Abstract
We describe a case of catatonia associated with hypernatraemia in an elderly lady with a background of moderate dementia. Catatonia has been described in association with a wide variety of metabolic disturbances, but we are not aware of any previous reports of an association between hypernatraemia and catatonia.
The patient was an 87-year-old female admitted to the Geriatrics Service from a nursing home for investigation and management of delirium, reduced oral intake and fever on the background of moderate dementia. Her medications included risperidone 1.5 mg bis die (bd) for control of agitation related to her underlying dementia, and sodium valproate 100 mg mane. Examination of notes from previous hospital admissions revealed that the patient had previously been on citalopram 10 mg mane for major depressive disorder, and this was recommenced. There was no documented reason why sodium valproate had been commenced, although the patient's daughter denied a history of bipolar affective disorder, seizure disorder, pain disorder, or previous head injury or intracranial pathology. Her CXR was suggestive of patchy opacification in the right middle zone, and she was therefore prescribed treatment for community-acquired pneumonia. Her fevers settled in the first 24 h of treatment. On the second day of her admission, routine bloods revealed hypernatraemia and in consultation with the Endocrinology Service she was charted for an infusion of 0.18% normal saline and 4% dextrose over 8 h. Her sodium valproate dose was halved to 50 mg once daily, in order to reduce her oral sodium intake. Due to an error in handover to the evening staff, the infusion was not commenced until the following day, just prior to which her sodium level was found to be 160 mmol/L. At that time, a variety of signs of catatonia were demonstrable, including mutism, waxy flexibility of her upper and lower limbs, psychological pillow, staring, grasp reflex, advertence reaction (‘reaction at the last moment’), posturing of her upper limbs and gegenhalten in her lower limbs. No echophenomena or signs of automatic obedience were demonstrable. The saline/dextrose infusion was commenced as originally intended, and risperidone was ceased in view of the well-documented risk of antidopaminergic medication exacerbating catatonic states. The following day, in response to the saline/dextrose infusion, her sodium level was 152 mmol/L. Her mutism had resolved, and the waxy flexibility in her upper limbs was less marked, but gegenhalten persisted in her lower limbs. Two days after this her sodium had normalized, and no catatonic signs were demonstrable. The following day she was discharged from hospital back into the care of her nursing home, and was able to spontaneously thank the medical and nursing staff for their care.
Hypernatraemia is common in hospital settings, and is a common complication of severe neurological disease such as dementia where oral intake may be compromised [1], as was the case in our patient. Neurological manifestations of hypernatraemia are common. These include seizures and depression of consciousness, progressing from lethargy to coma in a degree proportional to the severity of hypernatraemia [1]. However, our patient was not comatose, but catatonic. Catatonia has been described in the setting of a variety of metabolic abnormalities [2], but the association of hypernatraemia and catatonia has not been previously described. Although we cannot rule out the possible contributions of medications in this complex patient, especially the recommencement of citalopram and the reduction in her valproate dose, the resolution of her catatonic symptoms with the resolution of her hypernatraemia points to the hypernatraemia itself being the primary causative disturbance. Clinicians need to be aware that catatonia can complicate a variety of metabolic disturbances, including hypernatraemia.