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An Unusual Neurological Complication in a CAPD Patient

Editor: Neurological complications in dialysis patients include multi-infarct dementia, chronic subdural hematoma, hydrocephalus, and intracranial hemorrhage (1). Here we report an unusual neurological complication, subdural hygroma, of rapid onset in a patient on continuous ambulatory peritoneal dialysis (CAPD). A 68-year-old female vegetarian patient with diabetic end-stage renal disease and hypertension, who was on CAPD for the previous 30 months using 2 L Dianeal [Baxter (India) PVT; IMT Manesar, Gurgaon, Haryana, India] 3 or 4 exchanges/day, was admitted to hospital for treatment of protocolitis. On the third day, she developed a stroke while asleep; her Glasgow coma scale was 9/15, with difficulty in speech. Computed tomography (CT) scan of the brain showed a right corona radiata and caudate nucleus infarct, with no midline shift. Her neurological status, including speech, improved with treatment. She was able to ambulate after a week and was discharged home on subcutaneous insulin along with aspirin and clopidogrel. The patient was readmitted a month later with generalized edema and fluid overload; she weighed 68 kg. Blood pressure was 130/90 mmHg. She had normal neurological status. Her parameters revealed hemoglobin 7.8 g/dL, white blood cell count 10 100/ mm3, platelets 451 ×103/μL, red blood cell count 2.6 × 105/mm3, randon blood sugar 309 mg/dL, BUN 24 mg/ dL, serum creatinine 6.9 mg/dL, Na+ 128 mmol/L, K+ 3.6 mmol/L, HCO3 29 mmol/L, total protein 5.2 g/dL, and albumin 1.7 g/dL. Dialysis was done four times per day with hypertonic exchanges, and an infusion of human albumin 20% 100 mL was given for the hypoalbuminemia. Strict salt and water restriction was enforced. The edema began to subside rapidly and her weight came down to 59.2 kg at the end of the third day. She became drowsy and gradually lost her consciousness again by the fourth day. Her blood sugar was 156 mg/dL and Na+ was 143 mmol/L. A repeat CT scan of the brain showed a large bifrontal parietal subdural hygroma in addition to the previous CT scan findings (-5HU) (Figure 1). The hypertonic dialysis exchanges were stopped and the patient was given isotonic exchanges along with oral hydration. She improved and was discharged home ambulant. She was reviewed after 3 weeks and continues on aspirin and clopidogrel, and is doing well. Subdural hygroma is a collection of cerebrospinal fluid in the subdural space, occurring following trauma or rapid decompression of the ventricular system after shunting. Excessive dehydration may also result in passive development of subdural hygroma (2). Small subdural hygromas get reabsorbed on their own. Rehydration and expansion of the brain can result in resolution of subdural hygromas. Since the majority of patients with a subdural hygroma do not show a mass effect, surgery is rarely required (3). In our patient, the temporal onset of symptoms, signs, and CT findings suggest dehydration as a possible cause for the development of subdural hygroma. The improvement of the patient with hydration over a period of 1 week supports this hypothesis. This case report highlights the fact that patients with pre-existing neurological damage may develop symptomatic subdural hygroma following rapid removal of extracellular fluid.