Approach to Shock.” These Podcasts Are Designed to Give Medical Students an Overview of Key Topics in Pediatrics
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Differentiating Between Anxiety, Syncope & Anaphylaxis
Differentiating between anxiety, syncope & anaphylaxis Dr. Réka Gustafson Medical Health Officer Vancouver Coastal Health Introduction Anaphylaxis is a rare but much feared side-effect of vaccination. Most vaccine providers will never see a case of true anaphylaxis due to vaccination, but need to be prepared to diagnose and respond to this medical emergency. Since anaphylaxis is so rare, most of us rely on guidelines to assist us in assessment and response. Due to the highly variable presentation, and absence of clinical trials, guidelines are by necessity often vague and very conservative. Guidelines are no substitute for good clinical judgment. Anaphylaxis Guidelines • “Anaphylaxis is a potentially life-threatening IgE mediated allergic reaction” – How many people die or have died from anaphylaxis after immunization? Can we predict who is likely to die from anaphylaxis? • “Anaphylaxis is one of the rarer events reported in the post-marketing surveillance” – How rare? Will I or my colleagues ever see a case? • “Changes develop over several minutes” – What is “several”? 1, 2, 10, 20 minutes? • “Even when there are mild symptoms initially, there is a potential for progression to a severe and even irreversible outcome” – Do I park my clinical judgment at the door? What do I look for in my clinical assessment? • “Fatalities during anaphylaxis usually result from delayed administration of epinephrine and from severe cardiac and respiratory complications. “ – What is delayed? How much time do I have? What is anaphylaxis? •an acute, potentially -
Hypovolemic Shock and Resuscitation Piper Lynn Wall Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1997 Hypovolemic shock and resuscitation Piper Lynn Wall Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Sciences Commons, Physiology Commons, Surgery Commons, and the Veterinary Physiology Commons Recommended Citation Wall, Piper Lynn, "Hypovolemic shock and resuscitation " (1997). Retrospective Theses and Dissertations. 11754. https://lib.dr.iastate.edu/rtd/11754 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directly fi-om the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter &ce, while others may be from any type of computer printer. The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overiaps. -
Fluid Resuscitation Therapy for Hemorrhagic Shock
CLINICAL CARE Fluid Resuscitation Therapy for Hemorrhagic Shock Joseph R. Spaniol vides a review of the 4 types of shock, the 4 classes of Amanda R. Knight, BA hemorrhagic shock, and the latest research on resuscita- tive fluid. The 4 types of shock are categorized into dis- Jessica L. Zebley, MS, RN tributive, obstructive, cardiogenic, and hemorrhagic Dawn Anderson, MS, RN shock. Hemorrhagic shock has been categorized into 4 Janet D. Pierce, DSN, ARNP, CCRN classes, and based on these classes, appropriate treatment can be planned. Crystalloids, colloids, dopamine, and blood products are all considered resuscitative fluid treat- ment options. Each individual case requires various resus- ■ ABSTRACT citative actions with different fluids. Healthcare Hemorrhagic shock is a severe life-threatening emergency professionals who are knowledgeable of the information affecting all organ systems of the body by depriving tissue in this review would be better prepared for patients who of sufficient oxygen and nutrients by decreasing cardiac are admitted with hemorrhagic shock, thus providing output. This article is a short review of the different types optimal care. of shock, followed by information specifically referring to hemorrhagic shock. The American College of Surgeons ■ DISTRIBUTIVE SHOCK categorized shock into 4 classes: (1) distributive; (2) Distributive shock is composed of 3 separate categories obstructive; (3) cardiogenic; and (4) hemorrhagic. based on their clinical outcome. Distributive shock can be Similarly, the classes of hemorrhagic shock are grouped categorized into (1) septic; (2) anaphylactic; and (3) neu- by signs and symptoms, amount of blood loss, and the rogenic shock. type of fluid replacement. This updated review is helpful to trauma nurses in understanding the various clinical Septic shock aspects of shock and the current recommendations for In accordance with the American College of Chest fluid resuscitation therapy following hemorrhagic shock. -
Severe Sepsis and Septic Shock Antibiotic Guide
Stanford Health Issue Date: 05/2017 Stanford Antimicrobial Safety and Sustainability Program Severe Sepsis and Septic Shock Antibiotic Guide Table 1: Antibiotic selection options for healthcare associated and/or immunocompromised patients • Healthcare associated: intravenous therapy, wound care, or intravenous chemotherapy within the prior 30 days, residence in a nursing home or other long-term care facility, hospitalization in an acute care hospital for two or more days within the prior 90 days, attendance at a hospital or hemodialysis clinic within the prior 30 days • Immunocompromised: Receiving chemotherapy, known systemic cancer not in remission, ANC <500, severe cell-mediated immune deficiency Table 2: Antibiotic selection options for community acquired, immunocompetent patients Table 3: Antibiotic selection options for patients with simple sepsis, community acquired, immunocompetent patients requiring hospitalization. Risk Factors for Select Organisms P. aeruginosa MRSA Invasive Candidiasis VRE (and other resistant GNR) Community acquired: • Known colonization with MDROs • Central venous catheter • Liver transplant • Prior IV antibiotics within 90 day • Recent MRSA infection • Broad-spectrum antibiotics • Known colonization • Known colonization with MDROs • Known MRSA colonization • + 1 of the following risk factors: • Prolonged broad antibacterial • Skin & Skin Structure and/or IV access site: ♦ Parenteral nutrition therapy Hospital acquired: ♦ Purulence ♦ Dialysis • Prolonged profound • Prior IV antibiotics within 90 days ♦ Abscess -
When the Heart Kills the Liver: Acute Liver Failure in Congestive Heart Failure
December 14, 2009 Eu Ro PE an JouR nal oF MED I cal RE sEaRcH 541 Eur J Med Res (2009) 14: 541-546 © I. Holzapfel Publishers 2009 WHEn tHE HEaRt KIlls tHE lIvER: acutE lIvER FaIluRE In congEstIvE HEaRt FaIluRE F. H. saner1, M. Heuer1, M. Meyer1, a. canbay2, g. c. sotiropoulos1, a. Radtke1, J. treckmann1, s. Beckebaum1, c. Dohna-schwake2, s. W. oldedamink3, 4, a. Paul1 1Department of general-, visceral- and transplant surgery, university Hospital Essen, germany, 2Department of Pediatric Medicine, university Hospital Essen, germany, 3Department of surgery, university of Maastricht, netherlands, 4Department of surgery, university college london Hospital, ucl, uK Abstract gestive heart failure may be absent [5, 18]. Both, congestive heart failure as a cause of acute liver fail- chronic and acute congestive heart failure can lead to ure is rarely documented with only a few cases. hepatic dysfunction [10, 17]. although there is no although the pathophysiology is poorly under- classic pattern of abnormalities, a cholestatic bio- stood, there is rising evidence, that low cardiac output chemical profile is common, with a mild elevation in with consecutive reduction in hepatic blood flow is a total bilirubin (usually 3 g/dl), a mild elevation in al- main causing factor, rather than hypotension. In the kaline phosphatase and only occasional elevations in setting of acute liver failure due to congestive heart transaminases. another common observation is an in- failure, clinical signs of the latter can be absent, which crease in InR. the presumed causes of hepatic dys- requires an appropriate diagnostic approach. function in congestive heart failure are hepatic con- as a reference center for acute liver failure and liver gestion from venous outflow obstruction and result- transplantation we recorded from May 2003 to De- ing hypertension and decreased oxygen delivery from cember 2007 202 admissions with the primary diag- an impaired cardiac output [10]. -
Septic Shock V9.0 Patient Flow Map
Septic Shock v9.0 Patient Flow Map Approval & Citation Summary of Version Changes Explanation of Evidence Ratings Patient presents to the ED with fever and/or concern for infection and ED sepsis score ≥ 6 ! BPA fires Use the ED Suspected Septic Shock RN and Well-appearing patients should be placed pathway for all ill on the appropriate ED CSW pathway for Provider appearing patients their underlying condition (e.g. ED No including HemOnc/BMT, Huddle: HemOnc BMT Suspected Infection, ED Central Line Infection Is the patient ill Suspected Central Line Infection, ED and Neonates appearing? Neonatal Fever) Yes ED Septic Shock Pathway • Use ED Suspected Septic Shock Plan • Antibiotics and blood cultures for specific populations included Inpatient Admit Criteria Does NOT meet Inpatient Admit Minute criteria • Resolution of hypotension and no • Admit to ICU ongoing signs of sepsis after ≤ 40 ml / 60 Huddle: YES NO • Follow ICU Septic Shock Pathway kg NS bolus Does patient meet • Use PICU/CICU Septic Shock Admit • First dose antibiotics administered Inpatient admit Plan • RISK to follow criteria? • Antibiotics, blood cultures for specific populations included in sub plans Previously healthy > 30 days RISK RN to follow all • Admit to General Medicine patients admitted with • Follow Admit from ED Septic Shock concern for sepsis Pathway • Use Inpatient Septic Shock Plan ! Concern for evolving sepsis Previously healthy < 30 days Any • Admit to General Medicine admitted • Call RRT or Code Blue • Follow Neonatal Fever Pathway patient with • Follow Inpatient -
Evaluation and Management of the Polytraumatized Patient in Various Centers
World J. Surg. 7, 143-148, 1983 Wor Journal of Stirgery Evaluation and Management of the Polytraumatized Patient in Various Centers S. Olerud, M.D., and M. Allg6wer, M.D. The Akademiska Sjukhuset Uppsala, Sweden, and the Department of Surgery, Kantonsspital, Basel, Switzerland A questionnaire was sent to the following 6 trauma centers: Paris: Two or more peripheral, visceral, or com- University Hospital for Accident Surgery, Hannover, Fed- plex injuries with respiratory and circulatory fail- eral Republic of Germany (Prof. H. Tscherne); University ure. (This excludes patients who only have sus- of Munich, Department of Surgery, Klinikum Grossha- tained fractures.) dern, Munich, Federal Republic of Germany (Prof. G. Dallas: Multiply injured patient presenting le- Heberer); Akademiska Sjukhuset Uppsala, Sweden (Prof. sions to 2 cavities, associated with 2 or more long S. Olerud); University Hospital, Department of Surgery, bone failures; lesions to 1 cavity associated with 2 Basel, Switzerland (Prof. M. Allgiiwer); H6pital de la Piti~, or more long bone failures; or lesions to multiple Paris, France (Prof. R. Roy-Camille); and University of extremities (at minimum, 3 long bone failures). Texas Southwestern Medical School, Dallas, Texas, U.S.A. (Prof. B. Claudi). Their answers have been summarized in a few short paragraphs where tabulation was not possible, Do You Grade Polytrauma, and If So, How? and then mainly in tabular form for convenient comparison among the various centers. There seems to be considerable international agreement on the main points of early aggres- Hannover: Yes, with our own grading system along sive cardiopulmonary management to prevent multiple with ISS and AIS. -
Shock and Hemodynamic Monitoring
Shock and Hemodynamic Monitoring Matthew Bank, MD, FACS Assistant Professor Hofstra North Shore‐LIJ School of Medicine Director, Surgical Intensive Care Unit North Shore University Hospital I do not have any financial conflicts of interest to disclose for this presentation Shock • Multiple different strategies for classifying shock, but all forms of shock result in impaired oxygen delivery secondary to either one or both: – reduced cardiac output (cardiogenic, septic) OR – loss of effective intravascular volume (hypovolemic, neurogenic, anaphylactic, septic). Septic Shock –Gram Negative • Gram negative septic shock: —Very studied well studied in animal models —Lipopolysaccharide (LPS) in bacterial cell wall binds to LPS binding protein. —LPS‐LBP complex then binds to cell surface CD14 receptors on monocytes and macrophages. —The LPS‐LBP‐CD14 complex then activates cells via Toll‐like receptor‐4 (TLR4). —TLR4 then “activates” cells which produce a cytokine “cascade” of proinflamatory mediators. Septic Shock –Gram Negative • Tumor Necrosis Factor (TNF) – First cytokine produced in response to gram negative sepsis – Principal mediator for acute response to gram negative bacteria – Major source of TNF is from activated macrophages – High levels of TNF predict mortality and can cause apoptosis. Septic Shock –Gram Negative • Interleukin‐1 (IL‐1) – Levels of IL‐1 increase soon after TNF production in gram negative sepsis (second cytokine to be elevated) – IL‐1 produced by macrophages, neutrophils and endothelial cells – IL‐1 increases levels of next proinflammatory cytokines in cascade, IL‐2 and IL‐12. – IL‐1 does NOT cause apoptosis Septic Shock –Gram Negative • Interleukin‐10 – Anti‐inflammatory cytokine – Inhibits production of IL‐12 – Inhibits T‐cell activation Septic Shock –Gram Positive • Gram positive sepsis – Gram positive cell wall components are also known to be involved in septic response – Peptidoglycans – Teichoic Acid – Likely act in a similar manner as LPS, but less potent on a weight bases. -
Myocarditis in Acute Infective Diseases a Review of 200 Cases by C
Arch Dis Child: first published as 10.1136/adc.19.100.178 on 1 December 1944. Downloaded from MYOCARDITIS IN ACUTE INFECTIVE DISEASES A REVIEW OF 200 CASES BY C. NEUBAUER, M.D. Resident Medical Officer, City Hospital for Infectious Diseases, Newcastle upon Tyne The acute infective diseases constitute the most voltage in all three limb leads together. This sign important cause of myocarditis, the commonest occurs especially in cases of severe myocarditis. heart disease in childhood. Increasing amount of Pathological anatomy. Whenever possible the evidence from electrocardiographic investigations heart of a fatal case was examined in the Patho- of the heart in acute infective diseases shows that logical Department (Prof. B. Shaw) ofKing's College, there can be a myocarditis when clinical signs and Newcastle upon Tyne. Two illustrative cases are symptoms are slight, doubtful or completely absent. given: These investigations further revealed that many 1. convalescent cases whose unsatisfactory condition Sheila F., ten years, died on the eleventh day of diphtheria. Immediately beneath the ven- was accounted for by post-infective or secondary tricular anaemia were endocardium and also in the inner third of actually suffering from myocarditis. the wall are some scattered small foci of lymphoid Therefore, since this involvement of the myocardium and histiocytic cells. These foci sometimes occur is so common an event and liable to be missed or in association with shrunken muscle fibres and what misdiagnosed, it seems justifiable to give an account appear to be small delicate recent scars. of 200 cases of myocarditis occuring in acute 2. Iris N., eight years old,'died on the fourth day infectious diseases. -
Hypovolemic Shock
Ask the Expert Emergency Medicine / Critical Care Peer Reviewed Hypovolemic Shock Garret E. Pachtinger, VMD, DACVECC Veterinary Specialty & Emergency Center Levittown, Pennsylvania You have asked… What is hypovolemic shock, and how should I manage it? Retroperitoneal effusion in a dog The expert says… hock, a syndrome in which clinical deterioration can occur quickly, requires careful analy- All forms of shock share sis and rapid treatment. Broad definitions for shock include inadequate cellular energy pro- a common concern: Sduction or the inability of the body to supply cells and tissues with oxygen and nutrients and remove waste products. Shock may result from a variety of underlying conditions and can be inadequate perfusion. classified into the broad categories of septic, hemorrhagic, obstructive, and hypovolemic shock.1-3 Regardless of the underlying cause, all forms of shock share a common concern: inadequate per- fusion.1,2 Perfusion (ie, flow to or through a given structure or tissue bed) is imperative for nutri- ent and oxygen delivery, as well as removal of cellular waste and byproducts of metabolism. Lack of adequate perfusion can result in cell death, morbidity, and, ultimately, mortality. Hypovolemic shock is one of the most common categories of shock seen in clinical veterinary medicine.4 In hypovolemic shock, perfusion is impaired as a result of an ineffective circulating blood volume. During initial circulating volume loss, there are a number of mechanisms to com- pensate for decreases in perfusion, including increased levels of 2,3-Bisphosphoglycerate, result- ing in a rightward shift in the oxyhemoglobin dissociation curve and a decreased blood viscosity. -
Acute Kidney Injury in Cardiogenic Shock: an Updated Narrative Review
Journal of Cardiovascular Development and Disease Review Acute Kidney Injury in Cardiogenic Shock: An Updated Narrative Review Sohrab Singh 1 , Ardaas Kanwar 2, Pranathi R. Sundaragiri 3, Wisit Cheungpasitporn 4 , Alexander G. Truesdell 5, Syed Tanveer Rab 6, Mandeep Singh 7 and Saraschandra Vallabhajosyula 8,* 1 Department of Medicine, The Brooklyn Hospital, Brooklyn, NY 11201, USA; [email protected] 2 Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA; [email protected] 3 Section of Primary Care Internal Medicine, Wake Forest Baptist Health, High Point, NC 27262, USA; [email protected] 4 Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 5 Virginia Heart/Inova Heart and Vascular Institute, Falls Church, VA 22042, USA; [email protected] 6 Section of Interventional Cardiology, Division of Cardiovascular Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; [email protected] 7 Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 8 Section of Cardiovascular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27262, USA * Correspondence: [email protected] Abstract: Acute myocardial infarction with cardiogenic shock (AMI-CS) is associated with high mortality and morbidity despite advancements in cardiovascular care. AMI-CS is associated with multiorgan failure of non-cardiac organ systems. Acute kidney injury (AKI) is frequently seen in patients with AMI-CS and is associated with worse mortality and outcomes compared to those without. The pathogenesis of AMI-CS associated with AKI may involve more factors than previously Citation: Singh, S.; Kanwar, A.; understood. -
Clinical Assessment in Acute Heart Failure
Hellenic J Cardiol 2015; 56: 285-301 Review Article Clinical Assessment in Acute Heart Failure 1 2 NIKOLAOS S. KAKOUROS , STAVROS N. KAKOUROS 1University of Massachusetts, MA, USA; 2Cardiac Department, “Amalia Fleming” General Hospital, Athens, Greece Key words: eart failure (HF) is defined as “a clear precipitant or trigger. It is very im Heart failure, complex clinical syn drome that portant to establish the precipitating diagnosis, physical examination, H can result from any structural or causes, which may have therapeutic and congestion. functional cardiac disorder that impairs the prognostic implications. Approximate ability of the ventricle to fill with, or eject ly 60% of patients with AHF have doc blood.” HF has an estimated overall prev umented CAD. Myocardial ischemia in alence of 2.6%. It is becoming more com the setting of acute coronary syndromes mon in adults older than 65 years, because is a precipitant or cause, particularly in of increased survival after acute myocar patients presenting with de novo AHF.4 dial infarction (AMI) and improved treat AHF is also often precipitated by medica ment of coronary artery disease (CAD), tion and dietary noncompliance, as well val vular heart disease and hypertension.1 as by many other conditions, which are Acute HF (AHF) is an increasingly com summarized in Table 1. Once the diagno mon cause of hospitalizations and mortality sis of AHF is confirmed, initial therapy in worldwide. In the majority of patients, AHF cludes removal of precipitants; if this can Manuscript received: can be attributed to worsening chronic HF, be carried out successfully, the patient’s August 25, 2014; and approximately 4050% of this group have subsequent course may be stable.