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Emergency Medicine Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 83 CHAPTER 5 Emergency Medicine Meg Brison, Julian Owen, Dr. John Crossley, and Dr. Chris Hall ANAPHYLAXIS RATIONALE CLINICAL BOX • Anaphylaxis is a rapidly progressive, life-threatening allergic reaction. Anaphylaxis Statistics • In children, foods are the most common allergens. • Anaphylaxis is a clinical Dx based on Hx and P/E. • 50 fatalities per year in • Patient Tx demands rapid recognition of the condition, aggressive airway and CV Canada support, and prompt administration of meds. • True incidence is unknown due to under-reporting and differences in defining ‘‘ana- APPLIED SCIENTIFIC CONCEPTS phylaxis’’ • There is a spectrum to allergic/hypersensitivity reactions with local dermatologic mani- festations at one end and anaphylactic shock at the other. • Anaphylaxis is an IgE-mediated, immediate onset, hypersensitivity reaction to a protein ASC Box Ag. It requires a prior ‘‘sensitizing’’ exposure to the Ag. • Anaphylactoid reactions are clinically identical to anaphylaxis but are not IgE mediated. Cytokines Contributing Reactions can occur upon initial exposure to the Ag. (see Fig. 5.1) to the Late-Phase Response CAUSAL CONDITIONS IL-4–↑ IgE secretion Table 5.1 IL-5–recruitment and activation Common Anaphylaxis-Inducing Ags of leukocytes Foods Peanuts/nuts, seafood, eggs, cow’s milk TNF-α–contributes to systemic Hymenoptera envenomation Bees, wasps, fire ants anaphylactic shock Drugs/therapeutic agents β-Lactam Abx, NSAIDs, antineoplastic meds, ACEIs, vaccines, local anesthetics Human products Blood products, insulin Iatrogenic Latex, radiocontrast material CLINICAL BOX Anaphylaxis Differential Dx • Other types of shock: hypovolemic, sep- • ‘‘Restaurant’’ syndromes: MSG or sulfite sensitivity tic, cardiogenic • Excess endogenous production of histamine • Other causes of acute Resp failure: • Nonorganic disease: panic attack, Munchhausen¨ asthma, PE, epiglottitis • Other: vasovagal syncope, hereditary angioedema, • Flush syndromes: carcinoid, menopausal ACEI angioedema Sx, pheochromocytoma 83 Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 84 84 Essentials for the Canadian Medical Licensing Exam: Review and Prep for MCCQE Part I Figure 5.1 Anaphylaxis: cellular mechanisms, immune mediators, and physiologic s. APPROACH/KEY OBJECTIVES CLINICAL BOX • Anaphylactic shock is a form of distributive shock, and therefore requires aggressive fluid resuscitation to prevent CV collapse. Types of Anaphylaxis • Patients may initially present with mild Sx but will rapidly deteriorate without medical Biphasic Anaphylaxis Rx. Recurrence of Sx 4 to 32 h (mean • Most patients will present with Sx within 1 h of exposure to the offending Ag. However, 10 h) after the initial episode. some people may have a delayed response or will present hours later with a biphasic Occurs in up to 20% of patients ◦ anaphylactic response. and is due to the release of 2 • Anaphylaxis is a clinical Dx and there are no diagnostic tests of value in the emergent mediators and the late-phase setting. Classically, anaphylaxis is evidence of allergic reaction with either hypotension response. and/or Resp distress. Protracted Anaphylaxis PERTINENT HX Refractory Resp distress or Diagnostic Predictors hypotension despite appropriate medical Rx. • Known allergies and previous Hx of anaphylactic reactions • Hx of asthma or other atopic conditions (e.g., eczema) • Recent/current exposure to any suspected causative Ags Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 85 Chapter 5 • Emergency Medicine 85 Table 5.2 Common Presenting Signs and Sx in Anaphylaxis CNS Anxiety, headache, ↓ level of consciousness Resp Oropharyngeal swelling, chest tightness, dyspnea, wheezing, stridor, inability to speak, hypoxia, apnea CV Hypotension, palpitations, weak/absent pulses, tachycardia, cardiac arrest GI Dysphagia, abdominal pain or cramping, nausea, vomiting, diarrhea Dermatologic Pruritus, rash, urticaria, angioedema Figure 5.2 Acute Tx of anaphylaxis. Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 86 86 Essentials for the Canadian Medical Licensing Exam: Review and Prep for MCCQE Part I Prognostic Predictors • Prehospital use of EPI, antihistamines, or steroids following exposure CLINICAL BOX • Current meds–β-blockers and antihypertensives will blunt the effect of EPI and other resuscitative meds What saves lives? EPI, • Chronic CV or pulmonary disease–such patients may deteriorate much more rapidly EPI, EPI than others Q1 Adults: 0.3 to 0.5 mg IM All patients presenting with signs or Sx of anaphylaxis get: Children: 0.01 mg/kg IM • Measures to stop any continuing Ag exposure IV EPI: 0.1 mg, dilute 0.1 mL • Two large bore IVs 1:1,000 in 10 mL N/S • Supplemental O2 Give1to2mL/min • Cardiac and O2 sat monitoring • EPI IM or IV–to ↓ vascular permeability, relax bronchial smooth muscle, and ↑ cardiac and peripheral vascular resistance • Methylprednisolone 125 mg IV–to limit the production of leukotrienes in the late phase • Diphenhydramine 50 mg IV + ranitidine 50 mg IV–to block the action of histamine at the H1 and H2 receptors BURNS EPIDEMIOLOGY • Burns are common and range from minor cutaneous lesions to life-threatening injuries. • They are a significant source of morbidity in survivors. CAUSAL CONDITIONS THERMAL BURNS Types: fire (flash, flame), contact, and scalds (grease, steam, liquids spill, liquids immersion) ELECTRICAL BURNS Types: low voltage, high voltage, and lightning • DC–short duration of contact, but ↑ risk of trauma because victim often thrown from source • AC–exposure can be prolonged because source repetitively stimulates muscle contraction • First-, second-, and third-degree burns result from interaction of current with resistance of tissues Unique Features • Cardiac–arrhythmia occurs in 15% of injuries, rhythms are usually benign, but can result in Vfib • MSK–because of high resistance of muscle/ligament/bone, greatest amount of injury results here. Compartment syndromes may result +/− rhabdomyolysis Table 5.3 Unique features of Electrical Burns Cardiac Arrhythmia occurs in 15% of injuries, rhythms are usually benign, but can result in Vfib MSK High resistance of muscle/ligament/bone; therefore, greatest injury results here. Compartment syndromes may result +/− rhabdomyolysis Renal High concentration of CK combined with fluid losses may result in ATN. Tx involves ++ fluid administration +/− urine alkalinization CNS LOC, paralysis, Resp depression, amnesia can be transient effects Eye May result in keraunoparalysis and fixed, dilated pupils Other eye injuries such as cataracts are frequent after lightning injury Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 87 Chapter 5 • Emergency Medicine 87 Figure 5.3 A: Local effects of thermal burns. Full thickness burns consists of three distinct zones of tissue. Zone of coagulation: white, charred central portion. Consists of necrotic tissue. Zone of stasis: red, may blanch with pressure initially, but fragile blood supply gives way to AVN. Zone of hyperemia: red, blanches with pressure and has intact blood supply. Healing takes place in first wk. Image excerpted from the Textbook of Medical-Surgical Nursing, 9th Ed. B: Systemic effects of thermal burns. Image modified from the Textbook of Medical-Surgical Nursing, 9th ed. Chowdhury ch05.tex V1 - 01/28/2009 1:21 A.M. Page 88 88 Essentials for the Canadian Medical Licensing Exam: Review and Prep for MCCQE Part I • Renal–high concentration of CK combined with fluid losses may result in ATN. Tx involves ++ fluid administration +/− urine alkalinization • CNS–LOC, paralysis, Resp depression, amnesia can be transient effects Lightning may result in keraunoparalysis and fixed, dilated pupils. Other eye injuries such as cataracts are frequent after lightning injury. CHEMICAL BURNS Types: acid (nitric acid, sulfuric acid, HCl, oxalic acid, HF) and alkali (lime/cement, ammonia, NaOH, KOH) Alkali burns acid burns • Systemic effects have occurred with exposure to certain chemicals: because alkali dissolves pro- 1. Hypocalcemia with oxalic acid, HF tein and collagen and penetrates 2. Nephrotoxicity with tannic acid, phosphorus + deeper than acid burns 3. CNS depression hypotension with phenol exposure 4. Liver failure, ATN, and death from dichromate poisoning • Tx early and with ++ water. Neutralization with acid/alkali is not recommended because thermal injury is greater. RADIATION BURNS Types: UV, medical/therapeutic • Exposure through skin or ingestion/inhalation • Most common Sx involve GI and hematologic systems because of rapidly dividing cells, but high-dose exposure may also affect CNS • Absolute lymphocyte count within 48 h is best indicator for prognosis of whole body exposure • Tx involves removing clothing and irrigation as in other types of burns. Otherwise, supportive and symptomatic unless ingestion/inhalation suspected and chelating or blocking agents may help APPROACH MINOR BURNS • Generally can be handled as outpatients • Remove burn source promptly to halt burning process • Meticulous cleaning with soap and water or dilute antiseptic solution. Td immunization prn • Controversy exists over blister debridement, but in general those affecting mobile joints should be drained and cleansed thoroughly. However, blisters of the hands and feet should always be left intact. Traditional empiric Rx involves Rx with topical Abx in the form of 1% silver sulfadiazine (Dermazine) (avoid application to face or if patient has sulfa allergy), bacitracin (Baciguent), or bacitracin/neomycin/polymyxin B (Neosporin ointment). Remind patients
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