A 12-year-old girl was brought in to the Emergency Department by her parents for progressive weakness of all 4 limbs over 3 days. She had nausea and vomiting over the preceding 4 days but there was no fever, diarrhoea, or other positive history. She had a past history of smear positive pulmonary tuberculosis after coming into close contact with a school mate. Treatment was completed 7 months prior to presentation.
On examination she was tachypnoeic and exhibited paralysis over all 4 limbs with lower motor neuron findings. She was otherwise alert. Blood investigations revealed severe hypokalemia with normal anion gap metabolic acidosis. Serum potassium was 1.8mmol/L, sodium 145mmol/L, chloride 120mmol/L, pH 7.2mmol/L bicarbonate 12mmol/L and partial pressure carbon dioxide (pCO2) 16mmHg. Urea and creatinine was 5.1mmol/L and 71µmol/L respectively. Transtubular potassium gradient was raised at 14.
She was initially treated as acute gastroenteritis with hypokalemic periodic paralysis. However, after aggressive intravenous hydration with 0.9% normal saline and multiple doses of potassium correction amounting to a total of 6gm in 12 hours, serum potassium continued to remain low and metabolic acidosis worsened requiring intubation and mechanical ventilation in the intensive care unit (ICU). Further laboratory tests indicated a high urine pH at 8.0 and positive urine anion gap. A trace of past history via the hospital electronic medical records revealed a baseline low potassium of 2.3mmol/L more than 1 year prior to admission which had gone unnoticed with the patient being asymptomatic. A nephrology consult and a diagnosis of distal renal tubular acidosis was made.
She was then initiated on intravenous infusion of sodium bicarbonate. With the correction of acidosis, serum potassium gradually picked up at the expense of serum sodium which increased steadily, peaking at 180mmol/L even after discontinuation of sodium bicarbonate and sodium containing intravenous fluids. While the obvious cause was iatrogenic, she started to have polyuria, more than 3L per day. 2 doses of subcutaneous desmopressin 0.1mcg was given at 12 hours apart resulting in a slight increase of urine osmolality (221 to 350mOsm/kg) suggesting a partial nephrogenic diabetes insipidus. The sodium was slowly corrected by calculated replacements of water deficit with dextrose 5% solution.
Besides a deranged potassium, sodium and acid base status, she also had hypophosphatemia needing regular replacements with intravenous potassium dehydrogenase phosphate. Serum phosphate was 0.4mmol/l while fractional excretion was 25%. While ventilated, her pCO2 was maintained at a low level, ranging 22-32mmHg. Serum magnesium and uric acid was normal while urine glucose was negative. Ultrasound of the kidneys was normal with no evidence of nephrolithiasis. Once the acidosis and sodium levels were corrected, the phosphate level also normalized without needing supplements.
During the ICU admission her condition was complicated with multiple thromboses and sepsis. Imaging confirmed cavernous sinus thrombosis and right lower limb arterial and venous thromboses. Screening tests for autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren’s syndrome were negative. The contrasted CT Brain suggested tuberculoma. Tracheal aspirate sample sent for mycobacterium tuberculosis polymerase chain reaction was positive. Lumbar puncture for confirmation of neurological involvement was not done as her parents did not consent. She was treated with heparin infusion which was converted to warfarin and initiated on anti-tuberculosis treatment with the addition of oral prednisolone for tuberculous meningitis.
A final diagnosis of disseminated tuberculosis with distal renal tubular acidosis was made. She was extubated and transferred out to ward for physiotherapy and rehabilitation before being discharged home well. She is doing well on follow-up reviews and continues to be on potassium and sodium bicarbonate supplements with normal serum potassium, sodium, bicarbonate and phosphate.