Refractory hyperkalemia related to heparin abuse
A 26-year-old male patient was admitted in the emergency department with the complaint of weakness of all four limbs since 1 day prior to admission, which was rapidly progressive. He was a pharmacist at a private nursing home addicted to multiple medicines including tramadol, diclofenac, pheniramine, and dexamethasone along with heparin to maintain the venous patency since several years. He was a known case of bronchial asthma and was on and off steroids for the past several years.\nOn admission, patient was conscious and oriented, hemodynamically stable with a heart rate of 112 beats/min, non-invasive blood pressure of 130/80 mmHg, respiratory rate of 24/min and a temperature of 99°F. There was no pallor. No signs of clubbing or lymphadenopathy were there. Oral thrush was present. Chest, cardiovascular system and per abdomen examination were grossly normal. On central nervous system examination, power was grade 3/5 in upper limbs and 1/5 in lower limbs. Generalized areflexia was present. Planters were bilateral flexors. Sensory examination was normal. Laboratory investigations are tabulated in . Arterial blood gas (ABG) at admission showed a normal pH (7.437) with hyperkalemia (K+ = 6.01). Although the first lab sample did not show hyperkalaemia, all repeat values did. Also the hyperkalemia was subsequently treated after 6 hours or so when repeat samples confirmed hyperkalemia. Patient was admitted to intensive care unit for monitoring and within an hour of admission, he got tachypnoeic with respiratory rate of 36-40/min and was put on non-invasive ventilation. Heart rate went up to 130 beats/min, regular but pulses got feeble. His blood pressure dropped down to 100/56 mmHg. At this time, invasive lines were put in, in the form of central venous cannulation and arterial line. Central venous pressure was 6 cm H2O and mean arterial pressure (MAP) was 55 mmHg. Patient was resuscitated with a fluid bolus of 1 litre normal saline. His blood pressure improved with MAP going up to 64 mmHg. He was further given 500 mL of normal saline in the subsequent hour and was started on normal saline 100 mL/h infusion. Subsequently, a MAP of >65 mmHg was targeted. Urine output was >0.5 mL/kg at all times. His chest X-ray showed a patch of consolidation on the right middle and lower zones. Echocardiography showed global hypokinesia with severe left ventricular dysfunction with ejection fraction of 30%. Repeat ABG after 6 h showed metabolic acidosis with lactic acidosis and hyperkalemia (pH = 7.257, pCO2 = 27.2, pO2 = 98.6, HCO3− = 13.8, Lactate = 7.1, K+ = 7.0). Lab values of S. K+ were 6.7 mEq/L and anti-hyperkalemia treatment was started in the form of calcium gluconate, dextrose-insulin, and salbutamol nebulization. With nephrologist's opinion, patient was urgently taken up for slow low-efficiency dialysis (SLED) of 8 h. Within 20 min of starting dialysis, patient had an episode of pulseless ventricular tachycardia. Patient was defibrillated and cardiopulmonary resuscitation (CPR) was done. Anti-hyperkalemia regimen was repeated. Urgent serum K+ levels done at the time of event were 9.1 mEq/L. After 40 min of CPR, patient was revived with normal sinus rhythm, was intubated and put on invasive ventilatory support. He was started on inotropes and vasopressors. Subsequent ABG done before the end of planned duration of SLED still showed persistent hyperkalemia (K+ = 7.1), with slight improvement in pH values. On discussion with the nephrologist, we planned to extend the ongoing SLED. After another 4 h of extended SLED, blood gas still showed raised potassium values (K+ = 7.2) with constant pH. For persistent hyperkalemia, SLED was further extended making a total duration of 20 h. Post dialysis, patient still had lab serum K+ level of 7.6 mEq/L. Next morning, patient developed blisters all over the body. He had coagulopathy and thrombocytopenia (PT/INR increased from 1.21 to 6.8 and platelets dropped down to 33,000 from 1.55 lacs/mm3), which was thought to be related to sepsis. On admission, patient was started empirically on ceftriaxone but in view of deteriorating clinical condition, he was shifted to meropenem, teicoplanin and ampicillin. It was an emperical selection of broad spectrum antibiotics keeping in mind MRSA and ampicillin for coverage for leptospira, with plans to de-escalate after obtaining culture reports. With deterioration in blood gas showing acidosis and again rise in potassium levels, patient was taken up for SLED again. He was dialyzed for more than 32 h, out of his 40 h hospital stay but his hyperkalemia remained refractory to antihyperkalemic agents and dialysis. Serial blood gases done showed that patient continued to have high anion gap acidosis and hyperkalemia at all times during his hospital stay []. This refractory hyperkalemia made us think over its cause. After ruling out all possible causes, it was considered to be related to heparin abuse. Following this, fludrocortisone in the dose of 100 μg/day was also added on morning of day 2. Correlating thrombocytopenia and coagulopathy also with heparin, activated clotting time was monitored and protamine sulphate was also given. On the 3rd day morning, patient had an episode of upper gastrointestinal bleed, following which he went into asystole. CPR was done according to protocol but patient could not be revived and was declared dead. Blood cultures obtained after 72 h showed methicilin-resistant staphylococci.