A CASE REPORT ON THIAZIDE INDUCED HYPONATREMIA ADDRESSING AN UNDERESTIMATED COMPLICATION

Hyponatremia is a common and mostly unnoticed electrolyte imbalance in hospitalized patients. Attention and medical management depends on level of depletion below the normal sodium values and presence or absence of symptoms. Drug induced hyponatremia, arising from renal water retention is predominantly attributed to the Syndrome of Inappropriate Diuresis (SIAD). Hyponatremia manifest with signs of escalation in intracranial pressure such as headache, nausea and vomiting, particularly in case of acute onset with significant serum sodium reduction. Urgent medical interference is called for as symptoms ascend to altered consciousness encompassing confusion, drowsiness, seizures and coma. Various drugs such as Argenine Vasopressin Analogue (AVP analogues), Vasopressin Type II (V2) receptor agonist, diuretics, thiazide like agents induce hyponatremia by various mechanisms. Critical in restoring the serum sodium level is the cessation of implicated agent, coupled with the provision of necessary additional support including 3% NaCl, dexamethasone and fluid restriction. Here is a case report of  63 year old female patient with a diagnosis of euvolemic hyponatremia, induced by hydrochlorothiazide. The patient presented with complaints of drowsiness, altered sensorium and 8-10 episodes of vomiting. Laboratory investigation revealed a significant drop of 106 mmol/L in serum sodium, decreased serum chloride and an elevated D- Dimer. The patient was treated in ICU with 3%normal saline, antibiotics and antihypertensive along with prophylactic anticoagulants. Once the patient condition was satisfactory the patient was moved to wards and later discharged.