Ann Thorac Surg 2009;87:e1-e3. doi:10.1016/j.athoracsur.2008.07.055
© 2009 The Society of Thoracic Surgeons
Case Reports
Propofol Infusion Syndrome in Adult Cardiac Surgery
Mohammed Iyoob Mohammed Ilyas, MS, MRCSa,*,
Lognathen Balacumaraswami, FRCSa,
Christopher Palin, FRCAb,
Chandi Ratnatunga, FRCSa
a Department of Cardiothoracic Surgery, John Radcliffe Hospital, Oxford, United Kingdom
b Nuffield Department of Anesthesia, John Radcliffe Hospital, Oxford, United Kingdom
Accepted for publication July 9, 2008.
* Address correspondence to Dr Ilyas, Department of Cardiothoracic Surgery, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, United Kingdom (Email: driyoob{at}yahoo.com).
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Abstract
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We report a case of rapid and progressive severe metabolic acidosis in the postoperative period after coronary artery bypass grafting. After exclusion of potential causes for this phenomenon, it was attributed to perioperative intravenous propofol infusion causing propofol infusion syndrome. We discontinued this intravenous agent resulting in a prompt and considerable improvement in the lactic acidosis and clinical condition in the subsequent 6 hours resulting in an uneventful recovery and hospital discharge.
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Introduction
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Severe perioperative metabolic acidosis if not corrected promptly is associated with significant morbidity and mortality.
We present a case of unexplained severe lactic acidosis in the postoperative period after coronary artery bypass grafting (CABG) using cardiopulmonary bypass in a 67-year-old man weighing 76 kg. He had severe three-vessel disease and moderate left ventricular impairment with long-term, rate-controlled atrial fibrillation. His preoperative medications included digoxin for atrial fibrillation, prednisolone for asthma, verapamil, bisoprolol, ramipril, anti platelet agents, and nitrates.
General anesthesia was induced with midazolam, fentanyl, thiopentone, and vecuronium. Pre-cardiopulmonary bypass arterial blood gas analysis demonstrated serum lactate of 2.1 mmol/L and base excess of 3.6. Anesthesia was maintained initially with isoflurane and propofol infusion at an initial dose of 0.8 mg/kg/hr (60mg/hour), which increased to 5.2 mg/kg/hr (400 mg/hour) during cardiopulmonary bypass. The bypass was primed with 1,500 mL of Hartmann's solution and the patient was cooled to 32°C during bypass. Coronary artery bypass grafting was performed using left internal mammary artery to left anterior descending artery and three saphenous venous grafts to intermediate artery, first and second obtuse marginal arteries with 79 minutes of cardiopulmonary bypass, and a total of 33 minutes of aortic cross-clamp time using intermittent cross clamp and fibrillation technique. Intraoperative arterial blood gas monitoring showed progressively worsening metabolic acidosis (Table 1). He was separated from cardiopulmonary bypass with epinephrine 0.06 mcg/kg/min due to the presence of preoperative moderate left ventricular dysfunction. Propofol infusion was discontinued after sternotomy closure to facilitate fast track extubation. However, metabolic acidosis continued to deteriorate, and propofol infusion was re-started to allow further mechanical ventilation. His metabolic measurements continued to worsen to a serum lactate of 13.3 mmol/L and –12.3 of base excess. The inotropic support remained with epinephrine 0.06 mcg/kg/min and serum glucose level was maintained within acceptable range by continuous human actrapid infusion. Clinical examination was unremarkable with well-perfused extremities and good urinary output. There were no new electrocardiographic abnormalities and a transesophageal echocardiogram showed mild left ventricular dysfunction with no new regional wall motion abnormalities. A pulmonary artery catheter was inserted for continuous cardiac output monitoring and the cardiac index was measured at 3.7 L/min/m2 by thermodilution.
His urine became weakly positive for myoglobin and hemoglobin, and was negative for ketones. His serum creatine kinase levels were elevated to 260 mmol/L, with predominant skeletal muscle expressed fraction of creatine kinase (CK-MM) on isoenzyme electrophoresis. His troponin levels and liver enzymes were within the normal limits. His renal function tests were normal preoperatively and showed no significant changes in the entire postoperative period.
In view of the worsening metabolic measurements, without any obvious explanation, propofol infusion syndrome was suspected, and a decision was made to discontinue the drug. Morphine and midazolam infusions were commenced and the epinephrine infusion remained at the same rate. In the absence of any further intervention, there was a remarkable improvement in his metabolic measurements within 6 hours as seen in Table 1. He progressed with uncomplicated recovery and was eventually discharged from the hospital after 5 days (Fig 1).
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Comment
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Propofol is a commonly used short-acting intravenous anesthetic agent to induce and maintain general anesthesia in cardiac and general surgery. It is also used in intensive care units to facilitate mechanical ventilation in adults and pediatric patients. It provides a smooth and rapid recovery of consciousness making it suitable for both short-term and long-term sedation, as well as general anesthesia.
Propofol infusion syndrome has been described as a potentially fatal complication in the pediatric population on long-term, high-dose propofol infusion [1, 2]. Recently, this phenomenon has also been reported in adults on short-term, high-dose propofol infusion [3]. It may present with varied complications, such as severe metabolic acidosis, rhabdomyolysis, myoglobinuria, and cardiac arrhythmias. When unrecognized, this may lead to an inexorable decline resulting in cardiac failure, renal failure, and death [4, 5]. The principal clinical presentation associated with most reported cases is severe and progressive unexplained metabolic acidosis. Catecholamine infusions and steroids, when combined with propofol, may act as trigger factors for this syndrome. It is interesting to note that our patient was on regular steroids preoperatively for asthma, and had inotropic infusions during the perioperative period. The underlying pathophysiology is unknown, but genetic predisposition, mitochondrial inhibition, and increases in serum free fatty acids are believed to play a role [6].
In our patient, despite exclusion of potential causes of progressively worsening acidosis in the perioperative period, we were unable to identify a definitive reason for this clinical presentation after uneventful coronary artery bypass grafting. Although we instituted measures aimed at supporting cardiac function and improving organ perfusion, we failed to impede the progressive decline in the metabolic status. Hence, we considered the possibility of propofol infusion syndrome and promptly discontinued propofol. This resulted in a dramatic improvement in the metabolic acidosis and an uneventful postoperative course.
In the postoperative cardiac surgical environment, severe and progressively worsening lactic acidosis is of serious concern. Propofol infusion syndrome, although rare, can be potentially fatal. Early identification of this possible complication is critical to prevent progressive clinical deterioration and potential cardiac mortality.
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References
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- Bray BA. Propofol infusion syndrome in children Paediatr Anaesth 2004;14:435-438.[Medline]
- Kam PCA, Cardone D. Propofol infusion syndrome Anaesthesia 2007;62:690-701.[Medline]
- Liolios A, Guérit JM, Scholtes JL, Raftopoulos C, Hantson P. Propofol infusion syndrome associated with short-term large-dose infusion during surgical anesthesia in an adult Anesth Analg 2005;100:1804-1806.[Abstract/Free Full Text]
- Ernest D, French C. Propofol infusion syndrome—report of an adult fatality Anaesth Intensive Care 2003;31:316-319.[Medline]
- Trampitsch E, Oher M, Pointner I, Likar R, Jost R, Schalk HV. Propofol infusion syndrome Anaesthesist 2006;55:1166-1168.[Medline]
- Wolf A, Weir P, Segar P, Stone J, Shield J. Impaired fatty acid oxidation in propofol infusion syndrome Lancet 2001;357:606-607.[Medline]
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Abstract
Introduction
