Severe hepatotoxicity after sevoflurane anesthesia in a child with mild renal dysfunction

Jang, Young‐Eun; Kim, In-Soo

doi:10.1111/j.1460-9592.2005.01648.x

Cited by 36 publications

(19 citation statements)

References 23 publications

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“…For suspected volatile anaesthetic drug-induced liver injury, a time to onset of reaction of one to 14 days, with gradual evolution over the next 14 days, and gradual resolution were considered consistent based on previous literature (10,11). Scoring was by two independent observers (A. N. and J. L.).…”

Section: Data Collectionmentioning

confidence: 99%

Drug‐induced hepatotoxicity: incidence of abnormal liver function tests consistent with volatile anaesthetic hepatitis in trauma patients

Lin

Moore

Hockey

et al. 2013

Liver International

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Section: Data Collectionmentioning

confidence: 99%

Drug‐induced hepatotoxicity: incidence of abnormal liver function tests consistent with volatile anaesthetic hepatitis in trauma patients

Lin

Moore

Hockey

et al. 2013

Liver International

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“…11 Two to five percent of the administered sevoflurane is metabolized by the cytochrome P-450 system to hexafluoroisopropanol, inorganic flouride and formaldehyde. 11,12 Hexafluoroisopropanol has a low binding affinity to liver proteins and is rapidly gluconurated and eliminated by the kidneys. 12 Kharasch 11 postulated in 1995 that anesthetic metabolism and anesthetic toxicity can no longer be considered synonymous.…”

Section: Discussionmentioning

confidence: 99%

“…11,12 Hexafluoroisopropanol has a low binding affinity to liver proteins and is rapidly gluconurated and eliminated by the kidneys. 12 Kharasch 11 postulated in 1995 that anesthetic metabolism and anesthetic toxicity can no longer be considered synonymous. Martin 2 stated that, theoretically, patients sensitized to other volatile anesthetics could safely be anesthetized with sevoflurane.…”

Section: Discussionmentioning

confidence: 99%

“…He did not, however, recommend the use of sevoflurane in a patient with a history of volatile anesthetic induced hepatitis. 2 There are several reports [12][13][14][15][16][17][18] of sevoflurane induced hepatotoxicity, mostly in children, many of them published in Japanese. Compound A (2-fluoromethoxy-1,1,3,3,3-pentafluoro-1-propene) is produced by the reaction of sevoflurane with carbon dioxide absorbents.…”

Section: Discussionmentioning

confidence: 99%

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Case report: Fatal hepatic failure after aortic valve replacement and sevoflurane exposure

Lehmann

Neher

Kiessling

et al. 2007

Can J Anesth/J Can Anesth

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Purpose: To report a case of lethal hepatotoxicity possibly caused by sevoflurane. Clinical features:A 76-yr-old woman with a history of four previous minor surgical procedures developed acute liver failure after general anesthesia with sevoflurane, sufentanil and propofol for aortic valve replacement. After an uneventful procedure the patient was extubated 4.5 hr after surgery. On the second postoperative day, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased. On the third postoperative day liver failure occurred, ALT peaked at 10504 U·L -1 and AST at 15516 U·L -1 , and coagulopathy with an international normalized ratio of 4.6 developed. Liver transplantation was considered but rejected as a therapeutic option. The patient died three days after the operation in multiple organ failure triggered by hepatic failure. Other possible causes for liver failure were excluded. Conclusions:Sevoflurane hepatitis as a cause for liver failure may be implicated in this patient undergoing valve surgery. Unlike other halogenated anesthetic drugs, sevoflurane is not metabolized to hepatotoxic trifluroacetyl proteins. However, compound A may react with proteins and may be transformed into antigenic material. We suggest that all halogenated anesthetics may be implicated with acute liver injury.

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“…S ir —We thank Drs Khalil and Glorimar for their interest in our case (1). In their case, an 8‐month‐old child weighing 5 kg undergoing esophageal dilation developed acute severe liver failure following anesthesia with sevoflurane.…”

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confidence: 87%

Author's reply

Hyun¹,

Jang²

2006

Pediatric Anesthesia

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SIR IR-With interest we read the recent case report 'Severe Hepatotoxicity after Sevoflurane Anesthesia in a Child with Mild Renal Dysfunction' (1). In our institution, we had a child who developed severe acute liver failure after routine sevoflurane anesthesia from which she recovered. The child was 8-month-old female, trisomy 21, 5 kg scheduled for outpatient esoghageal dilatation. At birth, the child was 34-week gestation, with tracheoesophageal fistula which was surgically repaired. Unfortunately, the child developed secondary esophageal stricture. She had no allergies and was receiving zantac, raglan and poly-visol. Previously, she received several general anesthetics without apparent complications. She was status post-PDA ligation and J tube placement. She had no cardiac, hepatic or renal problems; however, she had a mild degree of developmental delay.On the day of the procedure, the child was NPO and received clear fluids 4 h before anesthesia induction. In the OR, after applying routine monitors, anesthesia was induced via a mask using sevoflurane and oxygen. Propofol, 25 mg i.v. were administered to facilitate orotracheal intubation. At the end of the procedure, the baby was awakened, the tracheal tube was removed, and the child moved to PACU. The child was well and required admission for 23-h observation. That evening the child developed respiratory distress. Later, she appeared listless with notable subcostal and suprasternal retractions that necessitated intubation and ventilation. A chest X-ray that evening demonstrated baseline chronic lung changes.She developed tachycardia and had poor perfusion with a capillary refill of approximately 5-6 s and low-grade fever with no apparent etiology. Blood gas results demonstrated severe metabolic acidosis with normal P a CO 2 and anemia. Normal saline, packed RBC and sodium bicarbonate were administered to correct hypovolemia, metabolic acidosis and anemia.On the second day after surgery, an extreme elevation of liver enzymes were noted, SGOT, 2546 UAEl )1 , SGPT, 2600 UAEl )1 , total bilirubin 34 lmolAEl )1 (2.0 mgAEdl )1 ), direct bilirubin 15.4 lmolAEl )1 (0.9 mgAEdl )1 ) indirect bilirubin 18 lmolAEl )1 (1.1 mgAEdl )1 ). Alkaline phosphate was 283 UAEl )1 . Serologic tests for hepatitis A, B or C were negative. There was no growth on blood cultures at 5 days. An abdominal ultrasound showed that the liver, gall bladder and the bile ducts appeared normal. An upper gastrointestinal X-ray series showed that there was no esophageal leak. With supportive medical care, the liver enzymes decreased gradually to normal levels after 1 week. The child was then discharged from the hospital.Two weeks after hospital discharge, she was rescheduled for esophageal dilation. A second anesthesia team administered the anesthesia. They were unaware of her previous postoperative complication. They administered uneventful general anesthesia using sevoflurane. Postoperatively the child was admitted to the hospital and her liver enzymes were checked on the following postoperative d...

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Severe hepatotoxicity after sevoflurane anesthesia in a child with mild renal dysfunction

Cited by 36 publications

References 23 publications

Drug‐induced hepatotoxicity: incidence of abnormal liver function tests consistent with volatile anaesthetic hepatitis in trauma patients

Drug‐induced hepatotoxicity: incidence of abnormal liver function tests consistent with volatile anaesthetic hepatitis in trauma patients

Case report: Fatal hepatic failure after aortic valve replacement and sevoflurane exposure

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