Cardiology Department, Concord Hospital, The University of Sydney, Sydney, Australia.
PLoS One. 2013 Apr 19;8(4):e61966. doi: 10.1371/journal.pone.0061966. Print 2013.
Baseline hyponatremia predicts acute mortality following pulmonary embolism (PE). The natural history of serum sodium levels after PE and the relevance to acute and long-term mortality after the PE is unknown.
Clinical details of all patients (n = 1023) admitted to a tertiary institution from 2000-2007 with acute PE were retrieved retrospectively. Serum sodium results from days 1, 3-4, 5-6, and 7 of admission were pre-specified and recorded. We excluded 250 patients without day-1 sodium or had <1 subsequent sodium assessment, leaving 773 patients as the studied cohort. There were 605 patients with normonatremia (sodium≥135 mmol/L throughout admission), 57 with corrected hyponatremia (day-1 sodium<135 mmol/L, then normalized), 54 with acquired hyponatremia and 57 with persistent hyponatremia. Patients' outcomes were tracked from a state-wide death registry and analyses performed using multivariate-regression modelling.
Mean (±standard deviation) day-1 sodium was 138.2±4.3 mmol/L. Total mortality (mean follow-up 3.6±2.5 years) was 38.8% (in-hospital mortality 3.2%). There was no survival difference between studied (n = 773) and excluded (n = 250) patients. Day-1 sodium (adjusted hazard ratio [aHR] 0.89, 95% confidence interval [CI] 0.83-0.95, p = 0.001) predicted in-hospital death. Relative to normonatremia, corrected hyponatremia increased the risk of in-hospital death 3.6-fold (95% CI 1.20-10.9, p = 0.02) and persistent hyponatremia increased the risk 5.6-fold (95% CI 2.08-15.0, p = 0.001). Patients with either persisting or acquired hyponatremia had worse long-term survival than those who had corrected hyponatremia or had been normonatremic throughout (aHR 1.47, 95% CI 1.06-2.03, p = 0.02).
Sodium fluctuations after acute PE predict acute and long-term outcome. Factors mediating the correction of hyponatremia following acute PE warrant further investigation.
基线低钠血症可预测肺栓塞（PE）后的急性死亡率。PE 后血清钠水平的自然史及其与 PE 后急性和长期死亡率的相关性尚不清楚。
回顾性检索了 2000 年至 2007 年期间在一家三级医疗机构因急性 PE 入院的所有患者（n=1023）的临床资料。入院第 1、3-4、5-6 和 7 天的血清钠结果预先指定并记录。我们排除了 250 名无入院第 1 天钠值或有<1 次后续钠评估的患者，留下 773 名患者作为研究队列。其中 605 名患者为正常钠血症（入院期间钠≥135mmol/L），57 名患者为纠正性低钠血症（入院第 1 天钠<135mmol/L，随后恢复正常），54 名患者为获得性低钠血症，57 名患者为持续性低钠血症。通过全州死亡登记处跟踪患者的结局，并使用多变量回归模型进行分析。
入院第 1 天的平均（±标准差）钠值为 138.2±4.3mmol/L。总死亡率（平均随访 3.6±2.5 年）为 38.8%（住院死亡率 3.2%）。研究（n=773）和排除（n=250）患者之间无生存差异。入院第 1 天的钠值（校正后的危险比[aHR]0.89，95%置信区间[CI]0.83-0.95，p=0.001）预测住院死亡。与正常钠血症相比，纠正性低钠血症使住院死亡的风险增加 3.6 倍（95%CI 1.20-10.9，p=0.02），持续性低钠血症使住院死亡的风险增加 5.6 倍（95%CI 2.08-15.0，p=0.001）。持续性或获得性低钠血症的患者比纠正性低钠血症或整个住院期间正常钠血症的患者长期生存更差（aHR 1.47，95%CI 1.06-2.03，p=0.02）。
PE 后钠的波动可预测急性和长期结局。急性 PE 后纠正低钠血症的中介因素值得进一步研究。
