Propofol infusion syndrome complicated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes: a case report.
MELAS syndrome
mitochondrial disease
propofol
propofol infusion syndrome
status epilepticus
Journal
Acute medicine & surgery
ISSN: 2052-8817
Titre abrégé: Acute Med Surg
Pays: United States
ID NLM: 101635464
Informations de publication
Date de publication:
Historique:
received:
24
07
2019
revised:
23
10
2019
accepted:
10
11
2019
entrez:
29
1
2020
pubmed:
29
1
2020
medline:
29
1
2020
Statut:
epublish
Résumé
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. 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. 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.
Sections du résumé
BACKGROUND
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
METHODS
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
CONCLUSIONS
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.
Identifiants
pubmed: 31988785
doi: 10.1002/ams2.473
pii: AMS2473
pmc: PMC6971469
doi:
Types de publication
Case Reports
Langues
eng
Pagination
e473Informations de copyright
© 2019 The Authors. Acute Medicine & Surgery published by John Wiley & Sons Australia, Ltd on behalf of Japanese Association for Acute Medicine.
Déclaration de conflit d'intérêts
Approval of the research protocol: N/A. Informed consent: Informed consent was obtained from the patient and patient’s family for publication of this case report and accompanying images. Registry and the registration no. of the study/trial: N/A. Animal studies: N/A. Conflict of interest: None.
Références
Crit Care Res Pract. 2015;2015:260385
pubmed: 25954513
Lancet. 2001 Feb 24;357(9256):606-7
pubmed: 11558490
Ann N Y Acad Sci. 2008 Oct;1142:133-58
pubmed: 18990125
Anesthesiology. 2015 Feb;122(2):343-52
pubmed: 25296107
Epilepsia. 2004 Jul;45(7):757-63
pubmed: 15230698
Int J Biochem Cell Biol. 2014 May;50:60-3
pubmed: 24534273
Br J Anaesth. 2019 Apr;122(4):448-459
pubmed: 30857601
Neurology. 2013 Aug 20;81(8):770-1
pubmed: 23873972
J Child Neurol. 2014 Aug;29(8):NP40-6
pubmed: 24026895
Int J Biochem Cell Biol. 2014 Mar;48:85-91
pubmed: 24412347