A53-09 A Fatal Cascade: Chlorthalidone-induced Refractory Hypokalemia, Resulting in Ileus, Stercoral Colitis, Septic Shock, and Multiorgan Failure

Background Severe hypokalemia may impair gastrointestinal smooth muscle function, causing ileus or pseudo-obstruction. When refractory to repletion, it can trigger a cascade of metabolic, mechanical, and inflammatory complications. We present a case of Chlorthalidone-induced refractory hypokalemia leading to paralytic ileus, severe colonic distention, stercoral colitis, and fatal septic shock. Case Presentation A 77-year-old man with hypertension, diabetes, and hyperlipidemia on chlorthalidone 50 mg daily presented with one week of constipation unrelieved by laxatives. CT abdomen/pelvis revealed severe fecal impaction, stercoral colitis, and colonic pneumatosis. Initial labs showed K+ 2.0 mEq/L, Mg 0.9 mg/dL, and WBC 19.5 × 109/L. Despite discontinuation of chlorthalidone and aggressive replacement (>450 mEq potassium through oral and IV routes), serum potassium remained <3.0 mEq/L for four days. Urine K+ 35 mEq/L and TTKG 9.0 confirmed renal potassium wasting, later improving to 5.7, reflecting depleting chlorthalidone effect. He underwent only partial fecal disimpaction in OR under limited anesthesia due to persistent hypokalemia. Repeat imaging showed continued impaction and colonic dilation. On hospital day 4, the patient developed tachypnea, hypoxemia (SpO2 86% on 6 L O2), and pCO2 53 mmHg, requiring ICU transfer for hypercapnic respiratory failure. Persistent abdominal distension reduced diaphragmatic excursion, resulting in gas-exchange impairment, worsened by volume overload from eventual shock. The patient developed shock requiring norepinephrine; labs showing WBC 22 K/µL, lactate 4.1 mmol/L, and troponin >23,000 ng/L, Cr 2.5, consistent with sepsis and multiorgan failure. Despite HFNC, trial of BiPAP and maximal medical management, he expired on day 5 under DNR/DNI status. Discussion Refractory hypokalemia was primarily renal in origin, due to chlorthalidone’s prolonged effect. Severe potassium depletion caused colonic hypomotility, leading to severe colonic dilation and ischemic bowel. Mucosal injury and bacterial translocation produced a sepsis-like inflammatory state. Extreme colonic distension also elevated the diaphragm, causing type II respiratory failure. The combination of sepsis physiology, shock, and metabolic derangement culminated in multiorgan failure. Conclusion This case highlights the lethality of chlortalidone-induced potassium derangement. Chlorthalidone’s long half-life and potent distal tubular action can sustain renal potassium wasting days after discontinuation, producing refractory hypokalemia unresponsive to conventional repletion. The ensuing smooth muscle paralysis precipitated severe ileus with catastrophic results. The trajectory from a correctable electrolyte disorder to fatal sepsis and multiorgan failure illustrates how quickly a cascade of metabolic, mechanical, and infectious complications can occur. Vigilance in identifying persistent diuretic-induced renal potassium loss and early, aggressive correction is critical to prevent this preventable and deadly sequence.