ArticleCureus2026
Post-craniotomy Troponin Elevation Without Ischemia After Traumatic Brain Injury: A Case Report and Management Framework.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Cardiac complications after neurosurgical procedures are uncommon but may present significant diagnostic and therapeutic challenges, particularly when anticoagulation carries a high risk of intracranial hemorrhage. We report the case of a 40-year-old woman with no prior medical history who sustained blunt craniofacial trauma from a heavy metallic object. Head CT revealed bilateral depressed frontal fractures with associated epidural hematomas and cerebral contusions. The patient underwent bilateral frontal craniotomy for hematoma evacuation and osteosynthesis. During the early postoperative period, she developed acute chest pain, marked tachycardia (up to 170 bpm), and a significant elevation in troponin levels (peak 244.7 ng/L). Serial electrocardiograms (ECGs) demonstrated sinus rhythm without dynamic ischemic changes, and echocardiography showed preserved biventricular function without regional wall motion abnormalities. Given the recent craniotomy and high bleeding risk, anticoagulation and antiplatelet therapy were deferred. The clinical presentation and diagnostic findings were consistent with acute myocardial injury likely secondary to hemodynamic stress and sympathetic overactivation rather than acute coronary syndrome. The patient improved with conservative management, achieving full recovery without neurological or cardiac complications. This case highlights the importance of distinguishing neurogenic or stress-related myocardial injury from true ischemia in postoperative neurosurgical patients. Mechanisms such as catecholamine surge and paroxysmal sympathetic hyperactivity (neuro-storm) may contribute to transient myocardial injury in this setting. A multidisciplinary approach integrating ECG trends, biomarker kinetics, and echocardiography can support accurate diagnosis while minimizing bleeding risk. These findings should be interpreted in the context of a single case, and further studies are needed to better characterize this phenomenon.
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