Propofol infusion syndrome: An unusual cause of renal failure

Casserly, Brian; O’Mahony, Elizabeth; Timm, Edward G.; Haqqie, Syed S.; Eisele, George; Urizar, Rodrigo E.

doi:10.1053/j.ajkd.2004.08.036

Cited by 47 publications

(30 citation statements)

References 25 publications

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“…These electrocardiographic changes precede the malignant ventricular arrhythmias that cause sudden cardiac death in these patients. More reports of unexplained early metabolic acidosis developing in patients who were not critically ill on high dose propofol infusions of short duration emerged [13,17,18,39]. A 31-year-old woman received propofol sedation for a radiofrequency ablation procedure for chronic atrial fibrillation [16].…”

Section: Historymentioning

confidence: 99%

“…Two reports have recorded the successful use of extracorporeal membrane oxygenation (ECMO) for oxygenation and circulatory support [31,32]. Haemodialysis or haemofiltration has been advocated to decrease the blood levels of metabolic acids and lipids, and has been the most effective treatment of severe PRIS when combined with cardiorespiratory support [13,19,[27][28][29][30][31][32].…”

Section: Managementmentioning

confidence: 99%

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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: Historymentioning

confidence: 99%

Section: Managementmentioning

confidence: 99%

Propofol infusion syndrome

2007

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“…There are some reports of rhabdomyolysis caused by propofol [6] and its interaction with other statins [7] , but this is the first case report documenting rhabdomyolysis after atorvastatin and midazolam administration.…”

Section: Discussionmentioning

confidence: 98%

Rhabdomyolysis after midazolam administration in a cirrhotic patient treated with atorvastatin

Gigante

Giraldi

Gasperini

et al. 2014

WJGPT

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The administration of statins in patients with liver disease is not an absolute contraindication. Hepatotoxicity is a rare and often dose-related event and in the literature there are only a few described cases of fatal rhabdomyolysis in patients with chronic liver disease after statin administration. During treatment with 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, the factors responsible for myopathy may either be related to the patient, or due to interactions with other medications that are metabolic substrates of the same isozymes and therefore able to increase blood statin concentration. The most important side effects consist of increased transaminase levels, abdominal pain or muscle weakness, increased serum levels of creatine kinase and rhabdomyolysis. In this article we report a case of fatal rhabdomyolysis with acute renal failure after gastric endoscopy, where midazolam was used as a sedation agent in a patient with chronic liver disease treated with a high dose of atorvastatin. Therefore, we suggest paying particular attention to the potential risks of associating atorvastatin and midazolam in patients with chronic liver disease who need to undergo gastric endoscopy.

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“…This may become evident in situations of (1) metabolic stress and high energy demand (a ''priming factor'' [14], such as critical illness with central nervous system activation and endogenous production of catecholamines, glucocorticoids, Fig. 2 Propofol and phenylephrine infusion doses and creatinine kinase levels of the third patient with PRIS and cytokines), (2) low availability of alternative sources of energy, such as carbohydrates (in children more than adults, because of higher dependence of the former on fatty-acid oxidation, due to lower glycogen storage capability [6,13,16]), and (3) high availability of lipids (due to the high-lipid content in the propofol emulsion and the additional catecholamine-mediated lipolysis [13,21,22]), which are inefficiently oxidized because of propofol. Risk factors for developing the syndrome include younger age, severe neuro-critical illness, inborn errors of mitochondrial fatty-acid metabolism (such as very long chain acyl-coenzyme A dehydrogenase deficiency), acquired carnitine deficiency (with administration of valproic acid, malabsorption syndrome, cirrhosis, or chronic renal failure [18]), ketogenic diet or low carbohydrate intake [13,14], exogenous catecholamine or steroid administration [13,14,[22][23][24], and high-dose, prolonged infusions of 2% propofol (>5 mg/kg/hour for more than 48 h [8,11]).…”

Section: Discussionmentioning

confidence: 99%