Metabolic Acidosis due to Propofol Infusion

Farag, Ehab; DeBoer, Glenn; Cohen, Bruce H.; Niezgoda, Julie

doi:10.1097/00000542-200503000-00042

Cited by 36 publications

(20 citation statements)

References 13 publications

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“…Under these conditions, they develop severe rhabdomyolysis, cardiac and hepatic insufficiency associated with hypoglycaemia [45,46]. Steiner et al [47] and Farag et al [48] recommended that propofol should not be used in patients with an inborn error of mitochondrial fatty-acid metabolism (very long chain acyl-coenzyme A dehydrogenase deficiency) because it interfered with fatty-acid oxidation and caused severe metabolic acidosis.…”

Section: Mechanism Of Prismentioning

confidence: 99%

Propofol infusion syndrome

2007

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SummaryThe clinical features of propofol infusion syndrome (PRIS) are acute refractory bradycardia leading to asystole, in the presence of one or more of the following: metabolic acidosis (base deficit > 10 mmol.l−1), rhabdomyolysis, hyperlipidaemia, and enlarged or fatty liver. There is an association between PRIS and propofol infusions at doses higher than 4 mg.kg−1.h−1 for greater than 48 h duration. Sixty‐one patients with PRIS have been recorded in the literature, with deaths in 20 paediatric and 18 adult patients. Seven of these patients (four paediatric and three adult patients) developed PRIS during anaesthesia. It is proposed that the syndrome may be caused by either a direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism mediated by propofol. An early sign of cardiac instability associated with the syndrome is the development of right bundle branch block with convex‐curved (‘coved type’) ST elevation in the right praecordial leads (V1 to V3) of the electrocardiogram. Predisposing factors include young age, severe critical illness of central nervous system or respiratory origin, exogenous catecholamine or glucocorticoid administration, inadequate carbohydrate intake and subclinical mitochondrial disease. Treatment options are limited. Haemodialysis or haemoperfusion with cardiorespiratory support has been the most successful treatment.

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Section: Mechanism Of Prismentioning

confidence: 99%

Propofol infusion syndrome

2007

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“…Bray [35] reported 18 critically ill children who under propofol sedation developed a typical clinical entity of metabolic acidosis, refractory cardiac failure, fever and muscle cell damage. Farag et al [36] reported that even short-term use of propofol in children with mitochondrial disorders may be associated with delayed recovery and the need for ICU admission. They proposed that children who develop metabolic acidosis and myocardial failure after propofol infusion may have subclinical forms of mitochondrial disorders.…”

Section: Mitochondrial Diseasesmentioning

confidence: 99%

Neuromuscular and mitochondrial disorders: what is relevant to the anaesthesiologist?

Driessen

2008

Current Opinion in Anaesthesiology

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“…As shown in table 1, lactate levels were already elevated and increasing within 1 h of induction in our case. It is interesting to note that a proposed mechanism for the propofol-induced acidosis is inhibition of mitochondrial respiration,18 and it has also been suggested that these cases may represent the reaction of a previously undiagnosed mitochondrial disorder to the oxidative stresses of propofol 21…”

Section: Discussionmentioning

confidence: 99%