الفهرس 
Sedation in icuOnly 14 pages are availabe for public view
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Abstract
Propofol is a simple phenol derivative with sedative hypnotic effect. It is insoluble in water; so many lipophilic and organic formulations appeared. Severe hypersensitivity and anaphylactoid reactions unfavoured use of cremphore El.So EDTA and metabisulfite were added to retard microbial growth and postoperative infection. Propofol can only be used as an intravenous agent. It is metabolized by liver and excreted by kidney. There is a significant extra hepatic metabolism especially in lungs. Recovery from its clinical effect is due to redistribution of the drug from highly perfused tissues (e.g brain) to poorly perfused tissues (fat and muscles).
Propofol rapidly induces hypnosis and its duration is dose dependant. At sub therapeutic doses, it provides anxiolysis and sedation. Propofol has myocardial depressant effect via its action on sympathetic drive of the heart resulting into hypotension and bradycardia. It has a respiratory depressant and an antioxidant effect. Propofol was mainly compared to midazolam, dexametomidine and remifentanil as regard sedation in ICU. Propofol provides more rapid recovery, midazolam provides better amnesia, dexametomidine unlike propofol reduces analgesic requirement and has no effect on respiration. However it produces more prolonged sedation. Remifentanil is characterized by rapid onset and offset with better hemodynamic stability and more rapid weaning.
Unfortunately propofol was associated with some adverse effects, pain upon injection, hypotension and bradycardia, hyperlipidemia, hypertriglyceremia, postoperative pancreatitis and propofol infusion syndrome. In 1992, Parke et al were first to record a serious problem related to propofol infusion in pediatrics. Multiple factors as critical illness (sepsis, trauma, burns and neurological insults) is considered a priming factor for the syndrome which has been triggered by some factors as use of high dose of propofol [>4mg/kg/hour for long period (>48hours) in most cases], use of IV catecholamines and corticosteroids. It is characterized by severe metabolic acidosis, rhabdomyolysis, hyperkalemia, lipemic serum, renal failure, hepatomegaly and cardiovascular collapse.
The most recent and likely mechanisms are inhibition of mitochondrial enzymes in respiratory chain, electron transport chain and oxidative phosphorylation pathway which eventually cause failure of ATP production and metabolic collapse. Early diagnosis and prevention precautions are of paramount importance to prevent the high mortality that accompanies undiagnosed propofol related infusion syndrome. This can be achieved by monitoring of early markers of (PRIS) via serial arterial blood gases to detect metabolic acidosis, lactate level in blood, CPK, triglycerides levels and other more specific markers of mitochondrial failure like acylcarnitine and malonylcarnitine. Serial ECG is recommended which may reveal Brugada like ECG pattern of raised coved ST segment in v1 to v3 which is considered very early sign of (PRIS).
So with simple and available tools like serial ABG and ECG and serum triglycerides, we can detect this serious problem as early detection of PRIS makes the prognosis much better for our patients. Management of propofol infusion syndrome is non-specific and its success relies on prompt recognition of early signs and markers of propofol infusion shift to other alternative and supportive treatment addressing the clinical manifestation. Cardiovascular support is either with crystalloid/colloid replacement, escalating dose of inotropes, cardiac pacing, or ECMO and renal hemodialysis.
Finally propofol is widely used all over the world. PRIS is rare but fatal adverse effect of propofol. All clinicians and anesthesiologist should be aware of it for early detection and management.