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Case Reports Indian Pediatrics 2002; 39:488-491 |
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Cerebral Salt Wasting |
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Kalpana Sengupta
Hyponatremia has long been recognized as a serious metabolic consequence of central nervous system insult in children. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) has until recently been thought to be responsible for the majority of cases of hyponatremia developing after neurological insult(1). However, a less well-known and recognized entity, termed cerebral salt wasting (CSW), may be responsible for the hyponatremia in some cases. CSW is characterized by polyuria and natriuresis, which is in contrast to SIADH characterized by oliguria and variable urinary sodium excretion. CSW can cause hyponatremia in some children following CNS insults such as trauma, infection or hemorrhage(2,3). We describe a case of CSW in an eighteen months old child with an intracranial granuloma. Case Report An 18-month-old boy presented with history of 4-5 episodes of vomiting per day and altered sensorium for 3-4 days. There was no history of fever or convulsions. The patient had been on two antituberculous drugs since 5 months for suspected pulmonary tuberculosis. On examination, he was dehydrated, marasmic and drowsy. The vital signs were normal and there were no signs of meningeal irritation, raised intracranial pressure or focal neurological deficit. Laboratory investigations showed hemoglobin of 10 g/dl, total leukocyte count 10200/mm3, 48% neutrophils and 52% lymphocytes and ESR of 60 mm. The Mantoux test was negative. The chest radiograph, CSF examination and CT scan of the brain were normal. The blood levels were : sodium - 114 mEq/L, potassium - 4.2 mEq/L, urea - 13 mg/dl, creatinine - 0.4 mg/dl and glucose - 150 mg/dl. The blood pH was 7.44, pCO2 38 mm, pO2 92 mm and bicarbonate 13.3 mEq/L. Intravenous fluids were given for correction of dehydration and hyponatremia but after 24 hours of treatment, the child still remained dehydrated. The serum sodium level fell further to 109 mEq/L. He was then treated with intravenous hydrocortisone without improvement of levels of serum sodium. The patient continued to be volume depleted without any gastrointestinal source of fluid loss. MRI of brain showed granulomas in posterior midbrain and right parietal lobe, which were thought to be suggestive of tuberculoma. The patient’s urine output was persistently more than 5 ml/kg/hour. Urinary electrolytes revealed massive natriuresis with 24-hour sodium excretion ranging from 774 to 1530 mEq. Urinalysis and ultrasonogram of the kidneys were normal. Antituberculous treatment was started in view of the MRI findings. The diagnosis of CSW was made in view of hyponatremia in association with polyuria and natriuresis, and an intracranial granuloma. Renal causes of hyponatremia were ruled out. Adrenal disease was not considered, as there was no pigmentation, hypertension and hypokalemia. The blood level of antidiuretic hormone was 14 pg/ml (normal, 1-14 pg/ml). The patient was managed with intravenous fluids with 30 mEq/kg/d of sodium in the form of 3% NaCl. The serum sodium gradually increased to 130 mEq/day on day 15 and was maintained thereafter. The natriuresis decreased to 65 mEq/24 hours on day 20. The patient developed a respiratory infection and septicemia and died three days later. Discussion It has become increasingly evident that in patients with intracranial disorders, such as hemorrhage and infection, hyponatremia can occur in a setting of volume depletion and natriuresis(2,3). The entity described as CSW is distinct from SIADH. It is of utmost importance to differentiate the two conditions. A wrong diagnosis might lead to inappropriate fluid restriction and worsen the hypovolemia, in patients with CSW. Clinicians must be aware of the clinical features that distinguish CSW from SIADH (Table I). Table I-Differentiation of Cerebral Salt Wasting (CSW) from Syndrome of Inappropriate ADH Secretion (SIADH)
ANP = Atrial natriuretic peptide Inappropriate atrial natriuretic peptide (ANP) secretion has been proposed as a possible pathogenetic mechanism for CSW in children with subarachnoid hemorrhage and tuberculous meningitis(3). Rappaport et al. described a salt losing state as a possible cause for hyponatremia in patients with tuberculous meningitis(4). Hyponatremia in these cases was thought to be caused by SIADH, till Narotam et al. described increased natriuresis with polyuria as a cause of hyponatremia and postulated that increased ANP may be the cause of this condtion(5). ANP can inhibit both renin and angiotensin II mediated aldosterone secretion in healthy adults(6). ANP is also reported to suppress the enzymatic activity of renin on angiotensin II in animal models(7). Aggressive replacement of urinary salt and water losses using normal saline or 3% saline, if necessary, is the mainstay of treatment of CSW. The amount of 3% saline infused is calculated by multiplying the total body water (0.6 × weight) by 5 mEq/L which is the desired increase in serum sodium. Ishikawa et al. reported the resolution of CSW with fludrocortisone acetate at a dose of 0.2-0.4 mg/day(8). This treatment was considered because of the associated hormonal pattern of suppressed renin angiotensin system in CSW(9). Kappy et al.(3) have reported the only pediatric patient with subdural bleeding and CSW who responded to treatment with fludrocortisone acetate. Sakaran et al.(10) demonstrated that mineralocorticoid supple-mentation could effectively control the natriuresis and polyuria secondary to inappropriately secreted ANP in such patients. However, mineralocorticoid have not been shown to be consistently effective(11). It is essential that in any child with hyponatremia and meningitis, an evaluation be undertaken to differentiate between SIADH and CSW. Natriuresis and hypovolemia warrant the estimation of urine output, plasma and urine osmolality, urine and serum sodium and plasma ANP. CSW must be recognized and treated appropriately. Oral supplements of sodium chloride and mineralocorticoids may be useful in managing these patients. Contributors: KS and USA coordinated the study and drafted the paper. KS will act as the guarantor for the paper. PA participated in data collection and also helped in drafting the paper. Funding: None. Competing interests: None stated.
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