the placenta from the uterine myometrium:
1. Separation may be partial or complete.
B. Painful hemorrhage:
1. 80% of patients present with painful dark red vaginal bleeding.
Obstetrical Emergencies Page 355 Notes 2. 20% of patients with abruptio have no apparent vaginal bleeding. 3. Those with concealed retroplacental hemorrhage may present with pelvic pain and rigidity, preterm labor, coagulopathy or fetal distress. 4. Abdominal pain is usually present to some degrees. 5. The uterus is usually tender and hypertonic. 6. Shock is often out of proportion to the apparent blood loss.
C. Risk factors:
1. Previous history of abruptio: a. 10 - 25% reoccurrence rate. b. Probably secondary to underlying disease. 2. Underlying disease processes that predispose to placental circulatory insufficiency: a. Chronic hypertension. b. Preeclampsia. c. Diabetes mellitus. d. Chronic renal disease. 3. States leading to vasoconstriction: a. Maternal shock. b. Abdominal trauma during last half of pregnancy. c. Abrupt hypertension. d. Venal caval compression.
D. Associated complications:
1. Preeclampsia. 2. DIC - Coagulopathy laboratory abnormalities seen in up to 1/3 of patients with abruption. 3. Acute renal failure: a. 1-4 % of cases. b. Incidence and severity directly correlated to the severity of the abruption.
E. Definitive care:
1. Expectant in-patient management: a. Immature fetus, mild hemorrhage. b. Requires close maternal and fetal monitoring. 2. Vaginal delivery in selected cases. 3. Emergency caesarean section necessary if vaginal delivery is not imminent in the presence of any of the following: a. Severe hemorrhage. b. Fetal distress. c. Maternal hemodynamic instability. d. Tetonic uterine contractions. e. Coagulopathy. Obstetrical Emergencies Page 356 Notes
F. Mortality:
1. Maternal mortality rate is <1%. 2. Perinatal mortality rate approaches 35% - 50%.
VI. PLACENTA PREVIA
A. The covering of all or part of the internal cervical os by the placenta - total, partial, marginal or low-lying.
B. Painless hemorrhage:
1. Classically presents as painless, bright red vaginal bleeding. 2. Bleeding tends to occur in late pregnancy due to mechanical shearing of the placenta as lower uterine segment undergoes effacement and dilatation. 3. Bleeding tends to reoccur and often worsens with each episode. 4. Abdominal pain is generally absent. 5. The uterus is usually soft and nontender. 6. Shock is usually in proportion to the degree of hemorrhage.
C. Risk factors and associated complication:
1. Unlike abruptio, placenta previa occurs in the previously healthy. 2. Risk factors for placenta previa include: a. Multiple gestation. b. Multiparity. c. Previous scarring: i. Prior caesarean section. ii. Multiple elective abortions. d. Previous placenta previa. 3. Placenta previa is associated with abnormal lie of the fetus.
D. Definitive care:
1. Diagnosis should be done by sonography if the patient is stable and there is no evidence of impending fetal distress. 2. Otherwise, the diagnosis should be made by an obstetrician in the operating suite. 3. Expectant management if immature fetus and minor hemorrhage. 4. Delivery by caesarean section if: a. Severe hemorrhage. b. Maternal instability. c. Fetal distress. d. Active labor develops. Obstetrical Emergencies Page 357 Notes
E. Mortality:
1. Maternal mortality rate is <1%. 2. Perinatal mortality rate is 15% - 30%.
TABLE 1: Differentiating Placenta Abruptio from Placenta Previa in Third Trimester Hemorrhage
PLACENTA ABRUPTIO PLACENTA PREVIA INCIDENCE 1/100 1/200 28 wks to term 28 wks to term multiparous multiparous upper uterus lower uterus prior history abnormal lie - 15% low C-section (3x)
PAIN + none
BLEEDING +/- + dark, like menses bright red blood
UTERUS hypertonic, tender soft, nontender
GIRTH may increase no change
FETUS +/- FHT +FHT +/- palpable + palpable
PLACENTA not palpable palpable
SHOCK out of proportion if in proportion to concealed blood loss
TOXEMIA + -
DIC + -
UA proteinuria, anuria normal
LABS decreased Hg/Hct decreased Hg/Hct increased WBC normal decreased Fibrinogen normal
US +/- (1% accuracy) + (98% accuracy)
TREATMENT delivery expectant
Obstetrical Emergencies Page 358 Notes
VAG DELIVERY + -
MORTALITY fetal-up to 50% fetal-15% maternal - very low maternal - 1/2 - 1%
Drugs and Radiation in Pregnancy
I. IONIZING RADIATION EXPOSURE IN PREGNANCY
A. Generally, a cumulative dosage of less than 5 rads has not been associated with congenital anomalies or fetal growth retardation. It is considered the upper limit of safe ionizing radiation exposure in pregnancy.
TABLE 2
FETAL RADIATION DOSAGE IN COMMON RADIOGRAPHIC STUDIES
X-RAY DOSAGE TO FETUS*
Skull series 4 millirads Cervical spine series 1-10 millirads Chest 8 millirads Thoracic spine 9 millirads Extremity series 2-3 millirads Abdomen (KUB) 300 millirads Pelvis 350 millirads Hip 300 millirads Lumbosacral spine 350 millirads IVP 500 millirads CT scan** Pelvis 2,000 millirads 2 inches from fetus 670 millirads 4 inches from fetus 223 millirads 6 inches from fetus 74 millirads Annual environmental exposure*** 140 millirads
*with maternal abdomen and pelvis shielded when possible **fetal dose decreases by a factor of 3 (from the maximal dose of 2000) for every 2 inches the fetus is away from the nearest maternal section scanned ***average annual individual exposure from cosmic irradiation and other natural sources, for comparison from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan-Wiggins, L(ed): Emerg Med Clin N Amer, WB Saunders, 1994:12(1):9-43.
Obstetrical Emergencies Page 359 Notes
TABLE 3
GUIDELINES FOR X-RAY EVALUATION IN THE PREGNANT PATIENT
* All fertile women should be considered to be possibly pregnant. * A negative RIA or ELISA pregnancy test does not rule out pregnancy < 3 weeks GA. * Pregnant patients with negative pregnancy tests sensitive to 50 mIU/mL hCG or less are at lower risk for teratogenic effects compared to later in the first trimester. * Teratogenicity is more likely during the period of organogenesis (4 to 12 weeks GA). * Radiation exposure should be limited when possible. * The abdomen and pelvis of all fertile and pregnant patients should be shielded. * Filtration, collimation and avoidance of low-yield views. * Elective x-rays should be postponed until after the first trimester. * Necessary radiologic studies should never be withheld. * Patients should be informed of the radiation risks involved whenever possible. * In pregnant patients who require extensive x-ray or CT scan studies, radiation dosimetry calculations for subsequent genetic counseling may be appropriate. from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan-Wiggins, L(ed): Emerg Med Clin N Amer, WB Saunders, 1994:12(1):9-43.
II. MAGNETIC RESONANCE IMAGING (MRI) IN PREGNANCY
A. Uses in pregnancy:
1. Evaluate pelvic mass when ultrasound is nondiagnostic. 2. Real-time MRI: a. Visualize fetal lung and kidneys. b. Assess myelinization of the fetal brain. c. Detect impaired placental perfusion. 3. Alternative to CT scan in studying non-pelvic pathology: a. Lack of ionizing radiation. b. Iodinated contrast agents not required.
B. Safety issues of MRI:
1. No evidence to suggest MRI will have any harmful effect on exposed fetus at the magnetic field strength and radio frequency currently used for clinical diagnostic studies. 2. Local heating of tissue is a theoretical concern. 3. Gadolineum (Class C) should be avoided in all trimesters,
Obstetrical Emergencies Page 360 Notes because of the long half life for the fetus.
III. SONOGRAPHY
A. Ultrasound:
1. No ionizing radiation. 2. Potential adverse effects: a. Heating of tissues. b. Acoustic cavitation. 3. Usage in pregnancy considered safe if FDA guidelines followed.
B. Color flow imaging:
1. Exposure virtually identical to that seen in grayscale sonography. 2. Poses no additional risk.
C. Pulsed Doppler:
1. Has potential to surpass maximum fetal energy exposure. 2. Additional guidelines are being proposed.
IV. DRUGS IN PREGNANCY
A. General:
1. Drugs should only be prescribed during pregnancy when there is a clear medical need, as all drugs have the potential to affect the developing fetus. 2. Untoward effects of neonatal drug exposure: a. Teratogenicity - risk is greatest during the period of organogenesis (4 to 12 weeks GA). b. Toxicity. 3. FDA classification: a. Class A - controlled studies have not demonstrated fetal risk. b. Class B: i. Animal studies indicate no fetal risk, but no human studies to date. ii. Animal studies show adverse effects, but human studies do not. c. Class C: i. Animal studies indicate teratogenic effects; no human studies to date. ii. Or, no human or animal studies to date. d. Class D - human studies show fetal risk, but benefits may outweigh the risks. Obstetrical Emergencies Page 361 Notes e. Class X - fetal risk clearly outweighs any benefit.
B. Analgesics:
1. Acetaminophen – Class B: a. Drug of choice during pregnancy: i. Antipyretic. ii. Analgesic. b. Crosses placenta and secreted in breast milk but no adverse effect known to fetus or infant. 2. Narcotics: a. Meperidine (Demerol) and morphine relatively safe. b. May cause CNS and respiratory depression in the newborn if given to the mother in labor. c. Chronic use during pregnancy may lead to withdrawal symptoms in the newborn. 3. Nitrous oxide: a. Not recommended in the first trimester of pregnancy. b. Blocks folate and Vitamin B-12 metabolism. c. Feto-toxic in long-term exposure in pregnant rats. 4. Salicylates and other nonsteroidal anti-inflammatory agents: a. Not recommended in any trimester of pregnancy. b. Increased incidence of abortions. c. Platelet inhibitors. d. Prostaglandin inhibitors: i. Inhibit uterine contractions. ii. Prolong labor. iii. Associated with post-mature deliveries. iv. May cause premature closure of the ductus arteriosus in the fetus.
C. Antibiotics:
1. Aminoglycosides - Class C: a. Not routinely recommended in pregnancy. i. Crosses placenta poorly. ii. BUT may cause fetal ototoxicity and nephrotoxicity. b. Reserved for life-threatening gram negative infections. 2. Cephalosporins - Class B: a. Considered safe during all trimesters of pregnancy. 3. Chloramphenicol - Class C: a. Contraindicated in third trimester pregnancy: i. Newborns with suppressed metabolism. ii. Gray baby syndrome is rate- and dose-dependent. 4. Clindamycin - Class B: a. No known adverse effects except do not use topical vaginal cream formulations in pregnancy. 5. Erythromycin - Class B: a. Erythromycin itself is safe during all trimesters of Obstetrical Emergencies Page 362 Notes pregnancy. b. Estolate form (i.e., EES) should NOT be used – hepatotoxicity. c. Crosses placenta poorly - does not offer fetal therapy. 6. Nitroimidazoles: a. Metronidazole: i. Class B. ii. Recommended in pregnancy for the treatment of bacterial vaginosis or symptomatic Trichomonas. b. Tinidazole: i. Class C. ii. Not recommended in pregnancy. 7. Nitrofurantoin: a. Class B. b. Safe to use in 2nd trimester (American College of Obstetricians and Gynecologists, 2011). c. Contraindicated in known G6PD deficiency and controversial in 3rd trimester: i. Hemolytic anemia. ii. Hyperbilirubinemia. 8. Penicillins - all Class B: a. Natural penicillins and semisynthetics. b. Considered safe in all trimesters of pregnancy. c. Crosses placenta, therefore offers treatment of fetus also. 9. Quinolones - Class C: a. Contraindicated in pregnancy. b. Produce arthropathy in fetus. 10. Sulfonamides: a. Dual classification: i. Class B in first and second trimester. ii. Class D - contraindicated in third trimester: Competes with bilirubin for albumin binding sites. May cause kernicterus in neonates. 11. Tetracyclines - Class D: a. Contraindicated in all trimesters of pregnancy. b. Readily crosses the placenta. c. Binds to developing fetal teeth and bone: i. Causes permanent discoloration of teeth. ii. Causes long bone growth retardation. d. Causes maternal hepatocellular necrosis. 12. Trimethoprim - Class C: a. Contraindicated in first trimester - folate antagonist.
D. Anticoagulants:
1. Heparin: a. Does not cross placenta due to its high molecular weight.
Obstetrical Emergencies Page 363 Notes b. Negligible fetal effects. c. May be reversed by protamine sulfate during labor. 2. Lovenox - Class B. 3. Warfarin (Coumadin) - Class X: a. Contraindicated in 1st and 3rd trimester of pregnancy. b. Readily crosses placenta. c. Associated with congenital malformations in first trimester. d. Associated with third trimester maternal and fetal hemorrhage.
E. Anticonvulsants:
1. The possible benefits of seizure control are thought to outweigh potential teratogenic risks. 2. Acidosis and hypoxia during seizure are detrimental to fetus. 3. Epilepsy is associated with a two- to three-fold increase in malformation rate: a. Facial clefts are most common malformation. b. Probably multifactorial. c. Difficult to determine teratogenicity of anticonvulsants since epilepsy itself produces adverse effects. 4. Monotherapy with newer anticonvulsant drugs suggests lower teratogenic risks and considered RELATIVELY SAFE with consideration of risk benefit ratio: a. Levetiracetam (Keppra) – Class C. Newer agent with better safety profile. Drug of choice in pregnancy. b. Lamotrigine (Lamictal) – Class C. Also, first line in pregnancy. c. Neurontin – Class C. d. Carbamazepine (Tegretol) e. Infants born to mothers taking anticonvulsants are at increased risk of clotting abnormalities: i. Clotting studies should be performed. ii. Vitamin K injection recommended. 5. Anticonvulsants generally contraindicated during pregnancy: a. Phenytoin (Dilantin) – Class D. Bradycardia and hypotension. Fetal hydantoin syndrome and bleeding. b. Phenobarbital – Class D. i. Newborn withdrawal has been described. ii. Newborn withdrawal not associated with seizures. c. Trimethadione (Tridione) - fetal malformations and mental retardation. d. Valproic acid (Depakene) – AVOID. Neural tube defects. e. Topamax – Class D (*change 2011). Oral cleft palate. 6. Status epilepticus should be treated early and aggressively: a. Diazepam (Valium) and Levetiracetam (Keppra). b. Consider magnesium sulfate and delivery for preeclampsia. Obstetrical Emergencies Page 364 Notes c. Poor fetal prognosis.
F. Antiemetics:
1. 5-HT3 receptor antagonists: a. Ondansetron (Zofran). b. Controversial due to concern for potential risks of VSD and cleft palate but data is limited. c. Benefits of treatment outweigh the risks of hyperemesis with severe nausea and vomiting in the ED setting. d. Second-line therapy after antihistamines and pyridoxine. 2. Antihistamines: a. Doxylamine: i. Class C alone (not tested). ii. Class A when used in combination with pyridoxine (Vit B6) known as Diclegis (Doxylamine 10 mg and pyridoxine 10 mg). iii. 20 mg doxylamine and 20 mg pyridoxine qhs. iv. If symptoms persist, increase to bid. v. Sedation is common side effect. b. Trimethobenzamide (Tigan): i. Class C. ii. No known teratogenicity. 3. Metoclopromide – Class B. 4. Phenothiazines: a. Prochlorperazine (Compazine) – Class C. b. Slight risk of hypotension and lower placental perfusion. c. Effective and probably safe.
G. Asthma medications:
1. Adrenergic agents: a. Albuterol - Class C: i. No adverse fetal effects to date. ii. Probably safer than fetal risk due to maternal hypoxia. iii. Aerosolized form preferred. b. Epinephrine: i. Associated with increased risk of fetal malformations. ii. May still be safer than maternal hypoxia in a patient unresponsive to inhaled Beta agonists. c. Isoproterenol and Ephedrine - Class D - not generally indicated. d. Metaproterenol - Class C: i. No adverse fetal effects in 25 years of clinical years. ii. Teratogenic in high doses in rabbits. iii. Aerosolized form preferred. e. Terbutaline - Class B - tocolytic agent - therefore avoid in term pregnancy. 2. Cromolyn sodium - Class B - no known adverse effects to date. Obstetrical Emergencies Page 365 Notes 3. Steroids: a. No adverse fetal effects known in humans. b. Maternal side-effects unchanged by pregnancy. c. Inhalation route may be preferred: Beclomethasone - Class C.
H. Cardiac drugs:
1. Antiarrhythmic agents: a. Agents considered safe in pregnancy: i. Atropine. ii. Lidocaine - Class B. iii. Procainamide - Class C. iv. Quinidine - Class C. b. Agents to avoid in pregnancy: i. Phenytoin. ii. Amiodarone - Class C/D. 2. Antihypertensive agents: a. Hydralazine and labetalol - drugs of first choice. b. Drugs to be avoided if possible in pregnancy: i. ACE inhibitors - Class D. ii. Diuretic agents - Class C/D. iii. Nitrates - Class C. iv. Nitroprusside - Class C/D. 3. Digoxin - considered safe in pregnancy - Class C.
I. Psychotropic drugs:
1. Avoid whenever possible in first trimester pregnancy. 2. Lithium known to cause cardiac defects in first trimester pregnancy.
J. Vaccinations:
1. Inactivated vaccines safe: a. Rabies. b. Tetanus. c. Hepatitis B. d. Polio. e. HPV – Class B 2. Live attenuated virus NOT recommended in pregnancy: a. MMR (mumps, measles, rubella). b. Varicella. c. Influenza (LAVE). d. Smallpox.
K. Immunoglobulins considered safe:
1. Rabies. Obstetrical Emergencies Page 366 Notes 2. Tetanus. 3. Hepatitis B. 4. Varicella zoster - should be given to a pregnant woman exposed to chicken pox if serology titer is negative.
Acute Appendicitis in Pregnancy
I. INCIDENCE
A. Occurs in 1/550 to 1/3,000 pregnancies.
B. Gestation does not predispose to appendicitis.
C. Occurs at same rate as general population, but diagnosis more difficult.
II. DIAGNOSIS
A. Increasingly difficult as pregnancy progresses.
B. Location of abdominal tenderness:
1. First trimester: a. Begins as poorly defined pain in the periumbilical region. b. Migrates to the right lower quadrant. c. May be superior to McBurney’s point in late first trimester. 2. Third trimester: a. May remain more diffusely localized. b. Or may be localized to right upper quadrant. c. Appendix moves upward and outward toward the flank in later pregnancy.
C. Anorexia:
1. Sensitive sign in normal appendicitis. 2. May be lacking in appendicitis in pregnancy.
D. Nausea and vomiting - may be less specific, because commonly seen in first 14-16 weeks of normal pregnancy.
E. Leukocytosis - may be less specific, because commonly seen in normal pregnancy also.
III. COMPLICATIONS
A. Increased rate of abortion and premature labor.
Obstetrical Emergencies Page 367 Notes B. Rate increased even further if peritonitis develops.
C. As appendix moves upward and outward, there is an increased risk of rupture, as “walling off” the area of inflammation is less possible.
D. Risk of complications is highest in third trimester of pregnancy.
IV. DIFFERENTIAL DIAGNOSIS
A. Acute pyelonephritis:
1. Most common misdiagnosis during late pregnancy. 2. Both pyelonephritis and appendicitis: a. Fever and chills - fever tends to be higher in pyelonephritis. b. Flank pain - in later pregnancy. c. Absence of peritoneal signs - in later pregnancy. 3. The diagnosis of pyelonephritis should be strongly doubted in the absence of bacteriuria or significant pyuria (over 10 WBC per HPF). 4. Ureteral irritation from appendiceal inflammation may lead to mild degrees of pyuria (i.e., 5-10 WBC per HPF or less), but no bacteriuria. 5. Pregnant women with pyelonephritis should be admitted for intravenous antibiotic therapy. Lack of response over 24 to 48 hours demands consideration of possible appendicitis or other disease process (pelvic or abdominal or renal abscess, etc.).
B. Cholecystitis and cholelithiasis:
1. Second most common cause of acute abdomen during pregnancy. 2. Incidence is slightly elevated during pregnancy. 3. Presents with right upper quadrant abdominal pain, exacerbation with meals, possible Murphy’s sign. 4. Although presents very similar as in non-pregnant patient, appendicitis and pyelonephritis must be considered. 5. Diagnosis may be made by sonography and liver function studies. 6. HIDA scan is usually not necessary. 7. Treatment is bed rest, bowel rest and analgesia. 8. Surgery, when indicated, is preferably performed in the second trimester, and avoided in the first and third trimesters.
V. TREATMENT OF APPENDICITIS IN PREGNANCY
A. Immediate surgical laparotomy in all three trimesters.
Obstetrical Emergencies Page 368 Notes B. Delay can worsen the prognosis, due to increased risk of rupture.
C. Caesarean section is rarely ever indicated at the time of appendectomy.
1. Recent abdominal incision poses no increased risk during labor and vaginal delivery. 2. Risk of prematurity is of concern.
Trauma in Pregnancy
I. GENERAL
A. Diagnosis:
1. 7% of pregnancies are complicated by trauma. 2. More common in the third trimester. 3. Trauma is the leading cause of non-obstetrical maternal deaths. 4. Motor vehicle collisions, falls, and assaults are most common causes: a. 31.5% of hospitalized, injured pregnant patients are secondary to domestic violence. b. Most common cause of fetal death is maternal death, followed by placental abruption, severe maternal injury and less commonly by direct fetal injury.
B. Pathophysiology:
1. Metabolic demands and oxygen consumption increases. 2. Tidal volume and minute ventilatory volume increase, causing a physiologic respiratory alkalosis. 3. Decreased gastric motility and increased laxity of the gastroesophageal junction increases the risk of aspiration. 4. The bladder becomes intra-abdominal after 12 weeks GA, increasing the risk of injury. 5. Maternal blood volume increases: a. Produces a physiologic anemia. b. Hemorrhagic shock can be masked until 30-35% of blood volume is depleted. 6. Normal cardiovascular changes: a. Cardiac output is increased by 40%. b. Pulse is increased by 20-30%. c. Mild decrease in blood pressure. 7. Enlarged uterus may obstruct the inferior vena cava when the patient is supine, reducing venous return to the heart by up to 30%, therefore decreasing cardiac output by up to 28%.
Obstetrical Emergencies Page 369 Notes C. Treatment:
1. Primary survey should be no different than the non-pregnant patient: a. Appropriate maternal resuscitation will help achieve best fetal outcome. b. Airway/breathing. c. Protect patent airway. d. Supplemental oxygen. 2. Circulation: a. Establish two large-bore intravenous catheters. b. Pulse and blood pressure may be unreliable. c. Because of increased blood volume, may lose 1500 cc of blood prior to signs of maternal shock. d. Fetal bradycardia is the earliest sign of impending maternal shock. e. Decreased capillary refill, decreased urine output and decreased pulse pressure also are useful in detecting hypoperfusion. f. Place in left lateral decubitus position (wedge under right side if on a backboard) - may increase venous return by up to 30%. g. Mast trousers - controversial - do NOT inflate intraabdominal compartment. h. Consider transfusion of PRBC for maternal shock (O negative). i. Consider transfusion of FFP for DIC (abruption). j. Continuous cardiac monitoring of mother. k. Monitor fetal heart tones: i. Normal = 120-160. ii. Fetal bradycardia is the earliest sign of impending maternal shock. iii. If fetus is viable, continue monitoring as fetal demise can occur later. 3. Nasogastric tube insertion to prevent aspiration. 4. Foley catheter insertion to monitor urinary output. 5. Secondary survey including vaginal speculum exam and assessment for amniotic fluid: a. Vaginal bleeding - seen in 80% of patients with placenta abruption. May lose up to 2 liters of blood in the uterine cavity in the 20% of patients with concealed hemorrhage. b. Nitrazine pH paper B vaginal secretions have a pH of 5; amniotic fluid has a pH of 7. 6. Abdominal exam is less reliable in later pregnancy due to the blunted response to peritoneal irritation. 7. Uterine tenderness is often present in placenta abruption and uterine rupture. 8. Tetanus toxoid and tetanus immune globulin as indicated. 9. RhoGAM B 300 ugh given to Rh negative women with < 30 cc Obstetrical Emergencies Page 370 Notes vaginal bleeding. 10. Kleihauer-Betke testing used to quantify amount of fetal- maternal hemorrhage. An additional 300 ug RhoGAM is given for each additional 30 ml of fetal blood detected. 11. Necessary X-rays should not be withheld: a. Shield fetus when possible. b. Cervical spine, chest X-ray and pelvis films are all < 1 rad. c. Low teratogenic risk when exposed to < 10 rads. 12. Ultrasound is safe and preferred to assess for intraperitoneal hemorrhage during first half of pregnancy in a stable patient. a. Used to rule out placenta previa in third trimester hemorrhage. 13. CT scan of the abdomen/pelvis is 3-10 rads. a. Preferred in second half of pregnancy to assess for intraperitoneal and retroperitoneal hemorrhage in the stable patient. 14. Diagnostic peritoneal lavage (DPL): a. Open supraumbilical approach in the first half of pregnancy. b. Rarely if ever performed in second half of pregnancy. 15. Chest tubes should be placed 1-2 interspaces higher in the pregnant patient secondary to diaphragmatic elevation. 16. Order basic lab studies as indicated: a. Trauma panel. b. Indirect Coombs test and Rh typing. c. DIC panel. d. Indication of fetal injury. e. Suggests placental abruption, amniotic fluid embolization or in utero fetal demise. 17. Cardiogenic (myocardial contusion) and neurogenic shock (spinal injury) are the only indications for vasopressors as they decrease uterine blood flow. 18. Tocolysis is indicated only after oxygen, hydration, left lateral position in the absence of placental abruption, hemorrhage, and hypoperfusion. 19. Obstetric and trauma surgery consults.
D. Disposition:
1. Transfer patient when appropriate: trauma ICU, neonatal ICU, and burn units all improve outcomes. 2. All patients with significant trauma in pregnancy need to transfer to L & D for a minimum of 4 hours of fetal monitoring prior to discharge. 3. If discharged, patients must return for abdominal pain, leaking fluid, vaginal bleeding, more than six uterine contractions per hour, or less than three fetal movements in a 12-hour period.
Obstetrical Emergencies Page 371 Notes II. BLUNT TRAUMA
A. Diagnosis:
1. Maternal death most often due to head injury or hemorrhagic shock. 2. Risk of splenic injury and retroperitoneal hematoma is greater due to increased vascularity. 3. Incidence of bowel injury is decreased because of uterine displacement. 4. Placental abruption occurs in 1-5% of minor trauma and 20- 50% of major trauma: a. Up to 2 liters of blood may be lost. b. Signs include vaginal bleeding, uterine rigidity and tenderness, cramping, hypoperfusion, and fetal bradycardia. c. <25% of placental separation associated with premature labor. d. >50% of placental separation results in nearly inevitable fetal demise. 5. Uterine rupture occurs <1% of all injuries: a. Fetal mortality @ 100% in uterine rupture caused by trauma.
B. Pathophysiology:
1. Hemodynamic changes and organ displacement change the presenting signs and symptom. 2. Uterine rupture and placental abruption are unique to pregnancy trauma.
C. Treatment:
1. Maternal resuscitation. 2. Fetal monitoring.
D. Disposition:
1. Fetal monitoring even for minor trauma. 2. Referral as in non-pregnant patients.
III. PENETRATING TRAUMA
A. Pathophysiology:
1. Gunshot wounds are more common than knife wounds. 2. Penetrating trauma inflicted in the first half of pregnancy are more likely to cause maternal gastrointestinal and vascular injuries. Obstetrical Emergencies Page 372 Notes 3. Penetrating trauma inflicted in the second half of pregnancy are more like to cause uterine and fetal injuries. 4. The fetus is injured in 60-70% of gunshot wounds. 5. Stab wounds have a better prognosis.
B. Diagnosis:
1. Surgical exploration in most cases. Diagnostic peritoneal lavage, ultrasound, and CT scan can offer non-surgical options.
C. Treatment and disposition:
1. Most require exploratory laparotomy.
IV. DOMESTIC VIOLENCE
A. 0.9% to 20.1% of pregnant women are victims of abuse.
B. Worsens as the pregnancy progresses.
C. Associated with low birth weights and drug/alcohol abuse.
Perimortem Cesarean Section
I. GENERAL
A. C-section indications:
1. Mother is in a state of cardiac arrest and does not respond within four minutes to resuscitative measures. 2. Identify fetal heart tones. 3. Identify potential fetal viability - gestational age estimated >23 weeks. 4. Survival at 22 weeks is 0%, 26 weeks is 54.7%, and 98.7% at 34 weeks.
B. Procedure:
1. Midline vertical incision from the upper uterine segment to the symphysis pubis. 2. Retract abdominal wall and bladder. 3. Vertical incision through lower uterine segment. 4. Extend incision vertically with scissors, using second hand as a shield for the fetus. 5. Deliver infant through the incision. 6. Vigorous resuscitation of the infant should be anticipated. 7. Resume maternal resuscitative efforts post delivery.
Obstetrical Emergencies Page 373 Notes C. Prognosis:
1. Infant survival is 10-40%. 2. Survival dependent on gestational age, birth weight, time from maternal death to delivery and presence of maternal CPR. 3. Good prognosis if time from maternal death to deliver < 5 minutes. 4. No reported survival if >25 minutes from maternal death to delivery. 5. Rare maternal survival reported after delivery.
Emergency Delivery
I. METHODS FOR EMERGENCY DELIVERY
A. Mechanism of vertex delivery:
1. Follows 7 cardinal movements: a. Engagement - biparietal diameter of fetal head passes through pelvic inlet: i. Occurs during labor – multiparous. ii. Occurs in last two weeks of pregnancy – nulliparous. b. Flexion of infant’s head. c. Descent. d. Internal rotation. e. Extension of head: i. Occurs when head reaches the vulva. ii. Head is delivered when full extension occurs. f. External rotation: i. Brings shoulders into anterior-posterior plane. g. Expulsion: i. Delivery of shoulders and then remainder of body. 2. Controlled technique is essential.
B. Technique for vertex delivery:
1. Modified Ritgin maneuver after crowning: a. Exert gentle upward pressure to the fetal head with gloved hand covered by a sterile towel. b. Simultaneously exert pressure superiorly on the infant’s occiput. c. This allows more control of the delivery of the head, thus reducing maternal injury. 2. Assess for loops of cord around infant’s neck. 3. Free such loops if found after delivery of the head and prior to delivery of the shoulders. 4. Bulb suction infant’s nares and oropharynx at the perineum. 5. If meconium present, intubation and tracheal suction indicated Obstetrical Emergencies Page 374 Notes post delivery. 6. Delivery of shoulders. 7. Usually occurs spontaneously: a. May exert gentle downward traction on infant’s head to ease delivery of the anterior shoulder. b. Then gentle upward traction on head to aid delivery of posterior shoulder. 8. Remainder of delivery follows rapidly. 9. Double clamp cord and cut in between clamps. 10. Infants are slippery until cleansed: a. Rest infant’s head in your antecubital fossa. b. While hooking hand around one of the infant’s legs. 11. Dry off infant and warm: a. Isolette when possible. b. Warm blankets, maternal heat until incubator available. 12. Delivery of placenta: a. Separation of placenta occurs within 1-5 minutes: i. Uterus changes from discoid to globular and firmer. ii. Often see a gush of blood. iii. Umbilical cord protrudes out of the vagina further. b. Gentle, steady umbilical traction while lifting uterus cephalad with the abdominal hand until placenta at introitus. c. Remove placenta from the vagina by lifting the cord up. d. Examine placenta for completeness and send to path lab. 13. Post-delivery: a. Gentle fundal massage. b. Oxytocin 20 IU in 1 liter crystalloid: i. Infuse at rate of 10 ml/minute until uterus contracted. ii. Then reduce rate to 1-2 ml/min. c. 5-10 IU Oxytocin may be given IM if no venous access. d. Methylergonovine maleate (Methergine) - 0.2 mg IM.
II. DYSTOCIA (DIFFICULT LABOR)
A. Precipitous labor:
1. Extremely rapid, tumultuous labor and delivery. 2. Complications include: a. Uterine rupture. b. Lacerations of the cervix, vagina, vulva or perineum. c. Amniotic fluid embolism – rare. d. Postpartum hemorrhage. e. Fetal distress - tumultuous uterine contractions prevent adequate uterine blood flow. f. Fetal intracranial trauma. 3. Management: a. Try to keep as controlled as possible: Obstetrical Emergencies Page 375 Notes i. Modified Ritgin maneuver for delivery of head. ii. Check for nuchal chord. iii. Attempt to suction nares and mouth at perineum. b. Do NOT attempt to delay delivery by holding the baby's head back or other physical maneuvers.
B. Shoulder dystocia:
1. Impaction of the shoulder in the pelvic canal, halting the progression of infant delivery after delivery of the head. 2. Incidence is 0.15%. 3. Incidence increases in post-term or >4000 gram infants (1.7%). 4. Suspect shoulder dystocia if fetal head “retracts” during delivery. 5. Treatment: a. Large mediolateral episiotomy. b. Adequate anesthesia. c. Suction the infant’s mouth and nose. d. Check and reduce nuchal cord. e. McRoberts manueuver – hyperflexion of the mother’s legs at the hip tightly to the abdomen while an assistant applies suprapubic pressure. f. Woods “screw” maneuver - apply pressure to the infant’s posterior scapula to rotate upward. The posterior shoulder then passes beneath the symphysis and is delivered as an anterior shoulder. g. If unsuccessful, sweep the posterior arm across the infant’s chest and deliver it. This rotates the shoulder girdle.
C. Breech presentation:
1. Incidence is 3% to 4%. 2. Incidence increased in prematurity, grand multiparity, multiple gestations, uterine and congenital abnormalities. 3. Complications: a. Increased perinatal morbidity and mortality: i. 12-fold increase in mortality rate (versus vertex birth). ii. Intracranial hemorrhage is most common cause of infant death. Also spinal cord, liver, adrenal glands and spleen. b. Prematurity. c. Prolapsed cord - especially in footling breeches (11%). d. Placenta previa. 4. Types: a. Frank breech - feet lie in close proximity to head - most common (legs flexed at the hips and extended at the knees). b. Complete breech - one or both knees are flexed. c. Footling (incomplete) breech - a foot or knee is lowest in Obstetrical Emergencies Page 376 Notes the birth canal. 5. In breech delivery, successive infant parts become harder to deliver (opposite of that seen with vertex deliveries). 6. Management: a. Caesarean section preferred - decreased morbidity and mortality. b. Partial or total breech extraction usually necessary in vaginal deliveries.
III. FETAL DISTRESS IN ACTIVE LABOR
A. Evaluate:
1. Fetal heart rate: a. Hand-held Doppler. b. Normal baseline at term is 120-160 beats per minute. 2. Fetal heart rate response to palpable maternal contractions - uses principles used in formal cardiotopography. 3. Evidence of fetal distress: a. Baseline fetal bradycardia (heart rate of 110 bpm or less). b. Late or variable decelerations: i. Late decelerations: Represents uteroplacental insufficiency. Fetal heart rate drops as contraction intensity peaks. Recovery to baseline heart rate does not occur until after the contraction is over. ii. Variable decelerations: Represents cord compression. Deceleration of fetal heart rate occurs but without correlation to the timing of contractions. 4. Early decelerations occur early during the contraction and are merely in response to fetal head compression during contractions. Occasionally they represent compression of the umbilical cord.
B. Management:
1. Supplemental oxygen. 2. Place mother in left lateral decubitus position. a. Displaces uterus away from the inferior vena cava. b. This increases maternal venous return, which will then increase placental perfusion. 3. Rule out prolapsed umbilical cord by vaginal exam. 4. Emergency obstetrical consultation. 5. Definitive therapy is delivery, possibly by caesarean section.
Obstetrical Emergencies Page 377 Notes IV. PROLAPSED UMBILICAL CORD
A. Definition:
1. Rupture of membranes with obvious prolapse of cord through the cervix. 2. Concealed prolapse - cord lies along side or in front of presenting fetal part with or without ruptured membranes.
B. Pathophysiology:
1. Incidence is 3-6 per 1000 deliveries. 2. Associated with prematurity, abnormal presentation, multiple gestation, hydramnios and grand multiparity.
C. Clinical presentation:
1. Usually membranes rupture first. 2. Patient reports feeling something in or coming out of their vagina. 3. Patient may or may not be in active labor. 4. Umbilical cord may be visualized at the introitus. 5. Umbilical cord may be palpable on digital exam. 6. If any doubt, do speculum exam.
D. Treatment:
1. Place mother in left lateral knee-chest or deep Trendelenburg position. 2. Supplemental oxygen. 3. Manually displace uterus to left using abdominal hand. 4. Apply continuous upward digital pressure through the vagina on the presenting fetal part while rushing patient up to the OR. 5. Definitive treatment is delivery, usually by caesarean section.
V. PREMATURE RUPTURE OF MEMBRANES
A. General:
1. Definition - leakage of amniotic fluid prior to the onset of labor. 2. Incidence: a. Normally rupture of membranes occurs during active labor. b. In 10% of cases it occurs prior to the onset of labor. 3. Etiology – unknown.
Obstetrical Emergencies Page 378 Notes B. Complications:
1. Intrauterine infection - risk increases if greater than 24 hours elapse between membrane rupture and delivery. 2. Precipitation of labor. 3. Increased incidence of cord prolapse, if presenting part is not engaged in pelvis. 4. The closer to term the membranes rupture, the less serious the complications are.
C. Diagnosis:
1. Patient may complain of a sudden gush of clear fluid. 2. Amniotic fluid may be present at the cervical os or vaginal fornix. 3. Nitrazine paper: a. Vaginal secretions with pH of 4.5 to 5.5 - paper stays yellow. b. Amniotic fluid with pH of 7 to 7.5 - turns paper blue. c. Blood gives false positive result (pH 7.4) - turns paper blue. 4. Ferning: a. Amniotic fluid with high sodium chloride content. b. Blood may interfere with ferning (false negative). 5. Heating: a. Amniotic fluid turns white. b. Cervical mucus turns brown. 6. Differentiate from “bloody show”: a. Extrusion of mucous plug which precedes labor. b. Small amount of blood-tinged mucous. c. Differentiate from third trimester hemorrhage.
D. Management:
1. Admit. 2. Minimize vaginal examinations: a. Single sterile speculum exam to diagnose fluid. b. Single sterile-gloved digital exam to rule out cord prolapse. 3. Definitive care - dependent on gestational age: a. >36 weeks - induction of labor within 12-24 hours. b. <36 weeks: i. Dependent on fetal maturity and evidence of infection. ii. Conservative approach: Admission with bed rest. Glucocorticoids to promote fetal lung maturity iii. Delivery - if infection occurs.
Obstetrical Emergencies Page 379 Notes
OBSTETRICAL EMERGENCIES
PEARLS
1. Patients with history of tubal ligation or recent elective or spontaneous abortion are at increased risk of death, because of failure to consider ectopic pregnancy.
2. Patients who present with a “complete Ab” should have all tissue sent to pathology to ensure presence of chorionic villi or fetal parts. 5% of patients with ectopic pregnancy shed a decidual cast, which may be misinterpreted for fetal tissue on gross inspection.
3. Cornual pregnancies may rupture later (14-16 weeks), while isthmic pregnancies may rupture earlier (6-8 weeks) than the classic 8-10 weeks.
4. The physical examination, including pelvic exam, is quite unreliable in the diagnosis of ectopic pregnancy. The absence of an adnexal mass in particular should not lessen one’s suspicion for ectopic pregnancy.
5. Clinical findings consistent with ectopic pregnancy should outweigh any single negative test result.
6. Clinical distinction between complete and incomplete abortion may be insufficient.
7. Any cause of first trimester hemorrhage may result in Rho(D) sensitization in the Rho(D) negative woman.
8. Unrelenting abdominal pain or hemorrhage after passage of tissue is indicative of incomplete abortion, and further therapy or observation is required.
9. Fetal heart tones are often detected at 10 weeks by hand-held Doppler.
10. Beta-HCG may be detected in the maternal serum as early as 8-9 days after fertilization.
11. HCG levels peak approximately 65 days after conception at about 50,000 mIU/mL.
12. Toxemia is most likely due to arteriolar vasospasm secondary to an imbalance between prostaglandin (PG'2) and thromboxane (TxA2).
13. Preeclampsia is diagnosed usually after 20 weeks gestation and should include hypertension (acute) with proteinuria.
Obstetrical Emergencies Page 380 Notes
14. Eclampsia criteria include preeclampsia plus convulsions and/or coma.
15. The two types of therapy for preeclampsia are delivery (the only definite form) and expectant (may be justified if immature fetus).
16. The two most common complications with expectant management of a severely preeclamptic patient are abruption (22%) and thrombocytopenia (20%).
17. MgSO4 is the pharmacologic mainstay for seizure prophylaxis in preeclampsia.
18. All antihypertensive agents also lower placental perfusion.
19. Hydralazine (5 mg IVP increments) is still the antihypertensive of choice since it probably lowers placental perfusion the least.
20. Pelvic exam stimulation can induce convulsions in a preeclamptic patient.
21. Ectopic pregnancy may occur even in absence of history of amenorrhea.
22. Some degree of abdominal and vaginal/cervical tenderness is present in 75% of ectopic pregnancies.
23. Abruption placenta and placenta previa are the major causes of third trimester bleeding.
24. Abruptions often present with vaginal bleeding, a board-like uterus, uterine tenderness, and varying levels of shock.
25. Advancing age and multiparity are associated with increased incidence of a placenta previa.
26. Placenta previa typically presents with painless vaginal bleeding after the seventh month.
27. A speculum exam during third trimester bleeding may be indicated but avoid bimanual and rectal exams especially with placenta previa.
Obstetrical Emergencies Page 381 Notes
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18. Haughey M, Calderon Y. Trauma in pregnancy: Optimizing maternal and fetal outcomes. Emerg Med Reports 2000;21:177-86.
19. Henderson S, Mallon WK. Trauma in pregnancy. Emerg Med Clin North Am 1998;16:209-28.
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22. Lavery JP, Staten-McCormick M. Management of moderate to severe trauma in pregnancy. Obstet Gynecol Clin North Am 1995;22:69-90.
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24. Mason E, Rosene-Montella K, Powrie R. Medical problems during pregnancy. Med Clin North Am 1998 Mar:82(2):249-69.
25. Mercer BM. Management of preterm premature rupture of the membranes. Clin Obstet Gynecol 1998 Dec:41(4):870-82.
26. Morris JA, Rosenbower TJ, et al. Infant survival after Cesarean section for trauma. Ann Surg 1996;223:481-91.
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Obstetrical Emergencies Page 383 Notes 29. Norris TC. Management of postpartum hemorrhage. Am Fam Phys 1997 Feb 1:55(2):635-40.
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Obstetrical Emergencies Page 385
Page 386
EENT/Ophthalmologic Emergencies
Marc Dorfman, MD, FACEP, MACP
Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center, Chicago; Assistant Clinical Professor, University of Illinois at Chicago
Page 387
Page 388 Notes
EENT/OPHTHALMOLOGIC EMERGENCIES
EENT Emergencies
I. THE EAR
A. Auricle:
1. Auricular hematoma: a. Blunt trauma (classically in wrestlers and boxers). b. Collection of blood between the perichondrium and the cartilage. c. Untreated may result in cartilage necrosis (“cauliflower” ear). d. Diagnosis is clinical: pain, tenderness, swelling. e. Treatment: drainage (I & D or needle aspiration), possible anti-staphylococcus oral antibiotics, and a compressive dressing. Should be reassessed in 24 hrs (re-accumulation). 2. Perichondritis and chondritis: a. Infection of the auricular soft tissues. b. Causes include uncontrolled otitis externa, auricular hematoma, and auricular abrasions or lacerations. c. TREATMENT IS ADMISSION FOR IV ANTIBIOTICS broad coverage. d. Pseudomonas aeruginosa - often causative agent. 3. Relapsing polychondritis: a. Disease of unknown etiology which may mimic perichondritis. b. Characterized by inflammation and destruction of cartilaginous tissues throughout the body. c. Ears and nose are affected in 80-90% of patients, resulting in floppy ears and a collapsed nose. d. Labs - elevated erythrocyte sedimentation rate (ESR). e. Diagnosis - auricle is inflamed but the lobe (i.e., no cartilage) is spared. Confirmed by biopsy. f. Treatment: steroids.
B. External auditory canal:
1. Otitis externa: a. Infection of the auditory canal usually preceded by excessive moisture, abrasions, or lacerations. b. Presentation is pain and otorrhea. c. The auditory canal is inflamed, swollen with tenderness in auricular motion or tragal pressure. d. Pseudomonas aeruginosa is common pathogen and less commonly Staph. aureus. e. Treatment is antibiotic/steroid combination ear drops (Cortisporin otic suspension) or an acetic acid solution EENT/Ophthalmologic Emergencies Page 389 Notes (Vosol). f. If the canal is too swollen to allow penetration of antibiotics, insert a compressed cellulose wick (i.e., “Pope” ear wick). g. If cellulitis or periauricular adenopathy is present, the patient should be started on an oral antibiotic. 2. Malignant otitis externa: a. Immunocompromised patients (i.e., elderly, diabetic, chemotherapy, high dose oral steroids) are at risk. b. Most commonly pseudomonas aeruginosa. c. Classical finding is granulation tissue on the floor of the auditory canal at the bony-cartilage junction. d. Facial nerve paralysis ensues as the disease reaches the stylomastoid foramen. The disease can progress to multiple cranial nerve involvement and meningitis. e. Treatment may include immediate referral to an otolaryngologist for surgical debridement and IV antibiotics. 3. Herpes zoster (Ramsay-Hunt Syndrome): a. Infection of the geniculate ganglion resulting in painful vesicular rash of the external auditory canal, auricle, and surrounding area. b. Usually an associated sensorineural hearing loss and facial nerve paralysis. c. Treatment is admission for IV antivirals. 4. Foreign body: a. Most common source of unilateral hearing loss is cerumen impaction. b. Tools for removal include irrigation (e.g., partially obstructing FB), alligator forceps, suction, hook, or cerumen loop. c. Do not irrigate vegetable matter because it may expand. d. Live insects should be stupefied by either lidocaine or mineral oil prior to removal. e. Removal can be complicated by traumatic tympanic membrane perforation and ossicular disruption; therefore, proximal foreign bodies or those in uncooperative patients should be removed under anesthesia by an otolaryngologist.
C. Tympanic membrane:
1. Perforation: a. Caused by sharp instrumentation, blunt trauma, or change in pressure. b. Most injuries occur to the anterior inferior portion of the TM (pars tensa). c. Findings include bloody otorrhea and partial conductive hearing loss. Weber tuning fork test will lateralize to the side of injury. d. Clean injury - no antibiotic is required and 95% will heal spontaneously. EENT/Ophthalmologic Emergencies Page 390 Notes e. Contaminated injuries require antibiotics (e.g., injury sustained while water skiing). f. Ossicular disruption is much more likely if the perforation is in the posterior superior quadrant (pars flaccida). Associated with pronounced hearing loss and possibly vertigo. They do not require immediate repair. g. Treatment is the same as above but otolaryngology referral is mandatory. h. With profound hearing loss (i.e., sensorineural) and vertigo, a perilymph fistula should be suspected. This results from displacement of the stapes from the oval window. This condition requires immediate otolaryngology referral and hospital admission. 2. Bullous myringitis: a. Characterized by clear or hemorrhagic blebs on the TM. b. Present with otalgia and usually have an associated URI. c. Etiologies are viral (most common) and mycoplasma. d. Treatment consists of systemic analgesics, macrolides.
D. Middle ear:
1. Acute suppurative otitis media: a. Most common between 6-36 months of age. b. Most common organisms in the pediatric age group are Streptococcus pneumoniae (29%), Haemophilus influenzae- nontypeable (23%), and Branhamella catarrhalis (13%). c. Treatment – antibiotics (amoxicillin). d. Most common complication is TM perforation, which usually heals spontaneously. e. Most serious complication is mastoiditis. Symptoms include purulent otorrhea with TM perforation, sagging of the posterior-superior external auditory canal, tenderness over the mastoid prominence, and post-auricular fluctuance. Radiography of the mastoid will reveal loss of normal air cells and a “ground glass” appearance. Treatment is admission for IV antibiotics and possible mastoidectomy. Complications include extension to the inner ear, meningitis, intracranial abscess, and lateral sinus thrombophlebitis. 2. Otitis media with effusion: a. Presents with a dull, often retracted, poorly mobile tympanic membrane. Bubbles or an air-fluid level may be visualized. b. Pneumatic otoscopy confirms decreased TM mobility. c. In children, it is usually associated with a URI, but allergy, immunologic disorder, and submucosal cleft palate can also be etiologies. d. Antihistamines and decongestants have been demonstrated to be ineffective. e. Although as many as 80% will spontaneously resolve within 2 months, most clinicians will treat with oral antibiotics. This EENT/Ophthalmologic Emergencies Page 391 Notes is supported by a 48-66% positive culture rate of middle ear aspirates. f. In adults, antihistamines and decongestants may be useful, especially when associated with upper respiratory allergies. g. Unilateral effusion may be the presenting sign of a nasopharyngeal tumor. 3. Barotrauma: a. Caused by rapid changes in atmospheric pressure such as in flying or scuba diving. b. Complains of a plugged feeling, pain, and decreased hearing. c. Treatment consists of analgesics, oral decongestants, and topical nasal spray decongestants. d. Antibiotics are not helpful unless secondary infection is suspected. e. Severe cases may require myringotomy for symptomatic relief.
E. Inner ear:
1. Presents with painless hearing loss developing over minutes to hours. a. Tinnitus and/or vertigo may be present. b. The etiology for unilateral loss is viral neuritis, acoustic neuroma, and Ménière’s disease. c. The etiology of bilateral loss is ototoxic drugs (aminoglycosides, erythromycin, vancomycin, antimalarials, ASA, NSAIDs, furosemide, ethacrynic acid, cisplatin) and loud noise. d. Refer to an otolaryngologist. 2. Perilymph fistula: a. Sudden onset hearing loss with tinnitus and severe vertigo is indicative of a perilymph fistula. b. The oval or round window is disrupted. This often occurs while straining (i.e., heavy lifting, coughing, barotrauma valsalva). c. Pressure applied with a pneumatic otoscope will induce vertigo, nystagmus, and sensorineural hearing loss. Straining (coughing, sneezing, and lifting) exacerbates symptoms. d. Treatment is usually conservative but surgical intervention may be necessary. 3. Acoustic neuroma: a. A rare cause of sensorineural hearing loss, the cerebellopontine angle tumor (i.e., acoustic neuroma). b. Symptoms include tinnitus followed by a gradual unilateral hearing loss over many months to years. c. Late symptoms include a constant, mild vertigo and finally, facial paralysis as the eighth and seventh cranial nerves, respectively, are compressed in the internal auditory canal. d. It should be suspected in an elderly patient with unilateral EENT/Ophthalmologic Emergencies Page 392 Notes sensorineural hearing loss. 4. Weber and Rinne tests: a. Weber test: i. 512 Hz tuning fork on the patient’s forehead. With a unilateral conductive hearing loss, the tone is perceived as louder in the ear with the hearing loss. ii. In a unilateral sensorineural hearing loss, the patient hears the tone louder in the better ear. b. Rinne test: i. 256 Hz tuning fork placed on the patient’s mastoid and then near the ear. The purpose is to compare loudness between the fork placed on the skin over the mastoid cortex (i.e., bone conduction) and the same fork held in the air near the patient’s ear canal (i.e., air conduction). Normal is for air conduction to be louder than bone conduction. ii. Air conduction (AC) is louder than bone conduction (BC). This is because the tympanic membrane and ossicles amplify sound to the inner ear. iii. With a conductive hearing loss (i.e., disruption of the TM or ossicles), it will be heard louder over the mastoid cortex. iv. Sensorineural hearing loss - the Weber test lateralizes to the better ear. The Rinne test will be louder in the air than on the mastoid cortex.
EXAMPLES:
RIGHT SIDED UNILATERAL RIGHT SIDE UNILATERAL CONDUCTIVE HEARING LOSS SENSORINEURAL HEARING LOSS Weber lateralizes to right Weber lateralizes to left Rinne BC > AC Rinne AC > BC
II. NOSE AND PARANASAL SINUSES
A. Epistaxis:
1. Anterior most common due to erosion of superficial blood vessels near the anterior end of the nasal septum (i.e., Little’s Area or Kiesselbach’s Plexus). 2. Etiologies are as follows: a. Local: i. Excessive dryness (mostly seen in winter months when there is low humidity). ii. Digital trauma (i.e., nose picking) or nose blowing. iii. Upper respiratory infection. iv. Nasal trauma.
EENT/Ophthalmologic Emergencies Page 393 Notes v. Nasal tumors. vi. Nasal foreign bodies. b. Systemic: i. Hypertension. ii. Arteriosclerosis. iii. Blood dyscrasia. iv. Coagulation disorder. v. Drugs (i.e., aspirin, Coumadin). vi. Hereditary hemorrhagic telangiectasia (Osler-Weber- Rendu Syndrome). Autosomal dominant trait characterized by multiple mucosal (i.e., nose, oral cavity, stomach, colon, lungs) and cutaneous telangiectasias. 3. If significant bleeding or a clotting disorder is suspected, then laboratory studies (i.e., CBC, PT< PTT) are indicated. 4. Management of anterior nasal bleeds: a. Patient in upright position and pinch nose for 10-15 minutes. b. If continued bleeding, inspect nose and cauterize bleeding site with silver nitrate or electrocautery. c. If bleeding continues, pack the nose with Vaseline strip gauze or a commercially available device. 5. Complications of anterior nasal packings include sinusitis, toxic shock syndrome. Applying antibiotic ointment may prevent the latter. Any patient with a packing for greater than 24 hours should be put on oral antibiotics. 6. Posterior nasal bleeds are usually seen in the elderly, diagnosed by failure of anterior nasal packs to control the hemorrhage. Management is as follows: a. Posterior nasal packing/intranasal balloon device or a Foley catheter. b. Admitted for humidified oxygen, analgesics, and antibiotics. Posterior packing may lead to hypoxemia. c. For uncontrollable hemorrhage, patients may require arterial ligation or arteriography with embolization.
B. Nasal foreign bodies:
1. Most common in children and the mentally ill. 2. Patients present with a malodorous, purulent, unilateral rhinorrhea. 3. Diagnosis is by inspection. 4. Treatment is removal with a nasal speculum, suction, forceps, and/or ear curette or right-angled hook.
C. SINUSITIS
1. Acute sinusitis (less than 3 weeks duration) most commonly caused by Haemophilus influenzae, Streptococcus pneumoniae, Group A Streptococcus, Staph. aureus, and Moraxella catarrhalis. EENT/Ophthalmologic Emergencies Page 394 Notes 2. Chronic sinusitis (greater than 3 weeks) is more likely caused by anaerobic bacteria, fungi, and mixed flora. 3. Complications of acute sinusitis result from extension of infection into contiguous structures- bone, CNS, eye, or vascular system. 4. Acute maxillary sinusitis - facial pain below the eyes, fever, purulent nasal discharge, and upper dental pain. Pain is often accentuated by leaning forward. 5. Acute ethmoid sinusitis is a disease of children, has a propensity to spread into the orbit or CNS. Complications include periorbital cellulitis, orbital abscess, meningitis, and cavernous sinus thrombosis. 6. Cavernous sinus thrombosis: high fevers and appear toxic. There is eyelid edema, proptosis and chemosis third and sixth nerve palsies, pupillary dysfunction, and papillary edema occur. CNS symptoms include lethargy, coma, or seizures. Diagnosis may be confirmed by CT scan or MRI. 7. Acute frontal sinusitis presents with frontal headache, fever, purulent rhinorrhea. The frontal sinus begins to develop at ages 6-8 and may never develop in a small proportion of the population. Therefore, frontal sinusitis is not seen in young children. The infection may cause an osteitis of the anterior sinus wall (Pott’s puffy tumor). 8. Acute sphenoid sinusitis is an uncommon disease. Pain is poorly localized to the vertex, occiput, or mastoid area of the skull. 9. CT of sinuses most sensitive for diagnosing sinus disease. 10. Treatment of acute sinusitis is topical nasal decongestants for 2-3 days, analgesics and oral decongestants. Antibiotics are indicated for severe or persistent symptoms > 1 week. 11. Immunocompromised patients are prone to a highly invasive rhinocerebral fungal sinusitis caused by the Phycomycetes class of fungi (e.g., Mucormycosis). a. Exam reveals nasopharyngeal necrosis, dark nasal discharge, ocular findings, and cranial nerve palsies. b. X-rays may show bony destruction.
III. SALIVARY GLANDS, OROPHARYNX, AND HYPOPHARYNX
A. Sialadenitis and sialolithiasis:
1. Sialadenitis refers to an infection of the salivary glands. It is most commonly seen in debilitated patients (i.e., elderly, dehydrated, diabetic). 2. Presents as a painful swelling of either the submandibular gland (most common), parotid. 3. Purulent discharge can often be seen from Stensen’s or Wharton’s duct. 4. Staph. aureus is the most common pathogen. 5. Treatment is hydration and anti-staphylococcus oral antibiotics. EENT/Ophthalmologic Emergencies Page 395 Notes 6. Mumps (paramyxovirus-most common viral pathogen) is usually seen in children ages 5-15 but may be seen at any age. a. Typically a prodrome of low-grade fever, anorexia, malaise, and headache, followed by bilateral diffuse, tender parotid swelling. b. The disease is usually mild and self-limited, and treatment is symptomatic. c. Orchitis is a common complication in postpubertal men and occurs with a 25% incidence. d. Unilateral hearing loss may occur at all ages with a 4% incidence. It is usually temporary. e. Encephalitis is a rare complication. 7. Sialolithiasis - obstruction of a salivary duct by a stone. a. 90% are located in Wharton’s duct, and 10% in Stensen’s. b. X-ray may be diagnostic since the majority of stones are radiopaque. c. Most pass spontaneously and treatment is sialogogues (i.e., lemon drops) to induce salivation. d. Antibiotics are reserved for secondary infection.
B. Pharyngitis:
1. Group A streptococci (i.e., Streptococcus pyogenes) accounts for 20-30% of all cases of acute pharyngitis. a. Treat because of risk of acute rheumatic fever. b. Rapid strep detection tests have a false negative rate of up to 20%. c. Antibiotic treatment is advocated for the following reasons: i. Shortens the course of illness. ii. Prevents suppurative complications (i.e., peritonsillar abscess and cellulitis, retropharyngeal abscess). iii. Prevents acute rheumatic fever (antibiotic treatment within 9 days of symptomatic pharyngitis has been proven effective). iv. Acute glomerulonephritis is not prevented by treatment with antibiotics. 2. Mononucleosis usually presents with exudative pharyngitis and fever. a. Splenomegaly occurs in approximately 50% of patients and predisposes to splenic rupture. b. Severe tonsillar swelling and exudate may rarely cause upper airway obstruction. c. Diagnosis is confirmed by a positive monospot test. d. Avoidance of contact sports is recommended when splenomegaly is present. 3. Gonococcal pharyngitis occurs from orogenital contact. a. It is usually asymptomatic but may present with tonsillar swelling, erythema, and exudate with cervical lympenopathy. b. Treatment – antibiotics. EENT/Ophthalmologic Emergencies Page 396 Notes 4. Diphtheria caused by Corynebacterium diphtheriae. a. An exudative pharyngitis with production of an exotoxin affecting the myocardium and peripheral nervous system. b. Characteristically, there is a blue-white membrane in the pharynx composed of bacteria, fibrin, and necrotic debris. c. Sudden airway obstruction may ensue from pharyngeal swelling and copious exudate. d. Mortality is directly related to delay in treatment with an antitoxin. e. Additional management includes antibiotics (i.e., penicillin or erythromycin), and admission for cardiac monitoring.
C. Deep tissue infections:
1. Peritonsillar abscess is usually a complication of acute suppurative tonsillitis. a. Present with severe sore throat, fever, odynophagia and drooling, “hot potato” voice, and variable degrees of trismus. b. Treatment is IV antibiotics (i.e., penicillin) and drainage. 2. Ludwig’s angina is a bilateral cellulitis of the floor of the mouth involving the sublingual and submandibular spaces. a. True emergency because rapidly progressive pharyngeal swelling and displacement of the tongue leads to upper airway obstruction. b. Most common in elderly, debilitated men. c. Usually caused by dental infections (lower molars) and bacterial cultures growing mixed anaerobic and aerobic flora. d. Diagnosis is made clinically by verifying brawny edema of the submandibular area in a febrile patient with a protruding elevated tongue and respiratory distress. e. Treatment is IV antibiotics (clindamycin or cefoxitin or pen + metronidazole) and the airway must be secured to prevent pending obstruction. 3. Retropharyngeal abscess is most common in children under 3 years of age (6 months-3 years). a. Present with fever, neck pain, muffled voice, dysphagia and snoring or stridorous breathing. b. Patients prefer to lie supine; forced sitting can increase airway compromise. c. Diagnosis is confirmed by soft tissue X-ray of lateral neck. d. CT scan may be helpful to assess the extent of involvement. e. Treatment is IV antibiotics, admission, and ENT referral for surgical drainage.
IV. SUPRAGLOTTIC LARYNX
A. Adult epiglottitis (pediatric epiglottitis is discussed elsewhere):
1. In contrast to children, complete upper airway obstruction is EENT/Ophthalmologic Emergencies Page 397 Notes infrequent probably because of a larger, more rigid airway. Peak incidences: age 20-40. a. Should be suspected in cases where symptoms of sore throat and dysphagia are out of proportion to findings on pharyngeal examination. b. Adults will often have prodrome of 1-2 day URI symptoms. c. H. influenzae is the most common pathogen, but adults have a greater incidence of gram positive and Branhamella catarrhalis infections. d. Lateral soft tissue neck X-rays reveal classic finding of “thumbprint-like” epiglottis. e. Airway equipment at bedside, ICU, immediate ENT consult, antibiotics.
B. Croup:
1. Inflammation of the larynx and subglottic airway. 2. Parainfluenza virus most common. Also RSV, adenovirus. 3. Children ages 3 to 36 months. Rare after age six. 4. Treatment - steroids, humidified oxygen (warm vs. cool), racemic epinephrine. 5. A randomized trial of a single dose of oral dexamethasone for mild croup: a. For children with “mild” croup, use of a single dose of dexamethasone (0.6 mg/kg) results in significant benefits, including being less likely to return for croup problems within seven days.
V. DENTAL EMERGENCIES
A. Nontraumatic:
1. Dental caries: a. Most common cause of odontogenic pain. b. Tooth decay should be evident on examination. c. Treatment: analgesics (or nerve block), antibiotics and referral to a dentist. 2. Alveolar osteitis (dry socket): a. Severe pain associated with a foul order and taste in the mouth two to three days after an extraction. b. Cause is loss of the healing blood clot and localized osteomyelitis. c. Treatment - saline irrigation of the socket and application of a medicated dental packing or iodoform gauze slightly dampened with eugenol (oil of cloves). d. Dental referral. 3. Periodontal abscess: a. Swelling of the gingiva secondary to entrapment of plaque and debris between the tooth and the gingiva. EENT/Ophthalmologic Emergencies Page 398 Notes b. Treatment consists of warm saline irrigation and antibiotics (i.e., penicillin or tetracycline). 4. Acute necrotizing ulcerative gingivitis (ANUG or trench mouth, Vincent angina - extension to the pharynx and tonsils): a. An acute destructive disease in which bacteria invade non- necrotic tissue. b. Etiology is fusobacteria and spirochetes. c. Gingiva appears edematous and fiery red; interdental papillae are swollen and covered with a grayish pseudomembrane. d. Accompanied by systemic illness including fever, malaise and regional lymphadenopathy. e. Treatment is antibiotics, warm saline rinses, systemic analgesics, and application of topical local anesthetics such as viscous lidocaine.
B. Traumatic:
1. Tooth fractures: a. Ellis Class I fractures - only involve the enamel portion of the tooth. This requires no treatment in the emergency department. b. Ellis Class II fractures - involve the enamel and the underlying dentin. There may be sensitivity to heat, cold or even air. i. Under the age of 12, place dressing of a calcium hydroxide paste on the exposed dentin, which is then covered by dry gauze, aluminum foil or dental dry foil. ii. Patient > 12 years of age are advised to avoid extremes in temperature and to seek dental care the following day. c. Ellis Class III fractures - involve the enamel, dentin and pulp. This is a true dental emergency and requires immediate attention from a general dentist or endodontist. If a dentist is not immediately available, cover the tooth with aluminum foil or seal with “cavet,” a temporary root canal sealer. 2. Tooth avulsion: a. Avulsed primary teeth in the pediatric population (i.e., ages 6 months to 5 years) are not replaced into their sockets. b. One percentage point for successful replantation is lost each minute that tooth is absent from the oral cavity. c. Do not handle any portion of the tooth other than the crown - disrupts periodontal ligament need for reimplantation. d. The tooth should be transported either in the patient’s mouth or in a cold glass of milk. e. Successful reimplantation is associated with survival of the periodontal ligament fibers on the root. f. Hank’s solution has been shown to maintain viability of the periodontal ligaments for four to six hours or longer. If a tooth has been avulsed for longer than 30 minutes, there is evidence that soaking in Hank’s solution for 20 to 30 minutes EENT/Ophthalmologic Emergencies Page 399 Notes prior to replantation may improve survival. g. The avulsed tooth should be replaced in the socket in the emergency department and seen by a dentist within 24 hours for stabilization. 3. Temporomandibular joint dislocation: a. Occur secondary to yawning, laughter, or trauma. b. If unilateral, the jaw deviates to the opposite side. c. To reduce, operator must overcome masseter contraction. d. Post reduction, avoid extreme opening of mandible, laughing or yawning. Soft diet for 1 week, warm packs, NSAIDs. e. Patients with chronic dislocations may be helped with a Barton bandage.
VI. VERTIGO
A. Vertigo is characterized by an illusion of motion where no motion exists (i.e., spinning sensation, imbalance or sensation of being pulled to one side or the other). Once it has been determined that the “dizzy” patient has vertigo, the history and physical should focus on differentiating central from peripheral etiologies.
B. Differentiating factors are as follows:
CENTRAL PERIPHERAL
Vertigo Mild/constant Severe/intermittent Nausea & Intermittent Frequent vomiting
Hearing loss & Absent May be present tinnitus
Nystagmus Multidirectional, nonfatigable, Unidirectional, fatigable, not positional, not inhibited by horizontal or rotary vertical, ocular fixation, may be vertical positional, inhibited by ocular fixation, never vertical
Neurological May be associated with ataxia, None symptoms diplopia, cranial nerve findings, hemiparesis Slow Onset Sudden
Etiologies Brainstem infarct or tumor Vestibular neuronitis Cerebellar infarct or bleed Labyrinthitis Perilymph fistula Ménière’s disease Benign positional vertigo Drug effects Posttraumatic vertigo Acoustic neuroma
EENT/Ophthalmologic Emergencies Page 400 Notes
C. If the history and physical do not clearly differentiate a peripheral etiology: CT scan.
D. Several features to remember are as follows:
1. Ménière’s disease or endolymphatic hydrops is characterized by recurrent attacks of vertigo with a progressive, fluctuating hearing loss. Tinnitus is usually present during attacks. ED treatment consists of medications shown to inhibit vertigo (i.e., meclizine, Valium, droperidol). 2. Acute labyrinthitis is presumed viral but the etiology is often unknown. The illness is self limited. 3. A perilymph fistula presents with severe vertigo and sensorineural hearing loss. Straining (i.e., coughing, sneezing, and lifting) exacerbates symptoms. Diagnosis can be presumed if symptoms worsen with pneumatic otoscopy. 4. Posttraumatic vertigo is common following closed head trauma. It is due to concussion of the labyrinth. 5. Benign positional vertigo is a self limited disease (i.e., few weeks) seen most commonly in the elderly. Patients have brief, repeated attacks of vertigo associated with movement or changes in head position. There is no hearing loss or tinnitus. Treatment is symptomatic and an exercise program designed to repetitively induce symptoms may be helpful. 6. Central-Wallenberg Syndrome - infarct of brain stem (lateral medullary). Symptoms include numbness, Horner’s, contralateral loss of pain, temp. 7. Other central-vertebral basilar insufficiency - multiple sclerosis.
Ophthalmologic Emergencies
I. PHYSICAL EXAM
A. Visual acuity - best corrected response:
1. Pinhole can approximate prescriptive eyewear (object is centered over visual axis through mid lens and to fovea) – squinting. 2. Snellen at 20 feet/Rosenbaum at 14 inches. 3. If necessary, document counting fingers (CF), hand motion (HM), or light perception (LP).
B. Pupils recall Marcus-Gunn pupil (afferent pupil defect) and Adies pupil (syphilis pupil - one that “accommodates but does not react”).
EENT/Ophthalmologic Emergencies Page 401 Notes
II. EYELID DISEASE
A. Blepharitis:
1. Inflammation of eyelids may be chronic. a. Scaly, erythematous, greasy lid margins. b. S. aureus most common agent. c. Symptoms - pruritus, redness, irritation, AM crustiness. 2. Treatment: a. Warm soaks/lid scrubs frequently (baby shampoo ideal). b. May consider sulfacetamide drops or antibiotic ointment to eyelid margins (erythromycin or bacitracin).
B. Hordeolum (sty):
1. Acute inflammation of lid margin. S. aureus most common. a. Internal: i. Infection meibomian gland. b. External: i. Eyelash follicle or lid margin tear gland. 2. Symptoms - redness, focal swelling with a tender nodule or pustule on the eyelid usually close to the margin, pain. 3. Treatment: a. Warm compresses. b. Soaps. c. Topical sulfa/erythromycin 7 days. d. May need incision and drainage if no improvement.
C. Chalazion:
1. Chronic granulomatous inflammation of Zeis or Meibomian tear gland. 2. Inflamed, nontender, lesion. 3. Commonly seen in patients with: a. Blepharitis. b. Rosacea. 4. Treatment: a. Warm compresses and massage. b. Incision and curettage/ steroid injection by ophthalmologist. c. If recurrent: i. Sebaceous cell, basal cell or meibomian gland carcinoma.
D. Dacryocystitis - acute infection of lacrimal sac, in infants and adults > 40 years of age:
1. Painful, red, swollen below medial canthus. 2. Most commonly Staph. aureus, then staph. epidermidis, strep, H. flu. EENT/Ophthalmologic Emergencies Page 402 Notes 3. Referral to ophthalmology, warm soaks, and systemic broad spectrum antibiotics (Augmentin), topical antibiotics.
E. Preseptal cellulitis:
1. Lid erythema, warmth, tenderness. 2. Absence of proptosis, restricted eye movement, pain with eye movement - if any of these, think orbital cellulitis.
III. THE RED EYE
A. Painless:
1. Conjunctivitis - most common cause of red eye. a. Definition - conjunctival inflammation which typically spares the cornea. b. Symptoms - itching, burning, tearing, FB sensation, gritty. c. Signs - redness, exudate, chemosis, follicular hyperplasia (cobblestoning), normal cornea, normal visual acuity. d. Viral - most common of all conjunctivitis: i. Initially unilateral (bilateral within 24-48 hours). ii. Copious clear secretions. iii. Contagious, viral prodrome, preauricular lymphadenopathy. iv. Agents – adenovirus is most common, Coxsackie, enterovirus. Epidemic keratoconjunctivitis (EKC) differs in that this may present with photophobia and corneal involvement. v. Treatment - cool compresses, antihistamine for pruritus. e. Bacterial: i. Similar to viral, discharge can be purulent, AM crust. ii. Different from blepharitis in discharge is continuous through the day. iii. Agents - Staph, Strep, H. flu, pneumococcus, Moraxella, or mixed. iv. Treatment: Broad spectrum antibiotics drops every 2 hours; ointment every 6 hours. Local hygiene. No steroids, no patching. v. Neisseria gonorrhoeae - real potential for vision loss: Can ulcerate or perforate cornea; true ocular emergency. Adults - parenteral ceftriaxone and topical antibiotics. Treat for concomitant chlamydia infection; ocular irrigation; consult ophthalmology; admit all but mildest cases. Concurrent urethritis common.
EENT/Ophthalmologic Emergencies Page 403 Notes vi. Neonatal (ophthalmia neonatorum) conjunctivitis within first month of life. N. Gonorrhea first 2-4 days (ceftriaxone). Chlamydia 5-13 days (topical erythromycin). vii. Chlamydial - not as serious as N. gon: Erythromycin P.O. and topical for 14 days. Maybe cause for refractory conjunctivitis, leading cause of preventable blindness worldwide. Must treat sexual contact(s). viii. Allergic - chief complaint is itching: Clear watery discharge with cobblestoning; bilateral. Typically seasonal, environmental. May see chemosis. ix. Treatment: Cold compresses. Topical decongestant (naphazoline) and/or antihistamine (pheniramine) - Naphcon A.
B. Painful:
1. Iritis - (AKA uveitis, iridocyclitis): a. Definition - internal inflammation without infection. b. Etiology - allergic, infectious, post-traumatic, foreign body, most commonly idiopathic. c. Symptoms - dull ocular pain, may or may not have blurred vision, reddened eye, photophobia. d. Signs - pupil constricted (secondary to spasm), injected bulbar conjunctiva, perilimbal/ciliary flush, anterior amber with flare and cell (F/C). e. Clues – will have consensual photophobia, pain not relieved with topical anesthetic. f. Differentiate from acute glaucoma in that iritis has “normal” cornea, constricted to mid-range pupil, and normal intraocular pressure. g. Treatment – cycloplegics such as homatropine, may use steroids after consulting ophthalmology, referral. 2. Acute narrow angle glaucoma (ANAG): a. Leading cause of blindness in the U.S. b. Definition - acute flow obstruction at canal of Schlemm in patients with congenital defect of angle or predisposed with shallow anterior chamber. c. Symptoms - severe unilateral ocular pain, red eye, blurry vision, photophobia, halos around lights, headache, nausea/emesis, cephalgia, abdominal pain (systemic symptoms often “cloud” syndrome). d. Signs - corneal edema, ciliary flush, increased IOP (>40 mmHg), rock hard globe, mid-range pupil, sluggish or nonreactive pupil, injected bulbar conjunctiva, decreased
EENT/Ophthalmologic Emergencies Page 404 Notes visual acuity. e. Treatment – EMERGENT consultation during treatment: i. Constrict pupil (remove iris from meshwork) pilocarpine 2% 1 drop every 15 minutes for 2 hours. ii. Decreased aqueous humor production: Beta blockers – Timolol 0.5% 1 drop and repeat in 10 minutes (beware of cardiac and pulmonary contraindications). Acetazolamide (CAI - carbonic anhydrase inhibitor) - Diamox – 500 mg IVPB. Adrenergic-imodipine 0.1% drop. iii. Hyperosmotics: Glycerol 50% 1-1.5 mg/kg P.O. (dilute with juice and remember diabetics), or: Mannitol 20% 1-2 gm/kg IV over 30 minutes (beware of osmolarity). iv. Antiemetics. v. Consult ophthalmology for surgery - peripheral iridectomy, laser iridotomy.
C. Corneal disorders:
1. Foreign body (FB): a. Symptoms - history usually guides; burning, redness, tearing, irritation. b. Signs - may visualize in upper/lower lids, embedded within cornea, or positive fluorescein staining; if none of the above, visualize all eyelashes. c. Removal – irrigation, spud, blade, needle, swab. d. Rust ring – iron containing FB, can cause chronic irritation, visual acuity disturbance, corneal staining, remove after 24 hours. e. Refer deeply embedded FB, old FB, and large FB over the visual axis. f. Antibiotics, analgesics, tetanus immunization and referral. 2. Corneal abrasion: a. Symptoms similar to foreign body. b. Normal exam unless abrasion over visual axis, positive fluorescein. c. Antibiotic, cycloplegics, topical anti-inflammatories, analgesics, tetanus immunization, potential referral (“dirty” abrasions from human or animal causes may require more aggressive therapy and referral). d. Avoid eye patching. 3. Contact lens syndrome: a. Very common. b. Painful, red eye; may have iritis. c. Usually not infected.
EENT/Ophthalmologic Emergencies Page 405 Notes d. Injected conjunctiva with fluorescein positive keratopathy. e. Stop lens usage, antibiotics and may need cycloplegic; referral. f. Ulcers almost invariably Pseudomonas a. and require ophthalmologic consultation and frequent antibiotics (ciprofloxacin a good choice). 4. UV keratitis (welders, sunbathers, skiers, tanning booths, high altitude): a. Typically bilateral, painful, red eyes; usually presents 6-8 hours after incident. b. Injected conjunctiva; decreased visual acuity, diffuse, punctate keratopathy with fluorescein; possible iritis. c. Antibiotics, analgesics, topical cycloplegic agent referral if iritis. d. Topical anesthetics unjustifiable - falsely protects and known cellular toxin. e. Oral pain management may be needed. 5. Viral corneal infection: a. Herpes simplex infection: i. May be primary outbreak or reactivation. ii. Symptoms - foreign body sensation, tearing, photophobia, pain. iii. Signs - may have typical vesicles on lids, conjunctiva; cornea may have dendritic or ulcerative process with fluorescein uptake; decreased visual acuity if over visual axis. iv. Treatment – referral to ophthalmologist, topical antiviral agents such as trifluridine or vidarabine, cycloplegics. 6. Herpes zoster ophthalmia - varicella virus: a. Symptoms - paraesthesia, burning, pain, rash; most common form of recurrent zoster. b. Signs - vesicular eruptions along CN V1, unilateral involvement, keratitis, scleritis, conjunctivitis, dendritic defect, lesions to the tip of the nose (Hutchinson’s sign) signal nasociliary nerve involvement and high likelihood of ocular lesions. c. Treatment: i. Oral acyclovir or famciclovir. ii. Topical steroids may decrease neuralgia but consult ophthalmologist. iii. Referral. 7. Pterygium: a. Fibrovascular tissue, usually wedged shaped. b. Extends onto cornea. c. Treatment - artificial tears, non-emergent referral.
D. Pupillary syndromes:
1. Horner’s Syndrome: EENT/Ophthalmologic Emergencies Page 406 Notes a. Ptosis. b. Miosis. c. Anhyrdosis. d. Opiates, brain stem stoke. 2. Argyll Robertson: a. Small irregular pupil. b. Neurosyphilis. c. Accommodates but doesn’t react. 3. Marcus Gunn: a. Afferent pupillary defect. i. Inadequate response to light in affected eye. b. MS, optic neuritis, retinal artery/vein occlusion, globe retina disease.
IV. OCULAR TRAUMA
A. Orbital fracture:
1. Blunt more common than penetrating trauma. 2. 10-25% have associated globe injury. 3. Blow-out fracture: a. Floor and medial wall most susceptible. b. Entrapment (fat, inferior rectus, and inferior oblique muscles). c. Hypesthesia ipsilateral cheek and lip, diplopia and limited upward gaze. d. Antibiotics only if fracture involves infected sinus. e. Surgical repair if persistent diplopia, cosmetic. f. Usually delayed 7-10 days. 4. Medial wall fractures-subcutaneous emphysema, ethmoid sinus, epistaxis.
B. Retrobulbar hemorrhage:
1. Orbital hemorrhage in potential space surrounding globe: a. May occlude central retinal artery (pressure phenomenon). b. Clinically - proptosis, visual loss, increased IOP. c. Diagnosis - CT scan. d. Treatment - CAI, beta blockers, mannitol, lateral canthotomy, immediate optho consult.
C. Lids/conjunctival injury:
1. Lid injuries typically from penetrating trauma; most primarily repaired but refer following: a. Lid margin injuries - require multilayer closure and often cosmetically poor result. b. Canalicular involvement - medial 1/3 of lid (upper or lower) can involve lacrimal system and may need stenting. EENT/Ophthalmologic Emergencies Page 407 Notes c. Levator/canthal tendon involvement - ptosis often results with poor repair. d. Puncture/laceration through orbital septum (fat protrusion in wound) - risk of infection. e. Rule out penetrating globe injury/ foreign body. f. Laceration/avulsion - those with significant skin loss. 2. Conjunctival injuries: a. Less than 1 cm left alone. b. Repair those greater than 1 cm. c. More important not to miss a foreign body or associated globe injury.
D. Anterior segment injury:
1. Corneal laceration: a. Symptoms - decreased vision, pain. b. May have shallow anterior chamber, tear drop iris, leaky aqueous humor, or prolapsed iris. c. Treatment - stop further exam, rigid metal eye shield and referral. 2. Scleral laceration/perforated globe: a. True ocular emergency. b. Blunt or penetrating trauma with significant force, commonly located in inferior aspect. c. Up to 20% of globe ruptures have no signs of perforation. d. Tear drop pupil, bloody chemosis, decreased visual acuity, flattening of anterior chamber, small fragments of iris at wound edges on exam. i. Seidel test – positive if fluorescein stain reveals efflux of aqueous humor in “river like” pattern from laceration on slit lamp exam. e. Treatment: i. Halt exam, no pressure to eye, metal eye shield, tetanus immunization, parenteral antibiotics, immediate referral, nothing topically. f. Sympathetic ophthalmia: i. Seen with severe injuries. ii. Occurs in unaffected eye. iii. Mechanism - autoimmune granulomatous reaction affecting contralateral eye forcing enucleation of injured eye if vision is to be preserved. 3. Hyphema - anterior chamber hemorrhage: a. Patient sitting up, blood layers and form meniscus. b. Blunt much more common than penetrating. c. 25-35% have an associated eye injury. d. Symptoms - pain, photophobia, blurry vision best examined in sitting/upright position. e. Complications: i. Rebleed in 2 to 5 days with worse prognosis. EENT/Ophthalmologic Emergencies Page 408 Notes ii. Corneal staining. iii. Secondary glaucoma. iv. Anterior and posterior synechia. f. Treatment: i. Small size, reliable patient outpatient, all others admitted. ii. Analgesics but avoid salicylates/NSAIDs, platelet inhibitors. iii. Referral; may or may not hospitalize. iv. Rest with head elevated 45º. v. Cycloplegics, miotics, mydriatics, antifibrinolytics, steroids. vi. Sickle cell – beta blockers, alpha agonist, CAI. 4. Lens injury: a. Dislocated/subluxed. b. Invariably visual disturbance - monocular diplopia. c. Iridodonesis - trembling of iris after rapid eye movements. d. Blunt trauma, Marfan’s, syphilis. e. Funduscopic exam different from contralateral eye, may be anterior or posterior dislocation. f. Immediate ophthalmology consult. 5. Pupil injury: a. Traumatic mydriasis. b. Often associated with blunt injury with selective neurapraxia of parasympathetic fibers of CN III affecting constrictors (hence dilated) and accommodation (hence visual disturbance). i. Note that mydriasis can imply: Significant intracranial pathology – “blown pupil.” Atropine administration. Accidental Neo-Synephrine administration when vasoconstricting nasal mucosa prior to nasotracheal intubation. Can reverse mydriasis caused by intracranial mass with pilocarpine; the same will not work initially for a. and b. above. Treatment - referral; typically spontaneously resolves. c. Traumatic miosis: i. Selective neurapraxia to sympathetic fibers to pupil dilators (hence unopposed constriction); may see with Horner’s syndrome. ii. Treatment - referral; typically spontaneously resolves. 6. Subconjunctival hemorrhage: a. Very common - typically asymptomatic. b. Can occur with minor (sneezing, screaming, Valsalva, coughing) or major (globe rupture) trauma. c. If history and physical examination dictate benign process, then reassure that this entity will spontaneously resolve within 10-14 days.
EENT/Ophthalmologic Emergencies Page 409 Notes d. May have associated facial/lid petechia.
E. Posterior segment injury:
1. Intraocular foreign body: a. History more helpful than physical examination. b. Search for entry wound, i.e., grinding wheel, working with metal. c. X-rays, sonography, CT, MRI, dictated by suspicion, exam, and type of FB. d. Treatment, immediate referral, tetanus immunization, metal shield, antibiotics. 2. Vitreous hemorrhage: a. Blunt injury, diabetic retinopathy. b. Symptoms – sudden painless unilateral loss of vision, floaters, visual disturbance. c. Signs - visual acuity deficit, may see hemorrhage. d. Treatment - rest, head elevation, immediate referral. 3. Preretinal, superficial retinal, and/or chorioretinal injury: a. Shaken baby syndrome. b. Retinal - tear/detachment. c. Treatment - rest, referral. 4. Complications: a. Infection. b. Ulcerations. c. Endopthalmitis - infection of deep eye structure, pain, decreased visual acuity. i. Treatment - intraocular and systemic antibiotic. d. Sympathetic opthalmia.
V. SUDDEN VISION LOSS
A. Trauma (see Section IX, A-D).
B. Vascular:
1. Central retinal artery occlusion (CRAO): a. Symptoms - sudden, painless, unilateral vision loss. b. Risks - carotid artery disease, sickle cell, acute glaucoma, retrobulbar hemorrhage, exophthalmos. c. Signs: i. Severe decreased visual acuity. ii. Afferent pupil defect. iii. Optic disk pallor, macular edema, bloodless arterioles, dark veins, “cherry-red spot” (choroidal vessels supply macula). iv. Treatment - (ischemic time 30-60 minutes) goal is to restore retinal artery blood flow by dislodging clot, dilating the artery and lowering IOP. EENT/Ophthalmologic Emergencies Page 410 Notes Immediate referral: •• Vigorous massage (5 second intervals). •• Enhance vasodilation – carbogen or paper bag breathing (beware of hypoxemia with latter). •• Acetazolamide and a topical β blocker. Surgical paracentesis of anterior chamber. 2. Central retinal vein occlusion (CRVO): a. Symptoms – sudden, painless, unilateral vision loss typically less severe than CRAO. b. Etiology – thrombosis of the central retinal vein. c. Signs: i. Decreased visual acuity: “Blood and thunder” retina, engorged veins, retinal hemorrhage. Differential diagnosis includes pseudotumor cerebri and papilledema. d. Treatment - referral, treat underlying cause, poor prognosis. 3. Miscellaneous - TIAs, ocular migraine, vitreous hemorrhage.
C. Idiopathic:
1. Retinal detachment: a. Symptoms - painless “veil over eyes” or “drawn curtain”; can have prodrome of floaters, cloudy vision, flashing lights, spider webs; typically >50 year old patients. b. Etiology - unknown cause for separation between sensory and pigmented retina. c. Signs: i. Decreased visual acuity if macula involved. ii. Detached undulating gray retina. iii. Tear, hole, bulla, fold. d. Treatment – immediate referral, rest; spontaneous reattachment rare. 2. Hysterical blindness: a. Normal exam except for complaint. b. Occipital CVA only confounder but differentiate with optokinetic reflex. c. A normal pupillary reaction, funduscopic exam, and lack of afferent pupillary defect is very suggestive of hysteria/ conversion disorder or malingering.
D. Inflammatory:
1. Optic neuritis: a. Symptoms - sudden, unilateral vision loss; can have pain with EOM. b. Signs - loss of central retinal vision with intact peripheral vision (central scotomata); decreased color vision; normal
EENT/Ophthalmologic Emergencies Page 411 Notes exam - “the patient sees nothing and the doctor sees nothing.” c. An association with multiple sclerosis; 25-65% will develop MS. d. Treatment – emergent referral, systemic and/or retrobulbar steroids. 2. Temporal (giant cell) arteritis: a. Vasculitis of medium and large arteries that can cause optic nerve infarction and permanent vision loss, female predominance, most > age 50. b. Symptoms - unilateral, boring pain; tenderness; may have sudden onset; may have flu-like prodrome consistent with polymyalgia rheumatic; visual disturbance that progresses. c. Signs - erythema, swelling, tenderness, and nodularity of artery involved; funduscopic exam can reveal pallor, hemorrhage, exudates; iritis; ESR > 70; temporal artery biopsy for diagnosis. d. Treatment - referral; high dose systemic steroids.
VI. OCULAR BURNS
A. Acid (the only eye emergency requiring treatment prior to visual acuity evaluation):
1. Coagulation necrosis of epithelium and usually self limiting. 2. Less devastating than alkaline burns. 3. Treatment – “irrigation, irrigation, irrigation”; fluorescein staining, cycloplegics, +/- antibiotics, +/- referral, reassess pH (Nitrazine paper), no neutralization.
B. Alkaline:
1. Drain cleaners, chemical detergents, fertilizers, ammonia derivatives. 2. Initially conjunctivitis but liquefaction necrosis continues burn process until alkali removed. 3. Signs - perilimbal blanching and corneal edema are poor prognostic indicators. 4. Treatment - copious irrigation; referral mandatory if any signs of injury from alkaline burn; reassess pH; no neutralization. 5. Long term complications - perforation, adhesions, glaucoma, cataracts.
C. Thermal:
1. Rare due to Bell’s phenomenon - in response to stimulus, eyes blink and roll up. Assess lid closure - if cornea is exposed, it must be kept moist.
EENT/Ophthalmologic Emergencies Page 412 Notes
EENT/OPHTHALMOLOGIC EMERGENCIES
PEARLS
EENT Emergencies
1. An auricular hematoma must be emergently drained and a compressive dressing applied to avoid the complication of “cauliflower ear.”
2. The most common pathogen in otitis externa is Pseudomonas aeruginosa followed by Staphylococcus aureus.
3. Relapsing polychondritis is an autoimmune inflammatory disease of cartilage. When the auricle is affected, the ear lobe is spared since it does not have cartilage.
4. The classic physical finding in malignant otitis externa is granulation tissue on the floor of the auditory canal at the bone-cartilage junction.
5. Malignant otitis externa is an osteomyelitis seen in immunocompromised patients requiring surgical debridement and IV antibiotics covering Pseudomonas.
6. Herpes zoster of the geniculate ganglion (Ramsay-Hunt Syndrome) may present with painful rash, hearing loss, and facial nerve paralysis.
7. Traumatic perforation of the tympanic membrane will heal spontaneously in 95% of patients within 3 months. Profound hearing loss or vertigo should raise suspicion of ossicular disruption and should be referred to ENT.
8. The most common pathogen in otitis media of children is Strep. pneumoniae followed by H. influenzae.
9. The most common site of nosebleeds is the anterior nasal septum (Kiesselbach’s plexus or Little’s area).
10. Patients with posterior nasal packings are at risk for hypoxemia and must be admitted to a monitored setting.
11. The most common pathogen in acute sinusitis is H. influenzae and Strep. pneumoniae. (Chronic sinusitis is caused by allergic, then infectious mixed flora, anaerobes and fungi.)
EENT/Ophthalmologic Emergencies Page 413 Notes
12. Cavernous sinus thrombosis is a complication of ethmoid sinusitis and presents with eyelid edema, proptosis, chemosis, 3rd & 6th cranial nerve palsies, pupillary dysfunction, and papillary edema. Diagnosis is confirmed by CT scan or MRI and treatment is IV antibiotics, not surgical.
13. Frontal sinuses develop at age 6-8; therefore, frontal sinusitis is not seen in children.
14. Ludwig’s angina is a cellulitis of the floor of the mouth. It is most common in older males with bad teeth. Treatment is IV antibiotics, possible intubation, possible surgery.
15. Retropharyngeal abscess is commonly seen in children less than 3 years of age due to atrophy of the retropharyngeal nodes with aging.
16. Antibiotic treatment of strep pharyngitis within 9 days of the onset of symptoms will prevent acute rheumatic fever, but not acute glomerulonephritis.
17. A permanent tooth avulsed intact should be replaced into the socket as soon as possible. The chance of survival drops approximately 1% every minute the tooth remains out of socket. Do not replace primary teeth in children.
18. Avulsed teeth should be transported to the ED in milk or the patient’s mouth.
19. Bullous myringitis is most commonly caused by viruses but also may be caused by Mycoplasma pneumoniae.
20. The most reliable sign of AOM is decreased mobility of the tympanic membrane on pneumatic otoscopy.
21. The most common source of posterior nosebleeds is the sphenopalatine artery.
Ophthalmologic Emergencies
1. The only indication for the emergent use of a miotic agent (green caps) is for acute angle closure glaucoma (pilocarpine 2%).
2. Topical corticosteroids can cause HSV reactivation.
3. S. aureus is the most common agent causing blepharitis and hordeolum (sty).
EENT/Ophthalmologic Emergencies Page 414 Notes
4. The most common cause of a painless red eye is viral conjunctivitis and the most common etiology is adenovirus.
5. Neisseria gonorrhea ophthalmic infection can cause loss of vision and perforate an intact cornea and is considered an ocular emergency. In general, should be admitted for parenteral ceftriaxone and topical antibiotics.
6. The most common cause of a painful red eye is iritis (AKA uveitis/iridocyclitis).
7. Classic iritis presents with the following signs: constricted pupil, injected conjunctiva (bulbar), perilimbal flush and inflamed anterior chamber (flare/cell).
8. Differentiate iritis from acute angle closure glaucoma by iritis having a normal cornea, small pupil, and normal tonometry.
9. Typical signs of acute narrow angle glaucoma (ANAG) include: corneal edema, ciliary flush, decreased visual acuity, mid-range and sluggish pupil, and increased IOP (>50 mmHg).
10. Treatment for ANAG includes: consultation, pupillary constriction, decrease aqueous humor production, hyperosmotics, antiemetics, and surgery.
11. Most common form of recurrent zoster is herpes zoster ophthalmia (varicella virus). Lesions on the tip of the nose (Hutchinson’s sign) from nasociliary nerve involvement indicate high likelihood of ocular lesions.
12. Ten to twenty percent of orbital fractures have an associated globe injury.
13. Complications of hyphema are re-bleed (2 to 5 days), corneal staining, and glaucoma.
14. Subconjunctival hemorrhage is very common, typically asymptomatic, and resolves without sequelae.
15. Central retinal artery and vein occlusions can present as sudden painless unilateral loss of vision.
16. Central retinal vein occlusion presents with decreased visual acuity and a blood and thunder appearance on funduscopic exam
17. Of all eye exposure injuries, alkaline injuries carry poorest prognosis due to the mechanism of liquefaction necrosis. EENT/Ophthalmologic Emergencies Page 415 Notes
REFERENCES
EENT Emergencies
1. “Acute Pharyngitis: How Effective is Therapy?” Emergency Medicine News, pg. 7-9, October, 1995.
2. Diseases of the Nose, Throat, Ear, Head, and Neck, Ballenger, John, Lea and Febiger, 1991.
3. “ENT Emergencies,” Emergency Medicine Clinics of North America, May, 1997.
4. Emergency Medicine, A Comprehensive Study Guide 6th ed, Tintinalli, Judith, McGraw-Hill, 2004.
5. Rosen’s Emergency Medicine, Concepts and Clinical, 6th Ed Rosen, P et al, 2006.
6. “Evaluation and Management of Acute Uvular Edema,” Annals of Emergency Medicine, 22(2):251-5, Feb., 1993.
7. “Removing Cockroaches from the Auditory Canal: Controlled Trial,” NEJM, 312(18), May, 1985.
8. “Pharyngitis: The Value of Laboratory Testing,” Emergency Medicine News, pg. 4-11, September, 1995.
Ophthalmologic Emergencies
1. Rosen’s Emergency Medicine, Concepts and Clinical, 6th Ed Rosen, P etal, 2006.
2. Bienfang DC, et al: Medical progress: Ophthalmology NEJM 1990; 323:958-959.
3. Janda RM: Ocular Emergencies, in Tintinalli; J (eds): Emergency Medicine, ed 6 2004. St. Louis, McGraw-Hill, Inc., 2004.
4. Drugs for viral infections. Medical Letter 1992; 34:31-36.
5. Brunette DD, et al: Ophthalmology, in Rosen P (eds): Emergency Medicine, ed 5. St. Louis, Mosby, 2002, Vol 2, pp.908-927.
6. Shingleton BJ: Eye injuries. NEJM 1991; 325:408-413.
EENT/Ophthalmologic Emergencies Page 416 Notes
7. Rhee D, Pyfer, M. The Wills Eye Manual. Office and Emergency Room Diagnosis and Treatment of Eye Disease. 3rd Ed 1999 Lippincott Williams & Wilkins.
08/17
EENT/Ophthalmologic Emergencies Page 417
Page 418
GI Emergencies
Brian Donahue, MD, FACEP
Clinical Assistant Professor, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, Presence Resurrection Medical Center, Chicago
Page 419
Page 420 Notes
GI EMERGENCIES
I. ABDOMINAL PAIN
A. General:
1. Very common cause for ED visits (10%); (8-11% of test). a. Nonspecific abdominal pain: i. (Most common) young-middle age, women of child- bearing age, low socioeconomic status, psychiatric disorders. b. Elderly: more likely to have a life-threatening process. 2. Presentations extremely variable, KNOW THE CLASSICS! 3. Always consider extra-abdominal causes. 4. High index of suspicion for children, elderly, and immunocompromised patients.
II. DISORDERS OF THE GALLBLADDER / BILIARY TREE
A. Cholelithiasis (gallstones):
1. Etiology: a. 20% females, 8% males have asymptomatic gallstones. 2. Risk factors: a. Female, as high as 4:1. b. Age. c. Family history. d. High estrogen state: female, fertile, forty, fat, contraceptives, clofibrate. e. IBD: Crohn’s, ulcerative colitis. f. Cystic fibrosis. g. Hemoglobinopathies. h. Sickle cell disease, thalassemia. i. Rapid weight loss/starvation. j. Elevated lipids/triglycerides. k. TPN. l. Post-op. 3. Types of stones: a. Cholesterol (pure or mixed): i. Most common! (> 75%) ii. Radiolucent (not visible) on X-ray. iii. Due to delayed GB emptying and bile stasis (increasing cholesterol concentration). b. Pigmented (black or brown): i. Unconjugated bilirubin + calcium salts. ii. Radiopaque (due to calcium). iii. Black stones:
GI Emergencies Page 421 Notes Advanced liver disease. Hemolytic disorders. Found exclusively in the GB. iv. Brown stones: Associated with infection. Found throughout biliary system. 4. History: a. RUQ/epigastric pain – constant or intermittent. b. Radiation to scapula or shoulder. c. N/V. d. Similar episodes in past. 5. Physical exam: a. RUQ/epigastric tenderness. 6. Diagnosis: a. Labs often within normal. b. X-ray – only 10% of GB stones visualized. c. US – test of choice: i. Highly sensitive for GB stones. 7. Treatment: a. For asymptomatic patients: i. No acute treatment needed. ii. 15-20% becomes symptomatic. iii. Outpatient elective surgery if: Frequent or severe attacks. Diabetic. Large biliary calculi. b. For symptomatic patients: i. Pain control. ii. Antiemetics. iii. Outpatient elective surgery. iv. 90% have recurrent symptoms within 2 years. v. 50% will develop acute cholecystitis.
B. Acute cholecystitis:
1. Etiology: a. Sudden inflammation of GB. b. Bacterial infection in 50-75%. c. E. Coli, Klebsiella, Enterococci predominant. 2. History: a. RUQ or epigastric pain; radiation to tip of (scapula). b. Pain becomes constant! c. Nausea / vomiting. d. +/- fever. 3. Physical exam: a. RUQ tenderness. b. Murphy’s sign (stops inspiratory breath upon deep palpation).
GI Emergencies Page 422 Notes i. Much lower sensitivity in elderly. 4. Diagnosis: a. CBC. b. Often elevated WBC with left shift. c. Alk Phos, Bilirubin, AST/ALT: i. Mildly elevated or normal. ii. Large elevations of Alk Phos, Bilirubin suggests stone in common bile duct (CBD). d. KUB: i. Poor sensitivity, stones seen ~ 10%. ii. Air in biliary tree … rare, but serious! (Gangrenous infx) e. Ultrasound: modality of choice: i. Gallstones. ii. Thickened GB wall. iii. Pericholecystic fluid. iv. Sensitivity 90-95%; specificity 75-85%. US can miss stones in cystic duct. f. CT scan: i. Sensitivity 92%, specificity 99%. ii. Especially helpful in emphysematous and hemorrhagic cholecystitis. iii. Excellent for diagnosing other intraabdominal disorders. g. HIDA scan – gold standard for this disease: i. Positive = no visualization of GB. ii. Identifies stones in cystic duct. iii. Very sensitive; neg scan essentially rules out diagnosis. 5. Treatment: a. Admit, NPO, IVFL. b. Pain, emesis control (NGT if multiple emesis). c. Antibiotics recommended: i. Bugs = gram negatives, anaerobes and Enterococcus. ii. Coverage with single broad-spectrum antibiotic (2-3rd generation Cephalosporin) adequate if not septic. iii. Triple coverage if septic. d. Surgical consultation: i. Surgery typically 24-72 hr after symptoms resolve. ii. Immediate surgery if toxic/gangrene/perforation. 6. Complications: a. Perforation (3-5%). b. Emphysematous cholecystitis (1%): i. Gangrene due to gas forming bacteria. E. Coli, Clostridium perfringens, Klebsiella. ii. Increased risk in diabetics, elderly. iii. High mortality. iv. Acalculous in 30% cases. c. Gallstone ileus. d. Pancreatitis (15-20%). e. Ascending cholangitis.
GI Emergencies Page 423 Notes f. GB empyema: i. Complete obstruction of cystic duct with bacteria. ii. Abscess formation within GB wall.
C. Acute acalculous cholecystitis:
1. No stones present in GB. 2. 2-12% of acute cholecystitis. 3. Rapid, malignant course, up to 41% mortality. 4. Bile stasis equivalent to common duct obstruction. 5. Risk factors: a. Elderly. b. Post-surgery. c. Diabetics. d. Trauma, burns. e. Sepsis. f. AIDS (due to CMV or Cryptosporidium Infx). g. Systemic vasculitic states. 6. Presentation: a. Similar to acute calculous cholecystitis EXCEPT: i. Gravely ill on presentation. ii. Frequently a complication of another process. 7. Diagnosis: a. HIDA scan: i. Poor filling of gallbladder without gallstones. b. Ultrasound: i. No gallstone. ii. Thickened GB wall, pericholecystic fluid. 8. Treatment: a. NPO, IVFL. b. Emergent surgical consultation for cholecystectomy vs. drain if unstable. c. Broad spectrum antibiotics.
D. Ascending cholangitis:
1. Obstructed bile flow causes retrograde infection up biliary tree (gram negatives, enterococci, anaerobic). 2. Causes/risk factors: a. Choledocholithiasis (CBD stone): #1 cause. b. Diabetes. c. Malignant strictures. d. Sclerosing cholangitis. 3. Presentation: a. Charcot’s triad: i. RUQ pain. ii. Fever/chills. iii. Jaundice. b. Reynolds’s pentad = Charcot’s triad plus: GI Emergencies Page 424 Notes i. Sepsis. ii. Mental status change. 4. Diagnosis: a. Labs: i. Elevated WBC. ii. Hyperbilirubinemia. iii. Elevated alkaline phosphatase. b. ERCP. c. Transhepatic cholangiography. d. Ultrasound: i. Shows common and intrahepatic ductal dilatation. ii. Often non-diagnostic. 5. Treatment: a. NPO, IVFL. b. Broad spectrum antibiotics. c. ERCP: i. Removal of stones, tract decompression. d. Emergency surgical consultation. e. Mortality nears 100% if untreated.
III. HEPATITIS
A. General:
1. Definition: general inflammation of liver. 2. Etiology: viral (Hep A, B, C or D, EBV), bacterial, alcoholic, immune, medications.
B. Hepatitis A virus:
1. RNA virus. 2. Fecal-oral transmission. 3. 33% of US with immunity secondary to exposure. 4. Greatest infectivity before onset of symptoms of disease. 5. Usually self-limited. 6. Acute disease, no chronic carrier state.
C. Hepatitis B:
1. DNA virus (3 major antigens): a. HepBsAg – surface antigen. b. HepCcAg – core antigen. c. HepBeAg – e antigen. 2. Effective vaccination has decreased prevalence. 3. Spread through parenteral/intimate exposure. 4. Highest among IVDA and homosexual males. 5. Onset of symptoms 60-90 days after exposure. 6. 10% infected adults (90% neonates) develop chronic hepatitis or carrier stage. GI Emergencies Page 425 Notes
D. Hepatitis C virus:
1. RNA virus. 2. Previously called non-A non-B. 3. Most common of blood borne infections in U.S.: a. Occupational exposure (i.e., needle sticks). b. IVDA. c. Transfusions: i. Prior to screening, risk was 0.45% / unit. ii. With screening, risk now 0.03% / unit. 4. Chronic HCV infection occurs in 85% of infected patients. a. 50% develop chronic hepatitis. b. Cirrhosis develops in 20% of this group within 10 years.
E. Hepatitis D virus:
1. Defective RNA virus. 2. Only co-infects patients with chronic or current Hep B. 3. High incidence in IVDA, homosexual males. 4. Increased risk of fulminant disease.
F. History (hepatitis in general):
1. Variable, many cases asymptomatic. 2. Malaise, low-grade fever, anorexia (most common complaints). 3. Other complaints: N/V, abdominal pain, diarrhea. 4. Jaundice most often reason for 1st physician visit. 5. If fulminant hepatitis: a. Acute onset (days) of liver failure and encephalopathy. b. Seen mostly in Hep B + Hep D. c. Hallmarks = altered mental status, mucosal bleeding.
G. Physical exam:
1. Low-grade temperature. 2. Icterus (yellowing of sclera when bili >2.5 mg/dl). 3. RUQ abdominal tenderness. 4. Often tachycardic when vomiting is present. 5. Hepatomegaly.
H. Diagnosis:
1. ALT > AST (Both 10 – 100 x normal!): a. AST > ALT seen in alcoholic hepatitis! 2. Bilirubin elevated (mild/severe). 3. Protime (PT): a. Elevated PT is a sign of significant hepatic disfunction and the first sign of a complicated course. GI Emergencies Page 426 Notes 4. Hepatitis A: a. Acute infection = presence of HAV-Ab (IgM antibody). 5. Hepatitis B: a. Acute HBV infection = presence of HBsAg + HBcAb (IgM). b. High infectivity = presence of HBeAg. c. Past infection or immunization = presence of HBsAb.
I. Treatment:
1. Treatment of viral hepatitis is primarily symptomatic. 2. Correct fluid / electrolyte imbalances. 3. Stop nonessential medications with potential hepatotoxicity. 4. Abstinence from alcohol. 5. Admit if altered sensorium or PT 5 seconds above normal.
J. Complications:
1. Fluid and electrolyte imbalances (acute disease). 2. GI bleed from multiple emesis. 3. Liver failure. 4. Hepatic encephalopathy. 5. Cirrhosis. 6. Death.
K. Prophylaxis:
1. Hepatitis A – provide to household or daycare contacts: a. Immune Serum Globulin (if serologic testing negative for prior immunity). b. Minimal risk of contracting to health care workers if universal precautions are followed (handwashing/hygiene). 2. Hepatitis B – provide to percutaneous or sexual contacts if previously unvaccinated: a. HBIG + start HB vaccine.
IV. SPONTANEOUS BACTERIAL PERITONITIS
A. Definition: Acute bacterial infection of cirrhotic ascitic fluid.
B. Pathophysiology:
1. Migration of enteric organisms through edematous bowel: a. E. coli (47-55% of cases). b. Streptococcus species (18-26%). c. Klebsiella species (11%). d. Streptococcus pneumoniae (8-20%). e. Polymicrobic/anaerobes NOT common (<1%).
GI Emergencies Page 427 Notes
C. History:
1. Variable presentations. 2. Abdominal pain (insidious or acute, mild or severe). 3. Fever/chills. 4. If septic: hepatic encephalopathy and hemodynamic instability.
D. Physical exam:
1. Variable: a. Ranges from mild abdominal tenderness to rigidity and guarding with rebound.
E. Diagnosis:
1. Paracentesis: a. WBCs > 500 cells/mm3. b. Treat if neutrophil count > 250 cells/mm3. i. Even if paracentesis culture negative! c. If coagulopathic (high PT), give FFP prior to procedure.
F. Treatment:
1. IV antibiotics: a. 3rd generation cephalosporin treatment of choice. b. OR ampicillin-sulbactam.
V. PANCREATITIS
A. Pathophysiology:
1. Release of activated digestive enzymes. 2. Autodigestion of pancreatic / parapancreatic tissues. 3. Edema and inflammatory cell infiltration.
B. Etiology in the U.S.:
1. Gallstone – most common cause. a. Women > men. b. Together account for 80% of cases in U.S. 2. Alcoholic – second most common cause. a. Men > women. 3. Gallstones & ETOH together account for 80-90% of cases in U.S. 4. Idiopathic. 5. Infectious: a. Viral: i. Mumps; coxsackie B (most common viruses). ii. EBV/ CMV. GI Emergencies Page 428 Notes iii. Hep A, B, C. iv. HIV. b. Bacterial: i. Mycoplasma. ii. Legionella. iii. M. avium complex. 6. Trauma. 7. S/p ERCP. 8. Pregnancy. 9. Scorpion stings. 10. Hyperlipidemia (>500). 11. Hypercalcemia (often from hyperparathyroidism). 12. Drugs: a. Lasix. b. Tetracycline. c. Thiazides. d. HIV medications.
C. History:
1. Abdominal pain (classically “a boring pain”): a. Epigastric/LUQ. b. Constant (colicky pain suggests alternate diagnosis). c. Radiation to midback. d. May find pain improved with sitting forward. 2. Nausea/vomiting.
D. Physical exam:
1. Vital signs: a. Tachycardia common. b. Shock/hypotension in serious disease. 2. Epigastric/LUQ tenderness: a. Guarding common. b. Rebound tenderness uncommon because the pancreas is a retroperitoneal organ. c. Pain often out of proportion to exam. 3. Palpable mass (phlegmon, pseudocyst). 4. Jaundice possible. 5. Grey-Turner sign: a. Ecchymosis at flank. b. Indicates severe hemorrhagic pancreatitis. 6. Cullen sign: a. Ecchymosis at umbilicus. b. Indicates severe hemorrhagic pancreatitis.
GI Emergencies Page 429 Notes
E. Diagnosis:
1. Amylase: a. Elevated in majority of acute pancreatitis. b. May be normal in chronic pancreatitis. c. Sensitivity 79-95%. d. Poor specificity; differential includes: i. Pancreatic/lung cancer. ii. Bowel obstruction/perforation/infarction. iii. Renal failure. iv. Parotid disease. v. Hepatitis. vi. Ruptured ectopic pregnancy. e. Specificity increased if 5x normal level used. f. Elevates within 6-24 hr, peak 48 hr, normal 5-7 days. 2. Lipase: a. Found mostly in pancreas. b. More specific than amylase (80-90%). c. Sensitivity equal to or better than amylase. d. Remains elevated 8-14 days. 3. Very high amylase/lipase suggests gallstone pancreatitis. a. Amylase/lipase levels do not correlate with prognosis/severity.
F. Ranson’s criteria – predicts outcome in acute alcoholic pancreatitis:
1. Criteria on admission: a. Age over 55 yo. b. Blood glucose > 200 mg/dl. c. WBC > 16,000. d. SGOT (AST) > 250. e. LDH > 350. 2. Criteria after 48 hours: a. HCT decreases >10%. b. BUN rises > 5 mg/dl. c. Calcium < 8 mg/dl. d. pO2 < 60 mmHg. e. Fluid sequestration > 6L. f. Base deficit > 4 mEq/L. 3. Mortality criteria: a. 0 – 2 criteria = 1% mortality. b. 3 – 4 criteria = 15% mortality. c. 5 – 6 criteria = 40% mortality. d. 7 -8 criteria = 100% mortality. ***Ranson’s criteria was developed at a time when we did not have the aggressive resuscitation measures that we do today. Mortality scores, therefore, are not as directly applicable to today’s practices. There are more recent scoring systems but their GI Emergencies Page 430 Notes use in the ED is not very applicable.
G. Imaging tests:
1. Abdomen plain films: little utility: a. Pancreatic calcifications = chronic disease. b. “Sentinel loop” seen if local ileus. c. Left pleural effusion/atelectasis possible. 2. Ultrasound: a. Pancreas poorly imaged: i. Retroperitoneal organ. ii. Seen in only 60% scans. b. Test of choice to evaluate if gallstone etiology. c. Good for pseudocyst, phlegmon, abscess. d. Overall inferior to CT for acute pancreatitis. 3. CT scan: contrast enhanced very useful: a. Can diagnose enlarged pancreas, necrosis/hemorrhage, pseudocyst or abscess formation. b. Rule out other diseases in abdomen.
H. Treatment:
1. IV hydration (fluids, fluids, fluids!): a. Consider CVP line if serious disease. b. Electrolyte replacement as needed. 2. NPO, pain control. 3. Antiemetics; NGT if persistent emesis. 4. Antibiotics if gallstone etiology, septic, or severe disease. 5. Surgical consultation for: a. Gallstone etiology. b. Severe disease. c. Abscess/hemorrhage/pseudocyst. 6. ERCP if common duct stone.
I. Complications:
1. Pancreatic pseudocyst or phlegmon: a. 1-8% of patients. b. Approx. 2-4 weeks after initial attack. 2. Hemorrhagic pancreatitis. 3. Pancreatic abscess, infected pseudocyst. 4. Pulmonary effusions (usually left-sided). 5. ARDS (mortality 60%). 6. Cardiovascular collapse. 7. Renal failure (ATN). 8. Acute GI bleeding, DIC. 9. Hypocalcemia, hyperglycemia. 10. Pancreatic insufficiency – exocrine and endocrine: a. Most commonly with chronic pancreatitis. GI Emergencies Page 431 Notes b. Fat malabsorption when 90% of pancreas is destroyed.
VI. DISORDERS OF THE ESOPHAGUS
A. Esophageal dysphagia:
1. Obstructive disease (85%): a. Foreign body/food impaction: i. Main areas of obstruction: Cricopharyngeus muscle (at C6) near upper esophageal sphincter. Aortic arch. Left mainstem bronchus. Lower esophageal sphincter. **Most impactions occur at the mid-distal third of the esophagus. b. Carcinoma: i. Squamous cell - 95%. ii. Risks factors: Alcohol. Smoking. Achalasia. Caustic lye ingestion. c. Webs: i. Mid – proximal esophagus. ii. Plummer-Vinson syndrome. Chronic iron deficient anemia. d. Schatzki’s ring: i. Distal esophagus. ii. Food impaction common. e. Strictures: i. Scarring from GERD or chronic inflammation. f. Thyroid enlargement/goiter. g. Diverticulum: i. Can occur anywhere along esophagus. ii. Zenker’s diverticulum: Proximal to upper esophageal sphincter (UES). After age 50. 2. Neuromuscular disorders (15%): a. Achalasia: i. Impaired relaxation of LES. ii. Odynophagia, CP, regurge, weight loss. b. Peristaltic dysfunction: i. “Nutcracker esophagus”. ii. Strong, prolonged peristaltic contractions. c. Scleroderma, myasthenia gravis, MS, dermatomyositis. d. Infectious: i. Polio. GI Emergencies Page 432 Notes ii. Diphtheria. iii. Botulism. iv. Rabies. v. Tetanus. e. ALS. f. CVA. g. Diabetic neuropathy. 3. History/physical exam: a. Determine if acute, subacute or chronic. b. Determine if obstructed to solids, liquids or both: i. Solids only = obstructive. ii. Solids and liquids = neuromuscular. c. If complete obstruction: i. Inability to swallow. ii. Drooling. iii. Induced retching. iv. Pain from neck to epigastric region. 4. Diagnosis: a. X-rays of neck/chest: i. Visualize FB. ii. Mediastinal air if perforated. b. EGD – gold standard: i. Diagnosis and treatment. c. Gastrografin/barium contrast studies: i. Used if EGD unavailable. ii. Use Gastrografin if suspected perforation! Gastrografin is water soluble; barium is not. Gastrografin is a pulmonary irritant…don’t use if aspiration risk. iii. Barium may interfere with later EGD visualization. 5. Treatment: a. Food impaction: i. Glucagon 1 mg IV (up to 2 mg): Relaxes lower esophageal smooth muscle. Do NOT use if history of pheochromocytoma, may precipitate hypertensive crisis. ii. Carbonated beverages: Avoid if complete obstruction or obstruction of > 24 hrs due to possible perforation. iii. Nifedipine 10 mg SL: Relaxes smooth muscle. iv. Nitroglycerin: Relaxes smooth muscle. Avoid if hypotensive. v. Meat tenderizers: Not recommended!! vi. EGD if readily available or all else fails: Gold standard. GI Emergencies Page 433 Notes b. Foreign bodies: i. If able to visualize, remove with forceps. ii. Esophageal FBs need EGD. iii. FBs passed into stomach can follow-up as outpatient (if not sharp/long). c. Strictures/webs/rings: i. Dilatation by gastroenterologist.
B. Esophagitis:
1. Etiology (many!): a. Infectious: i. Usually immunocompromised: Chemotherapy patients. HIV. Transplant. DM. ETOH. ii. Organisms: Candida (most common). HSV. CMV. b. Inflammatory. c. GERD: i. May lead to ulcers, strictures, Barrett’s esophagus. d. Medications – pills stick to esophagus: i. Doxycycline (most common). ii. NSAIDs. iii. KCl supplements. iv. Ferrous sulfate. 2. History: a. Odynophagia. b. Dysphagia (liquids and solids). c. CP, heartburn. d. Fever/bleeding in some immunocompromised patients. 3. Physical exam: a. Oropharynx may appear normal. 4. Diagnosis: a. EGD: i. White plaques seen in Candida. ii. Ulcerative lesions seen in HSV. iii. Definitive diagnosis is with biopsy. b. Air-contrast barium swallow: i. Reveals ulcerations/plaques. ii. Not definitive. iii. Bad idea if any perforations. c. X-rays not helpful. 5. Treatment:
GI Emergencies Page 434 Notes a. Candida infection: i. Oral fluconazole (other –azoles) 3-4 weeks. b. HSV: i. Acyclovir (Fam/Valacyclovir) 1-2 weeks. c. CMV: i. Ganciclovir or Foscarnet for 2-3 weeks. d. Admit for severe disease, dehydration. e. Topical anesthetics, antacids, sucralfate.
C. Boerhaave’s syndrome:
1. Spontaneous rupture of esophagus: a. Most commonly during forceful emesis. b. Classically seen in alcoholic patients. c. Also seen in severe coughing, straining during childbirth and weightlifting. d. **(Endoscopy now most common cause of overall esophageal perforation). 2. Esophageal perforation generally has highest mortality of all perforated GI viscus. 3. History: a. Episode of severe, violent emesis. b. Chest pain. 4. Physical: a. Hamman’s sign: i. “Crunching” on auscultation of heart due to mediastinal emphysema. b. Neck crepitans, subcutaneous emphysema. c. Septic shock (late presentation). 5. Diagnosis: a. CXR: i. Mediastinal air, subcutaneous emphysema, pneumothorax, air-fluid levels, pleural effusion (Rt > Lt). b. Gastrografin swallow study: i. Shows extravasation through perforation. ii. Do not use if risk for aspiration (causes pneumonitis). iii. ***Barium may be used with caution (can incite inflammatory response to tissues) if high suspicion and negative Gastrografin study. 6. Treatment: a. Broad spectrum antibiotics. b. Fluid resuscitation. c. Emergent surgical repair.
D. GERD (Gastroesophageal Reflux Disease):
1. Affects up to 25% adult population; higher in elderly. 2. Pathophysiology: a. Intermittent decrease in LES pressure. GI Emergencies Page 435 Notes b. Decreased esophageal motility. c. Prolonged gastric emptying time. 3. History: a. Burning sensation/discomfort/pressure in chest, neck. b. May radiate to arms, shoulders, back. c. Regurgitation (bitter or acid material in mouth). d. Symptoms worse after meals. e. Relief with antacids (often brief). f. Worse when lying down. g. May be aggravated with activity, better at rest. h. Asthma (reflux gastric contents into lungs). 4. Physical exam: a. Not very helpful. b. History is key. 5. Diagnosis: a. Clinical diagnosis (history) in ED. b. R/O cardiac cause of pain. c. EGD for definitive diagnosis. 6. Treatment: a. Lifestyle modifications: i. Sleep at angle (30°), not recumbent. ii. Do not eat within 3 hours of bedtime. iii. Avoidance of: Smoking/nicotine. Alcohol, caffeine, fatty foods, citrus. Tomato based foods, chocolate. b. Antacids. c. H2 blockers, PPIs. d. Surgery last resort. 7. Complications: a. Changes in esophageal mucosa lead to inflammation, ulcers, erosions and strictures. b. Barrett’s esophagus: i. Metaplasia from normal stratified squamous epithelium to metaplastic columnar epithelium. ii. Strong correlation with adenocarcinoma of esophagus. c. Asthma exacerbations. d. Dental erosions. e. Chronic cough.
VII. DISORDERS OF THE STOMACH
A. Acute gastritis:
1. Pathophysiology: a. Superficial gastric erosions (not into submucosa). b. Localized or generalized. 2. Causes:
GI Emergencies Page 436 Notes a. Helicobacter pylori. b. Drugs: i. ASA/NSAIDs. ii. Iron. iii. Potassium. iv. ETOH. c. Infectious (viral, bacterial, parasitic). d. Corrosive agents: i. Acids. ii. Alkali. e. Ischemia from severe illness: i. Shock, trauma, severe burns, organ failure. f. Crohn’s. g. Sarcoidosis. 3. Presentation: a. Epigastric pain – burning, midline. b. Pain increases with eating in 50%. c. Vomiting often relieves pain that occurs after eating. 4. Diagnosis: a. Usually clinical diagnosis in ED. b. Endoscopy is test of choice. c. Rule out other diseases. 5. Treatment: a. Antibiotics for H. pylori: i. Not usually started in ED. b. H2 receptor antagonists. c. Antacids, sucralfate. d. Discontinue contributing factors: i. NSAIDs, ETOH. ii. Stress. 6. Complications: a. Pernicious anemia: i. Macrocytic anemia, memory loss, peripheral neuropathy. ii. Pathophysiology: Destruction of gastric parietal cells, leads to… Loss of intrinsic factor production, which leads to… Malabsorption of vitamin B12 (pernicious anemia). b. Bleeding. c. Gastric outlet obstruction. d. Perforation.
B. Peptic Ulcer Disease (PUD):
1. Erosions into submucosal layer of stomach or duodenum. 2. Duodenal 80%; gastric ulcers 20%. 3. Risk factors: a. H. pylori – most common. b. NSAIDs – second most common.
GI Emergencies Page 437 Notes c. Zollinger-Ellison syndrome: i. Gastrin secreting tumor. ii. Causes up to 1% of PUD cases. d. Smoking. e. Alcohol. f. Family history of PUD. g. Male > female. h. Stress, e.g., ICU, trauma, and neurosurgery. 4. Duodenal ulcers: a. Common, seen in up to 10% of population. b. Recurs in up to 90% within 2 years. c. H. pylori present in 70-80% of patients. d. H. pylori eradication reduces the recurrence rate to 15%. 5. Gastric ulcers: a. 95% are within 2 cm of pylorus. b. Up to 20% also have duodenal ulcer disease. c. H. pylori present in 60-70% of patients. 6. Presentation: a. Epigastric pain seen in both types of ulcers: i. Duodenal: food relieves pain. ii. Gastric: classically worse with food. b. Constant, gnawing or aching pain: i. Pain may awaken the patient at night (increased gastric output). ii. Pain may radiate to the back. iii. Relief often with antacids. c. Weight loss. 7. Physical exam: a. Vague epigastric tenderness. b. Heme positive stools (not sensitive). 8. Diagnosis: a. Labs (primarily to rule out other diseases). b. Test for H. pylori: i. Not usually done in ED. ii. Biopsy, CLO test during EGD. iii. Urea breath test. iv. Antibody testing. Antibodies remain positive for years after eradication. c. EGD: gold standard. d. Radiographic studies (upper GI). 9. Treatment: a. General measures: i. Stop smoking. ii. Frequent small, bland meals. iii. Avoid alcohol, NSAIDs. iv. Decrease stress. b. Medications: i. Antibiotics for H. pylori:
GI Emergencies Page 438 Notes Not usually started in ED. Pylori antibiotic regimens often changing. ii. Antacids: May decrease absorption of warfarin, digoxin, some anticonvulsants/antibiotics. iii. PPI (preferred for NSAID related ulcers). iv. H2-receptor antagonists. v. Sucralfate. vi. Misoprostol (Prostaglandin E analog). c. Surgery indicated in medical failures. 10. Complications: a. Hemorrhage: i. Occurs in up to 15% of patients. ii. Accounts for 60% of UGI bleeds. iii. Factors predicting higher risk of death: Older age. Comorbid illnesses. Large initial bleed. Hemodynamic instability. Continued or recurrent bleeding. Failure to clear NG with lavage. iv. Emergency treatment: IV (2 large bore). Resuscitate with isotonic fluid/PRBCs. Transfuse with screened whole blood if patient deteriorating (don’t wait for cross-matched). NG lavage. IV H2 blockers. Emergent EGD if uncontrolled bleeding for sclerotherapy, coagulation, or laser therapy. b. Perforation: i. Less common (7% patients). ii. Most often on anterior surface of the duodenum/pylorus or lesser curve of stomach. iii. Abrupt onset of severe pain! Localized pain, quickly spreads to entire abdomen. Elderly with less pain, less impressive exam. iv. Duodenal ulcers: Perforate posteriorly into pancreas, retroperitoneum. v. Gastric ulcers: Perforate anteriorly into abdomen. vi. Upright Abd X-ray in anterior perforation shows subdiaphragmatic air. May insufflate 200-400 cc air through NG tube to accentuate – this is controversial. vii. Treatment of perforation with antibiotics, NGT, surgery. c. Gastric outlet obstruction:
GI Emergencies Page 439 Notes i. 2% patients. ii. Edema and scarring near gastroduodenal ulcers. iii. Presents as weight loss, reflux, pain, vomiting, early satiety. iv. Physical exam: abdominal distention, succussion splash. v. Treatment: IVFL, NGT, admit. Some obstructions will open as edema subsides. Others need surgical procedure.
VIII. PERFORATED VISCUS
A. Pathophysiology:
1. Results from acutely or chronically diseased viscus: a. Rare to occur in normal bowel (except trauma). b. Small bowel perforation: i. Mid-gut perforations are rare. c. Large bowel perforation: i. Usually due to: Diverticulitis. Carcinoma. Trauma. Colitis. Foreign bodies. ii. Rapid onset due to bacterial contamination. 2. Most perforations occur freely into peritoneum. 3. High mortality rate.
B. Presentation:
1. Abrupt onset of abdominal pain. a. Elderly may have little or no pain. 2. Frank peritoneal signs (mild to severe). 3. Vomiting. 4. +/- fever. 5. Hypovolemic, toxic late in course. 6. Severity depends on: a. Site of perforation: i. Gastric = chemical peritonitis. ii. Intestinal = bacterial peritonitis. b. Time from onset of perforation. c. Age. d. Comorbid diseases, immunocompetency.
C. Physical exam:
1. Decreased bowel sounds. 2. Tympany.
GI Emergencies Page 440 Notes 3. Rigid abdomen. 4. Tachycardia.
D. Diagnosis:
1. X-ray: a. Upright chest: i. Air under diaphragm. Can increase yield by adding 200-400 ml of air into NGT and retaking film – this is controversial. b. Left lateral decubitus abdominal film. i. Air over liver. c. Abdominal flat plate. i. Air around bowel wall. 2. CT scan - very sensitive for air! 3. Causes of pneumoperitoneum seen on X-ray or CT scan NOT from perforated viscus: a. Tracheostomy. b. S/p DPL, abdominal surgery. c. Pneumothorax. d. Infection from gas forming organisms. e. Urogenital insufflation during sex.
E. Treatment:
1. Fluid resuscitation. 2. IV antibiotics. 3. NGT. 4. Emergent surgical consultation/immediate surgery.
IX. DISORDERS OF THE SMALL AND LARGE INTESTINE
A. Intestinal obstruction (general):
1. Common cause of abdominal pain in ED: a. SBO represents 20% of hospital admissions for acute abdominal pain. 2. Overall mortality: a. 3-5% for SBO. b. 20% for LBO.
B. Mechanical small bowel obstruction (SBO):
1. Etiology: a. Adhesions – post surgical: i. Most common cause! (more than 50%). ii. Typically months to years after surgery; however, may occur within the first few weeks. b. Incarcerated hernias (15% of cases): GI Emergencies Page 441 Notes c. Neoplasms (15% of cases): i. Adenocarcinoma. ii. Polyps. iii. Lymphoma. d. Intussusception: i. Often lymphoma at the lead point in adults. e. Bezoars: i. In patients s/p pyloroplasty or pyloric resection. f. Crohn’s disease. g. Infection/abscess. h. Radiation enteritis. 2. Pathophysiology, H&P, diagnosis and treatment: included below under Large Bowel Obstruction.
C. Functional small bowel obstruction (adynamic ileus):
1. Etiology: No structural abnormality: a. Abdominal trauma, s/p laparotomy. b. Infection with local inflammation. c. Metabolic (hypokalemia!). d. Drugs (opiates). e. Others: MI, scleroderma, hypothyroidism. 2. Pathophysiology, H&P, diagnosis and treatment: included below under Large Bowel Obstruction.
D. Large bowel obstruction:
1. Etiology: a. Colorectal cancer 53% (most common cause!): i. Tumors on left = obstruct. ii. Tumors on right = bleed. b. Volvulus 17% (see next section for more detail): i. Sigmoid: 80 – 85% of cases. ii. Cecal: 10 – 15% of cases. c. Diverticulitis 12%. d. Fecal impaction: i. Elderly, nursing home patients. ii. Narcotic and laxative abusers. iii. Mentally delayed. e. FB. f. Crohn’s. g. Radiation or ischemic colitis. 2. Pathophysiology: a. Proximal bowel distends. b. Lymphatic and venous compromise with edema and stasis. c. Third spacing of fluids in distended loops of bowel. d. Bacteria propagate in distended loop. e. Increasing intra-luminal pressure impairs vascular supply. f. Bowel wall becomes ischemic, develops gangrene, perforates. GI Emergencies Page 442 Notes g. Peritonitis, sepsis, shock. 3. History: a. Crampy, colicky abdominal pain. b. Vomiting. c. Obstipation suggests complete obstruction (late finding). 4. Physical exam: a. Abdominal distention. b. High pitched bowel sounds, “rushes”. c. Tenderness (variable): minimal/diffuse or severe/localized. d. Peritoneal signs seen in gangrenous or perforated bowel. e. Fever, hypotension, tachycardia suggest sepsis. 5. Diagnosis: a. Obstructive series: flat and upright Abd, upright CXR, lateral decubitus film. i. SBO confirmed by X-ray in 50-60% cases: “Step ladder” air fluid levels. Absence of large bowel gas. ii. Dilated loops of bowel: Large bowel >10 cm = imminent perforation. Small bowel >3 cm = distention. b. Laboratory (very nonspecific). 6. Treatment: a. IV fluids!! b. Correct electrolyte abnormalities. c. NG suctioning. d. Broad spectrum antibiotics if strangulation, perforation or peritonitis. e. Emergent surgical consultation.
E. Sigmoid volvulus – most common volvulus (80- 85%):
1. Epidemiology: a. Elderly, bedridden. b. Psychiatric patients on anticholinergics. c. Neurologic disorders. d. History of constipation. 2. Pathophysiology: a. Lengthening of chronically distended colon. b. Leads to redundant sigmoid loop that twists on itself. 3. History: a. Crampy abdominal pain. b. N/V/dehydration. c. Constipation. d. SOB due to abdominal distention. e. Similar episodes in past that resolved with passage of flatus and stool. 4. Physical exam: a. Diffuse abdominal tenderness.
GI Emergencies Page 443 Notes b. Distention. c. Fever suggests possible peritonitis due to bowel strangulation or perforation in older patients. 5. Diagnosis: a. Must have high index of suspicion in incapacitated patients with abdominal pain. b. KUB confirms diagnosis in 80% of cases: i. Dilated loop of colon on left. ii. “Bent inner tube”. c. Barium enema = “Bird’s beak”. i. Use Gastrografin if perforation suspected. d. WBC > 20,000 suggests strangulation present. e. CT scan often useful. 6. Treatment: a. IV fluids. b. Antibiotics if peritonitis/strangulation. c. Surgery consult: i. Decompression with sigmoidoscopy and rectal tube 50-95% success rate: Recurrence rate 60%. Mortality = 20% overall (>50% if gangrene present). ii. Surgery: If unable to decompress. If signs of peritonitis. Elective surgical resection often after decompression.
F. Cecal volvulus:
1. Most common in ages 25-35. 2. NO history of chronic constipation. 3. Pathophysiology: a. Hypofixation of bowel to the posterior abdominal wall. i. Often congenital. b. Previous abdominal surgery, disrupting the fixation of cecum to posterior abdominal wall. c. Rotation of bowel leads to closed loop obstruction. 4. History: a. Severe, colicky abdominal pain. b. N/V/dehydration. 5. Physical exam: a. Diffusely tender abdomen with large distention. 6. Diagnosis: a. KUB: Large dilated loop of colon in midabdomen. i. Empty distal bowel. ii. “Coffee bean” deformity. iii. Free air indicates bowel perforation. 7. Treatment: a. Surgery is treatment of choice!
GI Emergencies Page 444 Notes b. Non-operative decompression is unavailable. c. Mortality rate is high if gangrene! i. 10% if bowel viable. ii. 30-40% if bowel gangrenous.
G. Hernias:
1. Types: a. Inguinal (most common): i. 75% of all U.S. hernia operations are inguinal. ii. Indirect (50%) = through inguinal ring, failure of obliteration of processus vaginalis. iii. Direct (25%) = through Hesselbach’s triangle, weakness of transversalis fascia. iv. Men > women. v. High risk of incarceration in kids. b. Femoral (5%): i. Women > men. c. Incisional (10%). d. Umbilical. i. Common in newborns: Incarceration very rare. 80% spontaneously close by 3-4 yo. ii. In adults, women > men. iii. Higher risk in obese, pregnant, ascites. e. Other: epigastric, spigelian, obturator. 2. Definitions: a. Incarcerated = unable to reduce. b. Strangulated = incarcerated with vascular compromise. 3. Clinical presentation: a. Vast majority asymptomatic. b. Pain at site if incarceration. c. Infants may just be irritable. d. Leads to SBO symptoms. e. Strangulation and necrosis may present as peritonitis and shock. 4. Treatment: a. Reduce if recent, non-tender incarceration: i. Trendelenburg, sedation, warm compresses. ii. Do NOT reduce if prolonged incarceration or possible dead bowel present! b. IV, NGT, labs, supportive care. c. Antibiotics if perforation or dead bowel suspected. d. All non-reducible, acutely incarcerated hernias or strangulated hernias need emergent surgical repair.
GI Emergencies Page 445 Notes
H. Mesenteric vascular disease:
1. Rare, but catastrophic; high mortality rate! (>50%). 2. Occurs primarily in elderly (>50 years old). 3. Etiology: a. Arterial embolus 50%. b. Arterial thrombus 25%. c. Non-occlusive disease 20%: i. CHF, hypovolemia, sepsis, shock. d. Venous occlusion 5%. 4. Risk factors: a. Increased age. b. CAD, vascular disease, valvular heart disease. c. Dysrhythmias (Afib!). d. Drugs: vasopressors, diuretics, digitalis, cocaine. e. Bleeding, dehydration, low cardiac output. f. Hypercoagulable states. 5. Pathophysiology: a. Impaired blood supply from SMA, IMA, and celiac trunk. b. Adynamic ileus due to lack of blood supply. c. Mucosal infarction/sloughing (occult or gross bleeding). d. Third-spacing of fluid in affected bowel. e. Bacterial invasion of bowel wall/ blood supply. 6. Presentation: a. Acute, severe colicky pain, poorly localized in pt > 50 yo with significant underlying vascular disease (i.e., Afib). b. Recent h/o postprandial pain (intestinal angina), weight loss, altered bowel habits in non-occlusive or arterial thrombus disease. c. N/V/D. d. 25% with predominant complaint of abdominal distention with rectal bleed (without abdominal pain). 7. Physical exam: a. Pain out of proportion to exam (classic!). b. Nonspecific exam. c. Abdominal distention. d. Heme positive stools (more than half of all cases). e. Tenderness progresses with time. f. Late findings = peritonitis, shock, hypothermia. 8. Diagnosis: a. Clinical suspicion is most useful! b. Tachycardia. c. WBC often > 15,000 (nonspecific). d. Metabolic acidosis (lactic acidosis). i. High sensitivity (but nonspecific). e. Elevated amylase, phosphate, LDH (nonspecific). f. Angiography is gold standard! i. Diagnostic and therapeutic. GI Emergencies Page 446 Notes ii. Contraindicated if patient in shock or receiving vasopressor therapy – each mimics disease. g. CT scan of abdomen: i. Edema of bowel wall and mesentery. ii. Demonstrates abnormal gas patterns. iii. Occasionally see mesenteric thrombus. iv. Normal CT scan does not rule out ischemia. h. Plain X-rays: i. Nonspecific. ii. Only late findings may be seen: Ileus. Bowel wall edema. Gas in portal venous system. Gas in bowel wall - “pneumatosis intestinalis” (classic). i. Barium studies: i. Thumb printing (thick mucosal folds). ii. Contraindicated because barium can limit visualization during angiography. 9. Treatment: a. Aggressive IV fluid hydration. b. Correct precipitating causes. c. NG tube. d. IV antibiotics – broad spectrum. e. Interarterial papaverine (reduces arterial spasms). f. Emergent surgical and radiographic consult: i. Laparotomy should be avoided in nonocclusive mesenteric ischemia. Anesthesia and operative manipulation can cause ischemia to progress to necrosis. ii. Angioplasty (especially for thrombosis of SMA, poor surgical candidates). iii. Surgical resection of necrotic bowel.
I. Acute appendicitis:
1. General: a. Common cause of abdominal pain. b. 250-300,000 new cases yearly in U.S. c. Approximately 7% of people in their lifetime will develop appendicitis. d. Low mortality: i. 0.1% in simple appendicitis. ii. 2-6% with perforation (general public). iii. 9% with perforation + elderly + comorbidities. e. Can affect all ages (peaks at 10-30 yo). f. Difficult to diagnose in young, old, pregnant and immunocompromised. i. Spontaneous fetal abortion = 5-15% in simple
GI Emergencies Page 447 Notes appendicitis; up to 37% if complicated. ii. Premature labor = 15-45%. 2. Pathophysiology: a. Appendiceal luminal obstruction leads to inflammation, bacterial invasion, infection, vascular compromise, appendiceal edema. b. May progress to gangrene, perforation, sepsis, and death. 3. History: a. Abdominal pain (98% of cases). i. “Classic” presentation (much less often): Vague epigastric, periumbilical pain later migrating to RLQ. Occurs in 20- 60% young adults, 30% elderly. < 48 hrs to localize to RLQ. b. Anorexia (70%). c. Nausea, vomiting (67%). d. Kids, elderly and pregnant perforate more often: i. Delay in diagnosis is greatest risk. ii. Nonspecific complaints and exam. iii. Elderly perforate up to 60% of cases. iv. Children < 3 years old perforate as high as 80%. v. 50% of kids diagnosed with appendicitis previously seen by physician with misdiagnosis: Gastroenteritis, UTI most common misdiagnoses. e. Pregnant patients often with RUQ tenderness: i. Appendix rises as uterus grows. 4. Physical exam: a. RLQ to right mid tenderness seen in nearly 95%. b. Rovsing sign: RLQ pain on palpating LLQ. c. Psoas sign: pain on elevation and extension of right hip. d. Obturator sign: flexion and internal rotation causes pain. e. Palpable mass felt in <5%. f. Rebound tenderness is late finding. g. Pelvic appendix may lead to rectal/vaginal tenderness. 5. Diagnosis: a. Laboratory: i. WBC > 10K (80-90% of patients): Normal value does NOT rule out diagnosis. Left shift common. ii. Urinalysis: Sterile pyuria common, especially if pelvic appendix. > 20 WBCs/hpf more likely to have genitourinary tract infection. b. X-ray: i. KUB not helpful, may help to r/o other diseases. c. Ultrasound: i. Sensitivity 75-90%, specificity 85-95%. ii. Best for kids, pregnant women.
GI Emergencies Page 448 Notes iii. Visualization of immobile, non-compressible appendix of greater than 6 mm diameter. iv. Drawbacks: results are operator dependent, difficult to visualize if retrocecal, obese, has strictures. v. Absence of abnormality does not rule out appendicitis unless appendix well visualized. d. CT scan: i. Test of choice! ii. Oral and IV contrast best. iii. Sensitivity 87-100%, specificity 89-98%. iv. Large appendix > 6 mm diameter. v. Pericecal inflammation. vi. Appendicolith. 6. Treatment: a. IV fluids. b. Antibiotics to cover abdominal flora. c. Surgery is definitive treatment. 7. Complications: a. Perforation, abscess. b. Localized wound infection, especially if perforated. c. Low complication rate if not perforated. d. SBO.
J. Irritable Bowel Syndrome:
1. Approx. 15% population with symptoms consistent with IBS. 2. Young to middle-aged adults. 3. Female: male = 2: 1. 4. Pathophysiology: a. Precipitating cause unknown. b. Alteration in intestinal motility and sensation. c. Thought to be neurophysiologic disorder. 5. History: a. Abdominal pain: i. Often relieved with passage of stools/flatus. b. Altered defecation: i. Constipation, diarrhea, or both. ii. Incomplete evacuation. iii. Mucus in stools. c. Many extracolonic symptoms: i. Bloating, belching, nausea, weakness. ii. Significant weight loss is UNUSUAL. 6. Physical exam: a. Nonspecific. b. Anxiety. c. Mild, diffuse, vague lower abdominal tenderness. d. No stool on rectal exam. 7. Diagnosis: a. No specific tests. GI Emergencies Page 449 Notes b. Diagnosis of exclusion. c. Outpatient work-up often includes: i. Sigmoidoscopy. ii. Stool examination: Occult blood. Bacteria, parasites (Giardia). iii. Food allergies. iv. Testing for lactose intolerance. 8. Treatment: a. Dietary: i. Increase stool bulk. ii. Avoid milk products. iii. Avoid caffeine. b. Anti-diarrheals prn. c. Reassurance. i. Avoid implying that problem is all psychological! d. Consider anticholinergics. e. Consider anxiolytics, antidepressants. Usually reserved for primary physician. f. Avoid narcotic analgesics! g. Regular appointments and therapeutic relationship with primary physician most helpful.
K. Diverticular disease:
1. Pathophysiology (general): a. Herniation of mucosa/submucosa through defects in muscular wall of bowel. b. Most common in sigmoid colon (not exclusively). c. Diverticulosis: i. Presence of one or more diverticulum. d. Diverticulitis: i. Inflammation of a diverticulum which is almost always symptomatic. ii. Develop in 10-30% with diverticulosis. 2. Acute diverticulitis: a. Inflamed diverticulum with microperforation: i. Left > right. ii. Incidence increases with age (2-4% under 40 yo). b. History: i. Pain, often in LLQ, worsened with bowel movements. ii. Change in bowel habits, often constipation. iii. N/V. c. Physical exam: i. Low-grade fever. ii. Abdominal distention. iii. Heme positive stools >50%. iv. LLQ abdominal tenderness:
GI Emergencies Page 450 Notes May have localized peritoneal finding. d. Diagnosis: i. Often clinical. ii. KUB nonspecific. iii. Sigmoidoscopy may show diverticula: Not done with acute diverticulitis for fear of perforation. iv. Barium enema often shows diverticula: Not done with acute diverticulitis for fear of perforation. v. CT scan: Test of choice. Show inflamed diverticula and local irritation to bowel/fat. Abscess. Evaluates for other disease processes. e. Treatment: i. If pain only: Clear liquid diet. Stool softeners. Pain meds. Oral antibiotics. Can manage as outpatient if no comorbidities. ii. If systemic symptoms, significant inflammation or abscess: Admit. Bowel rest (NPO, NG). IV antibiotics. Surgical consultation. After 2 episodes of acute diverticulitis, consider elective surgery for resection. f. Complications: i. Fistula. ii. Abscess. iii. Obstruction. iv. Perforation. 3. Painful diverticular disease: a. Pathophysiology: i. Increased muscular contraction leads to increased intraluminal pressure and stretching of bowel wall and pain. b. History: i. Recurrent, intermittent LLQ pain: Pain often post meals. Often relieved with defecation or flatus. ii. Diarrhea or constipation. May be increased with emotional stimuli.
GI Emergencies Page 451 Notes c. Physical exam: i. Mild LLQ tenderness: No rebound. No guarding. ii. No fevers. d. Diagnosis: i. Suspect if > 40 years old with above symptoms. ii. WBC wnl. iii. Barium enema. iv. Colonoscopy. e. Treatment – goal is to decrease bowel spasm: i. Anticholinergics. ii. Local heat. iii. High fiber diet. iv. Anxiolytics. v. Laxatives/stool softeners. vi. No antibiotics. 4. Diverticular bleeding: a. Most common cause of significant LGI bleed. b. Most patients asymptomatic until bleed. c. Prevalence increases with age. d. Diverticula cause stretching of vasa recta vessels: i. Bleeding occurs when the vasa recta rupture into the diverticulum. e. Presentation: i. Mild hematochezia to massive lower GI bleeding. ii. Most bleeds are painless (classic). iii. Many with previous episodes of diverticulitis/pain. f. Diagnosis: i. Sigmoidoscopy/colonoscopy: Proctosigmoidoscopy can r/o hemorrhoidal bleeding. ii. Tagged red blood cell studies: Need bleeding of 0.1-0.2 ml/min. iii. Selective arteriography: Need bleeding of 0.5 ml/min. g. Treatment: i. Resuscitation: 2 large bore IVs. Isotonic fluid. ii. Transfuse PRBCs if needed. iii. Surgical consultation. iv. Sigmoidoscopy/colonoscopy. Sclerotherapy. v. Arterial catheterization at bleeding site. Inject vasopressor to slow bleed.
GI Emergencies Page 452 Notes
L. Colonic tumors:
1. Presentation: a. Weight loss. b. Change in stool character. c. Rectal bleeding. d. Obstructive symptoms. 2. Adenocarcinoma most common tumor. 3. Lower GI: a. Apple core lesion (typically left sided). 4. Colonoscopy for definitive diagnosis.
M. Crohn’s disease:
1. Pathophysiology: a. Chronic inflammatory disease of the GI tract that can involve any part from mouth to anus. b. Segmental granulomatous inflammation “skip lesions”: i. Transmural inflammation. ii. Ileum is most common site. c. “Cobblestoning” by criss-crossing longitudinal ulcers. d. Confined to colon in 20%. e. Perianal complications 90%. 2. General: a. Peak incidence 15-22 yo. b. Secondary peak 55-60 yo. c. Prevalence: 10 cases/100,000. d. Increasing in U.S. over 20 years. e. Women increased risk by 20-30%. f. More common in Caucasians; 4x more prevalent in Jewish. g. Family history in 10-15%. h. Diagnosed by upper GI, air-contrast barium enema and colonoscopy. i. Recurrence rate 25-50% in 1 year for those that have responded to medical management. j. 75% require surgery within 20 years of onset. k. Presentation (Crohn’s exacerbation): i. Abdominal pain/cramps. ii. Diarrhea: May be bloody, but less common than ulcerative colitis. iii. Anorexia, weight loss. iv. Low-grade fever. v. Anemia, malabsorption. vi. Approximately ½ patients c/o perianal disease. 3. Treatment: a. IV fluids, NPO. b. Symptomatic care (analgesics, antipyretics, antiemetics). GI Emergencies Page 453 Notes c. Steroids. d. Sulfasalazine. e. Nutritional support. f. Broad-spectrum antibiotics if fulminant colitis. g. Evaluate for possible complications (below). h. Surgery may be needed for complications. 4. Complications (lifetime): a. Perianal abscess/fissure/fistula seen in 1/3 of patients. b. Internal abscess/fissure formation in 30%. c. Toxic megacolon – 6%. d. Extraintestinal manifestations in 25-30%: i. Gastrointestinal: Perforation. Peritonitis. Obstruction. Reason for surgery in 33% cases. ii. Rheumatologic: Arthritis. Ankylosing spondylitis. Sacroiliitis. iii. Dermatologic: Erythema nodosum. Pyoderma gangrenosum. iv. Hepatobiliary: Gallstones. Pericholangitis, cholangiocarcinoma. Pancreatitis. v. Ophthalmologic: Uveitis. Episcleritis. vi. Vascular: Vasculitis. Thromboembolic disease. vii. Cancer: Risk increased 3-5x as compared to the general population.
N. Ulcerative colitis:
1. Epidemiology (similar to Crohn’s): a. All age groups; peak in 2nd - 3rd decades of life. b. Industrialized nations; increasing in U.S. c. Family history in 10-15% cases. d. Caucasians 4x higher risk. e. Males slightly more prevalent. 2. Pathophysiology: a. Chronic inflammatory disease of colon and rectum. b. Continuous from rectum proximally. GI Emergencies Page 454 Notes c. Limited to mucosa and submucosa, shallow ulcers. d. Bloody diarrhea with mucoid stools due to friable, ulcerated mucosa - “crypt abscesses.” 3. Presentation: a. Broken into mild, moderate, severe disease: i. Mild (60%), < 4 BMs per day, few extraintestinal manifestations. ii. Moderate (25%). iii. Severe (15%), > 6 BMs per day, anemia, fever, wt. loss, low albumin, multiple extraintestinal manifestations. b. 10% usually present with: i. Low-grade fever. ii. Crampy abdominal pain. iii. Tenesmus. iv. Bloody, mucopurulent stool. c. Remainder with: i. Insidious onset. ii. Recurrent fevers. iii. Abdominal pain. iv. Anorexia. v. Mild diarrhea. 4. Diagnosis: a. Sigmoidoscopy/colonoscopy and biopsy. 5. Treatment: a. IV fluids, correct electrolyte abnormalities. b. Steroids or ACTH. c. Sulfasalazine. d. Enemas: i. Topical glucocorticoid. ii. 5-aminosalicylic. e. Antibiotics controversial, used primarily in severe dz. f. If mild disease: discharge on low residue diet, close medical F/U, possible medication adjustments. g. Admission if severe symptoms or toxic megacolon. 6. Complications: a. Toxic megacolon: i. Seen in 5% cases. ii. Etiology: Loss of neuromuscular tone leads to dilatation of transverse colon. iii. KUB = long segment of air-filled colon dilated more than 6 cm; possible thumbprinting. iv. Risks: Drugs that decrease bowel motility. Cathartics. Enemas. v. Presentation: Systemic toxicity. Marked abdominal distention.
GI Emergencies Page 455 Notes Peritonitis. vi. Treatment: IVFL, NG, steroids, antibiotics. Surgery if not improved 24-48 hours. b. Obstruction. c. GI bleed. d. Perforation (25%). i. 50% mortality. e. Perianal abscesses not as common as in Crohn’s. f. Iron deficiency. g. Stricture. h. Extracolonic complications: i. Same as those seen with Crohn’s.
X. ANORECTAL DISORDERS
A. Anal fissure:
1. General: a. Most common cause of painful rectal bleeding. 2. Pathophysiology: a. Tear in squamous epithelium of anal canal. 3. Presentation: a. Pain on defecation! b. Hematochezia – not massive! c. Often initiated by passage of a hard or sharp stool. 4. Physical exam: a. “Fissure triad”: i. Deep ulcer. ii. Sentinel pile. iii. Enlarged anal papillae. b. Sentinel pile: i. 90% posterior midline. ii. Central linear ulcer. iii. Hypertrophic papilla internally. iv. Hypertrophied skin externally, chronic inflammation. c. Treatment: i. Sitz baths. ii. Stool softeners. iii. Bulking agents. iv. Non-narcotic pain medications. v. Topical lidocaine. vi. Antispasmodic agents – nitroglycerin or calcium-channel blocker gel.
B. Hemorrhoids:
1. Pathophysiology:
GI Emergencies Page 456 Notes a. Dilated venules of hemorrhoidal plexus. b. Precipitating factors: i. Low bulk diet. ii. Erect posture. iii. Increased abdominal pressure (straining). iv. Chronic constipation. v. Pregnant. c. Can occur internally or externally. d. Anoscopy to evaluate for internal hemorrhoids. e. Dentate (pectinate) line: i. Defines junction of squamous and columnar epithelium. ii. Defines internal from external hemorrhoids. f. External hemorrhoids: i. Below dentate line. ii. Covered with skin. iii. Painful. g. Internal hemorrhoids: i. Above dentate line. ii. Covered with mucosa. iii. Painless. 2. External hemorrhoids: a. Presentation: i. Itching. ii. Burning. iii. Rectal bleeding with defecation. iv. Thrombosis (pain!). b. Treatment: i. NSAIDs for pain. ii. Sitz baths. iii. Stool bulking agents/stool softening agents. iv. Avoidance of straining. v. Excision of thrombosed hemorrhoid. 3. Internal hemorrhoids: a. Presentation: i. Painless, bright-red rectal bleed with defecation. Common cause of rectal bleeding. ii. Prolapse of internal hemorrhoid: Often while straining. May become permanent. May appear like thrombosed external hemorrhoid. Often painful. b. Treatment: i. Non-prolapsed: Hot sitz baths TID. Analgesics. Prevent prolonged sitting/straining. Bulk laxatives/stool softener. High fiber/bran diet. GI Emergencies Page 457 Notes ii. Prolapsed: Manual reduction! No excision or I&D! Surgery may be needed (band ligation) if continued bleeding or irreducible prolapsed hemorrhoid.
C. Rectal foreign body:
1. Seen in assault, self-administration, psych patients. 2. Fever, abdominal pain suggest perforation. 3. Diagnosis: a. Abdominal X-ray: i. See foreign body, position, shape. ii. Evaluate for free air/perforation. 4. Treatment: a. Soft, low-lying (< 10 cm from anal verge): i. Remove safely in ED: Sedation/muscle relaxant. Local anesthesia. Have patient bear down. Forceps. May try to pass a Foley beyond obstruction, then inflate balloon and provide gentle traction. b. Do not try to remove large, fragile, hard object, especially if >10cm from verge. c. Surgical consultation/general anesthesia often needed. d. Do not use cathartics! e. Indications for admission: i. Signs of perforation. ii. Rectal bleeding. iii. Torn sphincter.
D. Anorectal abscess:
1. Presentation: a. Pain! i. Worse with defecation, sitting. b. Fever +/-. c. Mucopurulent discharge. 2. Physical exam: a. Localized external tenderness: i. Painful swelling at anal verge = perianal. ii. Lateral pain, swelling = perirectal abscess. Perirectal abscesses may extend into surrounding potential spaces. Fluctuance. Painful digital exam with tender mass/induration. Anoscopy with pus and anal crypts. GI Emergencies Page 458 Notes 3. Complications: a. Fistulas. b. Gas gangrene. c. Necrotizing fasciitis. d. Sepsis. 4. Treatment: a. I & D necessary in virtually all cases: i. Simple perianal abscess = in ED. ii. Pilonidal cyst = in ED. iii. Perirectal abscess = in OR. b. Pack all drained abscesses. c. Antibiotics only if: i. Immunocompromised. ii. Toxic appearing. iii. Diabetic. iv. Marked cellulitis. d. Culture if antibiotics are given. e. Surgical consultation often necessary.
E. Infectious proctitis:
1. Seen in patients who have had receptive anal intercourse. 2. Initially: itching, seepage, mild pain/irritation. 3. Untreated: significant pain, bleeding, discharge. 4. Organisms: a. Gonococcus. b. Chlamydia. c. Syphilis. d. Condylomata acuminate (papillomavirus). e. Pinworms. f. Herpes simplex virus. g. Atypical organisms seen in AIDS: i. Mycobacterium avium. ii. CMV. 5. Treatment: a. Take cultures prior to treatment. b. Gonorrhea: i. Multiple choices of antibiotics. ii. 50% concomitant Chlamydia infection. c. Chlamydia: i. Doxycycline first line. d. Syphilis: i. PCN. e. Herpes: i. Acyclovir.
F. Radiation proctitis:
1. Presentation: GI Emergencies Page 459 Notes a. Immediate or delayed after irradiation. b. Diarrhea, tenesmus, urgency. c. Mild to moderate rectal bleeding. d. Constipation and obstruction. i. Usually late, secondary to strictures. e. Edematous, friable mucosa in anal canal. f. Fistulas, abscesses. 2. Diagnosis: a. Made clinically in one with diarrhea or rectal bleeding with h/o pelvic irradiation. 3. Treatment: a. Steroid enemas helpful in acute stages. b. Bulk forming agents. c. Antimotility agents. d. Iron supplements.
XI. INFECTIOUS DISORDERS OF THE GASTROINTESTINAL TRACT
A. Diarrhea:
1. Leading cause of death worldwide due to dehydration. 2. Second to “common cold” for lost days from work/school in U.S. 3. Dysentery = diarrhea with blood, pus, mucous. 4. Etiology: a. Infectious #1: i. Viral (70%). ii. Bacterial (24%). iii. Parasitic (6%). b. Drugs. c. Diet. d. Food allergies. e. Inflammatory bowel disease. f. Other: i. Malabsorption. ii. Malignancy. iii. Laxatives. iv. Obstruction. 5. Pathophysiology: a. Invasive: i. Alteration of GI mucosa. b. Enterotoxin: ii. Causes mucosal hypersecretion: Isotonic diarrhea in adults. Hypotonic diarrhea in children. 6. Presentation (variable): a. History of ill contacts. b. New meds or diet. c. Diarrhea (qualitative, quantitative):
GI Emergencies Page 460 Notes i. Watery. ii. Bloody. iii. Mucus. d. Abdominal pain: i. Generalized. ii. Crampy. e. Low grade fevers, myalgias, fatigue. 7. Diagnosis: a. Stool WBC > 5/hpf suggests possible invasive infection. b. Stool cultures: i. Who needs them? Public health concerns. Immunocompromised. Travel history. Prolonged symptoms. ii. Fecal leukocytes: Seen in invasive diarrhea; not seen with toxigenic diarrhea. iii. AM stool preferable. c. Stool O & P and special strains. 8. Treatment: a. Proper hydration without heavy osmotic loads (sugar). b. Antiemetics. c. Antidiarrheals – controversial! d. Antibiotics: i. High suspicion for invasive diarrhea. ii. Toxic appearing. iii. Positive culture. iv. Ciprofloxacin or TMP-SMX most common.
XII. BACTERIAL GASTROINTESTINAL DISEASE
A. Salmonella (invasive):
1. Second most common cause of bacterial enteritis in U.S. 2. Invasive bacteria. 3. Food and water borne, also transmitted by: a. Domestic pets (10%). b. Eggs. c. Unpasteurized milk. d. Pet turtles/reptiles. e. Chickens/turkeys. 4. 8-48 hour incubation. 5. Presentation: a. Bradycardic with fever. b. Colicky abdominal pain. c. Watery diarrhea, often with mucous/blood. d. Mild nausea or vomiting. GI Emergencies Page 461 Notes e. Can cause osteomyelitis, especially in sickle cell patients. f. Can cause septic arthritis in HIV and splenectomized patients. 6. Treatment: a. Uncomplicated: i. Rarely needs antibiotics. ii. Increases carrier state and resistance with antibiotics. b. Antibiotics (Ciprofloxin) in typhoid fever (serotype D).
B. Shigella (invasive):
1. Food and water borne. 2. Oral/fecal transmission. 3. As little as 50-100 bacilli can cause infection. 4. Invasive and exotoxin meditated disease: a. Seen in confined population. b. Nursing homes. c. Penal institutions. d. Indian reservations. 5. 24-48 hour incubation. 6. Presentation: a. Severe abdominal cramping. b. Mild watery and often bloody diarrhea. c. Dysentery possible. d. Fever. e. Seizures/neurologic effects (rare). 7. Treatment: a. No antibiotics needed unless severe disease or culture positive for Shigella dysenteriae. b. Consider Ciprofloxacin, TMP-SMX.
C. Yersinia (invasive):
1. Food (milk, pork) and water borne. 2. Oral/fecal transmission. 3. Invasive bacteria. 4. Domesticated animals. 5. Presentation: a. Fever. b. Watery and sometimes bloody diarrhea. c. Colicky abdominal pain. d. Anorexia and vomiting. e. Usually lasts 10-14 days. f. Cause of mesenteric adenitis, “pseudoappendicitis”. g. Can cause erythema nodosum. 6. Treatment: a. Supportive care. b. No antibiotics usually necessary. i. Reserved for refractory disease or immunocompromised.
GI Emergencies Page 462 Notes D. Campylobacter (invasive):
1. Overview: a. Most common bacterial causing diarrhea. b. Frequent cause of “Backpacker’s Diarrhea”. c. Water borne (streams). d. Raw milk, chicken, pigeons. e. Invasive bacteria. f. 2-5 day incubation. 2. Presentation – symptoms of rapid onset! a. Crampy abdominal pain. b. Bloody/loose/watery diarrhea 8-10/day. c. Constitutional symptoms are the rule: i. Anorexia. ii. HA. iii. Myalgias, malaise. iv. Fever. 3. Treatment: a. Ciprofloxacin. b. Erythromycin. c. Resistance pattern to TMP-SMX.
E. Vibrio parahaemolyticus (invasive):
1. General: a. Found in temperate coastal sea waters: i. Very common in Japan, U.S. b. Invasive bacteria. c. Raw fish/shellfish common source: i. Cruise ships! 2. Presentation: a. Incubation often 8-12 hours (range 4-48 hours). b. Diarrhea. c. Moderately severe abdominal cramping. d. Fever. e. HA. f. Vomiting not predominant. 3. Treatment: a. Most are self-limited (usually lasts 24-48 hours). b. Treatment with Cipro or TMP-SMX shortens duration.
F. E. coli serotype 0157:H7 (cytotoxin):
1. General: a. Toxin mediated: i. Cytotoxic to intestinal wall. b. Contaminated food: i. Undercooked meats. ii. Raw milk. GI Emergencies Page 463 Notes iii. Apple cider. iv. Raspberries. c. Person-to-person spread, especially: i. Day care centers. ii. Nursing homes. 2. Presentation: a. Incubation 4-9 days. b. Severe abdominal cramps. c. Watery stools initially. d. Becomes grossly bloody in 95% patients. 3. Treatment: a. Avoid anti-motility agents. b. Antibiotics often indicated. 4. Complications: a. Hemolytic-uremic syndrome (HUS): i. Seen in 20-25% of patients. b. Thrombotic thrombocytopenic purpura (TTP).
G. Traveler’s diarrhea (enterotoxin):
1. Enterotoxic E. coli most common cause (50-75%). 2. Seen throughout the world. 3. Contaminated food/water. 4. 18-72 hour incubation. 5. Presentation: a. Watery diarrhea without fecal leukocytes (classic). b. Vomiting seen in less than 50%. c. Mild abdominal pain. d. Possible bloody stools. 6. Treatment: a. Bismuth – large doses. b. TMP-SMX or tetracycline. c. Yogurt (natural “good” bacteria, i.e., lactobacillus).
H. Bacillus cereus (enterotoxin):
1. Aerobic, spore forming gram (+) rod. 2. Two forms: a. Emetic form – contaminated fried rice < 6 hours prior. b. Diarrheal – meats or vegetables. 3. Presentation: a. Emetic form: i. Incubation 2-3 hours. ii. Abdominal cramps. iii. Diarrhea in 25% patients. iv. < 10 hours duration. b. Diarrheal form: i. Incubation 6-14 hours. ii. Diarrhea 100%. GI Emergencies Page 464 Notes iii. Abdominal cramping 75%. iv. Vomiting 20%. v. Duration 20-36 hours. 4. Treatment: a. Mild and self-limited. b. No antibiotics. c. Antiemetics as needed.
I. Staphylococcal (enterotoxin):
1. Grows in protein-rich foods (picnic foods!): a. Mayonnaise. b. Potato salad. c. Eggs. d. Ham. 2. Only few hours needed for bacteria to grow/make enterotoxin. 3. Presentation: a. Explosive onset within 6 hours. b. Crampy, abdominal pain. c. Multiple vomiting. d. Diarrhea mild. e. Fever occasionally. f. Lasts 6-8 hours, possibly as long as 24 hours. 4. Treatment: a. Antiemetics. b. IV fluids. c. No antibiotics. d. Rapid uncomplicated recovery is rule.
J. Clostridium perfringens (enterotoxin):
1. Probably #1 cause of acute food poisoning in U.S. 2. Undercooked meat / poultry (esp. after sitting out > 24 hours). 3. Presentation: a. Onset after 6-12 hours, possibly up to 24 hours. b. Watery diarrhea. c. Moderate to severe abdominal cramping. d. Rarely fevers, N/V. 4. Treatment: a. Self-limited. b. Lasts < 24 hours.
K. Clostridium difficile (enterotoxin):
1. Pseudomembranous colitis. 2. Overgrowth of flora bacteria due to antibiotic use. 3. Toxin mediated – beware of toxin A. 4. All classes of antibiotics implicated, especially: a. Clindamycin. GI Emergencies Page 465 Notes b. Ampicillin. c. Cephalosporins. 5. Increased risk if using constipating agents. 6. Presentation: a. During or up to 3 weeks after antibiotic use. b. Watery, profuse diarrhea: i. Occasionally bloody. ii. Up to 30 stools/day. c. Crampy abdominal pain. d. Fecal WBC common. e. High WBC counts. 7. Diagnosis: a. Difficile toxin in stool. i. Takes lab 48-72 hours. 8. Treatment: a. Stop antibiotic! b. Flagyl PO or IV first line. c. Vancomycin PO only if second course needed. d. 25% relapse after 7-14 days.
XIII. VIRAL GASTROINTESTINAL INFECTIONS
A. Rotavirus:
1. Most common cause of gastroenteritis in young children. 2. Double stranded RNA virus. 3. Seasonal in winter. 4. Severe diarrhea and dehydration. 5. Vomiting early, then subsides. 6. High fever may be seen. 7. Self-limited. 8. Immunity develops.
B. Norwalk agent:
1. Adults, older children. 2. Single stranded RNA virus. 3. Acute onset diarrhea and mild abdominal cramps. 4. Usually no vomiting. 5. Possible low-grade fever. 6. Myalgias common. 7. Self-limited, rarely severe. 8. No immunity.
XIV. PARASITIC GASTROINTESTINAL INFECTIONS
A. Giardia lamblia:
1. Most common parasitic cause of diarrhea. GI Emergencies Page 466 Notes 2. Most common waterborne cause of diarrhea. 3. Water supplies infected with cystic-infected human or animal feces: a. Beavers. b. Dogs. c. Raccoons. 4. “Backpacker’s diarrhea”; foreign travel with bad water. 5. Giardia trophozoites infect small bowel. 6. Presentation: a. Colicky abdominal pain. b. Bloating and flatulence characteristic: i. Often audible borborygmi sounds. c. Explosive, foul-smelling stool. 7. Treatment: a. Metronidazole. b. Quinacrine.
B. Entamoeba histolytica:
1. In U.S., chronic disease more common than acute illness: a. Incubation 1 week – 1 year. 2. Fecal/oral transmission. 3. Vague abdominal cramping. 4. Flatulence. 5. Bloody diarrhea of gradual onset. 6. Can cause liver abscess. 7. O & P may take up to 6 stools to obtain cysts. 8. Treatment: a. Metronidazole plus tetracycline, or metronidazole plus iodoquinol for 5-10 days. b. If carrier: Iodoquinol 650 mg TID for 20 days.
XV. GASTROINTESTINAL TOXINS
A. Scombroid:
1. Heat stable toxin: a. Produced by bacterial action in certain types of dark-meat fish (improperly refrigerated): i. Dark meat of tuna. ii. Bluefish (mackerel, swordfish). iii. Mahi-mahi. 2. Presentation: a. Histamine-like reaction (key!): i. Flushing (facial sunburn). ii. Urticarial at times. b. Diarrhea. c. Headache. d. Abdominal cramping. GI Emergencies Page 467 Notes e. Peppery, metallic taste may be noted. f. Onset within 20-30 minutes of ingestion. g. Resolves in 5-6 hours. 3. Treatment: a. Self-limited. b. Antihistamines (diphenhydramine). c. H2 blockers.
B. Ciguatera:
1. Most common cause of fish-related poisoning in U.S. 2. Ciguatoxin: a. Heat stable neurotoxin made by dinoflagellate (small plankton that sit within algae). b. Accumulates in tissue of fish (larger, older fish): i. Red snapper. ii. Grouper. iii. Sea bass. iv. Sturgeon. v. Barracuda. vi. Moray eels. 3. Presentation: a. 2-6 hour incubation. b. Predominantly GI and neurologic findings. c. GI: i. N/V. ii. Profuse diarrhea. iii. Abdominal cramping seen early. d. Neurologic: i. Throat and perioral dysesthesias, paraesthesias. ii. Distorted temperature sensation “hot–cold reversal”- highly suggestive. e. Worsened by alcohol. f. Lasts 1-2 weeks on average. 4. Treatment: a. Supportive. b. IV mannitol may be helpful. i. 1g/kg of 20% solution over 30 minutes. c. Abstain from alcohol until all symptoms resolve.
XVI. GI BLEED
A. Overview:
1. Overall mortality 10%. 2. Upper vs. lower/ligament of Treitz. 3. Causes upper GI bleed: a. PUD (60%, most common etiology!). b. Gastritis/esophagitis (15%). GI Emergencies Page 468 Notes c. Varices: i. Portal hypertension, liver disease. d. Mallory-Weiss tear: i. Mucosal tear in lower esophageal region. ii. Classic: repeated retching, followed by bright red hematemesis. e. Aortoenteric fissure: i. History of aortic graft (AAA repair). ii. Classic: small self-limited “herald” bleed, subsequent massive hemorrhage. f. Others: i. Stress ulcers. ii. Malignancy. iii. AV malformation. g. ENT emergencies can masquerade as GI bleeds. 4. Causes of primary lower GI bleed: a. Hemorrhoids: i. Most common overall LGI bleed. b. Diverticulosis: i. Most common severe LGI bleed. c. Angiodysplasia: i. Usually of right colon. ii. Undiagnosed. d. Polyps/cancer. e. Rectal disease. f. IBD.
B. History:
1. Hematemesis seen in approximately 50% UGI bleeds. 2. Melena: a. 150-200 ml blood in GI tract for prolonged period. b. Seen in 70% patients with UGI bleed. c. Seen in 30% patients with LGI bleed. d. Iron, Bismuth can simulate (stool guaiac = Neg). 3. Hematochezia: a. Bright red/maroon stools. b. Most likely LGI bleed. c. Can be UGI bleed if rapid transit time. 4. Ask about NSAIDs, ASA, ETOH. 5. Weight loss, changes in bowel habits: a. Malignancy. 6. May complain solely of: a. Weakness. b. SOB. c. Dizziness. d. ICP. e. Abdominal pain.
GI Emergencies Page 469 Notes C. Physical exam:
1. Vital signs, orthostatics. 2. Skin: warmth, diaphoresis, color, rashes: a. Cool, clammy skin is sign of shock. b. Spider angiomata, palmer erythema, jaundice, bruises suggest underlying liver disease. 3. Abdomen. 4. Rectal.
D. Diagnosis:
1. Hemoccult: a. Can have guaiac positive stool up to 14 days after UGI bleed. b. False positives: i. Certain fruits (cantaloupe, grapefruit, figs), uncooked vegetables (broccoli, cauliflower, radish), or red meat. ii. Iodide. iii. Methylene blue. 2. Labs: a. CBC: i. Hgb/Hct—traditionally transfuse acute bleed if Hgb < 8. ii. Platelets. b. PT/PTT: i. Increased PT/INR may be from liver failure, vitamin K deficiency, Coumadin. c. Type & screen/type & cross: i. Type specific blood in 10-15 minutes. ii. Fully crossmatched blood in 45-60 minutes. d. Electrolytes: i. Decreased potassium; metabolic acidosis if vomiting. ii. Pre-renal azotemia: Reabsorption of blood from GI tract increases BUN. Hypovolemia increases BUN. 3. EKG – obtain when: a. >50 yo. b. Preexisting CAD. c. Patients with significant anemia. d. CP/SOB. e. May have asymptomatic MI. 4. X-rays: a. Not helpful. b. Barium studies limit use of endoscopy or angiograms. 5. Treatment: a. If unstable, initial resuscitation: i. 2 large bore IVs, O2, monitor. ii. Blood products. iii. GI consult for UGI bleed, surgery consult for LGI bleed.
GI Emergencies Page 470 Notes b. NGT and lavage: i. May help identify UGI vs. LGI bleed. ii. Evaluate for active UGI bleed. iii. Neg NG does not r/o UGI bleed. iv. Note: 14% of bright red/maroon blood per rectum unexpectedly from UGI. v. OK with varices. vi. Done with room temperature water. c. Anoscopy/proctosigmoidoscopy: i. For mild rectal bleeding. ii. Check for hemorrhoids. iii. Check if stool above rectum with blood. d. Colonoscopy: i. Diagnose diverticulosis, AV malformations. ii. Able to ligate or sclerose. e. EGD: i. Most accurate diagnostic tool for UGI bleeds. ii. Identifies lesions up to 95% patients. iii. Emergently at bedside if unstable, otherwise if stable may be done in 12-24 hours. iv. Band ligation or sclerotherapy for varices. f. Octreotide/Somatostatin: i. Patients with varices, peptic ulcer disease. ii. IV infusion at 50 mcg/hr for 24 hours in ICU. g. Vasopressin: i. Patients with varices. ii. Many catecholamine side effects. iii. Consult with GI before using. h. Balloon tamponade (Sengstaken-Blakemore tube): i. Controls variceal hemorrhage in 40-80%. ii. Many serious side effects. iii. Use has decreased significantly. i. Surgery indications: i. Hemodynamically unstable. ii. Unresponsive to volume resuscitation, endoscopy and correction of coagulopathy. iii. Transfused > 5 units within 4-6 hours, OR 2 units every 4 hours after replacing initial loss. iv. Mortality approaches 23% when taken emergently to operating room. j. May discharge home if: i. Currently asymptomatic. ii. No comorbidities. iii. Normal vital signs, normal hgb/hct. iv. NG aspirate negative. v. Heme negative or trace heme positive stools. vi. Patient with understanding of disease with good follow- up within 24 hours and ability to return if worse. vii. Admit all others. GI Emergencies Page 471 Notes
GI EMERGENCIES
PEARLS
1. Appendicitis is the most common cause of acute abdominal pain requiring emergency surgery (37%).
2. Elderly patients are more prone to perforation from appendicitis (44- 70% compared to 10-17% for adults under 60 years) due to the poor blood supply to the appendix and the thin appendix wall. Children under 6 years also have a high appendix perforation rate (65%) due to atypical presentation and inability to communicate.
3. Intermittent abdominal pain and vomiting with a prior surgery or trauma - think obstruction.
4. The most common causes of small bowel obstruction are postoperative adhesions (50%), hernia (15%) and malignancy (15%).
5. The most common causes of large bowel obstruction (excluding fecal impaction) are carcinoma (50-69%), volvulus (10-25%) and diverticular disease (10-15%).
6. Adynamic (paralytic) ileus is the most common cause of ileus overall.
7. Acalculous cholecystitis due to biliary stasis and obstruction has an atypical presentation with higher morbidity and mortality than calculous cholecystitis.
8. Charcot’s triad for ascending cholangitis is fever, jaundice and RUQ pain.
9. Air in the biliary tree is associated with emphysematous cholecystitis and gallstone ileus.
10. There are many causes of pancreatitis but the most common by far are alcoholism and biliary tract disease.
11. No clinical features are pathognomonic for pancreatitis.
12. Know Ranson’s criteria (on admission): Age over 55. Blood sugar greater than 200 mg/dl. WBC greater than 16,000 mm3. SGOT greater than 250 SF units/L. LDH greater than 700 IU/L. (during initial 48 hours):
GI Emergencies Page 472 Notes HCT fall > 10%. BUN rise > 5 mg/dL. Serum calcium < 8 mg/dL. Base deficit > 4 mEq/L. Estimated fluid sequestration > 6L. Arterial pO2 < 60 mmHg.
13. Risk factors for peptic ulcer disease include cigarettes, alcohol, coffee, cola, aspirin, NSAIDs, family history, Helicobacter pylori infection. Posterior duodenal ulcers penetrate into the pancreas while anterior ulcers perforate into the peritoneum.
14. A normal viscus will not perforate.
15. The most common cause of visceral perforation overall is ulcers. The most common cause of colonic perforations is diverticular disease.
16. The classic presentation for perforated ulcer is sudden onset of severe pain with a predisposing cause for perforation. Pneumoperitoneum is found in up to 50-80%.
17. Pain out of proportion to physical findings suggests mesenteric ischemia, particularly in the elderly with an arrhythmia.
18. Weight loss, change in bowel habits and abdominal pain—think mesenteric ischemia or cancer.
19. Avoid digoxin, beta blockers and vasopressors in a patient with mesenteric ischemia as they all decrease splanchnic blood flow.
20. The sigmoid colon is involved in 90% of diverticular disease; 80% of patients with diverticular disease are asymptomatic.
21. Bleeding diverticula are painless, usually from the right colon, and are the most common cause of massive LGI bleed overall.
22. Crohn’s disease has segmental granulomatous lesions involving all layers of the intestinal wall with skip areas of normal intestine in between; 75% involve the ileum and perianal disease is common.
23. Ulcerative colitis and Crohn’s disease have similar systemic symptoms and both can result in toxic megacolon.
24. Inguinal hernias are the most common hernias for both sexes.
25. Gastrointestinal “flags”: Pet turtles, fever but bradycardic, osteomyelitis: - Salmonella.
GI Emergencies Page 473 Notes Fever, diarrhea, seizure: - Shigella. Mesenteric adenitis, erythema nodosum: - Yersinia. Cruise ship, raw fish/shellfish: - Vibrio. Bad meat, crampy pain, H-U Syndrome: - E. coli 0157:H7. Contaminated fried rice: - Bacillus cereus. Picnic, potato salad, explosive diarrhea: - Staphylococcal. Antibiotic use, diarrhea: - C. diff. Child, winter, severe watery diarrhea: - Rotavirus. Backpacker, bloating/gas, foul-smelling diarrhea: - Giardia. Fish, flushing/urticaria: - Scombroid. Fish, paresthesias, hot/cold reversals: - Ciguatera.
GI Emergencies Page 474 Notes
REFERENCES
Abdominal Pain
1. Kelly E. King, John M. Wightman. Abdominal Pain. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 209 – 219.
2. Leslie S. Zun, Amardeep Singh. Nausea and Vomiting. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 200 – 208.
Acute Appendicitis
1. Jeannette M. Wolfe, Philip L. Henneman. Acute Appendicitis. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1451 – 1459.
Anorectal Disease
1. Wendy C. Coates. Anorectum. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1507 – 1523.
Colonic Disease
1. Michael A. Peterson. Large Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1490 – 1506.
Gall Bladder Disease
1. David A. Guss. Liver and Biliary Tract. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1402 – 1425.
Gastroenteritis
1. Robert A. Bitterman, David K. Zich. Acute Gastroenteritis. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1460 – 1489.
2. John E. Gough, Phillip A. Clement. Diarrhea. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 227 – 236.
GI Emergencies Page 475 Notes
Gastrointestinal Bleeding
1. Philip L. Henneman. Gastrointestinal Bleeding. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 220 – 226.
2. Mark J. Lowell. Esophagus, Stomach, and Duodenum. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1382 – 1401.
Hepatic Disease
1. David A. Guss. Liver and Biliary Tract. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1402 – 1425.
Inflammatory Bowel Disease
1. Michael A. Peterson. Large Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1490 – 1506.
Ischemic Bowel Disease and Bowel Infarction
1. Susan P. Torrey, Philip L. Henneman. Disorders of the Small Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1440 – 1450.
2. Michael A. Peterson. Large Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1490 – 1506.
Intestinal Obstruction
1. Michael A. Peterson. Large Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1490 – 1506.
2. Susan P. Torrey, Philip L. Henneman. Disorders of the Small Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1440 – 1450.
Pancreatitis
1. Sally A. Santen, Robin R. Hemphill. Pancreas. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1426 – 1439.
GI Emergencies Page 476 Notes
Peptic Ulcer Disease / GERD
1. Mark J. Lowell. Esophagus, Stomach, and Duodenum. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1382 – 1401.
Small Intestinal Disease
1. Susan P. Torrey, Philip L. Henneman. Disorders of the Small Intestine. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th Edition; 1440 – 1450.
08/17
GI Emergencies Page 477
Page 478
Infectious Disease
Paul E. Casey, MD, FACEP
Emergency Medicine Board Review Intensive Course Committee; Medical Director, Process Improvement & Patient Experience, Director of Resident Education, Associate Chief Medical Informatics Officer, Department of Emergency Medicine, Rush University Medical Center, Chicago
Page 479
Page 480 Notes
INFECTIOUS DISEASE
I. HIV/AIDS
A. HIV – Human Immunodeficiency Virus:
1. Reverse transcriptase retrovirus infects and kills CD4+ T-cells. 2. Two strains of virus: a. HIV-1: Majority of HIV infections worldwide. b. HIV-2: West Africa. 3. 50,000 new diagnoses in United States annually. 4. HIV transmission risks: a. Blood exposure (e.g., IVDU). b. Sexual intercourse. c. Breastfeeding. d. Pregnancy.
B. Primary HIV infection: Acute Retroviral Syndrome:
1. Develops in 40-90% patients within 28 days of exposure. 2. Clinical features: fever, malaise, lymphadenopathy, pharyngitis, rash lasting 1-2 weeks, but may last up to 6 wks. 3. Diagnosis: HIV RNA assay (first choice) or HIV p24 Ag assay (second choice).
C. HIV testing and disease markers:
1. Seroconversion: presence of anti-HIV antibodies, occurs 3-8 weeks after initial infection. 2. ELISA: screening test, sensitivity > 99.9%. 3. Western Blot: confirmatory test, 100% sensitivity/specificity. 4. CD4 count: predictor of susceptibility to opportunistic infections. 5. Viral load: most important predictor of disease progression to AIDS and death.
D. AIDS – Acquired Immunodeficiency Syndrome:
1. Definition: HIV infection with AIDS Defining Condition or CD4 count <200. 2. AIDS Defining Conditions (most common bolded): a. Bacterial infections, multiple or recurrent. b. Candidiasis of bronchi, trachea, or lungs. c. Candidiasis of esophagus. d. Cervical cancer, invasive. e. Coccidioidomycosis, disseminated or extrapulmonary. f. Cryptococcosis, extrapulmonary. g. Cryptosporidiosis, chronic intestinal (>1 month’s duration). h. Cytomegalovirus disease (other than liver, spleen, or nodes), Infectious Disease Page 481 Notes onset at age >1 month. i. Cytomegalovirus retinitis (with loss of vision). j. Encephalopathy, HIV related. k. Herpes simplex: chronic ulcers (>1 month’s duration) or bronchitis, pneumonitis, or esophagitis (onset at age >1 month). l. Histoplasmosis, disseminated or extrapulmonary. m. Isosporiasis, chronic intestinal (>1 month’s duration). n. Kaposi sarcoma. o. Lymphoid interstitial pneumonia or pulmonary lymphoid hyperplasia complex. p. Lymphoma, Burkitt (or equivalent term). q. Lymphoma, immunoblastic (or equivalent term). r. Lymphoma, primary, of brain. s. Mycobacterium avium complex or Mycobacterium kansasii, disseminated or extrapulmonary. t. Mycobacterium tuberculosis of any site, pulmonary, disseminated, or extrapulmonary. u. Mycobacterium, other species or unidentified species, disseminated or extrapulmonary. v. Pneumocystis jiroveci pneumonia. w. Pneumonia, recurrent. x. Progressive multifocal leukoencephalopathy. y. Salmonella septicemia, recurrent. z. Toxoplasmosis of brain, onset at age >1 month. aa. Wasting syndrome attributed to HIV. 3. In-depth information about the AIDS Defining Conditions can be found in the Appendix.
E. Current treatment concepts:
1. Treatment requires multi-drug therapy from 5 different classes of anti-retrovirals as monotherapy creates resistance. 2. Indications for initiation of therapy: a. Current practice to start ART on all HIV-infected patients regardless of CD4 count. b. Prior recommendations to initiate HAART if CD4 < 350 cells/mm3 or: i. History of an AIDS-defining illness. ii. Pregnancy. iii. HIV-associated nephropathy. iv. Co-infection with hepatitis B. 3. Antibiotic prophylaxis: a. < 50 MAC, CMV (macrolide prophylaxis once weekly for MAC). b. <100 thrush, esophagitis, cryptococcus, toxoplasmosis. c. <200 PCP (Bactrim prophylaxis, covers toxoplasmosis as well). 4. Common medication side effects: Infectious Disease Page 482 Notes a. Zidovudine (AZT) - marrow suppression, myopathy. b. Ds—ddI, ddC, d4T - Pancreatitis, peripheral neuropathy. c. Abacavir - Fatal hypersensitivity reaction. d. Indavir - Kidney stones. e. Efavirenz - Teratogenic. f. Lamivudine - Pancreatitis. 5. Monitoring treatment and goals: a. Viral load: useful in determining response to therapy and prognosis. b. CD4 count: demonstrates immune reconstitution, guides prophylaxis for opportunistic infections. c. Goals: non-detectable viral load, up-trending CD4+ count. 6. IRIS: Immune Reconstitution Inflammatory Syndrome: a. Flu-like symptoms or worsening of previous infections due to improving immune system. b. Increasing CD4 count. c. Usually within 60 days of starting HAART. d. MAC.
F. Post-exposure prophylaxis:
1. PEP reduces risk of seroconversion by 80% if initiated within 36 hours (no efficacy after 72 hours). 2. Risk of seroconversion following exposure to known HIV positive source: a. Needlestick or cut - 0.3%. b. Eye, nose, mouth (splash) - 0.1%. c. Intact skin exposure - < 0.1%. d. Unprotected sexual encounter - 0.1 – 30%. 3. Baseline testing of exposed patient for HIV, HBV, HCV. 4. Factors for risk of seroconversion in occupational exposure: a. Higher risk: i. Deep injury. ii. Visible blood on device. iii. Hollow needle, large-bore. iv. Needle was placed in vessel of source patient. v. Source patient with high viral load, late-stage AIDS, or acute seroconversion. b. Lower risk: i. Superficial injury or mucosal exposure. ii. Solid needle (suture). iii. Small amount of blood from source. iv. Non-blood body fluid. v. Low viral load. 5. Who receives PEP? a. Indicated for those with at least 0.1% risk of transmission from a high-risk or known HIV positive source patient. b. General rule: if known HIV source, fluid bloody and skin compromised - treat. Infectious Disease Page 483 Notes 6. PEP treatment: a. Combination nucleoside regimen (e.g., zidovudine + lamivudine) for 28 days. b. Close follow-up.
II. SEPSIS
A. Defining terms:
1. Sepsis II definitions (for purposes of exam): a. SIRS-Systemic Inflammatory Response Syndrome (2 of 4 criteria must be met): i. Temp >38C or <36C. ii. HR > 90/min. iii. RR > 20/min or PaCO2 < 32 mmHg. iv. WBC > 12,000, <4000 or > 10% bands. b. Sepsis = SIRS + documented infection. c. Severe sepsis = sepsis + signs of hypoperfusion or organ dysfunction (including elevated lactate). d. Septic shock = severe sepsis + hypotension despite adequate fluid resuscitation. 2. New Sepsis III definitions: a. Sepsis = suspected infection + (q)SOFA ≥ 2. b. Septic shock = sepsis and despite adequate IVF resuscitation: i. Persistent hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg. ii. Lactate ≥ 2 mmol/L.
B. Epidemiology:
1. Gram positive sepsis: a. Increased incidence with pneumonia/central lines. b. More common than gram negative sepsis in the U.S. 2. Gram negative sepsis: a. More lethal. b. Usually endotoxin mediated. 3. High risk populations: a. Elderly or very young. b. Immunocompromised (including diabetics).
C. Treatment (based on international guidelines for management of severe sepsis and septic shock:
1. Initial resuscitation goals: a. CVP 8-12 mmHg. b. MAP > 65 mmHg. c. Urine output > 0.5 mL/kg/hr. d. Central venous oxygen saturation > 70%. 2. Antibiotics within the first hour of recognition of severe sepsis Infectious Disease Page 484 Notes and septic shock. 3. Initial IV crystalloid challenge if suspect sepsis-induced tissue hypoperfusion or hypovolemia of 30 mL/kg. 4. Vasopressor (if necessary) of choice is norepinephrine - goal MAP 65 mmHg. 5. Use of corticosteroids remains controversial. 6. Glucose control - ideally <150 mg/dL.
III. VIRAL INFECTIONS
A. Influenza:
1. Acute respiratory illness caused by influenza A, B during winter months, further classified by serotypes (e.g., H1N1, H5N1). 2. Respiratory large particle droplet transmission. 3. Incubation period 1-4 days. 4. Viral shedding starts 24-48 hours before illness onset and ends on day 7-10. 5. Clinical presentation: Abrupt onset fever, HA, myalgias, malaise and respiratory tract symptoms. 6. Complications: a. Pneumonia (most common – primary viral or secondary bacterial). b. Myositis and rhabdomyolysis. c. Encephalitis, transverse myelitis, aseptic meningitis, Guillain- Barre. d. Myocarditis and pericarditis. 7. Treatment: a. Oseltamivir or zanamivir – treats both influenza A and B. b. Zanamivir not to be used with asthma/COPD patients, as it causes bronchospasms. c. Amantadine and rimantadine treat only influenza A and have high rates of resistance; thus, no longer recommended. d. Can shorten the duration of illness by 1-3 days (greatest benefit if started within first 24-30 hours of illness). e. Thought to also decrease severity of illness and viral shedding. f. Who should be treated: i. COPD / asthma. ii. Adults > 65 years of age, kids < 2 years of age. iii. Pregnant women (and those who are less than 2 weeks postpartum). iv. Chronic renal, hepatic, hematologic and metabolic (including DM) conditions. v. Residents of chronic care facilities. vi. Morbidly obese patients. vii. Illness requiring hospitalization.
Infectious Disease Page 485 Notes B. Coronavirus family (SARS and MERS):
1. Severe Acute Respiratory Syndrome (SARS): a. China (2002), Toronto (2003). 2. Middle East Respiratory Virus (MERS): a. Saudi Arabia (2014). 3. Clinical presentation: viral upper respiratory infection prodrome followed by respiratory phase of cough, dyspnea and may progress to respiratory failure. (MERS may also cause renal failure.) 4. Treatment: early quarantine and supportive management.
C. West Nile infections:
1. RNA virus discovered in Uganda in 1937; appeared in the U.S. in 1999. 2. Human illness peaks in late summer and early fall. 3. Transmission: a. Host: wild birds, horses, dogs. b. Vector: mosquito bites. c. Blood transfusion. d. Organ transplantation. e. Transplacental. 4. Clinical features: a. Asymptomatic (80%). b. West Nile symptoms (20%): fever, headache, malaise, myalgia, maculopapular rash. c. Severe neurologic symptoms (1%): muscle weakness, flaccid paralysis, seizures, mental status changes. 5. Diagnosis: a. CSF shows pleocytosis, elevated protein and normal glucose. b. ELISA IgM Ab confirmatory test. 6. Treatment: supportive.
IV. MALARIA
A. Mosquito-borne protozoan infection of RBCs:
1. Plasmodium falciparum (most severe, chloroquine resistant, banana gametophytes). 2. Plasmodium vivax (may live dormant in liver for years). 3. Plasmodium ovale (may live dormant in liver for years). 4. Plasmodium malariae.
B. Endemic regions (40% of world’s population live in these areas):
1. Africa. 2. Asia. 3. Oceania. Infectious Disease Page 486 Notes 4. Central and South America.
C. Transmission:
1. Mosquito bites (female Anopheles). 2. Blood transfusions. 3. Organ transplantation. 4. IVDU. 5. Perinatal transmission.
D. Clinical presentation: anemia, headache, cyclic fevers, fatigue, dry cough, vomiting.
1. P. falciparum may cause severe disease: seizures, coma, metabolic acidosis, severe anemia, renal failure, pulmonary edema, death.
E. Diagnosis: thick and thin peripheral blood smears.
F. Treatment:
1. Non-falciparum forms: chloroquine or hydroxychloroquine. 2. P. falciparum or chloroquine resistant: atovaquone-proguanil or mefloquine or quinine with doxycycline or clindamycin.
V. SOFT TISSUE INFECTIONS
A. Cellulitis and abscess:
1. Strep pyogenes (group A beta-hemolytic strep): a. Strep pharyngitis. b. Toxic shock syndrome: i. Fever (temp ≥ 38.9°C or 102.0°F). ii. Rash (diffuse macular erythroderma). iii. Desquamation (1-2 weeks after onset of rash). iv. Hypotension (SBP ≤ 90 mmHg). v. Multi-system involvement. c. Cellulitis, erysipelas, impetigo. d. Necrotizing fasciitis. 2. Staph aureus (MSSA or MRSA): a. Bacteremia (indwelling catheters, IVDU). b. Toxic shock syndrome. c. Scalded skin syndrome. d. Cellulitis, abscess, furuncles, carbuncles (staph more likely than strep if purulence). 3. Treatment: a. Uncomplicated cellulitis: cephalexin, doxycycline, clindamycin. b. Cellulitis concern for MRSA: clindamycin or Bactrim with Infectious Disease Page 487 Notes any of above. c. Dog/cat/human bite: amoxicillin-clavulanate (pcn allergy: moxifloxacin. d. Pre-septal cellulitis: amoxicillin-clavulanate, cefpodoxime or cefdinir. 4. Abscess: definitive treatment incision and drainage - consider antibiotics in addition if extensive disease (multiple sites), rapid progression, signs/symptoms or severe illness, very young or advanced age, or difficult area to achieve adequate drainage (e.g., face, hands, genitalia).
B. Necrotizing fasciitis:
1. Three types: a. Poly-microbial (most commonly). b. Group A strep (“flesh-eating bacteria”). c. Clostridial myonecrosis (“gas gangrene”). 2. Clues to diagnosis: a. Pain out of proportion to clinical findings. b. Failure to respond to antibiotic therapy. c. Hard, wooden feel to subcutaneous tissue. d. Systemic toxicity (e.g., altered mental status). e. Bullous lesions or skin necrosis. 3. Treatment: a. Aggressive IVF resuscitation (vasopressors as needed). b. Broad spectrum antibiotics (ampicillin-sulbactam, clindamycin, ciprofloxacin +/- vancomycin). c. Emergent general surgery consultation. d. Consider IVIG, hyperbaric oxygen.
VI. HELMINTHS
A. Cysticercosis (tapeworm):
1. Acquired by eating undercooked pork (tinea solium). 2. Eggs hatch in GI tract, embryos burrow through gut wall and embolize to distant locations (eye, brain). 3. Larvae in brain cause neurocysticercosis (primary cause of new- onset seizures in many parts of the world). 4. Diagnosis: stool samples. 5. Treatment: praziquantel.
B. Enterobius vermicularis (pinworm):
1. Most common helminthic infection in U.S. 2. Eggs develop in large intestine; gravid females migrate to anus at night to deposit eggs. 3. Outbreaks in schools, day care centers. 4. Symptoms: nocturnal pruritus, insomnia. Infectious Disease Page 488 Notes 5. Diagnosis: scotch tape test. 6. Treatment: mebendazole, repeat in 2 weeks.
C. Necator Americanus (hookworm):
1. Tropics and southeastern U.S. 2. Larvae penetrate through intact skin from feces-contaminated soil. 3. Larvae enter bloodstream, ascend trachea, descend esophagus to differentiate into adult works, then migrate to upper intestine. 4. Clinical features: abd pain, diarrhea, weight loss, eosinophilia, anemia and cutaneous larvae migrans. 5. Diagnosis: ova in stool. 6. Treatment: mebendazole or albendazole.
D. Ascaris lumbricoides (roundworm):
1. Large nematode normally found in ileum (15-30 cm long). 2. Rare in U.S. - modern sanitation/waste treatment (1900s). 3. Most infections are asymptomatic. 4. Worms migrate from the GI tract through the bloodstream. 5. Clinical symptoms: a. Gut - obstruction, volvulus, malnutrition. b. Biliary tree - cholecystitis, ascending cholangitis, pancreatitis. c. Brain – impaired cognitive function in kids. d. Lungs - cough, SOB, fever, hemoptysis. 6. Diagnosis: visible worms and eggs in feces and/or vomit. 7. Treatment: albendazole, mebendazole or pyrantel pamoate.
E. For additional helminths (whipworms and Strongyloides), please see the Appendix.
VII. TETANUS AND PROPHYLAXIS:
A. Usually from soft tissue injuries with skin breakage.
B. High risk in elderly, diabetics, IVDU and immunosuppressed.
C. Tetanospasmin (exotoxin) causes muscle spasms (lockjaw) and hypersympathetic state.
D. Treatment:
1. Tetanus immune globulin (TIG) – neutralizes toxin. 2. Metronidazole. 3. Muscle relaxants. 4. Neuromuscular blockade.
Infectious Disease Page 489 Notes E. Vaccination:
1. Minor, clean wounds: a. Td only if > 10 years since vaccination/last booster. b. Do not administer TIG for minor wounds. 2. Tetanus-prone wounds: a. Nothing if vaccinated/booster < 5 years. b. Td if >5 years since vaccination/booster. c. If no previous vaccination, administer Td and TIG. 3. Tdap—one dose between ages 11 and 65.
VIII. RABIES:
A. Fatal viral encephalitis.
B. Infected saliva.
C. High incidence worldwide, 29 cases in US since 2001.
D. Common carriers in U.S.:
1. Raccoons. 2. Bats. 3. Skunks. 4. Foxes. 5. Cats (most common domestic animal).
E. Average incubation period 1-2 months.
F. Can range from 10 days to 2 years.
G. Post-exposure prophylaxis is 100% effective if started before symptoms begin:
1. Indicted with bite, scratch or mucus membrane contamination from high-risk animal. 2. As much of RIG dose as is anatomically feasible should be infiltrated in the area around and in the wounds; remaining should be given IM. 3. Passive immunity achieved using human rabies immune globulin. 4. Active immunity achieved with human diploid cell vaccine on days 0, 3, 7, 14 (and 28 for immunosuppressed).
Infectious Disease Page 490 Notes
INFECTIOUS DISEASES
PEARLS
1. AIDS = HIV infection with either presence of AIDS Indicator Condition or CD4 < 200.
2. Acute Retroviral Syndrome is a mono-like syndrome that occurs 2-4 weeks post HIV exposure.
3. Treatment should be started: CD4 count < 350 , or Regardless of CD4 count with: o History of an AIDS-defining illness. o Pregnancy. o HIV-associated nephropathy. o Co-infection with hepatitis B.
4. PCP is the most common opportunistic infection. Prophylaxis should be started if CD4 < 200 or patients has had previous PCP infection.
5. PEP reduces risk of seroconversion by 80%. No benefit after 72 hours post-exposure.
6. Sepsis management: Early recognition and aggressive supportive care. Early Goal-Directed Therapy: o CVP 8-12 cm. o Scvo2 > 70%. o Vasoactive medications to maintain MAP >65 mmHg. o Hematocrit > 30%. o Lactate clearance. Broad-spectrum antibiotic use. Steroids remain controversial.
7. Influenza: Abrupt onset fever, HA, myalgias, malaise and respiratory tract symptoms. Pneumonia is the most common complication.
8. Consider MERS and SARS with travel to Middle East or Asia, respectively.
Infectious Disease Page 491 Notes
9. West Nile disease - CSF shows pleocytosis with lymphocytosis and elevated protein concentration and normal glucose. Treatment is supportive.
10. Malaria: consider if periodic fevers. P. falciparum can cause severe disease; diagnose with peripheral smear.
11. Cellulitis and abscess most likely group A strep or staph aureus (must consider MRSA).
12. Consider necrotizing fasciitis if failure to respond to initial antibiotics, systemic toxicity, ‘woody’ feeling to subcutaneous tissue or skin necrosis.
13. Neurocysticercosis is one of the primary causes of new-onset seizures in many parts of the world.
14. Enterobiasis (pinworm) is the most common helminthic infection in U.S.
15. Tetanus management includes Td vaccine, immunoglobulin, muscle relaxants and metronidazole.
16. Rabies carriers in U.S. include (in order of most to least common): raccoons, skunks, bats, foxes and cats.
Infectious Disease Page 492 Notes
REFERENCES
1. Marx J, et al. Rosen’s emergency medicine: concepts and clinical practice 7th ed. Mosby Elsevier: 2010.
2. Tintinalli JE, et al. Tintinalli’s Emergency Medicine: A comprehensive study guide, 7e. McGraw-Hill: 2010.
3. Quinn TC. Acute primary HIV infection. JAMA 1997; 278:58.
4. Brooks JT, Kaplan JE, Holmes KK, et al. HIV-associated opportunistic infections--going, going, but not gone: the continued need for prevention and treatment guidelines. Clin Infect Dis 2009; 48:609.
5. Rivers CS, et al. Preparing for the written board exam in emergency medicine, 5e. Emergency medicine educational enterprises, Inc: 2006.
6. Shelburn SA, et al. Incidence and risk factors for immune reconstitution inflammatory syndrome during highly active antiretroviral therapy. AIDS 2005, Vol 19 No 4.
7. Greenwald JL, et al. A Rapid Review of HIV Antibody Tests. Current Infectious Disease Reports 2006, 8: 125-131.
8. Newell ML, Prevention of mother-to-child transmission of HIV: challenges for the current decade. Bulletin of the World Health Organization, 2001, 79(12).
9. Centers for Disease Control and Prevention. (2014). from http://www.cdc.gov.
10. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions of sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20:864.
Infectious Disease Page 493 Notes
11. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Eng J Med 2001; 345:1368.
12. Glezen WP. Clinical Practice. Prevention and treatment of seasonal influenza. N Engl J Med 2008; 359:2579.
13. Peiris, JS, Yeun KY, Osterhaus AD, Stohr K. The severe acute respiratory syndrome. N Eng J Med 2003; 349:2431.
14. Greenwood BM et al. Malaria. Lancet 2005; 365:1487.
15. Rivers CS, et al. Preparing for the written board exam in emergency medicine, 5e. Emergency medicine educational enterprises, Inc: 2006.
16. K Buchacz, RK Baker, FJ Palella, and others (HOPS Investigators). AIDS-Defining Opportunistic Illnesses in U.S. Patients, 1994-2007: A Cohort Study. AIDS 24(10): 1549-1559 (Abstract). June 19, 2010.
17. Landovitz RJ, Currier JS. Postexposure prophylaxis for HIV infection. N Engl J Med. 2009;361(18):1768-1775.
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Infectious Disease Page 494 Notes
APPENDIX
I. AIDS DEFINING OPPORTUNISTIC INFECTIONS
A. PCP: Pneumocystis jiroveci (carinii) pneumonia:
1. Most common opportunistic infection. 2. Gradual onset over weeks of fever, SOB, DOE, non-productive cough, tachypnea, +/- rales. 3. Lab findings: a. Increased LDH. b. Decreased PaO2. 4. Imaging: a. CXR: i. Diffuse, bilateral infiltrates. ii. Mild disease—normal. iii. PTX and pneumatoceles are common. b. High resolution CT—ground glass appearance. 5. PCP classification: a. Mild: i. PaO2 > 70, A-a gradient < 35. ii. PO meds +/- output therapy. b. Severe: i. PaO2 < 70, A-a gradient >35. ii. IV antibiotics, steroids, admit. 6. Treatment: a. All treatment— 21 days: i. Trimethoprim/sulfamethoxazole (TMP/SMX). ii. Alternatives: pentamidine IV (if Bactrim allergic). b. Steroids: i. Reduce risk of respiratory failure and death. ii. Recommended if PaO2 < 70 mmHg, A-a gradient >35 (or pulse ox < 90% on room air). iii. Contraindicated for suspected TB or disseminated fungal infection. 7. PCP prophylaxis: a. CD4 < 200. b. Previous PCP. c. Oral TMP/SMX 1 double strength tab QD or 3 times/week.
B. Mycobacterium tuberculosis:
1. Incidence 200-500x higher than general population. 2. Risk factors: prison, shelters, IVDU, inner city. 3. Fever, cough, hemoptysis. 4. Diagnosis: a. Sputum AFB smear and cultures. b. PPD: Infectious Disease Page 495 Notes i. PPD positive in early HIV. ii. PPD often negative in late HIV. iii. HIV patient with PPD > 5 mm is considered to have clinical infection. c. CXR: often atypical lower lobe, diffuse infiltrates or marked adenopathy. 5. Extrapulmonary involvement common: lymph nodes, liver, blood, bone marrow, meninges. 6. Treatment: a. Triple-drug therapy; four-drug therapy in resistant areas. b. INH, rifampin, pyrazinamide, ethambutol (or streptomycin).
C. Mycobacterium avium complex:
1. Persistent bacteremia with widespread systemic symptoms. 2. Disseminated MAI: a. Most common opportunistic BACTERIAL infection. b. CD4 < 50. c. Treatment: clarithromycin + ethambutol or rifabutin. d. Prophylaxis: clarithromycin or azithromycin +/- rifabutin.
D. Bacterial pneumonia:
1. Occurs frequently in HIV. 2. Recurrent bacterial pneumonia is AIDS identifying condition. 3. Bacteremia very common. 4. Treatment same as in normal host.
E. AIDS dementia:
1. Secondary to long-term HIV infection. 2. Most common neurologic problem in patients with AIDS. 3. No treatment but antiretroviral therapy may delay onset.
F. Cryptococcus neoformans meningitis:
1. CD4 count usually < 100. 2. May be disseminated or isolated. 3. Subtle presentation: a. HA. b. Fever. c. Slow changes in personality or mentation. d. CNS often involved. e. Photophobia, neck stiffness, seizures, focal deficits rare. 4. Diagnosis: a. CT scan: usually non-diagnostic; may see cryptococcomas. b. CSF examination and culture: i. India ink (CFS) smear positive 60%-80%. ii. Opening pressure > 200 mm in 70%. Infectious Disease Page 496 Notes iii. Serum and CSF Cryptococcal antigen. 5. Treatment: Amphotericin B +/- flucytosine for 2 weeks, then fluconazole or itraconazole po X 8-10 weeks. 6. Prophylaxis: life-time with fluconazole.
G. Toxoplasmosis:
1. Most common cause of FOCAL encephalitis. 2. Parasite transmitted by cats, flies, cockroaches and undercooked meat. 3. Encephalitis seen with CD4 count < 100. 4. Fever, HA, confusion, lethargy, seizures, focal neuro deficit. 5. Diagnosis: a. CT/MRI: single or multiple ring-enhancing lesions with surrounding edema (CNS lymphoma usually single, large lesion). b. CSF: nonspecific and may be normal. c. Toxoplasmosis titers: very nonspecific. d. Brain biopsy: definitive. 6. Treatment: a. Treat for 8 weeks or until negative CT. b. Pyrimethamine plus folinic acid plus sulfadiazine. c. Steroids - may be required to decrease edema. 7. Lifetime prophylaxis required.
H. CNS lymphoma:
1. HA, seizures, focal deficits, encephalopathy, CN polyneuropathy, fever. 2. Diagnosis: a. Requires brain bx to confirm. b. CT - solitary lesion/s with peripheral enhancement. 3. Treatment: a. Radiation or multiagent chemotherapy. b. If edema, consider Decadron/mannitol. 4. Often mistaken for toxoplasmosis and then identified after no improvement in 7-10 days of antibiotic therapy. 5. Prognosis poor.
I. CMV encephalitis:
1. CD4 count < 100. 2. Fever, +/- delirium, rapidly progressive confusion, apathy, malaise and HA, no focal neuro deficits. 3. Diagnosis by CMV PCR or CMV antigen in CSF. 4. Treatment - Ganciclovir, Foscarnet.
Infectious Disease Page 497 Notes
J. HIV meningitis: aseptic encephalitis:
1. Direct consequence of HIV; may be self-limited. 2. HA, meningismus. 3. Diagnosis of exclusion. 4. Treatment - supportive with high-dose AZT.
K. Bacterial meningitis:
1. Uncommon in HIV. 2. Consider Listeria if suspicious.
L. CMV retinitis:
1. Most frequent and serious ocular opportunistic infection. 2. Most common cause of blindness in AIDS patients. 3. CD4 < 50. 4. Cottage cheese and ketchup lesions on funduscopy. 5. Treatment - foscarnet or ganciclovir. 6. Blindness occurs in 10% despite therapy.
M. Oral candidiasis:
1. Most common infection of the GI tract of AIDS. 2. Usually asymptomatic but may cause odynophagia. 3. Rx with clotrimazole or nystatin.
N. Esophagitis - intraoral lesions may or may not be seen.
O. Diarrhea:
1. Most common symptom in HIV. 2. Significant factor contributing to morbidity and AIDS wasting syndrome. 3. Medications are a frequent cause. 4. Specific agent not found in 30-50% of patients: a. Salmonella. b. Shigella. c. Campylobacter. d. E. coli. e. C. diff. f. Giardia. g. Viruses. h. MAC. i. Cryptosporidium. j. Microsporida.
Infectious Disease Page 498 Notes
P. CMV:
1. Diarrhea, bleeding or perforation. 2. Treatment: Ganciclovir IV or po, Foscarnet po. 3. All patients should have eye exam to exclude retinitis.
Q. Proctitis:
1. Etiology: Herpes simplex, gonorrhea, candida, syphilis, Chlamydia trachomatis, HPV, Enterobius vermicularis, Phthirus pubis, Sarcoptes scabiei, trauma. 2. Clinical: tenesmus, mucoid, suppurative discharge. 3. Treatment: as per cause; stool softeners prn; for HSV: oral acyclovir.
R. Bowel obstruction: May be secondary to lymphadenopathy with TB, CMV, HIV, lymphoma.
S. AIDS cholangiopathy:
1. Causes: Cryptosporidium, Microsporidia, CMV. 2. Clinical: RUQ abdominal pain without diarrhea, fever, elevated alkaline phosphatase, normal bilirubin; acalculous cholecystitis; may be result of portal lymphadenopathy from opportunistic infections and neoplasm.
T. Pancreatitis:
1. Very common. 2. Causes: direct viral injury, secondary to gall bladder disease, extrinsic compression due to retroperitoneal nodes or neoplasm or side effect of medications.
U. Kaposi’s sarcoma (KS):
1. Most common malignancy in patients with AIDS. 2. Purple, non-blanching, painless patches on skin, MM and viscera. 3. Uncommon in heterosexual HIV patient. 4. Treatment: anti-retroviral therapy, radiation, alpha-interferon, chemotherapy.
V. Mucocutaneous HSV:
1. Clinical: painful grouped vesicles or non-healing ulcers around nose, mouth, perineum. 2. Diagnosis: viral culture. 3. Treatment: acyclovir po; if ocular involvement, may need IV.
Infectious Disease Page 499 Notes
W. Varicella zoster:
1. May herald the diagnosis of AIDS, especially if seen in a young patient or with diffuse, bilateral disease. 2. Treatment – PO or IV acyclovir.
II. HELMINTHS
A. Whipworm (Trichiura):
1. Colon inhabitant. 2. Multiple small worms. 3. Diagnosis: Blood and mucus in stool, rectal prolapse. 4. Treatment: mebendazole or albendazole.
B. Trichinosis:
1. Roundworm that burrows into striated muscle. 2. Acquired by eating undercooked pork. 3. Clinical features: a. Early (1 week): diarrhea, N/V, crampy abdominal pain. b. Later (1-2 months): myalgias and periorbital edema. 4. Diagnosis: a. Eosinophilia. b. Elevated CPK level. c. ELISA becomes positive 3 weeks after infection. d. Muscle biopsy. 5. Treatment: mebendazole + steroids (reduce the muscle inflammatory response).
C. Strongyloides:
1. Threadworm endemic to tropical and subtropical regions. 2. Very rare in SE U.S., immigrants and military personnel. 3. Unlike all other helminthic parasites, Strongyloides can complete its entire life cycle within the human host. 4. Clinical features: a. Usually asymptomatic. b. Dermatitis, weight loss, nausea, coughing, hemoptysis. c. “Hyperinfection Syndrome” flare-up during diminished host defenses (steroids, chemo or malnutrition) which can lead to disseminated disease with septic shock. Occurrence in WWII vets. 5. Diagnosis: ova and parasites in stool sample. 6. Treatment: ivermectin or thiabendazole.
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