|Year : 2003 | Volume
| Issue : 1 | Page : 110--111
Cerebral salt wasting syndrome in a patient with a pituitary adenoma
SK Singh, AG Unnikrishnan, VS Reddy, RK Sahay, SK Bhadada, JK Agrawal
Department of Endocrinology and Metabolism, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005, India
S K Singh
Department of Endocrinology and Metabolism, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005
Cerebral salt wasting syndrome (CSWS) is often an unrecognized cause of hyponatremia that occurs in the setting of intracranial lesions. It is important to differentiate CSWS from the syndrome of inappropriate ADH secretion, as this would alter the management of hyponatremia. We describe a case of CSWS that occurred in association with a nonfunctioning pituitary adenoma.
|How to cite this article:|
Singh S K, Unnikrishnan A G, Reddy V S, Sahay R K, Bhadada S K, Agrawal J K. Cerebral salt wasting syndrome in a patient with a pituitary adenoma.Neurol India 2003;51:110-111
|How to cite this URL:|
Singh S K, Unnikrishnan A G, Reddy V S, Sahay R K, Bhadada S K, Agrawal J K. Cerebral salt wasting syndrome in a patient with a pituitary adenoma. Neurol India [serial online] 2003 [cited 2023 Mar 31 ];51:110-111
Available from: https://www.neurologyindia.com/text.asp?2003/51/1/110/1052
Cerebral salt wasting syndrome (CSWS) is a clinical syndrome, which is characterized by hyponatremia, hypovolemia and natriuresis.[l] It occurs in the setting of various intracranial disorders. We report an unusual case of CSWS occurring in association with a pituitary adenoma.
A 68-year-old male , after returning from a fortnight-long pilgrimage, developed malaise, became incoherent on the next day and lost consciousness on the third day. There was no history of convulsions or other localizing neurological features. CT-scan revealed an intrasellar mass. On clinical examination, he was dehydrated, but other vital parameters were stable. The patient was unconscious, but had no focal neurological deficits. Systemic examination revealed no other abnormality.
Hematological investigations were normal. Serum investigation results were as follows: sodium 118 mmol/L, potassium 3.8 mmol/L, chloride 98 mmol/L, blood glucose 75 mg/dl, blood urea 78 mg/dl, creatinine 1.5 mg/dl, T3 0.7 mmol/L (1.1-2.9), T4 3.5 mmol/L (64-154), TSH 0.8 mU/L (0.5-3.5), morning (8 am) cortisol 3.2 ug/dl (5-25), LH 3 IU/L (5-20), FSH 1.2 IU/L (5-20) and prolactin 20 ng/ml (
Hyponatremia in association with a sellar mass poses a clinical challenge, because both a decrease in ACTH or an increase in anti-diuretic hormone levels (SIADH) can be the etiological factors. As mineralocorticoid secretion is primarily controlled by the renin angiotensin axis, ACTH deficiency, unless very severe and longstanding, is not usually a cause of hyponatremia. SIADH can occur with sellar lesions; in addition, secondary hypothyroidism as well as ACTH deficiency can worsen preexisting hyponatremia by inducing ADH excess.
CSWS is an often-unrecognized cause of hyponatremia in intracranial disorders. Its presentation is similar to SIADH, as both present with hyponatremia, and a high urinary sodium concentration. However, there are subtle differences [Table:1]. Classical causes of CSWS include intracranial lesions, especially head injury, tumors and aneurysm surgery. CSWS is attributed to the release of natriuretic peptide from the brain, through stimuli that are unknown.
It is important to distinguish between CSWS and SIADH, as the former is managed with aggressive fluid therapy (usually with normal saline) while the treatment of SIADH aims at reduction of free water (generally by fluid restriction). In fact, if treatment indicated for one condition is instituted for the other, it aggravates the illness.
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