Introduction:
Allergic acute coronary syndrome, or Kounis syndrome is the occurrence of chest pain with allergic reaction and accompanied by clinical and laboratory findings of classic angina caused by inflammatory mediators released during the allergic insult. EKG changes often include ST segment elevations in the anterior and inferior leads. The mediators involved include tryptase, histamine, arachidonic acid metabolites and platelet activating factor, which are thought to contribute to one of the three presentations: Type I with vasospasm of otherwise normal coronaries; Type II with plaque rupture in patients with inactive lesions; and Type III with in stent thrombosis in patients with a significant cardiac history. We present a patient who had intraoperative hemodynamic collapse likely secondary to anaphylaxis (however without classic respiratory or cutaneous manifestations) with ST elevations and cardiac catheterization showing residual spasm concerning for allergic acute coronary syndrome.
Case Description:
A 55 year old man with a past medical history notable for bladder cancer status post surgical resection, chemotherapy and radiation, hydronephrosis, nephrolithiasis and mild obstructive sleep apnea with a history of anaphylaxis to vecuronium who was scheduled for cystoscopy and nephrolithotomy. The patient was given midazolam as premedication, induced with lidocaine, propofol and fentanyl (no muscle relaxant was used) and intubated uneventfully. Post induction hemodynamics were treated with ephedrine, phenylephrine and glycopyrrolate. He was given cefazolin for surgical prophylaxis. Soon after procedure start, the patient had an acute drop in end tidal CO2, became tachycardic and hypotensive. While blood pressure was being supported he lost pulses and developed marked tombstone ST elevations. ACLS was initiated per PEA protocol. He went into ventricular tachycardia and was defibrillated. Soon after he had ROSC after 13 minutes of ACLS.
He was taken to the cardiac catheterization lab which showed clean coronaries and mild spasm in his right coronary artery. CT scan was completed which was negative for pulmonary embolism. He was taken to the ICU intubated and on vasopressors for hemodynamic support. Tryptase was drawn which was markedly elevated, suggesting likely anaphylaxis to one of the agents given in the OR.
Discussion:
Severe intraoperative anaphylaxis is a rare occurrence, and when it does occur, diagnosis can be difficult. Intraoperative agents most likely to cause reactions include muscle relaxants, antibiotics and latex. Anaphylaxis can present with hemodynamic collapse alone, but more commonly alongside cutaneous or respiratory manifestations. When hemodynamic collapse is associated with signs and symptoms of acute coronary syndrome such as ST segment elevation, and angiographic evidence of vasospasm, one should consider allergic acute coronary syndrome as the etiology, a rare presentation of anaphylaxis with specific cardiac findings.
