Propofol infusion syndrome

The propofol infusion syndrome ( PRIS ) is a very rare symptom complex of severe adverse drug reactions that may occur as a result of intravenous administration of the anesthetic propofol. In addition to the induction and maintenance of anesthesia in the anesthetic propofol is widely used as a sedative in intensive care. The Propofolinfusionssyndrom is, among other things characterized by disorders of the cardiovascular system, rhabdomyolysis, and lactic acidosis.

Frequency

The propofol infusion syndrome is a very rare, life- threatening complication of anesthesia with propofol. By 2004, a total of 45 cases have been published. The incidence is a prospective study, in adult intensive care patients who were treated with propofol at least 24 hours, at 1.1 percent, and the mortality rate at 18 %.

Especially on long-term infusion of propofol or at very high doses, a propofol infusion syndrome occur. The complication, however, was already described in an approximately 5 hour long Propfol anesthesia. Children are particularly vulnerable to develop such a syndrome.

Formation

The emergence of Propofolinfusionssyndroms has not been clarified in detail. There are several factors play a role, with probably a disturbed fatty acid metabolism with uncoupling of the respiratory chain is the main cause. High-dose and long-lasting Propofolinfusionen promote the development of PRIS. It is unclear whether the intermediate dose or whether short-term high doses favor the development.

Clinical features

As part of a propofol infusion syndrome usually occurs heart failure and cardiac arrhythmias as well as metabolic acidosis. In addition, it occurs relatively frequently to rhabdomyolysis and acute renal insufficiency or acute renal failure, usually prevent the hypertriglyceridemia.

The arrhythmia Brugada -like ECG changes are typical. Furthermore, it may lead to atrioventricular blocks, spacers of the QRS complex and bradycardia. The latter can lead to asystole.

The metabolic acidosis is caused by lactic acidosis and the consequences of renal failure. The damage to the heart muscle can be demonstrated by increases in cardiac enzymes. In rhabdomyolysis creatine kinase and myoglobin in serum rise and it is myoglobin in the urine ( myoglobinuria ) detectable. The renal failure is probably caused by the increased myoglobin.

Therapy

The most important measure in the presence of a Propofolinfusionssyndroms is the immediate discontinuation of sedation with propofol and switching to another sedative. Even with a recovery or improvement of symptoms after discontinuation of propofol re- use is not recommended, as is suspected especially after Langzeitantanwendung an accumulation and redistribution of propofol. The latter can lead to a significantly longer influencing the metabolism than is to be expected in the short half -life of propofol.

In addition, supportive measures must be taken if necessary. These include the administration of fluids and catecholamines to maintain a sufficiently high blood pressure, treatment of bradycardia - when medication is not sufficient possibly by pacing - as well as a balance of matabolischen acidosis. The use of renal replacement therapy ( hemofiltration or hemodialysis) should be turned recommend this early stage considered as clinically severe cases have been reported in which this treatment option has not addressed. In particular, the continuous hemofiltration often leads to a rapid improvement of symptoms, possibly because a suspected metabolite of propofol is dialysable. Also an adequate caloric intake in the form of carbohydrates is recommended from the point of suspected fatty acid oxidation disorder.