JRSM >
Volume 94, Number 12 >
Pp. 637-638
Endocrine Clinic, Friarage Hospital, Northallerton, North Yorkshire DL6 1JG, UK
Correspondence to: Dr A Waise E-mail: awaise{at}nash-tr.northy.nhs.uk
Elderly patients, because of poor renal concentrating ability and impaired thirst mechanisms, are prone to hypernatraemia from various causes.
CASE HISTORIES
Case 1
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.
Case 2
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.
COMMENT
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.
Acknowledgments
We thank Dr B H Davies for his contribution to preparation of this report.
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