Propofol infusion in children: when does an anesthetic tool become an intensive care liability?

Wolf, Andrew; Potter, Frank Hamilton

doi:10.1111/j.1460-9592.2004.01332.x

Cited by 75 publications

(63 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Medium chain and short chain fatty acids diffuse into the mitochondria and inhibit the respiratory chain (at complex II), resulting in a rise in C5, C4 or C2-acylcarnitine [27,30,43]. This causes a failure of ATP production in the mitochondria, leading to a build up of long chain, medium chain and short chain fatty-acid metabolic by-products.…”

Section: Mechanism Of Prismentioning

confidence: 99%

“…Soya bean (added to propofol to enhance its solubility) increases the medium and long chain triglyceride fat load. As a consequence of impaired fatty-acid oxidation, a rapid build up of toxic fatty-acid intermediates results and when this is coupled with cellular hypoxia, it worsens the acidosis [30,43]. Excess serum fatty-acid concentrations cause ventricular arrhythmias [31,44].…”

Section: Mechanism Of Prismentioning

confidence: 99%

“…In critically ill patients, an inadequate supply of carbohydrate to the patient promotes the mobilisation of fat stores and increases fat metabolism [43]. This increases the circulating fatty-acid load and predisposes to PRIS.…”

Section: Preventing Pris In the Critically Illmentioning

confidence: 99%

“…This is equivalent to a fat load conferred by a 1% propofol infusion running at 4 mg.kg )1 .h )1 . As most of the reported cases of PRIS were associated with infusion rates greater than 4 mg.kg )1 .h )1 , it is postulated that the excessive lipid load may be a contributory factor [43]. The use of a more concentrated propofol solution (60 mg.ml )1 ) can reduce the lipid load [54]. )…”

Section: Preventing Pris In the Critically Illmentioning

confidence: 99%

See 3 more Smart Citations

Propofol infusion syndrome

2007

View full text Add to dashboard Cite

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.

show abstract

Section: Mechanism Of Prismentioning

confidence: 99%

Section: Mechanism Of Prismentioning

confidence: 99%

Section: Preventing Pris In the Critically Illmentioning

confidence: 99%

Section: Preventing Pris In the Critically Illmentioning

confidence: 99%

See 2 more Smart Citations

Propofol infusion syndrome

2007

View full text Add to dashboard Cite

show abstract

“…The predominantly suprathalamic actions of propofol did not delay recovery of the muscle tone in the clinical case in question in which the use of muscle relaxants should be minimized or abolished. The use of propofol should be avoided in prolonged procedures or sedation in intensive care due to the risk of propofol infusion syndrome, promoting metabolic acidosis, rhabdomyolysis, hyperlipidemic plasma, and cardiac arrest 17,20,21 . The mechanism is unknown, but the presence of mitochondrial toxicity by propofol metabolites, or direct propofol effects that requires prolonged high-dose infusion, or a genetic variance of the clearance and metabolism of this drug has been especulated 22 .…”

Section: Discussionmentioning

confidence: 99%