Collapse After Rocuronium and Cefazolin: Anaphylaxis Under General Anesthesia
A 42-year-old woman (BMI 32, no known allergies) is undergoing elective laparoscopic cholecystectomy under general anesthesia. After preoxygenation, fentanyl 100 µg, propofol 180 mg, and rocuronium 50 mg, the trachea is intubated easily. Five minutes after cefazolin 2 g and rocuronium, while the abdomen is being prepped, blood pressure falls from 118/70 to 62/34 mmHg, heart rate rises from 72 to 132/min, and SpO2 falls to 88% despite FiO2 1.0. Peak airway pressure increases from 18 to 38 cmH2O, expiratory wheeze is audible, and a diffuse urticarial rash appears on the abdomen. EtCO2 is 22 mmHg. The surgeon has not made an incision. One liter of crystalloid has been infused, and the resident has given 100 µg phenylephrine with only transient improvement.
1. Outline your immediate management and the differential diagnosis you are considering. Explain how you would distinguish anaphylaxis from the alternatives at the bedside.
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This is a perioperative crisis with hypotension, bronchospasm, high airway pressures, and skin changes after two likely triggers. I would call for help, stop the cefazolin infusion and any other potential trigger, deliver 100% oxygen, confirm the endotracheal tube is patent and not displaced, and give epinephrine 50–100 µg IV immediately, repeated every 1–2 minutes as needed. I would give rapid crystalloid boluses, keep the patient supine with legs elevated, remove surgical drapes, and start an epinephrine infusion early if repeated boluses are required.
The differential includes anaphylaxis, severe bronchospasm from another cause, tension pneumothorax, pulmonary embolism, aspiration, acute left ventricular failure, and a vasovagal reaction. Anaphylaxis is most likely because the reaction began within minutes of rocuronium and cefazolin and involves skin, airway, and circulation together. Tension pneumothorax would produce unilateral absent breath sounds, tracheal deviation, and often a more abrupt rise in airway pressure without urticaria. Pulmonary embolism causes sudden hypoxemia and hypotension with a low EtCO2 but no rash or wheeze. Aspiration may cause hypoxemia and high airway pressures but not immediate generalized urticaria. Bronchospasm alone does not explain the rash and profound vasodilation. The presence of urticaria plus multi-organ involvement strongly favors anaphylaxis and justifies immediate epinephrine rather than waiting for confirmation.
2. The patient remains hypotensive after two 50 µg epinephrine boluses. Discuss the next steps, including vasopressor choice, fluid strategy, and the role of sugammadex and tryptase testing.
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I would start a continuous epinephrine infusion at approximately 0.05–0.2 µg/kg/min and titrate to blood pressure, because epinephrine is the only drug that treats both vasodilation and bronchospasm. I would continue rapid but monitored crystalloid resuscitation, reassessing for pulmonary edema and response to fluids rather than giving an arbitrary fixed volume. If hypotension persists despite epinephrine, I would add a vasopressin bolus of 1–2 units followed by an infusion of 2–4 units/hour; vasopressin is useful in refractory vasodilatory shock because it acts through V1 receptors and does not rely on catecholamine responsiveness. I would avoid relying on phenylephrine alone because it lacks beta-2 bronchodilator activity. Hydrocortisone and antihistamines are adjuncts, not first-line treatment.
Sugammadex should not be used as a treatment for anaphylaxis. It binds rocuronium and has been reported to improve some cases, but it does not reliably treat the established reaction, may itself cause anaphylaxis, and must not delay epinephrine. If rocuronium is strongly suspected, the antigen load can be reduced by allowing the drug to clear, but sugammadex is not standard rescue therapy. For tryptase, I would draw a sample as soon as possible after resuscitation and a second sample 4–6 hours later, because tryptase peaks within 1–2 hours and may normalize by 6 hours. Later allergy testing to rocuronium and cefazolin should be arranged before any future exposure.
3. While the epinephrine infusion is being prepared, the patient becomes asystolic. Outline the modifications to standard resuscitation in this setting.
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I would start high-quality chest compressions immediately, ventilate with 100% oxygen, and give standard adult cardiac arrest doses of epinephrine 1 mg every 3–5 minutes. In anaphylactic arrest, the same ACLS algorithm applies, but resuscitation often requires large volumes of fluid and may be prolonged. I would continue the epinephrine infusion after return of spontaneous circulation and avoid abruptly stopping it, because recurrent vasodilation and recurrent anaphylaxis can occur. I would also give rapid crystalloid boluses, consider sodium bicarbonate only for prolonged arrest, and look for reversible causes such as tension pneumothorax or tube dislodgement.
If return of spontaneous circulation is not achieved after 30–45 minutes of good-quality CPR, extracorporeal membrane oxygenation should be considered if the institution has that capability, because anaphylactic arrest can be reversible with adequate support. After resuscitation, the patient needs ICU admission, continuous vasopressor support, serial tryptase samples, and allergy follow-up. The key judgement is not to abandon resuscitation early in a previously healthy young patient with a reversible cause, and not to omit epinephrine because of fear of tachycardia; in arrest, epinephrine is standard and necessary.