I. Airway, Breathing & Circulatory Support

Rapid recognition of airway compromise and hemodynamic collapse in anaphylaxis saves lives. Early intervention with airway protection, lung-protective ventilation, fluid resuscitation, and vasopressors is critical.

1.1 Indications for Mechanical Ventilation

The decision to intubate is clinical, based on the trajectory of airway compromise. Key indicators include:

• Progressive Upper-Airway Edema: Observable swelling of the tongue or lips, audible stridor, or subjective voice changes (hoarseness, “hot potato” voice).
• Respiratory Failure: Inability to maintain oxygen saturation (SpO2 < 90%) despite high-flow supplemental oxygen, or signs of severe work of breathing (accessory muscle use, retractions).
• Elective Intubation Triggers:
  • Rapidly advancing angioedema despite initial epinephrine doses.
  • Hypoxemia (PaO2 < 60 mm Hg) or hypercapnia (PaCO2 > 50 mm Hg) on arterial blood gas analysis.

Intubation and Ventilator Strategy

Intubation in the setting of angioedema is a high-risk procedure. The most experienced provider should perform it, with a difficult airway cart immediately available. An awake fiberoptic technique is often the safest approach. For ventilation, especially with bronchospasm, a lung-protective strategy is key: low tidal volumes (6 mL/kg predicted body weight), slower respiratory rates (10–12 breaths/min) to allow for prolonged expiratory time, and permissive hypercapnia (allowing PaCO2 to rise as long as pH remains ≥7.20) to prevent auto-PEEP.

1.2 Hemodynamic Support

Anaphylactic shock is a form of distributive shock caused by massive vasodilation and capillary leak, leading to profound relative and absolute hypovolemia. Management requires aggressive fluid resuscitation and vasopressors.

• Fluid Resuscitation: Begin with a rapid bolus of 20 mL/kg of an isotonic crystalloid (e.g., Lactated Ringer’s or Normal Saline). Repeat boluses as needed to achieve a systolic blood pressure (SBP) ≥ 90 mm Hg or a mean arterial pressure (MAP) ≥ 65 mm Hg. Patients may require large volumes (30–60 mL/kg or more) in the first hour.
• Vasopressor Selection: Epinephrine is the first-line vasopressor due to its potent alpha-1 (vasoconstriction) and beta-1 (inotropic/chronotropic) effects.

Special Considerations

For patients on beta-blockers who may have a blunted response to epinephrine, glucagon should be administered (5–10 mg IV push, followed by an infusion of 1–5 mg/h). Glucagon bypasses the beta-receptor to increase intracellular cAMP, restoring inotropy and chronotropy.

II. Prophylactic ICU Measures

Patients with severe hypersensitivity reactions requiring ICU admission are at risk for complications of critical illness. Prophylaxis against venous thromboembolism (VTE) and stress-related mucosal bleeding is standard of care, guided by individual risk factors.

2.1 Infection Control & Antibiotic Stewardship

Strict adherence to infection control bundles, particularly for central venous catheters, is crucial. Prophylactic antibiotics are not indicated for anaphylaxis. If an infection is suspected, obtain cultures before starting empiric, guideline-directed therapy, and de-escalate promptly based on culture results and clinical improvement. The clinical pharmacist plays a key role in dose optimization, renal adjustments, and monitoring for drug interactions.

III. Iatrogenic Complication Management

High-dose corticosteroids, while essential for managing inflammation in severe or biphasic reactions, can cause significant iatrogenic complications. Proactive monitoring and management are necessary to mitigate their adverse effects.

3.1 Steroid-Induced Hyperglycemia

Corticosteroids increase hepatic gluconeogenesis and induce insulin resistance, frequently leading to hyperglycemia. A proactive insulin regimen is superior to reactive sliding-scale-only approaches.

• Monitoring: Check capillary glucose every 4-6 hours, typically before meals and at bedtime.
• Insulin Regimen: For patients on intermediate-acting steroids (like prednisone), a morning dose of an intermediate-acting insulin (e.g., NPH 0.1–0.15 units/kg) can match the steroid’s glycemic effect. This is supplemented with correctional rapid-acting insulin for any pre-meal elevations. The NPH dose can be adjusted by ±20% daily based on glucose trends.

3.2 Corticosteroid-Related Myopathy

Critical illness myopathy is exacerbated by high-dose corticosteroids. It presents as diffuse, symmetric, proximal muscle weakness, particularly affecting the shoulders and hips. Patients may report difficulty lifting their arms or rising from a chair.

• Diagnosis: The diagnosis is primarily clinical. Creatine kinase (CK) levels are often normal, distinguishing it from other myopathies like rhabdomyolysis.
• Management: The cornerstone of management is to taper steroids as quickly as the underlying condition allows. Early physical and occupational therapy is vital to preserve muscle function and facilitate recovery. Anabolic agents are not proven to be effective.

IV. Goals of Care & Multidisciplinary Coordination

Severe critical illness necessitates clear communication and shared decision-making. Complex decisions regarding the initiation or withdrawal of invasive support require ethical deliberation among the ICU team, the patient, and their family.

4.1 Ethics and Shared Decision-Making

The primary goal is to align medical interventions with the patient’s values, goals, and prognosis. This involves early and repeated discussions about code status, acceptable quality-of-life thresholds, and the potential burdens versus benefits of continued intensive care.

4.2 Team Communication

Structured, daily interdisciplinary rounds are essential for coordinated care. These rounds should include physicians, nurses, respiratory therapists, pharmacists, and, when appropriate, palliative care specialists. Documenting clear daily goals—such as targets for weaning from ventilation, tapering vasopressors, and advancing nutrition—ensures the entire team is aligned.