Stunned Myocardium Syndrome Following Severe Traumatic Brain Injury with Multisystem Complications: A Neurocritical Care Challenge

Abstract

Stunned myocardium syndrome (SMS) is a reversible myocardial dysfunction occurring after ischemia and reperfusion, commonly described in cardiac contexts but underrecognized in traumatic brain injury (TBI). We present a case of severe TBI complicated by SMS after cardiac arrest, underscoring the importance of early recognition and multidisciplinary management.

Keywords

neurocritical care - severe traumatic brain injury - SMS - stunned myocardium syndrome

Introduction

Stunned myocardium refers to transient, reversible ventricular dysfunction persisting after reperfusion despite the absence of permanent myocyte injury.[1] Initially described in ischemic heart disease, it has since been reported in acute neurological disorders, particularly subarachnoid hemorrhage and severe traumatic brain injury (TBI).[1] [2] [3] Proposed mechanisms include catecholamine-mediated myocardial injury, sympathetic overdrive, and microvascular dysfunction.[1] [2] In neurocritical care, stunned myocardium syndrome (SMS) may exacerbate hemodynamic instability, complicating cerebral perfusion management. Early diagnosis using echocardiography and cardiac biomarkers is crucial for guiding treatment and improving outcomes.

Case Report

A 38-year-old male was found unconscious following a suspected road traffic accident. On arrival (Glasgow Coma Scale [GCS] E1V1M5), he was hemodynamically stable but had bilaterally nonreactive pupils. Computed tomography brain showed left occipital contusion, bifrontal subarachnoid hemorrhage, and frontal bone fractures. Magnetic resonance imaging revealed diffuse axonal injury with hemorrhagic contusions.

He was intubated, monitored for intracranial pressure (6–15 mm Hg), and managed in the intensive care unit (ICU). On day 2, he suffered asystolic cardiac arrest, requiring cardiopulmonary resuscitation. Postresuscitation, troponin T was 1228 and CPK-MB (creatine phosphokinase-myocardial band) 185; echocardiography showed global left ventricular hypokinesia, confirming SMS. Dobutamine and noradrenaline were initiated to support myocardial function and maintain mean arterial pressure > 65 mm Hg.

Prolonged ventilation necessitated tracheostomy. He developed acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI), managed with diuretics and one hemodialysis session. On ICU day 8, right lower limb ischemia appeared; Doppler revealed distal anterior tibial artery thrombosis, likely iatrogenic from vasopressors and arterial line trauma. Anticoagulation with enoxaparin, later rivaroxaban, was initiated.

By day 10 postarrest, neurological status improved to GCS E4VTM6; inotropes were tapered, and he was gradually weaned from ventilatory support. After an 80-day hospital stay, he was discharged stable.

Discussion

SMS after TBI reflects complex neurocardiogenic injury. Mechanisms involve excessive sympathetic discharge and catecholamine-mediated myocardial toxicity, impairing contractility without irreversible myocyte damage.[1] [3] While classically linked to subarachnoid hemorrhage, SMS in TBI—especially postcardiac arrest—is increasingly recognized.[2]

Management balances maintaining cerebral perfusion with minimizing myocardial strain. Dobutamine enhances contractility without significantly increasing afterload,[4] while noradrenaline supports perfusion but requires cautious titration due to vasoconstriction and ischemia risk.[5]

This case illustrates systemic complications—ARDS, AKI, and vascular thrombosis—common in prolonged critical illness.[6] Vasopressor use, immobility, and invasive lines contribute to thrombotic risk, necessitating preventive strategies and early detection.[7] Multidisciplinary coordination among neurosurgery, cardiology, intensive care, and vascular teams was pivotal for recovery.

Conclusion

SMS is a reversible but potentially life-threatening complication in TBI. Early echocardiographic diagnosis, targeted hemodynamic support, and vigilant management of systemic complications can yield favorable outcomes. Cardiac monitoring should be integral to neurocritical care, particularly after cardiac arrest in TBI patients.

Conflict of Interest

None declared.

• References

• 1 Bolli R. Mechanism of myocardial “stunning”. Circulation 1990; 82 (03) 723-738
• 2 Banki NM, Kopelnik A, Tung P. et al. Prospective analysis of prevalence, incidence and severity of electrocardiographic abnormalities in subarachnoid hemorrhage. J Neurosurg 2005; 102 (03) 416-422
• 3 Nguyen HB, Polderman KH. Catecholamine stress-induced cardiomyopathy. Crit Care 2009; 13 (05) 220
• 4 Marik PE, Zaloga GP. Catecholamines and the critically ill: what is the role of dobutamine?. Chest 2002; 121 (01) 340-341
• 5 Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369 (18) 1726-1734
• 6 Kantharia BK. ARDS management in polytrauma patients. Indian J Crit Care Med 2012; 16 (04) 186-190
• 7 Polderman KH, Girbes AJ. Central venous catheter use. Part 1: mechanical complications. Intensive Care Med 2002; 28 (01) 1-17

Publication History

Article published online:
13 November 2025