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* From the Departments of Anesthesiology, and
Heart Surgery, Montreal Heart Institute, Montreal, Quebec, Canada.
Address correspondence to: Dr. André Y. Denault, Department of Anesthesiology, Montreal Heart Institute, 5000 Belanger Street East, Montreal, Quebec H1T 1C8, Canada. Phone: 514-376-3330, ext. 3709; Fax: 514-376-8784; E-mail: denault{at}videotron.ca
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Clinical features: A 57-yr-old female patient underwent repeat cardiac surgery to treat prosthetic valve endocarditis. She had received aprotinin during her first surgery 60 days ago. Despite a negative test dose of iv aprotinin 20,000 KIU, when aprotinin loading was initiated during the repeat surgery, the patient developed bronchospasm and hypotension secondary to acute distributive shock. Bronchospasm responded to inhaled salbutamol and ipatropium. The hypotension was refractory to high doses of phenylephrine. Two doses of iv vasopressin 5 U reversed the vasodilation and reestablished normal blood pressure.
Conclusion: Vasopressin, in association with alpha-agonists, can reverse acute refractory distributive shock following aprotinin administration.
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Two months later, the patient presented to the emergency room with chills and an altered level of consciousness. The patient was disoriented, stuporous, but arousable. She was tachycardic and had a temperature of 39°C without signs of meningismus or focal neurological findings. Laboratory tests revealed leukocytosis and acute azotemia with a serum creatinine of 221 µmol•L-1. Cranial computerized tomography showed two small hypodensities compatible with embolic cerebral infarcts in the territories of each middle cerebral artery. Transesophageal echocardiography demonstrated a large vegetation on the mitral valve prosthesis, for which an emergency repeat cardiac surgery was scheduled. The patient was rehydrated, started on iv heparin, and treated with vancomycin, rifampin and gentamicin. Eight of ten blood cultures were eventually positive for Staphylococcus epidermidis.
The patient was premedicated with morphine 7.5 mg im and also received allopurinol 300 mg po twice prior to the surgery. On arrival in the operating room, blood pressure (BP) measured from a radial arterial line was 110/70 mmHg, heart rate (HR) was 85 beats•min-1, and oxygen saturation was 100%. General anesthesia was induced uneventfully with iv midazolam 3 mg, sufentanil 80 µg, and pancuronium 10 mg. The trachea was intubated and mechanical ventilation with 100% oxygen was begun. Central venous lines and a pulmonary artery catheter were inserted. Anesthesia was maintained with an infusion of iv midazolam 0.04 mg•kg-1•hr-1, ketamine 0.5 mg•kg-1•hr-1 and sufentanil 1 µg•kg-1•hr-1. As per the preoperative antibiotic administration schedule, iv vancomycin and gentamicin were slowly infused over 30 min. During and following induction of anesthesia, the hemodynamic profile remained stable (Figure
), with a BP of 110/55 mmHg, a pulmonary artery pressure (PAP) of 40/25 mmHg, a central venous pressure (CVP) of 13 mmHg, a cardiac index (CI) of 2.6 L•min-1•m-2 and a systemic vascular resistance index (SVRI) of 24 mmHg•min•m2•L-1.
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Cardiopulmonary bypass was instituted without difficulty. During CPB, a mean arterial pressure between 50 to 80 mmHg was maintained using only small intermittent doses of phenylephrine. At sternotomy, an intense mediastinal inflammation from the previous surgery was noted and the presence of a bivalvular endocarditis with massive vegetations was confirmed. The patient underwent a complex repair of the aortomitral junction with bovine pericardium and combined aortic (Carbomedics 21®, Austin, TX, USA), and mitral (St. Jude 27®, Minneapolis, MN, USA) valve replacement. Duration of CPB was five hours; the patient was successfully weaned from CPB with an iv bolus of milrinone 5 mg and an iv infusion of norepinephrine 0.1 to 0.2 µg•kg-1•min-1. Perioperative transesophageal echocardiography demonstrated an excellent result with no valvular leak and normal left ventricular function. The infusion of norepinephrine was gradually tapered over 24 hr. The patient was extubated the next morning and her postoperative course was uneventful. She was discharged ten days after admission with home iv antibiotic therapy.
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Other medications administered within the hour prior to administration of aprotinin included midazolam, ketamine, sufentanil, pancuronium, vancomycin, and gentamicin. Midazolam, ketamine, and sufentanil infusions were continued throughout the surgery; thus, they were unlikely to be the cause of the hypotension. A reaction to pancuronium was unlikely, since it was re-administered as a 2-mg bolus 30 min after a 0.05-mg test dose without adverse effect. Vancomycin is known to cause hypotension when given rapidly; however, in this case it was administered over 30 min, and several doses of vancomycin and gentamicin were administered postoperatively without hemodynamic compromise.
To our knowledge, this case is the first to report the use of vasopressin in the context of a clinical presentation consistent with anaphylaxis. Vasopressin acts as a non-adrenergic peripheral vasoconstrictor by direct stimulation of smooth muscle vasopressin1 receptors. It produces vasoconstriction in skin, skeletal muscle, intestine and fat, with relatively less constriction of coronary and renal vasculature, and causes a cerebral vasodilatation.11 Vasopressin has been integrated into the Advanced Cardiac Life Support resuscitation guidelines as an alternative pressor agent in the treatment of cardiac arrest.12 Vasopressin has been demonstrated to be effective in the management of catecholamine-resistant hypotension in the context of post-CPB vasodilatory shock1,3,4 and septic shock. Our group has previously reported its effectiveness for treating catecholamine resistant hypotension during CPB.13 A recent laboratory study demonstrated that the addition of vasopressin to epinephrine reverses histamine-induced vasodilation of human internal mammary arteries more completely than either agent alone,14 providing a physiological basis for the use of both types of pressor agents in the context of anaphylaxis.
In this case, vasopressin was administered before epinephrine because the vasodilation responsible for the hypotension was not corrected by large doses of an alpha-adrenergic agonist. Epinephrine would have been the next line of treatment had vasopressin not corrected the patient’s hemodynamics. Administration of vasopressin contributed as a powerful alternative vasopressive mechanism. Also, in the context of septic endocarditis with valvular vegetations, it was hoped that the use of vasopressin would avoid a potentially deleterious epinephrine-induced tachycardia.
In conclusion, we report the case of a patient undergoing cardiac surgery, who presented with bronchospasm and refractory distributive shock following the administration of aprotinin 750,000 KIU. Bronchospasm was successfully treated by inhaled beta-2 agonists but hypotension was refractory to alpha-adrenergic stimulation with high doses of phenylephrine. Systemic vascular resistance, BP, and HR were normalized by a concomitant administration of vasopressin. Based on this report, we suggest that, in association with alpha-agonists, vasopressin may be an effective drug for the treatment of acute distributive shock compatible with the clinical diagnosis of anaphylaxis. The efficacy and safety of vasopressin associated with phenylephrine compared to epinephrine for the treatment of anaphylaxis should be further confirmed through experimental studies followed, if appropriate, by a randomized controlled trial.
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2 Tsuneyoshi I, Yamada H, Kakihana Y, Nakamura M, Nakano Y, Boyle WA 3rd. Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock. Crit Care Med 2001; 29: 487–93.[Medline]
3 Argenziano M, Chen JM, Choudhri AF, et al. Management of vasodilatory shock after cardiac surgery: identification of predisposing factors and use of a novel pressor agent. J Thorac Cardiovasc Surg 1998; 116: 973–80.
4 Morales DL, Gregg D, Helman DN, et al. Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock. Ann Thorac Surg 2000; 69: 102–6.
5 Royston D, Bidstrup BP, Taylor KM, Sapsford RN. Effect of aprotinin on need for blood transfusion after repeat open-heart surgery. Lancet 1987; 2: 1289–91.[Medline]
6 Lemmer JH Jr, Stanford W, Bonney SL, et al. Aprotinin for coronary bypass operations: efficacy, safety, and influence on early saphenous vein graft patency. A multicenter, randomized, double-blind, placebo-controlled study. J Thorac Cardiovasc Surg 1994; 107: 543–51.
7 Levy JH, Pifarre R, Schaff HV, et al. A multicenter, double-blind, placebo-controlled trial of aprotinin for reducing blood loss and the requirement for donor-blood transfusion in patients undergoing repeat coronary artery bypass grafting. Circulation 1995; 92: 2236–44.
8 Dietrich W, Spath P, Ebell A, Richter JA. Prevalence of anaphylactic reactions to aprotinin: analysis of two hundred forty-eight reexposures to aprotinin in heart operations. J Thorac Cardiovasc Surg 1997; 113: 194–201.
9 Diefenbach C, Abel M, Limpers B, et al. Fatal anaphylactic shock after aprotinin reexposure in cardiac surgery. Anesth Analg 1995; 80: 830–1.[Medline]
10 Dietrich W, Spath P, Zuhlsdorf M, et al. Anaphylactic reactions to aprotinin reexposure in cardiac surgery: relation to antiaprotinin immunoglobulin G and E antibodies. Anesthesiology 2001; 95: 64–71.[Medline]
11 Anonymous. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 1: introduction to ACLS 2000: overview of recommended changes in ACLS from the guidelines 2000 conference. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102(8 Suppl): I86–9.[Medline]
12 Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU, Lindner IM, Lurie KG. Vasopressin administration in refractory cardiac arrest. Ann Intern Med 1996; 124: 1061–4.
13 Talbot MP, Tremblay I, Denault AY, Belisle S. Vasopressin for refractory hypotension during cardiopulmonary bypass. J Thorac Cardiovasc Surg 2000; 120: 401–2.
14 Tsuda A, Tanaka KA, Huraux C, et al. The in vitro reversal of histamine-induced vasodilation in the human internal mammary artery. Anesth Analg 2001; 93: 1453–9.
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