Delayed Hemopericardium Due to Non-Penetrating Chest Trauma: A
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Disseminated Intravascular Coagulation (DIC) and Thrombosis: the Critical Role of the Lab Paul Riley, Phd, MBA, Diagnostica Stago, Inc
Generate Knowledge Disseminated Intravascular Coagulation (DIC) and Thrombosis: The Critical Role of the Lab Paul Riley, PhD, MBA, Diagnostica Stago, Inc. Learning Objectives Describe the basic pathophysiology of DIC Demonstrate a diagnostic and management approach for DIC Compare markers of thrombin & plasmin generation in DIC, including D-Dimer, fibrin monomers (FM; aka soluble fibrin monomers, SFM), and fibrin degradation products (FDPs; aka fibrin split products, FSPs) Correlate DIC theory and testing to specific clinical cases DIC = Death is Coming What is Hemostasis? Blood Circulation Occurs through blood vessels ARTERIES The heart pumps the blood Arteries carry oxygenated blood away from the heart under high pressure VEINS Veins carry de-oxygenated blood back to the heart under low pressure Hemostasis The mechanism that maintains blood fluidity Keeps a balance between bleeding and clotting 2 major roles Stop bleeding by repairing holes in blood vessels Clean up the inside of blood vessels Removes temporary clot that stopped bleeding Sweeps off needless deposits that may cause blood flow blockages Two Major Diseases Linked to Hemostatic Abnormalities Bleeding = Hemorrhage Blood clot = Thrombosis Physiology of Hemostasis Wound Sealing break in vesselEFFRAC PRIMARY PLASMATIC HEMOSTASIS COAGULATION strong clot wound sealing blood FIBRINOLYSIS flow ± stopped clot destruction The Three Steps of Hemostasis Primary Hemostasis Interaction between vessel wall, platelets and adhesive proteins platelet clot Coagulation Consolidation -
Managing a Rib Fracture: a Patient Guide
Managing a Rib Fracture A Patient Guide What is a rib fracture? How is a fractured rib diagnosed? A rib fracture is a break of any of the bones that form the Your doctor will ask questions about your injury and do a rib cage. There may be a single fracture of one or more ribs, physical exam. or a rib may be broken into several pieces. Rib fractures are The doctor may: usually quite painful as the ribs have to move to allow for normal breathing. • Push on your chest to find out where you are hurt. • Watch you breathe and listen to your lungs to make What is a flail chest? sure air is moving in and out normally. When three or more neighboring ribs are fractured in • Listen to your heart. two or more places, a “flail chest” results. This creates an • Check your head, neck, spine, and belly to make sure unstable section of chest wall that moves in the opposite there are no other injuries. direction to the rest of rib cage when you take a breath. • You may need to have an X-ray or other imaging test; For example, when you breathe in your rib cage rises out however, rib fractures do not always show up on X-rays. but the flail chest portion of the rib cage will actually fall in. So you may be treated as though you have a fractured This limits your ability to take effective deep breaths. rib even if an X-ray doesn’t show any broken bones. -
Delayed Traumatic Hemothorax in Older Adults
Open access Brief report Trauma Surg Acute Care Open: first published as 10.1136/tsaco-2020-000626 on 8 March 2021. Downloaded from Complication to consider: delayed traumatic hemothorax in older adults Jeff Choi ,1 Ananya Anand ,1 Katherine D Sborov,2 William Walton,3 Lawrence Chow,4 Oscar Guillamondegui,5 Bradley M Dennis,5 David Spain,1 Kristan Staudenmayer1 ► Additional material is ABSTRACT very small hemothoraces rarely require interven- published online only. To view, Background Emerging evidence suggests older adults tion whereas larger hemothoraces often undergo please visit the journal online immediate drainage. However, emerging evidence (http:// dx. doi. org/ 10. 1136/ may experience subtle hemothoraces that progress tsaco- 2020- 000626). over several days. Delayed progression and delayed suggests HTX in older adults with rib fractures may development of traumatic hemothorax (dHTX) have not experience subtle hemothoraces that progress in a 1Surgery, Stanford University, been well characterized. We hypothesized dHTX would delayed fashion over several days.1 2 If true, older Stanford, California, USA be infrequent but associated with factors that may aid adults may be at risk of developing empyema or 2Vanderbilt University School of Medicine, Nashville, Tennessee, prediction. other complications without close monitoring. USA Methods We retrospectively reviewed adults aged ≥50 Delayed progression and delayed development of 3Radiology, Vanderbilt University years diagnosed with dHTX after rib fractures at two traumatic hemothorax (dHTX) have not been well Medical Center, Nashville, level 1 trauma centers (March 2018 to September 2019). characterized in literature. The ageing US popula- Tennessee, USA tion and increasing incidence of rib fractures among 4Radiology, Stanford University, dHTX was defined as HTX discovered ≥48 hours after Stanford, California, USA admission chest CT showed either no or ’minimal/trace’ older adults underscore a pressing need for better 5Department of Surgery, HTX. -
Rib Fracture Management Guideline
Rib Fracture Management Guideline The main goals of treatment for patients with multiple rib fractures, with or without flail segments, are pain control, support of respiratory function, and chest wall stabilization. ICU admission for two or more of the following: Age >65 years History of COPD and/or heart failure, home oxygen use, current smoker, or other significant pulmonary condition 4 or more rib fractures Flail segment (at least 3 consecutive ribs with 2 fractures) IS volumes <50% of predicted volume (see chart) Inadequate pain control Pain Management: Non-ICU patients should receive a multimodal regimen with PRN opioids (also see pain management algorithm for verbal patients) ICU patients should receive a PCA (morphine preferred) in addition to multimodal regimen Multimodal Pain Regimen (include all as appropriate): o Acetaminophen 1000mg PO/IV q8h (po preferred) o Ketoralac 15-30mg IV q6h x 5 days or ibuprofen 600mg po q6 hours PRN (avoid if bleeding or renal dysfunction) o Methocarbamol 500-1000mg PO/IV q8h (po preferred; avoid IV if renal dysfunction) PCA guidelines o PCA should NOT have a continuous rate or be administered with any other opioids o Recommended dose for morphine: 1 mg q6 minutes, max dose 10 mg/hour o Recommended for hydromorphone: 0.1 mg q15 minutes, max dose 0.4 mg/hr o Transition to an oral regimen as soon as possible . Determine the amount of opioid given over the previous 24 hours by PCA . If ≥ 40 mg morphine equivalents, start long-acting oxycodone (can’t be given through a feeding tube) BID with a 50% taper. -
Heart – Thrombus
Heart – Thrombus Figure Legend: Figure 1 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A thrombus is present in the right atrium (arrow). Figure 2 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 1). Multiple layers of fibrin, erythrocytes, and scattered inflammatory cells (arrows) comprise this right atrial thrombus. Figure 3 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A large thrombus with two foci of mineral fills the left atrium (arrow). Figure 4 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 3). This thrombus in the left atrium (arrows) has two dark, basophilic areas of mineral (arrowheads). 1 Heart – Thrombus Comment: Although thrombi can be seen in the right (Figure 1 and Figure 2) or left (Figure 3 and Figure 4) atrium, the most common site of spontaneously occurring and chemically induced thrombi is the left atrium. In acute situations, the lumen is distended by a mass of laminated fibrin layers, leukocytes, and red blood cells. In more chronic cases, there is more organization of the thrombus (e.g., presence of vascularized fibrous connective tissue, inflammation, and/or cartilage metaplasia), with potential attachment to the atrial wall. Spontaneous rates of cardiac thrombi were determined for control Fischer 344 rats and B6C3F1 mice: in 90-day studies, 0% in rats and mice; in 2-year studies, 0.7% in both genders of mice, 4% in male rats, and 1% in female rats. -
Thrombotic Thrombocytopenic Purpura
Thrombotic thrombocytopenic Purpura Flora Peyvandi Angelo Bianchi Bonomi Hemophilia and Thrombosis Center IRCCS Ca’ Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Disclosures Research Support/P.I. No relevant conflicts of interest to declare Employee No relevant conflicts of interest to declare Consultant Kedrion, Octapharma Major Stockholder No relevant conflicts of interest to declare Speakers Bureau Shire, Alnylam Honoraria No relevant conflicts of interest to declare Scientific Advisory Ablynx, Shire, Roche Board Objectives • Advances in understanding the pathogenetic mechanisms and the resulting clinical implications in TTP • Which tests need to be done for diagnosis of congenital and acquired TTP • Standard and novel therapies for congenital and acquired TTP • Potential predictive markers of relapse and implications on patient management during remission Thrombotic Thrombocytopenic Purpura (TTP) First described in 1924 by Moschcowitz, TTP is a thrombotic microangiopathy characterized by: • Disseminated formation of platelet- rich thrombi in the microvasculature → Tissue ischemia with neurological, myocardial, renal signs & symptoms • Platelets consumption → Severe thrombocytopenia • Red blood cell fragmentation → Hemolytic anemia TTP epidemiology • Acute onset • Rare: 5-11 cases / million people / year • Two forms: congenital (<5%), acquired (>95%) • M:F ratio 1:3 • Peak of incidence: III-IV decades • Mortality reduced from 90% to 10-20% with appropriate therapy • Risk of recurrence: 30-35% Peyvandi et al, Haematologica 2010 TTP clinical features Bleeding 33 patients with ≥ 3 acute episodes + Thrombosis “Old” diagnostic pentad: • Microangiopathic hemolytic anemia • Thrombocytopenia • Fluctuating neurologic signs • Fever • Renal impairment ScullyLotta et et al, al, BJH BJH 20122010 TTP pathophysiology • Caused by ADAMTS13 deficiency (A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, member 13) • ADAMTS13 cleaves the VWF subunit at the Tyr1605–Met1606 peptide bond in the A2 domain Furlan M, et al. -
Rib Cartilage Injuries
PHYSIO4ALL revitalise – bounce – be healthy Rib Cartilage Injuries Structure of the ribcage The ribcage supports the upper body, protects internal organs including the heart and lungs, and assists with breathing. It consists of 24 curved ribs arranged in 12 pairs. Each pair is attached to a vertebra in the spine. At the front of the body, the first seven pairs of ribs are attached directly to the sternum (breastbone) by cartilage known as costal cartilage. These ribs are often called ‘true ribs’. The next three pairs aren’t connected to the sternum. Instead, costal cartilage attaches these ‘false ribs’ to the last pair of true ribs. The remaining two pairs aren’t attached at the front of the body at all and are known as ‘floating ribs’. The ribcage is supported by ligaments and muscles, including the muscles between the ribs (intercostal muscles). These muscles allow the ribcage to expand when you breathe in, and drop when you breathe out. Rib injuries include bruises, torn cartilage and bone fractures. Shop No. P16, NorthPoint, 100 Miller St. North Sydney. NSW – 2060 T – (02) 99222212 F – (02) 99225577 W: www.physio4all.com.au E: [email protected] ABN: 77 548 297 578 PHYSIO4ALL revitalise – bounce – be healthy Symptoms of rib cartilage injury Symptoms of rib injuries depend on the type and severity of the injury, but can include: • Pain at the injury site • Pain when the ribcage flexes – for example when you breathe, cough, sneeze or laugh • Pain when rotating or side flexing your spine • Crunching or grinding sounds (crepitus) when the injury site is touched or moved • Muscle spasms of the ribcage • Deformed appearance of the ribcage • Breathing difficulties. -
32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies
32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies Introduction Antiphospholipid antibodies (aPL) are related to thrombosis in the antiphospho- lipid syndrome (APS) [1, 2] and numerous pathophysiological mechanisms have been suggested involving cellular effects, plasma coagulation regulatory proteins, and fibrinolysis [3, 4]: aPL may act as blocking agents directly inhibiting antigen enzymatic or co-factor function of hemostasis; may bind fluid-phase antigens of hemostasis involved proteins and then decrease plasma antigen levels by clearance of immune complexes; may form immune complexes with their antigens that may be deposited in blood vessels causing inflammation and tissue injury; may cause dysregulation of antigen–phospholipid binding due to cross-linking of membrane bound antigens; and may trigger cell mediated events by cross-linking of antigen bound to cell surfaces or cell surface receptors [3, 4]. Moreover, several characteris- tics of the aPL, such as the concentration, class/subclass, affinity or charge, and several characteristics of the antigens, as the concentration, size, location or charge, may influence which of the theoretical autoantibody actions will occur in vivo [3]. Among the cellular mechanisms supposed to be involved, platelets have been considered as one of the most promising potential target for circulating aPL that may cause antibody mediated thrombosis as a part of the clinical spectrum of the autoimmune disorder of the APS. In the present chapter we will focus on the inter- actions that involve aPL binding to platelet membrane or platelet membrane bound antigens. Platelets as Target for aPL Platelets play a central role in primary hemostasis involving platelet adhesion to the injured blood vessel wall, followed by platelet activation, granule release, shape change, and rearrangement of the outer membrane phospholipids and proteins, transforming them into a highly efficient procoagulant surface [5]. -
Rib Fracture Management in the Older Adult; an Opportunity for Multidisciplinary Working
Subspecialty Section Rib fracture management in the older adult; an opportunity for multidisciplinary working Lauren Richardson and Shvaita Ralhan The elderly will soon make up the largest number of patients sustaining major trauma; a fall from standing height is their most common mechanism of injury1. Rib fractures are a common consequence of blunt chest trauma and are important to recognise and diagnose as complications can be fatal. They can be considered a surrogate for major trauma as up to 90% of patients will Lauren Richardson is an ST7 Registrar go on to have additional injuries identified2. The older in Geriatric and General Medicine working in the Thames Valley. Whilst adult presents a unique challenge. Their injuries are often undertaking a fellowship in Perioperative under-estimated and therefore under-triaged. Delays to Medicine she helped to develop the diagnosis are not uncommon3. Major Trauma Geriatric service at the John Radcliffe Hospital in Oxford. he mortality and thoracic deal with. Decisions regarding which team morbidity in the elderly as these patients should be admitted under can a result of rib fractures is therefore be contentious. Nationally, there is double that of their younger significant variation, and even in institutions counterparts. In elderly patients, such as ours where pathways do exist, Tfor each additional rib fracture, mortality conflicts often arise as to where the patient increases by 19% and the risk of pneumonia should be managed and by whom. increases by 27%4. It is therefore not surprising that older adults who sustain rib This article aims to address the key issues fractures have increased lengths of stay and that arise when managing older adults with more prolonged intensive care admissions5–7. -
Theappearanceof Bonescansfollowingfractures,Inciudingimmediateand Long@-Termstudies
CLINICAL SCIENCES DIAGNOS11C NUCLEAR MEDICINE TheAppearanceof BoneScansFollowingFractures,InciudingImmediateand Long@-TermStudies Philip Matin RosevilleCommunityHospital,Roseville,andUniversityof California,Davis,California Bone scans were performed on 204 patients at Intervals ranging from 6 hr to several years after traumatic fractures. The minimum time for a bone scan to be come abnormal following fracture was age-dependent; however, 80% of all frac tures were abnormal by 24 hr, and 95 % by 72 1w,after Injury. Three distinct tempo rally related phases were noted on bone scans as sequential studies showed a gradual return to normal. The minimum tIme for a fracture to return to normal on a bone scan was 5 mo. Approximately 90% of the fractures returned to normal by 2 yr after injury. J NuciMed 20:1227—1231,1979 Bone scans performed with technetium-99m phos were performed within 2 wk after fracture, including 60 phate compounds have proven to be among the most patients who had bone scans within the first week of in useful nuclear medicine procedures. The bone scan jury. The studies on these patients were performed until provides a sensitive method of detecting primary and their fractures became abnormal or until 7 days after metastatic skeletal neoplasms, and it has been useful in injury. In this group, nine patients were studied within evaluating metabolic bone disease and various joint 6 hr of their injury, and 20 within 24 hr. abnormalities (1—8).Although the procedure is helpful The subacute studies were performed during the in in evaluating skeletal trauma (9—12,14)little informa terval from 4 wk to 4 mo after injury; and the long-term tion is available about how bone scans change in ap or healing-stage studies were performed at periods pearance following fracture, and there have been es varying from 6 to 36 mo after fracture. -
Thrombosis and Embolism After Injury J Clin Pathol: First Published As 10.1136/Jcp.S3-4.1.86 on 1 January 1970
J. clin. Path., 23, Suppl. (Roy. Coll. Path.), 4, 86-101 Thrombosis and embolism after injury J Clin Pathol: first published as 10.1136/jcp.s3-4.1.86 on 1 January 1970. Downloaded from S. SEVITT From the Birmingham Accident Hospital Thrombosis is frequent in injured patients. It classified as follows, namely, local thrombosis, takes different forms, and at least one of them, deep vein thrombosis, pulmonary microem- deep vein thrombosis in the lower limbs, is a bolism, glomerular microthrombosis, allied to common cause of morbidity and death through the Schwartzman reaction, occasional cases of embolic detachment. The different kinds may be arterial thrombosis, and rarely, abacterial vege- tative endocarditis. Thrombi form in flowing blood and are layered structures, unlike blood clots which form copyright. in static blood. They contain platelets, fibrin, red cells, and leucocytes, or a variable mixture, the differences depending on size, genesis, age, and venous or arterial location; but whatever the origin, the building blocks of enlarging thrombi are closely packed clumps of platelets with narrow fibrin borders (Fig. 1). Two main pro- http://jcp.bmj.com/ cesses are involved, namely, coagulation and platelet aggregation. These are interlinked and local release of thrombin is probably the key factor; thrombin promotes platelet clumping at a low concentration and fibrin formation at a higher concentration. Further, the release of substances from platelets can set in motion the coagulation on September 30, 2021 by guest. Protected process. Local Thrombosis and Haemostasis Thrombosis is frequent as a direct response to injury. In burned skin, for example, small venous thrombi may become prominent in the subdermis and subcutaneous tissue. -
Vertebroplasty
Association for Radiologic & Imaging Nursing Clinical Practice Guideline Vertebroplasty Overview Vertebroplasty is a percutaneous procedure performed to treat painful vertebral compression fractures. The procedure uses Polymethlymethacrylate (PMMA) through a needle percutaneously inserted into the body of the vertebrae to stabilize the compression fracture. This procedure is commonly performed as an outpatient procedure for treatment of osteoporotic, metastatic, and benign lytic lesions such as hemangiomas of the spine. It is not typically used to treat the non- osteoporotic acute traumatic compression fracture. Target Audience RNs working in the Interventional Radiology Division Content/Strategies Osteoporosis is present in one out of every four women and one out of every eight men, over the age of 50. Along with the aging baby boomer generation, it is being identified by the public in greater numbers as a health risk. Neoplastic disease can metastasize to the vertebrae causing compression fractures. Treating these painful lesions in a palliative manner can improve end-of-life quality. Hemangiomas destabilize the body of the vertebrae leading to compression fracture. Eighty to 90 percent of patients obtain significant pain relief. Nursing Considerations: Pre procedure- Adequate intravenous access Proper positioning—often these patients are frail elders who must be positioned prone for the procedure. Bony prominences must be protected. Care must be taken when moving these patients to prevent causing fragility fractures to legs and ribs. Adequate airway maintenance in the prone position must be assured. Most procedures can be done under conscious sedation with some local anesthetic, although some might require general anesthesia depending on their acuity level. Intra procedure- Absolute sterility of this procedure is imperative—full surgical scrub of site, cap/mask for all in room.