Role of vasopressin in the treatment of anaphylactic shock in a child undergoing surgery for congenital heart disease: a case report

We describe the case of a child who was undergoing surgery for ventricular septal defect, with an anaphylactic reaction to heparin that was refractory to epinephrine infusion and was effectively treated by low dose vasopressin infusion.In case of anaphylactic shock, continuous infusion of low-dose vasopressin might be considered after inadequate response to epinephrine, fluid resuscitation and corticosteroid administration.The incidence of anaphylactic reactions during anesthesia is between 1:5000 and 1:25000 and it is one of the few causes of mortality directly related to general anesthesia [1]. The most important requirements in the treatment of this clinical condition are early diagnosis and maintenance of vital organ perfusion. Epinephrine administration is generally considered as the first line treatment of anaphylactic reactions [1]. However, recently, new pharmacological approaches have been described in the treatment of different forms of vasoplegic shock [2]. We describe a case in which low dose vasopressin promply re-established hemodynamic stability in a vasoplegic state due to an anaphylactic reaction that was refractory to epinephrine infusion.A 6-year-old 18 kg male with a ventricular septal defect and history of asthma was scheduled for surgical correction. The patient had never undergone general anesthesia and had a past medical history of bronchial asthma treated with inhaled salbutamol. General anesthesia was induced with 0.2 mg/kg of midazolam, 0.2 mg/kg cisatracurium besylate and 0.5 mcg/kg remifentanil. Intravenous general anesthesia was maintained with continuous infusion of remifentanil (0.25–0.5 mcg/kg/min), cisatracurium besylate (0.2 mg/kg/hr) and midazolam (0.2 mg/kg/hr). Continuous monitoring included electrocardiogram, invasive systemic arterial pressure (SAP) and central venous pressure (CVP), transcutaneous arterial oxygen saturation (SatO2), end tidal CO2 (Et CO2), cerebral saturation detected by near infrared spectroscopy monitoring