Beck Nam-Seon, Jeong Yeon-Oh, Lee Kyung-Hee, Jun Eun-Mi, Im Joung-Il, Hong Sae-Yong
Department of Pediatrics, Chung-Ang Jeil Hospital, Chungbuk, South Korea.
Department of Gastroenterology, Chung-Ang Jeil Hospital, Chungbuk, South Korea.
Case Rep Gastroenterol. 2025 Mar 17;19(1):165-172. doi: 10.1159/000544099. eCollection 2025 Jan-Dec.
Most patients with compensated cirrhosis remain asymptomatic. However, with the onset of decompensation, electrolyte and acid-base disturbances are frequent in patients with chronic liver disease, including hypokalemia. We encountered a case of chronic liver disease with portal hypertension, primarily presenting with motor weakness caused by intractable hypokalemia, hypoxia-associated respiratory alkalosis, and chronic diarrhea.
A 54-year-old male presented to the emergency department with motor weakness. He reported experiencing exertional dyspnea and watery diarrhea for the past 3 months, approximately ten times daily. Arterial blood gas analysis indicated hypoxia and hypocapnia compatible with chronic respiratory alkalosis. The transtubular potassium gradient was 1.69, and the aldosterone/renin ratio was 17.6 (ng/dL)/(ng/mL/h). The patient had a 30-year history of consuming 360-720 mL of 20% alcohol almost daily. Abdominal computed tomography revealed multiple regenerative and dysplastic nodules in the liver, splenomegaly, ascites, esophageal varices, and diffuse edematous wall thickening in the bowel, suggesting portal hypertensive enteropathy. Computed tomography of the lungs showed no specific abnormalities in the lungs, pleura, or thoracic wall.
We present a case of liver cirrhosis complicated by intractable hypokalemia, respiratory alkalosis, portal hypertension, and chronic diarrhea. A 24-h urine analysis showed renal excretion levels of Na, K, and Cl at 6.0, 2.5, and 11.0 mmol, respectively, suggesting renal retention of these electrolytes. Meanwhile, the serum levels of Na, K, and Cl were 136, 1.8, and 98 mEq/L, respectively, indicating a preserved balance of sodium and chloride but not potassium. This case underscores the importance of clinicians considering both liver cirrhosis-associated hypoxia and chronic liver disease-induced chronic diarrhea as potential underlying causes, especially when more common causes of hypokalemia have been excluded.
大多数代偿期肝硬化患者无症状。然而，随着失代偿的发生，慢性肝病患者常出现电解质和酸碱紊乱，包括低钾血症。我们遇到一例慢性肝病合并门静脉高压患者，主要表现为顽固性低钾血症、低氧相关性呼吸性碱中毒和慢性腹泻所致的肌无力。
一名54岁男性因肌无力就诊于急诊科。他报告在过去3个月中出现劳力性呼吸困难和水样腹泻，每天约10次。动脉血气分析显示低氧血症和低碳酸血症，符合慢性呼吸性碱中毒。跨肾小管钾梯度为1.69，醛固酮/肾素比值为17.6（ng/dL）/（ng/mL/h）。该患者有30年几乎每日饮用360 - 720 mL 20%酒精的病史。腹部计算机断层扫描显示肝脏有多个再生结节和发育异常结节、脾肿大、腹水、食管静脉曲张以及肠道弥漫性水肿性肠壁增厚，提示门静脉高压性肠病。肺部计算机断层扫描显示肺部、胸膜或胸壁无特异性异常。
我们报告一例肝硬化合并顽固性低钾血症、呼吸性碱中毒、门静脉高压和慢性腹泻的病例。24小时尿液分析显示肾钠、钾、氯排泄水平分别为6.0、2.5和11.0 mmol，提示这些电解质的肾潴留。同时，血清钠、钾、氯水平分别为136、1.8和98 mEq/L，表明钠和氯保持平衡但钾并非如此。该病例强调了临床医生将肝硬化相关低氧血症和慢性肝病引起的慢性腹泻视为潜在病因的重要性，尤其是在排除了更常见的低钾血症病因时。
