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Propofol Infusion Syndrome (PRIS)

History

The term “Propofol Infusion Syndrome” (PRIS) was coined by Bray in 1998. Although first death due to PRIS occurred in Denmark in 1990, it was Park et al who suggested the link between propofol infusion and mortality in children. First case report of PRIS in adult was in 1996, but mortality was reported in 1998.

Pathophysiology

Old Theory

Impaired hepatic lactate metabolism leading to lactate accumulation and metabolic acidosis causing accumulation of inactive propofol metabolites and lipid micro-embolization

New theory

There is disruption of mitochondrial fatty acid oxidation causing impaired mitochondrial respiratory chain function resulting in failure of ATP production-cellular hypoxia-metabolic acidosis.This leads to myocyte disruption and disintegration, further causing myocardial failure and cardiovascular collapse. Also,metabolic acidosis and cellular hypoxia leads to rhabdomyolysis and myoglobinurea resulting in acute renal failure (ARF) and secondary hyperkalaemia.

Predisposing and triggering factors

  • High dose of propofol,>4mg/kg/hr for more than 72h
  • Young age
  • Critical illness
  • Congenital errors of metabolism;mitochondriopathy
  • Exogenous catecholamine administration
  • Glucocorticoids
  • Systemic inflammation
  • Cytokine production
  • Head injury

Clinical Picture

  • Unexplained metabolic acidosis with base deficit >-10 mEq/l
  • Hepatomegaly
  • Rhabdomyolysis
  • ARF
  • Hyperkalemia
  • Progressive myocardial failure
    • Refractory bradycardia unresponsive to high dose of atropine
    • Cardiomyopathy
    • Acute cardiac failure
    • Arrhythmias such as AF/VF and SVT/Bundle branch block
    • ECG changes;coved ST elevation in V1-V3leads
  • Serum lactate more than 2.2nMol/l
  • Increased creatine kinase ,>200 U/LIncreased serum myoglobin levels ,>95 ng/ml
  • Hypertriglyceredemia ,>250 mg/dl

Management

  • Recognition of early signs and stop propofol immediately
  • Cardio respiratory support
  • Cardiac pacing may be required
  • ECMO for oxygenation and circulatory support
  • Hemofiltration to decrease blood levels of metabolic acids and lipids

Prevention

  • Avoiding high doses (>4mg/kg/hr) and minimize duration of infusion in high risk patients (<48hrs)
  • Change of sedatives,when prolonged sedation required
  • Sedation holidays
  • Avoiding lipid overload by assessing all the sources of fat including TPN
  • Having adequate provision of carbohydrates for nutrition in critically ill
  • Monitoring serum triglyceride in at risk patients receiving propofol >4mg/kg/hr or for >48hrs

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