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Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma
J L Canivet1, K Gustad, P Leclercq
1Department of Anesthesia and Intensive Care, University Hospital of Liège, Belgium.
Insights
Propofol sedation can cause severe ketonuria in children with brain injury, especially with restricted glucose intake. Monitoring for ketones is advised during prolonged propofol infusions.
Area of Science:
- Neuroscience
- Metabolic Medicine
Background:
- Propofol is a common anesthetic agent used for deep sedation.
- Brain injury can necessitate prolonged sedation and intensive monitoring.
- Restricted caloric intake is sometimes employed in critical care settings.
Observation:
- A 12-year-old girl with brain injury developed severe ketonuria (8+ Ketostix) during deep propofol sedation (5.1 mg/kg/h) with restricted glucose (5 Kcal/h).
- Metabolic parameters, including pH, HCO3-, and anion gap, remained within normal limits, indicating no metabolic acidosis.
- Indirect calorimetry showed that 70% of energy expenditure was derived from fat consumption.
Findings:
- Reducing propofol infusion and increasing glucose intake shifted energy metabolism from fat (39%) to carbohydrates within 8 hours.
- Ketone body excretion normalized (negative Ketostix) after metabolic adjustments.
- This suggests a direct link between propofol infusion, restricted glucose, and induced ketonuria.
Implications:
- Prolonged propofol sedation, particularly with limited glucose, poses a risk of significant ketonuria in pediatric patients.
- Monitoring urinary ketone bodies is crucial in patients receiving long-term propofol infusions.
- This finding highlights the importance of tailored nutritional support during critical care sedation to prevent metabolic disturbances.
Abstract:
Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances.