[Severe rhabdomyolysis secondary to severe hypernatraemic dehydration]
Ignacio Mastro-Martínez1, Ana María Montes-Arjona1, Margarita Escudero-Lirio1
1Servicio de Pediatría, Fundación Jiménez Díaz, Madrid, España.
Insights
Severe hypernatraemia, a rare cause of rhabdomyolysis, can occur in infants with acute diarrhea. Early detection of rhabdomyolysis through creatine phosphokinase monitoring is crucial for critically ill children.
Area of Science:
- Pediatric Nephrology
- Critical Care Medicine
- Biochemistry
Background:
- Rhabdomyolysis is an uncommon pediatric condition.
- This case highlights rhabdomyolysis secondary to severe hypernatraemic dehydration post-acute diarrhea.
Observation:
- An 11-month-old infant presented with severe dehydration, hypernatraemia (181 mEq/L), metabolic acidosis, and pre-renal kidney failure.
- The infant developed hypotonia and elevated creatine phosphokinase (75,076 IU/L) on day three, indicative of rhabdomyolysis.
- Management in the Intensive Care Unit involved intravenous rehydration, leading to clinical and renal function improvement.
Findings:
- Severe hypernatraemia is identified as a rare etiology for rhabdomyolysis and renal failure in pediatric patients.
- Prompt diagnosis and treatment of rhabdomyolysis are essential for favorable outcomes.
Implications:
- Clinicians should maintain a high index of suspicion for rhabdomyolysis in critically ill children with severe hypernatraemia.
- Serial creatine phosphokinase measurements aid in the early detection and management of rhabdomyolysis.
Introduction:
Rhabdomyolysis is a rare paediatric condition. The case is presented of a patient in whom this developed secondary to severe hypernatraemic dehydration following acute diarrhoea.
Case Report:
Infant 11 months of age who presented with vomiting, fever, diarrhoea and anuria for 15 hours. Parents reported adequate preparation of artificial formula and oral rehydration solution. He was admitted with malaise, severe dehydration signs and symptoms, cyanosis, and low reactivity. The laboratory tests highlighted severe metabolic acidosis, hypernatraemia and pre-renal kidney failure (Sodium [Na] plasma 181 mEq/L, urine density> 1030). He was managed in Intensive Care Unit with gradual clinical and renal function improvement. On the third day, slight axial hypotonia and elevated cell lysis enzymes (creatine phosphokinase 75,076 IU/L) were observed, interpreted as rhabdomyolysis. He was treated with intravenous rehydration up to 1.5 times the basal requirements, and he showed a good clinical and biochemical response, being discharged 12 days after admission without motor sequelae.
Conclusions:
Severe hypernatraemia is described as a rare cause of rhabdomyolysis and renal failure. In critically ill patients, it is important to have a high index of suspicion for rhabdomyolysis and performing serial determinations of creatine phosphokinase for early detection and treatment.
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