Abstract
Patrick Tolan, Denis O'Loughlin and John Botha, Frankston Hospital, Frankston, Australia:
We report the case of AB, a 41-year-old single female admitted to the intensive care unit with seizures secondary to severe hyponatremia, who subsequently developed rhabdomyolysis.
She had a 10-year history of paranoid schizophrenia. At no time prior to this episode were problems with excessive water intake or hyponatremia noted.
In the weeks prior to her admission with seizures she had been receiving assertive community treatment with a case manager visiting daily and monitoring her medication compliance. (Olanzapine 10 mg per day and sertraline 50 mg per day.)
In the days prior to her admission she reported that she consumed about 10 glasses of water per day which she said was normal for her.
On the morning of her admission she was found at home unconscious and unrouseable and had several generalised tonic-clonic seizures. She was intubated by ambulance staff and transferred to the emergency department.
On arrival in the emergency department her Glasgow Coma Score was 3/15. She was hypothermic temperature of 34.8°C, pulse 90 beats per minute and blood pressure 120/70 mmHg. There were no focal neurological signs and with the exception of bi-basal crepitations in the lung fields and a rash on both legs examination was unremarkable.
She had a low serum sodium 104 mmol/L (135–145 mmol/L) and a low urinary osmolarity. A head computerized tomography scan was normal.
The differential diagnoses made at initial assessment were a syndrome of inappropriate antidiuretic hormone secretion or water intoxication secondary to psychogenic polydipsia. A low urinary osmolarity, however, made SIADH unlikely.
She was transferred to the intensive care department on artificial ventilation with the electrolyte imbalance corrected over the following 48 h with hypertonic saline and diuresis.
Creatinine kinase (CK) was normal on admission rising slowly to peak at 91 970 IU/L (1–170 IU/L) on day 5 although there were no other features of neuroleptic malignant syndrome (i.e. no pyrexia, confusion, rigidity or autonomic instability). Creatinine kinase MB fraction troponin and electrocardiogram were all normal. Urinary myoglobin was strongly positive suggesting significant rhabdomyolysis. Despite neuroleptic malignant syndrome being unlikely it was felt prudent to cease both olanzapine and sertraline.
During the following 4 days in hospital she remained well, the biochemical abnormalities correcting themselves. She refused inpatient psychiatric admission following discharge from the medical ward and did not satisfy criteria for involuntary treatment at that time. She was discharged home for outpatient follow up on no psychotropic medication and at the time of writing had been re-admitted to hospital for a trial of clozapine. During this admission her serum sodium was within the normal range.
If NMS is discounted as playing a role in this case then the cause of the rhabdomyolysis remains unclear. Possibilities are rhabdomyolysis secondary to seizures or dilutional hyponatremia (DH).
In the literature there has been a number of reports of rhabdomyolysis secondary to water intoxication. In one case from Japan [1], a 44-year-old woman consumed 3 L of water after drinking alcohol. She became stuporous with sodium of 115 mEq/L and subsequently had a CK rise to 28 560 IU/L. In this case the occurrence of rhabdomyolysis was attributed to water intoxication. In another case also from Japan [2], a 32-year-old woman with schizophrenia had a sodium level of 102 mEq/L and developed a CK of 39 900 on day 5 of admission. The timing of this rise would appear to coincide with that of AB's present case. Another case from Switzerland was a 42-year-old man with schizophrenia who developed seizures secondary to DH and rhabdomyolysis [3].
These cases indicate that seizures and rhabdomyolysis can be a potentially serious complication of hyponatremia due to polydipsia.