PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Propofol Related Infusion Syndrome: Ultrastructural Evidence for a Mitochondrial Disorder.

Abstract The objective of this report of a fatal propofol-related infusion syndrome in a young adult was to present-to our knowledge for the first time-direct ultrastructural evidence for the central role of mitochondrial damage in the pathogenesis of this syndrome.
PMID
Related Publications

Propofol infusion syndrome in a super morbidly obese patient (BMI = 75).

Propofol Is Mitochondrion-Toxic and May Unmask a Mitochondrial Disorder.

Propofol infusion syndrome.

Impaired fatty acid oxidation in propofol infusion syndrome.

The syndrome of irreversible acidosis after prolonged propofol infusion.

Authors

Mayor MeshTerms
Keywords
Journal Title critical care medicine
Publication Year Start




PMID- 29252954
OWN - NLM
STAT- In-Process
LR  - 20171218
IS  - 1530-0293 (Electronic)
IS  - 0090-3493 (Linking)
VI  - 46
IP  - 1
DP  - 2018 Jan
TI  - Propofol Related Infusion Syndrome: Ultrastructural Evidence for a Mitochondrial 
      Disorder.
PG  - e91-e94
LID - 10.1097/CCM.0000000000002802 [doi]
AB  - OBJECTIVE: The objective of this report of a fatal propofol-related infusion
      syndrome in a young adult was to present-to our knowledge for the first
      time-direct ultrastructural evidence for the central role of mitochondrial damage
      in the pathogenesis of this syndrome. DATA SOURCES: Histological and electron
      microscopical analysis of liver, skeletal, and heart muscle obtained by autopsy
      and blood obtained from patient. STUDY SELECTION: Case report. DATA EXTRACTION:
      In addition to conventional macroscopical and histological investigations,
      electron-microscopical analysis of myocardial- and skeletal muscle and liver
      tissue obtained at autopsy from a young man was performed in order to search for 
      ultrastructural changes of mitochondria. Acylcarnitine concentrations of his
      blood were determined by ultra-high performance liquid chromatography mass
      spectrometry. DATA SYNTHESIS: A 19-year-old male was admitted with acute
      left-side hemiparesis. The patient was intubated, then propofol infusion started,
      and a craniotomy was performed to remove an intracerebral hematoma. In the
      postoperative period, the patient presented with elevated intracranial pressure
      and brain edema. After repeat surgery, the patient showed impaired systolic left 
      ventricular function, increasing fever, anuria, hyperkalemia, and metabolic
      acidosis, and he finally expired. Electron microscopy revealed dark, electron
      dense amorphous structures associated with mitochondria in heart muscle and liver
      tissue obtained at autopsy. Peripheral blood analysis revealed increased levels
      of acetyl-, propionyl-, butyryl-, malonyl-, and valeryl-carnitine as an indicator
      for propofol-related infusion syndrome, as well as for propofol-mediated
      inhibition of free fatty acid uptake into mitochondria, affecting beta-oxidation.
      CONCLUSIONS: Electron dense bodies found in association with mitochondria in
      muscle and liver cells probably correspond to accumulation of free fatty acid
      provide direct morphological evidence for the mitochondrial damage in
      propofol-related infusion syndrome.
FAU - Vollmer, Jorg-Peter
AU  - Vollmer JP
AD  - Institute of Anaesthesiology, Klinikum Stuttgart, Germany.
FAU - Haen, Susanne
AU  - Haen S
AD  - Institute of Pathology and Neuropathology, University of Tubingen, Germany.
FAU - Wolburg, Hartwig
AU  - Wolburg H
AD  - Institute of Pathology and Neuropathology, University of Tubingen, Germany.
FAU - Lehmann, Rainer
AU  - Lehmann R
AD  - Clinical Chemical Central Laboratory, University of Tubingen, Germany.
FAU - Steiner, Jochen
AU  - Steiner J
AD  - Department of Neurosurgery, University Hospital of Tubingen, Germany.
FAU - Reddersen, Silke
AU  - Reddersen S
AD  - Department of Neurosurgery, University Hospital of Tubingen, Germany.
FAU - Fend, Falko
AU  - Fend F
AD  - Institute of Pathology and Neuropathology, University of Tubingen, Germany.
FAU - Fallier-Becker, Petra
AU  - Fallier-Becker P
AD  - Institute of Pathology and Neuropathology, University of Tubingen, Germany.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Crit Care Med
JT  - Critical care medicine
JID - 0355501
EDAT- 2017/12/19 06:00
MHDA- 2017/12/19 06:00
CRDT- 2017/12/19 06:00
PHST- 2017/12/19 06:00 [entrez]
PHST- 2017/12/19 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
AID - 10.1097/CCM.0000000000002802 [doi]
AID - 00003246-201801000-00046 [pii]
PST - ppublish
SO  - Crit Care Med. 2018 Jan;46(1):e91-e94. doi: 10.1097/CCM.0000000000002802.