Abstract: SA-PO0538
Campylobacter Cascade: Hypokalemia-Induced Rhabdomyolysis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Patel, Dhara D., Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Bernabei, Luca L, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Nguyen, Thuy, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Comitalo, Kelianne, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Dhakarwal, Pradeep, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
Introduction
Rhabdomyolysis is characterized by muscle injury and breakdown that leads to leakage of intracellular contents. Rhabdomyolysis caused by hypokalemia is a rare phenomenon with only a few published case reports. Here, we present a case of non-traumatic, hypokalemia-induced rhabdomyolysis as a complication of Campylobacter diarrhea.
Case Description
A 53-year-old female with a PMH EtOH use presented to the ED with 4 weeks of watery, non-bloody diarrhea, poor PO intake and progressive upper and lower extremity weakness. Vital signs were normal. Initial labs were notable for K <1.5, Cl 82, bicarb >50, creatinine 0.54, BUN 4, CK 6939, EtOH <10 and pH 7.61 pCO2 55 via VBG. UA showed 2+ blood and 1 RBC/hpf. ECG showed T wave inversions and U waves. On day 2, her CK peaked at 8820 and urine sodium, potassium and chloride were 59,15 and 50, respectively. Stool was positive for Campylobacter jejuni. She was treated with IV fluids, a total of 780 mEq of potassium and IV antibiotics with improvement.
Discussion
Rhabdomyolysis can arise from traumatic causes like muscle injury and immobilization or from non-traumatic causes like infection, electrolyte abnormalities, alcohol use and certain medications. Although chronic alcohol use leads to hypokalemia, our patient’s duration of watery diarrhea and poor PO intake suggests Campylobacter as the primary etiology of hypokalemia. The severity of hypokalemia and hypochloremia from GI losses ultimately led to compensatory ammoniagenesis and increased bicarbonate reabsorption in the proximal tubule, contributing to alkalosis. The typical triad of rhabdomyolysis includes muscle pain, weakness, and dark urine due to myoglobinuria. Rhabdomyolysis commonly presents with hyperkalemia as intracellular contents, most notably, potassium, leak from ischemic myocytes. However, the mechanism of rhabdomyolysis from hypokalemia is poorly understood. In a hypokalemic state, the lack of potassium release favors vasoconstriction, thus causing an oxygen supply-demand mismatch and eventually muscle ischemia and degradation. This is thought to lead to myocyte leakage and thus rhabdomyolysis. A brief literature review revealed most cases of hypokalemic rhabdomyolysis were from hyperaldosteronism. We found very few cases of rhabdomyolysis as a result of GI losses and hypokalemic hyperchloremic metabolic alkalosis as in our case.