背景:钾异常在重症监护中很常见,但在急诊科的发生率尚不清楚。
目的:我们描述了三级儿科急诊科的钾异常谱。
方法:回顾性病例对照研究,纳入单中心三级急诊科2.5年的所有患者。我们将低钾血症(<3.0mEq/L)和高钾血症(>6.0mEq/L)的患者与以3:1比例招募的正常随机人群进行了比较,钾水平在3.5至5mEq/L之间。
结果:在2013年1月1日至2016年8月31日之间,我们收治了108,209名患者进入急诊科。共检测血样9342份,发现血钾测定结果如下:低钾血症60例(2.8±0.2mEq/L),高钾血症55例(6.4±0.6mEq/L)。总的来说,纳入200例正常钾血症患者(4.1±0.3mEq/L)。这些疾病的主要原因是非特异性的:低钾血症的下呼吸道感染(23%)和骨折(15%)。下呼吸道(21.8%)和耳鼻喉感染(20.0%)为高钾血症。高钾血症患者的肌酐水平升高(0.72±1.6vs.0.40±0.16mg/dL,P<0.0001),碳酸氢盐较低(19.4±3.8vs.21.8±2.8mmol/L,P=0.0001)和更高的磷水平(1.95±0.6vs.1.42±0.27mg/dL,P=0.0001)。低钾血症患者的肌酐水平升高(0.66±0.71vs.0.40±0.16mg/dL,P<0.0001)和较低的磷水平(1.12±0.31vs.1.42±0.27mg/dL,P=0.0001)。我们没有观察到pH的显着差异,PCO2,碱过量和乳酸,或根据PIM和PRISM评分,普通病房和儿科重症监护病房的平均住院时间。
结论:Dyskalemia在急诊科患者中很少见:低钾血症为0.64%,高钾血症为0.58%。这种情况可以通过短暂的体积紊乱引起的一定程度的肾衰竭来解释。主要机制是消化损失导致的脱水,年轻患者的呼吸困难,摄入量差。在低钾血症的情况下,摄入不良和消化损失可能是主要原因。这些疾病通过进食或灌注很容易解决,并且不会损害发育。
结论:Dyskalemia在急诊科患者中很少见,通过喂养或灌注很容易解决。一种可能的病因机制是瞬时容量干扰。贫血症并不能预测急诊儿科人群的不良发展。
BACKGROUND: Potassium abnormalities are frequent in intensive care but their incidence in the emergency department is unknown.
OBJECTIVE: We describe the spectrum of potassium abnormalities in our tertiary-level pediatric emergency department.
METHODS: Retrospective case-control study of all the patients admitted to a single-center tertiary emergency department over a 2.5-year period. We compared patients with hypokalemia (<3.0mEq/L) and patients with hyperkalemia (>6.0mEq/L) against a normal randomized population recruited on a 3:1 ratio with potassium levels between 3.5 and 5mEq/L.
RESULTS: Between January 1, 2013 and August 31, 2016 we admitted 108,209 patients to our emergency department. A total of 9342 blood samples were tested and the following potassium measurements were found: 60 cases of hypokalemia (2.8±0.2mEq/L) and 55 cases of hyperkalemia (6.4±0.6mEq/L). In total, 200 patients with normokalemia were recruited (4.1±0.3mEq/L). The main causes of the disorders were non-specific: lower respiratory tract infection (23%) and fracture (15%) for hypokalemia, lower respiratory tract (21.8%) and ear-nose-throat infections (20.0%) for hyperkalemia. Patients with hyperkalemia had an elevated creatinine level (0.72±1.6 vs. 0.40±0.16mg/dL, P<0.0001) with lower bicarbonate (19.4±3.8 vs. 21.8±2.8mmol/L, P=0.0001) and higher phosphorus levels (1.95±0.6 vs. 1.42±0.27mg/dL, P=0.0001). Patients with hypokalemia had an elevated creatinine level (0.66±0.71 vs. 0.40±0.16mg/dL, P<0.0001) and a lower phosphorus level (1.12±0.31 vs. 1.42±0.27mg/dL, P=0.0001). We did not observe significant differences in pH, PCO2, base excess and lactate, or in the mean duration of hospitalization in general wards and pediatric intensive care units according to the PIM and PRISM scores.
CONCLUSIONS: Dyskalemia is rare in emergency department patients: 0.64% for hypokalemia and 0.58% for hyperkalemia. This condition could be explained by a degree of renal failure due to transient volume disturbance. The main mechanism is dehydration due to digestive losses, polypnea in young patients, and poor intake. In the case of hypokalemia, poor intake and digestive losses could be the main explanation. These disorders resolve easily with feeding or perfusion and do not impair development.
CONCLUSIONS: Dyskalemia is rare in emergency department patients and is easily resolved with feeding or perfusion. A plausible etiological mechanism is a transient volume disturbance.
Dyskalemia is not predictive of poor development in the emergency pediatric population.