Case Presentation: A 19-year-old male with no significant medical or psychiatric history presented for evaluation of altered mental status and agitation in the setting of cannabis ingestion. The patient reported consuming a cannabis edible followed by 24 bottles of water due to excessive thirst. He presented to the emergency department by ambulance and required chemical and brief physical restraints during transport due to agitation. Exam was significant for obtundation with no other focal findings. Initial labs were significant for a sodium of 116 mmol/L, WBC of 19.2, creatine phosphokinase (CPK) of 3251 U/L and serum osmolality of 243 mOsm/kg. Urine toxicology screen was positive for marijuana and benzodiazepines (given in transit). Head CT and lumbar puncture were performed and results were unremarkable. The patient was admitted to the intensive care unit and started on 3% normal saline with rapid correction of sodium to 129 mmol/L within 4.5 hours. Mental status returned to baseline within 24 hours of admission. CPK levels were mildly elevated on admission as noted above and gradually increased to a peak of 29,286 U/L three days’ post admission. Renal function remained stable throughout hospital course. Patient was treated with intravenous fluids and discharged home on day 5 after CPK levels continued to trend down.
Discussion: We present an unusual case of rhabdomyolysis associated with hyponatremia. Hyponatremia is an electrolyte abnormality commonly encountered by pediatricians, but rhabdomyolysis is a less commonly recognized complication that has been previously noted in case reports and observational studies.The etiology of rhabdomyolysis in our patient was likely multifactorial. The polydipsia which caused his hyponatremia likely contributed as acute serum sodium fluctuations may have led to failure of cellular volume regulatory mechanisms with cellular swelling and subsequent lysis. The rapid overcorrection of his serum sodium likely also played a role as this has previously been documented in the literature. The etiology is likely related to failure in regulation of muscle cell volume and increased membrane fragility in the setting of rapid fluctuations in sodium concentrations. This complication appears to be grossly under-recognized in patients with polydipsia with one retrospective cohort study noting an incidence as high as 62.5%.Previous studies have also shown that rhabdomyolysis secondary to overcorrection of hyponatremia is a delayed phenomenon as seen in our patient. The peak CPK levels are estimated to be seen at 48-96 hours in primary polydipsia. This again shows that the rapid correction likely played a role as his CPK level was mildly elevated on admission but became markedly increased after intravenous fluid resuscitation. Also, while not the case with our patient, it should be noted that patients who present with primary polydipsia may often be taking antipsychotic medications. These have also been found to be independently associated with rhabdomyolysis, however it usually occurs later with a time of onset of 5 days to 2 years.
Conclusions: This case highlights the importance of monitoring for possible rhabdomyolysis in patients with hyponatremia in the setting of primary polydipsia and concurrent overcorrection of sodium. This complication may be under-recognized in the hospital and could contribute to increased morbidity with kidney injury and prolonged hospitalizations.