Crop Meindert J, Hoorn Ewout J, Lindemans Jan, Zietse Robert
Deprtment of Internal Medicine,Erasmus Medical Center, Rotterdam, The Netherlands.
Nephrol Dial Transplant. 2007 Dec;22(12):3471-7. doi: 10.1093/ndt/gfm471. Epub 2007 Sep 10.
The objective was to study the epidemiology of hypokalaemia [serum potassium concentration (S(K)) <3.5 mmol/l] in a general hospital population, specifically focusing on how often and why patients develop subsequent hyperkalaemia (S(K) > or =5.0 mmol/l).
In a 3-month hospital-wide study we analysed factors contributing to hypokalaemia and subsequent hyperkalaemia.
From 1178 patients in whom S(K) was measured, 140 patients (12%) with hypokalaemia were identified (S(K) 3.0 +/- 0.3 mmol/l). One hundred patients (71%) had hospital-acquired hypokalaemia. Common causes of hypokalaemia included gastrointestinal losses (67%), diuretics (36%) and haematological malignancies (9%). In 104 patients (74%), hypokalaemia was multifactorial. Hypokalaemia frequently coexisted with hyponatraemia (24%) and, when measured, hypomagnesaemia (61%). Twenty-three patients (16%) developed hyperkalaemia (highest S(K) 5.7 +/- 0.7 mmol/l) following hypokalaemia. In these patients, potassium suppletion was not more common (70 vs 59%, P = 0.5), but when potassium was given, the total amount administered was significantly higher (median 350 mmol vs 180 mmol, P = 0.02). Furthermore, these patients more often received total parenteral nutrition (17 vs 4%, P = 0.02) and magnesium suppletion (30 vs 9%, P = 0.009), and more often had haematological malignancies (22 vs 6%, P = 0.03).
Hypokalaemia is a multifactorial and usually hospital-acquired condition associated with hyponatraemia and hypomagnesaemia. One out of every six patients with hypokalaemia developed subsequent hyperkalaemia. Besides potassium suppletion, total parenteral nutrition (source of potassium), magnesium suppletion (may reduce kaliuresis) and haematological malignancy (may cause cell lysis) contribute to hyperkalaemia following hypokalaemia. Caution with potassium suppletion and frequent monitoring of S(K) may prevent iatrogenic hyperkalaemia.
目的是研究综合医院人群中低钾血症[血清钾浓度（S(K)）<3.5 mmol/L]的流行病学，特别关注患者发生后续高钾血症（S(K)≥5.0 mmol/L）的频率及原因。
在一项为期3个月的全院范围研究中，我们分析了导致低钾血症及后续高钾血症的因素。
在1178例测量了S(K)的患者中，确定了140例（12%）低钾血症患者（S(K) 3.0±0.3 mmol/L）。100例（71%）患者发生医院获得性低钾血症。低钾血症的常见原因包括胃肠道失钾（67%）、利尿剂（36%）和血液系统恶性肿瘤（9%）。104例（74%）患者的低钾血症是多因素导致的。低钾血症常与低钠血症（24%）并存，且在测量时，常与低镁血症（61%）并存。23例（16%）患者在低钾血症后发生高钾血症（最高S(K) 5.7±0.7 mmol/L）。在这些患者中，补钾情况并非更常见（70%对59%，P = 0.5），但在补钾时，补钾总量显著更高（中位数350 mmol对180 mmol，P = 0.02）。此外，这些患者更常接受全胃肠外营养（17%对4%，P = 0.02）和补镁（30%对9%，P = 0.009），且更常患有血液系统恶性肿瘤（22%对6%，P = 0.03）。
低钾血症是一种多因素导致的疾病，通常为医院获得性，与低钠血症和低镁血症相关。每六例低钾血症患者中有一例随后发生高钾血症。除补钾外，全胃肠外营养（钾的来源）、补镁（可能减少尿钾排泄）和血液系统恶性肿瘤（可能导致细胞溶解）是低钾血症后发生高钾血症的原因。谨慎补钾并频繁监测S(K)可预防医源性高钾血症。
