Anaphylaxis on the operating table: differentiating and escalating
A 45-year-old woman with no known drug allergies is undergoing elective laparoscopic cholecystectomy under general anaesthesia. Ten minutes after induction, and 2 minutes after intravenous cefazolin and skin preparation with chlorhexidine, her blood pressure falls from 118/70 to 68/34 mmHg, heart rate rises from 72 to 132/min, and peak airway pressure increases from 22 to 38 cmH2O. SpO2 falls to 86% despite FiO2 1.0. There is a diffuse erythematous rash on the trunk and urticaria on the arms. End-tidal CO2 is 2.8 kPa. The surgeon asks whether this could be light anaesthesia or a pneumoperitoneum-related problem. She takes ramipril for hypertension and had an uneventful anaesthetic 5 years ago.
1. How do you distinguish the likely cause from the alternatives, and what are your immediate actions?
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This is anaphylaxis until proved otherwise. The combination of sudden hypotension, tachycardia, a marked rise in airway pressure, desaturation and urticaria, occurring minutes after antibiotics and chlorhexidine, is typical. The timing implicates cefazolin, chlorhexidine or a neuromuscular blocker; chlorhexidine is a notorious cause and can sensitise after previous exposure. Light anaesthesia can cause hypertension and tachycardia but not urticaria or a rising airway pressure. Pneumoperitoneum raises airway pressure and can reduce venous return, but does not explain the rash or the severity of the cardiovascular collapse. Malignant hyperthermia is not plausible here, and local anaesthetic toxicity does not fit.
Immediate actions: call for help, stop all likely triggers including the cefazolin infusion and chlorhexidine preparation, give 100% oxygen, and lie the patient flat with legs elevated. Give adrenaline 50 µg intravenously (0.5 mL of 1:10,000) and repeat every 1–2 minutes as needed, while starting rapid crystalloid boluses of 500–1000 mL. Stop the pneumoperitoneum if it is compromising venous return. Give a beta-2 agonist through the circuit for bronchospasm. Antihistamines and steroids are adjuncts only after the patient is stabilised and must not delay adrenaline. Note that she takes ramipril, which is associated with more refractory hypotension.
2. The blood pressure remains 70/40 mmHg after three boluses of adrenaline and 2 litres of crystalloid. What next?
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I would start a continuous adrenaline infusion, typically 0.05–0.2 µg/kg/min and titrated to effect, rather than repeated boluses alone, and secure additional large-bore access. There is a risk of adrenaline-induced tachyarrhythmia and myocardial ischaemia, so continuous cardiac monitoring and frequent blood gas and electrolyte checks are needed. The airway should be rechecked, and the pneumoperitoneum released.
Add a vasopressin bolus of 1–2 units followed by an infusion, which acts through a different receptor and is particularly useful in catecholamine-resistant anaphylaxis, especially in a patient taking an ACE inhibitor. If there is severe refractory bronchospasm, consider magnesium and nebulised adrenaline. Glucagon may be considered if the patient were beta-blocked, but that is not the case here. Hydrocortisone is reasonable as an adjunct. Methylene blue has been used in refractory vasoplegia but is a rescue therapy, not a routine step.
If perfusion does not improve despite these measures, consider that the diagnosis may be wrong or incomplete: look for pneumothorax, cardiac tamponade, haemorrhage or sepsis, and use echocardiography. Escalate early to a second senior anaesthetist and intensive care; extracorporeal support has been used in refractory cases. Do not send the patient to recovery until the haemodynamics are stable and the airway is secure.
3. What investigations and follow-up would you arrange after the event?
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The diagnosis should be confirmed and the culprit identified, because future exposure could be fatal. Serial serum mast cell tryptase samples are the key test: an acute sample as soon as feasible after resuscitation, a second at 2–4 hours, and a baseline sample at least 24 hours later. A rise above the baseline supports mast cell activation, although a normal result does not exclude anaphylaxis, particularly in severe or rapidly treated cases. Blood should also be sent for routine investigations, and a sample stored for later specific testing if local arrangements allow.
Document the timing and dose of every drug given, including chlorhexidine skin preparation and any dyes or latex exposure, and record the clinical features and treatment. Refer to an allergy clinic for skin prick testing and specific IgE, usually 4–6 weeks after the event. Advise the patient to avoid the suspected agents in the meantime and provide a written record and an emergency plan. Report the reaction through the national pharmacovigilance system and inform the patient's general practitioner.
Debrief the theatre team, review whether the response followed the anaphylaxis algorithm, and check that adrenaline, airway equipment and a printed protocol are immediately available in every anaesthetic room.