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Year : 2001  |  Volume : 49  |  Issue : 2  |  Page : 197--9

Chasing hyponatraemia : unusual presentation.

M Tripathi, CC Sanjeev, AK Roy 
 Department of Neurology, St. John's Medical College Hospital, Bangalore, India., India

Correspondence Address:
M Tripathi
Department of Neurology, St. John«SQ»s Medical College Hospital, Bangalore, India.


Two females, in their sixth decade, presented with recurrent episodes of headache, vertigo, vomiting and altered sensorium. Both patients had persistent hyponatraemia as the only clue. Detailed investigations revealed a pituitary aetiology in both. One patient had a pituitary microadenoma while the other had an empty sella syndrome. The diagnosis and management is discussed and the relevant literature reviewed.

How to cite this article:
Tripathi M, Sanjeev C C, Roy A K. Chasing hyponatraemia : unusual presentation. Neurol India 2001;49:197-9

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Tripathi M, Sanjeev C C, Roy A K. Chasing hyponatraemia : unusual presentation. Neurol India [serial online] 2001 [cited 2022 Jan 20 ];49:197-9
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  ::   IntroductionTop

The clinical manifestations of hypopituitarism are diverse and variable, depending to a large degree on the extent and duration of pituitary hormone deficits. In most patients, the onset of symptoms is insidious and the clinical signs and symptoms are nonspecific or related to hormone deficiency, or due to mass effect. Occasionally, patients may present with features of apoplexy,[1] psychiatric manifestations[2] or have altered sensorium.[3] We present two cases, which on detailed investigations showed a panhypopituitary state.

  ::   Case reportsTop

Case 1 : Mrs P, a 65 years old lady presented with recurrent episodes of headache, vomiting and altered sensorium. The headache was occipital, throbbing and episodic, occurring once in 2-3 months, since 2 years. It was occasionally associated with vomiting and altered sensorium. She had 3 episodes of sudden onset unconsciousness lasting 6-12 hours, recovering spontaneously or with treatment. On one such occasion, she had respiratory arrest and was on ventilatory support for 3 days. She was not a hypertensive or diabetic. On examination she was obese, had a pulse rate of 82/min, blood pressure of 110/70 mmHg and had pedal oedema. Neurologically, she was in altered sensorium with minimal flexor nonpurposive response to painful stimuli, would blink occasionally, and had no vocal response. Extraocular movements were frozen, pupils were 3 mm sluggishly reactive, deep tendon reflexes were sluggish and plantars were non-responsive. She had respiratory distress and had to be put on mechanical ventilation. Investigations revealed normal haemogram and persistent hyponatraemia. Plain and contrast CT was normal. MRI showed a mildly enlarged pituitary gland, suggestive of a pituitary microadenoma (of size 0.71-0.65 cm3).The tumour was isointense on T1WI becoming hyperintense on T2WI and was enhancing on gadolinium contrast [Figure 1].

Case 2 : Mrs. N, a 67 years old lady presented with history of headache, vomiting, vertigo and altered sensorium. Headache was episodic and throbbing of one year duration. It was occasionally associated with vomiting, and vertigo.These episodes would last 2-6 hours. One such episode was associated with altered sensorium, which lasted for about 24 hours. She was a diabetic and hypertensive of 5 years duration. On examination, she was obese, with a pulse rate of 80/min and blood pressure of 140/100 mmHg. Her cardiovascular and respiratory systems were normal. Neurologically, she was in altered sensorium, vocalising, and moving limbs purposively, with blinking of eyes to painful stimuli. There was no papilloedema. Pupils were 4 mm equal and reactive. Extraocular movements were full, deep tendon reflexes were normal and plantars flexor. Investigations revealed persistent hyponatraemia. Plain and contrast CT was normal. MRI revealed hypointense (T1WI) cavity within the pituitary fossa becoming hyperintense on T2WI. This was suggestive of an empty sella syndrome. The optic chiasma was not prolapsed, however the pituitary stalk was pushed backwards, against the dorsum sella [Figure 2].

After persistent hyponatraemia was established in both the patients, investigations for the cause for the same were done [Table I]. Both patients did not fit into the criteria of SIADH. Though there was hypoosmolality of serum, urine osmolality was not increased, renal excretion of sodium was normal. Adrenocortical function was impaired with positive response to ACTH stimulation, indicating hypothalamic/pituitary involvement. Hence, a total endocrinological profile was done which showed a panhypopituitary state. Hypo natraemia was corrected with intravenous isotonic saline supplementation along with oral salt administered through ryles tube. Administration of replacement therapy with steroids (prednisolone 1mg/kg/day), and eltroxin managed the hypopituitary state. Both patients had made remarkable improvement at the time of discharge. They were conscious, oriented and had no focal deficits. There were no further episodes of headache or altered sensorium. The patient with pituitary adenoma refused surgery and has been regularly followed up for 2 years. Case 2 is also doing well on follow up with no further episodes, for over 1 and a 1/2 years.

  ::   DiscussionTop

Hyponatraemia is not a disease in itself but a manifestation of a variety of disorders. Common causes for this include syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting syndrome.[4] SIADH is characterised by a hypo-osmotic hyponatraemia in a setting of inappropriately concentrated urine, with a very high concentration of urinary sodium (.20 meq/L). A normal renal, adrenal, and thyroid function is the rule. Both the patients described here had hyponatraemia with a hypo-osmolar serum and hyperosmolar urine. Urinary spot sodium was normal. Hence, other causes of hyponatraemia were investigated.[4] An endocrinological profile showed decreased levels of almost all hormones in both the patients ([Table ] I). In the first case, TSH was low and in case 2, cortisol response to ACTH supression was positive, indicating a central cause for the hypopituitary state. MRI of the brain also suggested a central cause of the patient's clinical syndrome. Hyponatraemia may, hence, be the only manifestation of hypothyroidism and panhy-popituitarism.[5] Superiority of magnetic resonance imaging (MRI) in the diagnosis is well known.[6] The unusual features in these patients was their mode of presentations almost mimicking a stroke, both having a deceptively normal CT scans of the brain and persistent hyponatraemia. The first patient had a microadenoma, which was detected only on MRI. She also, however, had hypofunction of the pituitary gland. Hypofunction of a pituitary microadenoma is rare, but may occur if the adenoma is situated close to the stalk and producing a stalk sectioning effect, even in small tumours.[6] She was put on replacement therapy and had no further episodes. The second patient had an empty sella syndrome. It occurs from 8-35% of the normal population, and may be primary or secondary. They may present with neurological symptoms like headache (50-80%) memory loss, vertigo, seizures, CSF rhinorrhea, idiopathic intracranial hypertension and papilloedema, decreased visual acuity and visual field defects. Endocrinological symptoms like amenorrhoea, galactorrhoea, diabetes mellitus, hypofunction of the pituitary and systemic symptoms like hypertension, obesity, which may be related to hypothalamic alterations may also be there.[7] A panhypopituitary state may be seen in 10-20% of cases, as seen in our patient. In these cases, replacement therapy is very essential.[8]


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