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Published on: January 28, 2020
Could cardiac biomarkers predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?
Tijana Nastasovic1, Branko Milakovic2,3, Jelena Eric Marinkovic3
1Department of Anesthesiology and Resuscitation on Clinic for Neurosurgery, Center for Anesthesiology and Resuscitation, Clinical Center of Serbia, Pasterova 2, Belgrade, Serbia. tijananas@ptt.rs.
Background:
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after a significant central nervous system (CNS) insult. NPE occurs as a result of release of catecholamines into the blood immediately after aneurysm rupture. The aim of this study is to investigate the connection between the value of cardiac biomarkers on admission and incidence of NPE in patients with aneurysmal subarachnoid hemorrhage (SAH).
Methods:
A total of 262 SAH patients (162 women, 100 men) were prospectively included in the study. Clinical characteristics, electrocardiographic (ECG) changes, serum cardiac and inflammatory biomarkers were measured on admission and on the day of development of NPE. These data were analyzed in order to predict the development NPE.
Results:
Nineteen patients (7.25%) developed NPE. Comparison revealed that patients who subsequently developed NPE, sustained more severe SAH. Cardiac damage was more severe in these patients, as represented by significantly higher mean values of all examined cardiac biomarkers (P = 0.000), except for troponin I value that was significantly lower (P = 0.000). Multivariate regression analysis revealed that elevated troponin I (OR, 4.980; 95% CI, 1.27-19.49; P = 0.021) and white blood cell count (OR, 22.195; 95% CI, 3.99-123.50; P = 0.000) are predictors of NPE.
Conclusions:
Significantly higher values of cardiac biomarkers were observed in SAH patients complicated with NPE. Elevated values of cardiac biomarkers appear to play an active role in prediction of NPE, although white blood cell count may be involved in the prediction of NPE. There is an influence of SAH therapy on predictors of NPE.
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