Frustaci A, Scoppetta C
Postgrad Med J. 1984 Oct;60(708):679-81. doi: 10.1136/pgmj.60.708.679.
A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed.
报告了一例伴有昏迷、骨骼肌和心肌损伤的严重低钾血症病例。最初输注葡萄糖 - 胰岛素 - 钾(GIK)使临床症状暂时改善,肌酸激酶(CKMB)降低,血清钾升高。治疗第4天,出现神经肌肉和心血管功能恶化,同时CKMB进一步升高。这种恶化与血清磷酸盐浓度为0.26 mmol/l同时出现。使用超声心动图测量左心室(LV)功能并检测射血分数(EF)。停用GIK并开始输注磷酸钾。随着磷酸盐和钾缺乏得到纠正,神经肌肉和心脏异常消失,CKMB降至正常,左心室射血分数从40%升至72%。我们认为该患者可能因低磷血症而出现了额外的心脏损伤,该患者原本就因严重低钾血症而存在心脏损害。文中讨论了可能的机制。