Cerebral salt wasting syndrome in craniopharyngioma
A 45-year-old, 60 kg, male complaining of moderate degree headache for 15 days attended our out-patient department. Magnetic resonance imaging of brain revealed that he had sellar-suprasellar space occupying lesion (24 mm × 20 mm × 26 mm), predominantly solid in nature, without hydrocephalus, suggesting craniopharyngioma []. While waiting for elective surgical removal of that lesion, he became drowsy and admitted in our hospital. He was a patient of known hypothyroidism and was on oral thyroxin (0.1 mg daily). There was no history of convulsion or localising neurological deficit and patient was non-diabetic and non-hypertensive. Following admission, patient was found dehydrated (decreased in skin turgor), his pulse rate was 94/min; blood pressure was 96/60 mm Hg and Glasgow coma scale was 13/15. On investigation, haemoglobin was 10.8 g% and among other findings, total leucocyte count was 6600/cumm, blood glucose was 109 mg/dl, blood urea and serum creatinine were 58 mg/dl and 1.5 mg/dl respectively. Serum electrolyte studies revealed sodium 117 mmol/L and potassium 4 mmol/L. Chest X-ray and electrocardiogram detected no abnormality. Thyroid hormones and serum cortisol were within the normal limit. A central venous line through subclavian route was done and central venous pressure (CVP) was noted 3-4 mm of Hg. As patient was hyponatremic and dehydrated, we started normal saline (NS) infusion at the rate of 150 ml/h (change in serum Na+ equals to the replacement fluid Na+- serum Na+ divided by total body water + 1 and we wanted to correct serum by 0.5 mmol/L with a total increase of serum Na+ 8 mmol/L/24 h)[] to make the patient euvolemic. His urine output in 24 h was also recorded and found to be 3.5 L. At the same time, urine and blood samples were sent for further studies to detect the cause of hyponatremia. Investigations showed serum osmolality 264 mOsm/kg H2O, urinary osmolality 430 mOsm/kg H2O and urinary spot sodium 132 mmol/L and a diagnosis of CSWS was made. Infusion of NS was continued along with every 2 h monitoring of serum sodium. Even after 24 h of NS infusion, as serum Na+ level got slightly increased to 119 mmol/L, we preferred to infuse hypertonic saline (3% sodium chloride) at a rate of 45 ml/h. Patient gradually became conscious and oriented as serum sodium level increased to 130 mmol/L over next 48 h. Following improvement, patient was put up for definitive surgery. During the surgery, conventional neuroanaesthetic technique was used and the patient was reversed well. Intraoperative and immediate post-operative period remained uneventful. On the 4th post-operative day, patient again became drowsy. Although post-operative computed tomography scan revealed nothing abnormal, serum sodium was found to be 122 mmol/L and urine spot sodium 92 mmol/L. Sodium replacements was started immediately with NS infusion. Waxing and waning of the state of hyponatremia persisted for next 27 days and managed accordingly with sodium replacement through nasogastric tube, NS and occasional 3% saline infusion. However, with this treatment his high urinary sodium gradually became normal and serum sodium gradually reached normal level and patient became clinically stable. Patient was discharged, after 2 weeks of observation as he had been maintaining normal serum sodium level throughout that period.