Propofol Infusion Syndrome (PRIS)

Propofol basics:

• Short acting, intravenous general anesthetic
  
• Sedation dose typically 0.3-4 mg/kg/hr
  
• Anesthesia dose 4-12 mg/kg/hr
  
• Rapid onset and short duration
• Propofol infusion syndrome first described in 1990

 
Mechanism PRIS:

• Propofol inhibits transport of fatty acids into the mitochondria and inhibits electron transport chain causing build up of fatty acid metabolites and decreased ATP
  
• Made worse by a patient who is critically ill, has depleted carbohydrate stores, and thus relies on fatty acid breakdown for energy
  

 
Clinical features:

• Metabolic acidosis
  
• Cardiovascular collapse: Hypotension, treatment resistant bradycardia, and Brugada pattern on EKG

• Rhabdomyolysis/acute renal failure
  
• Elevated triglycerides
  
• Hepatomegaly
  
• Elevated lactate
  
• 30% mortality
  

 
Risk factors:

• Younger age (think higher doses propofol and less carbohydrate stores)
  
• People on high doses/long duration of propofol
  
• Exogenous glucocorticoids and vasopressors
  

 
Prevention:

• Limit propofol to 4 mg/kg/hr for less than 48 hours
  
• Note: cases of PRIS have still been described even with short duration/doses of propofol
  
• Consider screening high risk patients with lactate, CPK, EKG, or triglycerides
  

 
Treatment:

• Stop the propofol
  
• Provide carbohydrates
  
• Hemodialysis for acidosis
  
• ECMO if all else fails
  

 
References:
Diedrick, D, Brown D. Propofol Infusion Syndrome in the ICU. Journal of  Intensive Care Medicine. 2011; 26 (2) 59-72. .
 
Rosen DJ, Nicoara A, Koshy N, Wedderburn RV. Too much of a good thing? Tracing the history of the propofol infusion syndrome.  J Trauma. 2007;63(2):443-447.