Cardiac Troponin I and Acute Lung Injury After Subarachnoid Hemorrhage

• Published in: Neurocritical care Vol. 11; no. 2; pp. 177 - 182
• Main Authors: Naidech, Andrew M., Bassin, Sarice L., Garg, Rajeev K., Ault, Michael L., Bendok, Bernard R., Batjer, H. Hunt, Watts, Charles M., Bleck, Thomas P.
• Format: Journal Article
• Language: English
• Published: New York Humana Press Inc 01-10-2009; Springer Nature B.V
• Subjects: Acute Disease; Acute Lung Injury - diagnostic imaging; Acute Lung Injury - epidemiology; Adult; Aged; Aneurysms; Blood pressure; Cardiovascular disease; Catheters; Critical Care Medicine; Edema; Ejection fraction; Erythrocyte Transfusion - adverse effects; Female; Hemorrhage; Humans; Intensive; Internal Medicine; Medicine; Medicine & Public Health; Middle Aged; Mortality; Myocardium - metabolism; Neurology; Original Article; Patients; Pneumonia; Prospective Studies; Radiography; Regression Analysis; Respiratory distress syndrome; Respiratory Distress Syndrome, Adult - complications; Review boards; ROC Curve; Subarachnoid Hemorrhage - complications; Subarachnoid Hemorrhage - diagnostic imaging; Surgeons; Tomography, X-Ray Computed; Troponin I - metabolism; Variables; Acute lung injury; Subarachnoid hemorrhage; Troponin
• ISSN: 1541-6933; 1556-0961
• DOI: 10.1007/s12028-009-9223-y

Introduction
There are few predictors of acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) after subarachnoid hemorrhage (SAH). We hypothesized that cardiac troponin I, which is associated with cardiovascular morbidity, would also predict ALI.
Methods
We prospectively enrolled 171 consecutive patients with SAH. Troponin was routinely measured on admission and the next day and subsequently if abnormal. We prospectively recorded the maximum troponin, in-hospital events, and clinical endpoints. ALI and ARDS were defined by standard criteria.
Results
Acute lung injury was found in 10 patients (6%), ARDS in an additional 14 (8%), and pulmonary edema without lung injury in 9 (5%). Maximum troponin was different in patients without lung injury or pulmonary edema (0.03 [0.02–0.12] mcg/l), ALI (0.17 [0.04–1.4]), or ARDS (0.31 [0.9–1.8],
P
 < 0.001). In ROC analysis, a cutoff of 0.04 mcg/l had 91% sensitivity and 42% specificity for ALI or ARDS (AUC = 0.75,
P
 < 0.001). Troponin was associated with ALI or ARDS after accounting for neurologic grade in multivariate models without further contribution from pneumonia, packed red cell transfusion, gender, tobacco use, coronary artery disease, vasospasm, depressed ejection fraction on echocardiography, or CT grade. Lung injury was associated with worse functional outcome at 14 days, but not at 28 days or 3 months.
Conclusion
Troponin I is associated with the development of ALI after SAH.