What are the diagnostic criteria and management for propofol infusion syndrome?

Diagnosis of Propofol Infusion Syndrome

Propofol infusion syndrome (PRIS) should be diagnosed based on a constellation of clinical features including worsening metabolic acidosis, hypertriglyceridemia, hypotension with increasing vasopressor requirements, cardiac arrhythmias, acute kidney injury, hyperkalemia, rhabdomyolysis, and liver dysfunction in critically ill patients receiving propofol infusions. 1

Diagnostic Criteria

• PRIS presents with variable clinical manifestations, making early diagnosis challenging but crucial for patient survival 1
• Key diagnostic features include:
  • Unexplained metabolic acidosis (primary indicator) 1, 2
  • Cardiac dysfunction (arrhythmias, ECG changes including coved ST segment elevation similar to Brugada syndrome) 3, 1
  • Rhabdomyolysis (elevated creatine kinase) 1, 2
  • Hypertriglyceridemia 1, 4
  • Acute kidney injury 1, 2
  • Hyperkalemia 1, 5
  • Liver dysfunction (elevated liver enzymes) 1, 2
  • Increasing vasopressor requirements 4, 1

Laboratory Monitoring for Diagnosis

• Serial laboratory monitoring is essential for early detection and includes: 1
  • Serum creatine kinase (CPK) - values >5000 IU/L are concerning 6
  • Arterial blood gases (to detect metabolic acidosis) 1, 2
  • Serum triglycerides 1, 7
  • Serum lactate (values >4 mmol/L warrant concern) 6
  • Electrolytes (particularly potassium) 1, 5
  • Liver function tests 1, 2
  • Renal function tests 1, 2

Risk Factors for PRIS

• The incidence of PRIS with propofol infusions is approximately 1% 4
• Major risk factors include:
  • Prolonged administration (>48 hours) of high-dose propofol (>70 μg/kg/min or >5 mg/kg/h) 1, 3
  • Critical illness, particularly acute neurological or inflammatory conditions 1, 8
  • Concomitant administration of catecholamines and/or corticosteroids 1, 8
  • Decreased oxygen delivery to tissues 3
  • Serious neurological injury and/or sepsis 3, 8
  • Carbohydrate depletion 2

Management of PRIS

• Immediate discontinuation of propofol infusion upon suspicion of PRIS 1, 2
• Supportive care focused on organ dysfunction: 1
  • Management of metabolic acidosis 1, 2
  • Hemodynamic support for cardiovascular dysfunction 1, 2
  • Renal replacement therapy for acute kidney injury 1
  • In refractory cases, extracorporeal membrane oxygenation may be necessary 2

Prevention Strategies

• Limit propofol infusion rates to <5 mg/kg/h when possible 1, 8
• Avoid prolonged infusions (>48 hours) 1, 8
• Consider alternative sedatives for patients with risk factors: 1
  • Dexmedetomidine has minimal respiratory depression and different mechanism of action 1
  • Benzodiazepines can be used with monitoring for propylene glycol toxicity 1
• Implement prospective screening protocols in high-risk patients: 6
  • Daily monitoring of CPK and lactate levels 6
  • Discontinue propofol if CPK >5000 IU/L or lactate >4 mmol/L 6

Clinical Pitfalls and Caveats

• PRIS can be difficult to diagnose due to overlap with common ICU complications 1
• Mortality from PRIS is high (up to 33%) even after discontinuation of propofol 4, 7
• Increasing triglyceride levels may serve as an early biomarker of impending PRIS 7
• The syndrome can occur with low-dose infusions, though less commonly 4
• PRIS can develop during short-term infusions during surgical anesthesia, not just in ICU settings 3

Early recognition through systematic laboratory monitoring and prompt discontinuation of propofol upon suspicion of PRIS are critical for improving outcomes in this potentially fatal syndrome.