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Elderly patients, because of poor renal concentrating ability and impaired thirst mechanisms, are prone to hypernatraemia from various causes.
A man of 76 had been receiving treatment for prostate cancer and hypertension. His medication included cyproterone acetate and bendrofluazide. After the onset of severe uncontrolled urinary frequency and nocturia with incontinence he consulted his general practitioner. No abnormality was found on urine analysis and intranasal desmopressin was prescribed. Two days later he remained thirsty and polyuric, and the general practitioner, suspecting diabetes insipidus, stopped the cyproterone acetate and bendrofluazide and increased the dose of desmopressin. A renal ultrasound scan was arranged. Three days after the initial presentation his serum sodium was 153 mmol/L (reference range 135-145), potassium 3.1 mmol/L (3.5-5.5), creatinine 212 μmol/L (71-133) and urea 11.0 mmol/L (3.2-7.1). Hospital admission was recommended but the patient refused. Ten days after initial presentation he was still troubled by polyuria and polydipsia. Serum sodium was then 156 mmol/L, potassium 3.7 mmol/L, bicarbonate 32 mmol/L (22-30), chloride 111 mmol/L (98-107), urea 9.5 mmol/L, and creatinine 242 μmol/L and urine osmolality was 282 mosmol/kg— i.e. the patient had severe hypernatraemia, renal impairment and a renal concentration defect. An ultrasound scan demonstrated bladder outlet obstruction with bilateral renal hydronephrosis and a distended bladder, although the patient had no sensation of the latter. Two weeks later he underwent transurethral prostatectomy and a suprapubic catheter was inserted. Two weeks postoperatively serum sodium was 142 mmol/L, potassium 5.1 mmol/L, urea 8.1 mmol/L and creatinine 171 μmol/L. Hypernatraemia never recurred. Three months later he was able to go back to work, but he eventually succumbed to metastatic prostate cancer.
A farmer aged 73 was referred to an outpatient clinic with dryness of the mouth, polydipsia and nocturia. There was no complaint of hesitancy, dribbling or poor stream. Diabetes mellitus was suspected but a fasting plasma glucose was 5.9 mmol/L. Serum sodium was 152 mmol/L, potassium 4.2 mmol/L and creatinine 142 μmol/L. Plasma osmolality was 327 mosmol/kg and urine osmolality 369 mosmol/kg, suggesting impaired renal concentrating ability due to cranial or nephrogenic diabetes insipidus. A magnetic resonance scan of the pituitary and hypothalamus was normal. The patient was treated with oral desmopressin but felt that the tablets disagreed with him. He remained polyuric and complained of a dry mouth but denied thirst as such. Serum sodium rose to 159 mmol/L. He was therefore admitted to hospital for intravenous rehydration. During the investigation of a separate complaint he was found on abdominal tomography to have bilateral hydronephrosis, and an ultrasound scan showed a bulky prostate gland. Insertion of a urinary catheter was followed by diuresis of about 2000 mL and his serum sodium returned to normal— 148 mmol/L the next day and 137 mmol/L four days after catheterization. His serum sodium remained normal subsequently and renal function improved, with serum creatinine falling to around 110 μmol/L.
Hypernatraemia has been defined as a serum sodium concentration greater than 145 mmol/L1. Our definition of severe hypernatraemia, perhaps arbitrary2, is a serum sodium > 150 mmol/L. In both primary and secondary care, hypernatraemia is almost always due to water loss3,4. Several mechanisms contribute to sustained hypernatraemia including impairment of thirst, reduced renal concentrating ability, the use of inappropriately hypertonic intravenous infusion fluids and lack of free access to water, especially in individuals who are obtunded or being ventilated4. Elderly patients are believed to be at special risk of severe hypernatraemia because with advancing age their renal response to dehydration alters and they have a poorer thirst response5,6; also, renal concentrating ability declines7. As hypernatraemia progresses, patients who are initially very thirsty may lose their thirst partly or entirely. This seems to have been the case in the second patient, who was not particularly thirsty after the first few days despite severe hyperosmolality. Both of these factors put patients at a greater danger of cellular dehydration, with consequent cerebral dysfunction in the form of confusion and disorientation.
Chronic obstructive uropathy, with consequent nephron loss, may lead to tubular dysfunction in the form of nephrogenic diabetes insipidus9; but the resultant polyuria and polydipsia, if prominent, can overshadow the manifestations of outflow obstruction.
We thank Dr B H Davies for his contribution to preparation of this report.