Open AccessPropofol infusion syndrome complicated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes: a case report
Author(s) -
Shimizu Junji,
Tabata Takahisa,
Tsujita Yasuyuki,
Yamane Tetsunobu,
Yamamoto Yutaka,
Tsukamoto Takahito,
Ogawa Nobuhiro,
Kim Hyou,
Urushitani Makoto,
Eguchi Yutaka
Publication year - 2019
Publication title -
acute medicine and surgery
Language(s) - English
Resource type - Journals
ISSN - 2052-8817
DOI - 10.1002/ams2.473
Subject(s) - propofol , lactic acidosis , medicine , status epilepticus , encephalopathy , rhabdomyolysis , mitochondrial myopathy , metabolic acidosis , anesthesia , myoclonus , acidosis , metabolic disorder , epilepsy , psychiatry , biochemistry , chemistry , mitochondrial dna , gene
Background Propofol infusion syndrome (PRIS) is a rare but lethal complication of propofol use. It has been suggested that the pathological mechanism of PRIS involves mitochondrial disorder caused by propofol. Case Presentation A 24‐year‐old woman who had been diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes was admitted to our hospital with impaired consciousness and myoclonus. To control the non‐convulsive status epilepticus, propofol was administered. Arterial blood gas revealed metabolic acidosis, and creatinine kinase was elevated. The patient was diagnosed with PRIS. We treated her with interruption of propofol. She required mechanical ventilation for 25 days. After rehabilitation, she recovered and was discharged. Conclusion Mitochondrial disorder is a risk factor for PRIS. It is important for clinicians to be aware that mitochondrial disorder is a risk factor for PRIS, especially under conditions of critical illness and status epilepticus.