Anaphylaxis Five Minutes After Cefazolin at Induction

Most likely: IgE-mediated anaphylaxis, with cefazolin the leading culprit given the 5-minute onset after the infusion, though rocuronium is a close second and propofol is possible. The combination of hypotension, tachycardia, bronchospasm, falling EtCO2 (low cardiac output), and rash is the classic grade 3 picture.

Alternatives to exclude:

• Venous air embolism: no insufflation, no open venous source, no central line-unlikely; also rash is not typical.
• Histamine/vancomycin flush: vancomycin was not given; histamine reactions cause erythema and hypotension but usually not severe bronchospasm, and they are rate-related.
• Severe asthma exacerbation: would produce high airway pressures and desaturation first, with hypotension only as a late consequence; rash would be absent.
• Tension pneumothorax: unilateral absent breath sounds, high airway pressure, tracheal shift, no rash.
• Hemorrhage: no surgical source, no insufflation, no distension.
• Propofol or opioid anaphylaxis: possible; the timing and exposure history determine attribution, and all suspected agents must be stopped.

Sequence:

1. Stop all suspected triggers (cefazolin, propofol, rocuronium), call for help, and give 100% oxygen. Abandon surgery.
2. Epinephrine 50 mcg IV boluses (0.05 mg) every 1–2 minutes, titrated to BP and airway pressures; escalate to 100–200 mcg if needed. If no IV access, give 0.5 mg IM into the lateral thigh.
3. Rapid crystalloid 20–30 mL/kg (1–2 L) via a large-bore line and supine position with legs elevated.
4. For refractory hypotension: epinephrine infusion 0.05–0.2 mcg/kg/min, vasopressin 1–2 units, and consider methylene blue 1–2 mg/kg for vasoplegia; glucagon 1–5 mg if the patient is beta-blocked.
5. Inhaled salbutamol and increasing PEEP for bronchospasm; consider magnesium and ketamine.
6. After stabilization: H1 blocker (diphenhydramine 25–50 mg), H2 blocker (famotidine 20 mg), and hydrocortisone 200 mg.

Rationale: epinephrine is the only drug that reverses both the vasodilation and the bronchospasm; small titrated IV boluses avoid severe hypertension in a patient who may have underlying cardiac disease, while IM dosing is the safe default without IV access. Fluids counter the profound capillary leak. Antihistamines and steroids treat skin and late-phase components but do not treat the acute airway or shock.

Case: the procedure is canceled and the patient is transferred to a monitored setting with continuous hemodynamics, capnography, and repeated reassessment, because anaphylaxis can be biphasic in up to 20% of cases. Maintain the epinephrine infusion until stable, then wean while observing.

Documentation and follow-up:

• Record the exact timing and doses of every drug given, the clinical signs, and the treatment response.
• Draw serum tryptase within 1 hour of onset and again at 24 hours to support the diagnosis.
• Provide a written allergy alert, advise a medical alert bracelet, and refer to an allergist for skin testing 4–6 weeks later, when mast cell mediators have normalized.
• Warn that cefazolin and other beta-lactams may cross-react (low but not zero), and that rocuronium cross-reacts with other neuromuscular blockers; the allergist should test both.
• Routine premedication is not a reliable prophylactic strategy for future anesthetics; avoidance of the confirmed trigger is. Sugammadex should be immediately available at any future case if rocuronium is implicated.