Presentation

Classic presentation

• The severity of the presentation may vary depending on the degree of hypersensitivity, the quantity and route of exposure, and the sensitivity and responsiveness of the target organs.
  
• Rapid onset of symptoms (5–30 minutes) after parenteral exposure.
  
• Generalized warmth and tingling of the face, mouth, chest, hands, and areas of exposure.
  
• Pruritis.
  
• Generalized flushing and urticarial rash.
  
• Nasal congestion, sneezing, tearing.
  
• Crampy abdominal pain, nausea, vomiting, diarrhea, tenesmus.
  
• Cough, chest tightness, dyspnea, and wheezing.
  
• Lightheadedness or syncope.

Critical presentation

• Most fatalities occur within 30 minutes of antigen exposure.
  
• The rapidity of onset of symptoms after exposure is usually indicative of the severity of the reaction.
  
• Hoarseness, stridor, and hypersalivation may indicate oropharyngeal angioedema or laryngeal edema.
  
• Cough, wheezing, ronchi, and decreased air movement indicate lower respiratory tract bronchoconstriction.
  
• Hypotension and tachycardia suggest circulatory collapse due to vasodilation and increased vascular permeability; dysrhythmias may also occur.
  
• Altered mental status or seizure may occur due to decreased cerebral perfusion.
  
• Fibrinolysis and disseminated intravascular coagulation, manifesting with abnormal bleeding or bruising, may develop as the reaction continues.

Diagnosis and evaluation

• Vital signs
  
  
  
  • Tachycardia and hypotension indicate impending cardiovascular collapse.
    
  • Hypoxia may result from upper or lower airway compromise due to edema, bronchoconstriction, and excessive secretions.
  
  
• Physical examination
  
  
  
  • Cutaneous findings: urticaria, flushing, angioedema.
    
  • Upper airway: rhinitis, congestion, sneezing, hoarseness, hypersalivation, stridor, oropharyngeal edema.
    
  • Lower airway: cough, wheezing, dyspnea, decreased air movement.
    
  • Eye: conjunctivitis.
    
  • Hematological: mucous membrane bleeding, bruising.
  
  
• Diagnostic tests
  
  
  
  • Anaphylaxis is a clinical diagnosis. However, some laboratory tests may be helpful in evaluating the severity of the reaction, guide treatment, and rule out concurrent emergencies.
    
  • Laboratory studies: complete blood count (CBC), metabolic panel.
    
  • Electrocardiogram (ECG) to rule out dysrhythmias.
    
  • Chest radiograph.
    
  • Depending on the clinical situation: cardiac enzymes, serial blood gases, cultures, computed tomography (CT) of the head, neck soft tissue radiographs, indirect or direct laryngoscopy.

Critical management

• Initial steps
  
  
  
  • Secure the airway.
    
  • Remove the offending agent if still present.
    
  • Place the patient in Trendelenburg position if hypotensive.
    
  • Intravenous (IV) access and crystalloid administration.
    
  • Cardiac monitoring, pulse oximetry.
  
  
• Interventions
  
  
  
  • Epinephrine is the primary treatment of anaphylaxis.
    
  • The route of epinephrine administration depends on the severity of the clinical presentation.
    
  • For typical presentations of anaphylaxis, epinephrine should be administered intrasmuscularly (IM); the adult dose is 0.3–0.5 mL of 1:1000 concentration.
    
  • Indications for IV epinephrine include severe upper airway obstruction, acute respiratory failure, or systolic BP <80 mmHg. Patients receiving epinephrine should be placed on cardiac monitors.
    
  • IV epinephrine should be administered as 10 mL of a 1:100 000 dilution over 10 minutes; if there is no response, a continuous infusion of 1–10 micrograms/minute may be started.
    
  • Much confusion exists over proper epinephrine dosing: extreme care must be taken not to mistakenly administer the cardiac arrest dose (1 mg of 1:10 000 concentration) in anaphylaxis, as it may lead to potentially lethal cardiac complications.
  
  
• Antihistamines such as diphenhydramine should also be administered.
  
  
  
  • H2 antagonists such as famotidine and rantidine have been shown to potentiate the effect of H1 antagonists and can be used as well.
  
  
• Inhaled beta-agonists may be used for bronchospasm refractory to epinephrine.
  
• Systemic corticosteroids are of limited benefit in the acute treatment of anaphylaxis as the onset of action is approximately 4–6 hours; however, they may be useful for persistent bronchospasm and to prevent delayed reactions.
  
• Patients on beta-blockers may be refractory to epinephrine. In these cases, glucagon may be used to counteract the beta-blockade (1–5 mg IV over 5 minutes, followed by 5–15 micrograms/minute by continuous infusion).
  
• Disposition
  
  
  
  • Most patients with mild to moderate anaphylaxis who respond appropriately to initial treatment may be discharged home.
    
  • Due to the potential for rebound reaction, patients should be observed for 2–6 hours prior to discharge, depending on the severity of the reaction.
    
  • Patients should be provided with oral antihistamines and corticosteroid therapy for 7–10 days.
    
  • Indications for admission include any hypotension, upper airway involvement or prolonged bronchospasm.

Sudden deterioration

• Hypotension
  
  
  
  • Additional crystalloid should be considered; colloid solutions such as 5% albumin may also be considered given the increased vascular permeability involved in anaphylaxis.
    
  • If the patient remains hypotensive after fluid resuscitation, a vasopressor infusion should be initiated. Epinephrine is the first agent.
    
  • Dobutamine may be used if myocardial depression is suspected.
  
  
• Respiratory failure or airway obstruction
  
  
  
  • Patients with anaphylactic reactions and airway compromise should be managed expeditiously in order to prevent their airway from obstructing.

Vasopressor of choice: epinephrine.

References

Related posts:

Burns Chronic obstructive pulmonary disease Post–cardiac arrest care Monitoring Acute respiratory distress syndrome Severe pelvic trauma