Refractory Hypokalemia, Hypomagnesemia Following Hydrochlorothiazide Use in a Patient With Inclusion Body Myositis Secondary to HTLV

Abstract INTRODUCTION: Diuretic therapy is a leading cause of hypokalemia seen in 15-50% of patients. Hypokalemia,hypomagnesemia and hypercalcemia are common with Hydrochlorthiazide use which usually resolves on stopping. Wepresent an unusual case of refractory hypokalemia, hypomagnesmia and hypophosphatesemia secondary toHydrocholorthiazide.CASE PRESENTATION: 67 Year old African American female presented to ED with altered mental status. She had historyof Inclusion Body Myositis (IBM) secondary to HTLV since 1995 and was bedbound due to muscular weakness. Medicalhistory included hypertension for which she was on Hydrochlorthiazide 25mg daily. She had presented to the ED a week agocomplaining of headache and high blood pressure of 180/99. She was treated in the ER and later discharged onHydrochlorthiazide 50mg daily. Four days later home health attendant noticed change in mentation and confusion whichprompted the ED visit. Patient was taking both Hydrochlorthiazide 25mg and 50 daily.Admission serum sodium was 106meq/l, potassium 2.7 meq/l and ionized calcium 1.04 mmol/l. Complete blood count and liver function tests were normal.She was admitted to MICU for symptomatic Hyponatremia. On therapy with hypertonic saline, her mental status improvedgradually. Admission X ray revealed bi basilar pneumonia. On the second ICU day she developed acute on chronicrespiratory failure and was intubated and mechanical ventilated. ICU course was complicated by septic shock and ARDSsecondary to aspiration pneumonia. CT chest ruled out pulmonary embolism and showed extensive bilateral lower lobe lobarinfiltrates. Patient developed thrombocytopenia and coagulopathy secondary to sepsis that resolved. By second week in ICUthere was resolution of septic shock and ARDS. She failed multiple attempt of weaning and underwent tracheostomy. Duringthe entire hospital stay she had persistent hypokalemia, hypomagnesaemia and hypocalcemia. Potassium was aggressivelyreplaced but levels remained low. Trans-tubular potassium gradient (TTKG) was 9 consistent with renal potassium wasting.Plasma renin activity was 3.1 ng/mL/h and serum aldosterone level was 1ng/dl. Her Cortisol and thyroid profile was normal.She continued to have persistent hypokalemia despite aggressive electrolyte replacement of potassium, magnesium, andcalcium daily. TTKG repeated remained high. During her hospital stay she has received a total of 2793 meq of potassium,80600 mg of magnesium and 45750 mg of calcium. Despite these replacements she continues to have low potassium andher electrolytes are monitored daily with additional replacements.DISCUSSIONS: TTKG is a useful tool in the diagnosis of hypokalemia. TTKG of > 3 generally indicate renal potassiumlosses. Renal potassium wasting related to tubular defects is seen in various conditions such as RTA, Liddles syndrome,syndrome of apparent mineralocorticoid excess, Bartter's syndrome and Gitelman's syndrome. Endocrinopathies resulting inrenal potassium wasting include Conn's syndrome, Cushing syndrome and thyrotoxicoxis. Hydrochlorthiazide can causeHyponatremia, hypokalemia, hypomagnesemia but however results in hypercalcemia. In our patient there was no evidence ofany electrolyte imbalance prior to admission which excluded the congenital syndromes. Work up for endocrinopathies wasnegative. Hydrochlorthiazide was attributed as the causal agent for refractory hypokalemia and hypomagnesemia and thehypocalcemia was attributed to Vitamin D deficiency.