Singhal P C, Abramovici M, Venkatesan J
Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York 11042.
Am J Med. 1990 Jan;88(1):9-12. doi: 10.1016/0002-9343(90)90120-3.
We undertook this study to determine the occurrence of rhabdomyolysis in the hyperosmolal state.
We reviewed 130 hospital admissions due to diabetic ketoacidosis or hyperosmolal coma, or both. Thirty-one patients (12 men and 19 women) were found to be in the hyperosmolal state. Sixteen of 31 patients showed biochemical evidence of rhabdomyolysis. The clinical and biochemical features of the patients with rhabdomyolysis (Group I) and the patients without rhabdomyolysis (Group II) were compared.
Patients in Group I showed a 100-fold increase (7,156 +/- 2,820 IU/L) in serum creatine phosphokinase (CPK) when compared to the patients in Group II (61 +/- 11 IU/L). The mean serum osmolality was much higher (p less than 0.001) in patients with rhabdomyolysis (381 +/- 12 mOsm/kg) than in those without rhabdomyolysis (324 +/- 4 mOsm/kg). The serum sodium level was elevated (p less than 0.001) in Group I patients (151 +/- 4 mEq/L) but not in Group II patients (133 +/- 2 mEq/L). There was a linear association between serum CPK versus serum sodium (r = 0.62, p less than 0.05) and serum CPK versus serum osmolality (r = 0.05, p less than 0.05). The mean serum potassium level was lower (p less than 0.01) in Group I than in Group II. Only two patients (12%) in Group I and almost half the patients (seven of 15) in Group II were hyperkalemic. The mean serum phosphorus level was lower in Group II than in Group I. Four patients in Group I and one patient in Group II developed acute renal failure.
Subclinical rhabdomyolysis is a common finding in the hyperosmolal state. Absence of hyperkalemia in the presence of muscle injury, hyperosmolality, hyperglycemia, and acidosis suggested pre-existing total-body potassium deficiency in many of these patients. In addition to hypokalemia, the hyperosmolal state predisposes to the development of rhabdomyolysis.
我们开展这项研究以确定高渗状态下横纹肌溶解症的发生率。
我们回顾了130例因糖尿病酮症酸中毒或高渗性昏迷或两者兼有的住院病例。发现31例患者(12名男性和19名女性)处于高渗状态。31例患者中有16例显示出横纹肌溶解症的生化证据。比较了发生横纹肌溶解症的患者(I组)和未发生横纹肌溶解症的患者(II组)的临床和生化特征。
与II组患者(61±11 IU/L)相比,I组患者的血清肌酸磷酸激酶(CPK)升高了100倍(7,156±2,820 IU/L)。发生横纹肌溶解症的患者(381±12 mOsm/kg)的平均血清渗透压远高于未发生横纹肌溶解症的患者(324±4 mOsm/kg)(p<0.001)。I组患者的血清钠水平升高(151±4 mEq/L)(p<0.001),而II组患者(133±2 mEq/L)则未升高。血清CPK与血清钠之间(r = 0.62,p<0.05)以及血清CPK与血清渗透压之间(r = 0.05,p<0.05)存在线性关联。I组的平均血清钾水平低于II组(p<0.01)。I组中只有2例患者(12%)血钾过高,而II组中几乎一半的患者(15例中有7例)血钾过高。II组的平均血清磷水平低于I组。I组有4例患者和II组有1例患者发生了急性肾衰竭。
亚临床横纹肌溶解症在高渗状态下是常见的发现。在存在肌肉损伤、高渗、高血糖和酸中毒的情况下无高钾血症表明这些患者中的许多人预先存在全身钾缺乏。除低钾血症外,高渗状态易引发横纹肌溶解症。