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Departements of *Anaesthesia and Intensive Care,
Pediatric Nephrology, and
Urology, University Hospital Münster, Münster, Germany
Address correspondence and reprint requests to Alexander Reich, MD, DEAA, Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Münster, Albert Schweitzer-Str. 33, D-48129 Münster, Germany. Address e-mail to reich{at}anit.uni-muenster.de
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Abstract |
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IMPLICATIONS: Sevoflurane is a frequently used inhaled anesthetic in pediatric anesthesia and is regarded as a drug with low organ toxicity. This case report demonstrates a possible connection of the use of this drug and hepatic injury.
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Introduction |
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Case Report |
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The patient had an increased serum creatinine level (194 µmol/L) and a borderline serum calcium concentration of 2.8 mmol/L; all other laboratory values were found to be within normal ranges. Liver function tests and hepatic size were normal before surgery.
General anesthesia was induced with thiopentone 5 mg/kg IV and fentanyl 10 µg/kg IV, and rocuronium bromide was administered to facilitate endotracheal intubation. Anesthesia was maintained by the administration of sevoflurane in end-tidal concentrations of 1.8–2.2 vol% with a mixture of oxygen and air (fraction of inspired oxygen, 0.4) and a fresh gas flow of 0.8 L/min.
Throughout the entire surgical procedure, all vital variables were within normal ranges (heart rate, arterial blood pressure, temperature, and peripheral oxygen saturation), and no significant blood loss was observed. At the end of the operation, the child was tracheally extubated. After a short stay in the recovery room, the patient was transferred to the regular ward.
Two days after surgery, hepatomegaly was diagnosed by physical examination. A considerable increase in liver enzymes (aminoalanine transferase (ALT) from 5 to 543 IU/L, aminoaspartate transferase (AST) from 5 to 683 IU/L, and lactate dehydrogenase from 179 to 960 IU/L) was observed (Fig. 1).
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Two weeks after surgery, a second elective nephroureterostomia was performed on the contralateral side. General anesthesia was induced and maintained with fentanyl 8 µg/kg IV and a total dose of 0.4 mg/kg midazolam IV, supplemented by a caudal anesthesia with 9 mL of ropivacaine 0.2%. The second operation also went smoothly, and the child was tracheally extubated at the end of the operation. Both operations lasted 2.5 h each. Postoperatively no pathologic changes in liver function or size were found.
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Discussion |
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Trifluoroacetyl chloride can induce an immunological response that eventually leads to hepatic injury in susceptible patients (3). This hepatotoxic potential seems to be related to the extent of metabolic bioactivation to reactive metabolites that bind covalently to hepatic proteins (3).
Compound A, a substance formed after contact of sevoflurane with alkaline CO2 absorbent, is considered to be nephrotoxic. Eger et al. (4) postulated a mild hepatotoxicity of Compound A that has not been reproduced in other studies (5). Despite this controversial issue, a significant increase of Compound A levels in our case seems unlikely because of the use of Amsorb® (Armstrong Medical, Coleraine, Northern Ireland). This type of CO2 absorbent is not capable of producing significant levels of Compound A (6).
Sevoflurane may induce a mild hepatic injury 3–30 days after exposure as shown by a transient increase in ALT and AST (7–9). We observed a peak in injury after two days. Although there have been several reports of hepatic injury after anesthesia with sevoflurane, no causal connection has been suggested apart from a possible predisposition from the administration of other drugs known to be hepatotoxic (e.g., acetaminophen) (10,11).
Acetaminophen 15 mg/kg was given four times daily on the first two postoperative days, coinciding with the peak increase in liver enzymes. The increase subsided with cessation of acetaminophen administration. In the second case, the same amount of acetaminophen was administered during the first two postoperative days. However, it seems unlikely that acetaminophen caused the hepatic injury, because the total dose (60 mg/kg) was far less than the recommended upper daily limit.
PH 1, an inborn error of metabolism, is characterized by an isolated enzyme deficiency of alanine glyoxalate aminotransferase of the liver. Because of this genetically determined defect, glyoxalate is converted to oxalate and glycolate, which can be found in all organs but especially in the kidneys, retina, and skeletal organs. The course of the disease eventually results in renal failure and systemic oxalosis and, thus, will require combined hepatic and renal transplantation at a later stage (12,13). Although a metabolic defect is present, there are no reported toxic interactions between anesthesia and PH 1. In our case, with the administration of sevoflurane during the first operation, temporary liver injury was observed.
In summary, we report a patient who had PH 1 and developed hepatic injury after anesthesia with sevoflurane, but not after a subsequent anesthesia that avoided sevoflurane. Nothing in this patient’s disease or the conduct of the anesthesia would suggest a cause for the injury other than an idiosyncratic response to sevoflurane.
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This article has been cited by other articles:
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  A. Lehmann, M. Neher, A.-H. Kiessling, F. Isgro, A. Koloska, and J. Boldt Case report: Fatal hepatic failure after aortic valve replacement and sevoflurane exposure: [Presentation de cas : Insuffisance hepatique fatale apres un remplacement de la valve aortique et une exposition au sevoflurane] Can J Anesth, November 1, 2007; 54(11): 917 - 921. [Abstract] [Full Text] [PDF]
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 E. Turillazzi, S. D'Errico, M. Neri, I. Riezzo, and V. Fineschi A Fatal Case of Fulminant Hepatic Necrosis Following Sevoflurane Anesthesia Toxicol Pathol, October 1, 2007; 35(6): 780 - 785. [Abstract] [Full Text] [PDF]
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-glutamyl transferase; LDH = lactate dehydrogenase.
