P051: STRESS INDUCED CARDIOMYOPATHY FOLLOWING INTRACRANIAL HEMORRHAGE IN A YOUNG ATHLETE. CASE REPORT
Daniel Erwin Schmidt; Richard Silverman, MD; Nicolas P Caram, MD; Mariana Acosta, MD
Jackson Memorial Hospital / University of Miami
Introduction: Takotsubo cardiomyopathy (TC) or stress-induced cardiomyopathy, is a transient cardiac condition characterized by acute left ventricular dysfunction, typically triggered by intense emotional or physical stress. The clinical presentation of TC often mimics acute coronary syndrome, posing diagnostic and management challenges, especially in critical care settings.This case report describes the anesthetic and critical care management of a young, athletic male patient who developed TC following head trauma.
Patient Presentation: An 18-year-old male patient, with no known past medical history, was brought to the emergency department after being struck on the right side and collapsing shortly after, experiencing a brief loss of consciousness. Upon arrival at the ED, he was conscious, complaining of a headache, and exhibiting elevated blood pressure. Electrocardiogram was notable for ST segment elevation on leads D2, D3 and AVF.
While being transferred for a CT scan, his condition deteriorated, developing pink frothy sputum, acute hypoxemic respiratory failure, and myoclonic jerks, raising suspicion for neurogenic pulmonary edema requiring intubation and mechanical ventilation.
Critical Care Management and Diagnostic Findings: Following intubation, a bedside echocardiogram was performed, and unexpectedly revealed a severely reduced ejection fraction (EF) of 25-30% and a distinctive wall motion abnormality pattern indicative of TC
From a critical care standpoint, the priorities were to maintain hemodynamic stability, protect the lungs, and prevent further neurological deterioration. Vasopressor infusion was initiated to ensure adequate cerebral perfusion pressure and intracranial pressure monitoring was used via the external ventricular drain. Protective lung ventilation strategies with low tidal volumes were also employed.
Discussion: The likely mechanism of TC involves a surge of catecholamines, stress hormones released in response to the trauma, leading to myocardial stunning and transient left ventricular dysfunction. This catecholamine surge can overwhelm the heart, particularly the apical region, which has a higher density of beta-adrenergic receptors, resulting in the characteristic apical ballooning observed in TC.
The occurrence of acute pulmonary edema and heart failure underscores the potential for severe complications associated with TC. The pathophysiology of these complications is multifactorial, likely involving the sudden decrease in cardiac output, increased afterload due to peripheral vasoconstriction, and the release of inflammatory mediators. The patient's young age and athletic background are particularly noteworthy, as TC is more commonly observed in older individuals, especially post-menopausal women. This case emphasizes the importance of considering TC in the differential diagnosis of acute heart failure, even in young and healthy individuals, especially when significant physiological stress is involved.
In the critical care setting, close monitoring and prompt intervention were crucial in managing the patient's complex condition. The placement of an EVD allowed for continuous ICP monitoring and drainage of cerebrospinal fluid, aiding in the management of elevated ICP. The initiation of vasopressor support helped maintain adequate cerebral perfusion pressure and hemodynamics
Conclusion: This case reinforces the importance of a multidisciplinary approach in managing complex patients with TC, particularly in the context of acute neurological injury. Early recognition of TC and prompt initiation of appropriate supportive care are vital to improve patient outcomes.