Troponins and echocardiography: role in detecting myocardial injury in burn patients

Figures

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  Figure 1.. Pathophysiology of burn-related myocardial injury. Major burn injury triggers a cascade of hemodynamic, metabolic, and inflammatory changes that contribute to myocardial injury. The acute burn shock phase (0–24 h) is characterized by systemic capillary leak, plasma extravasation, and microvascular dysfunction leading to hypovolemia. Within days, a sustained hypermetabolic phase develops, driven by elevated catecholamines and mitochondrial inefficiency, increasing cardiac oxygen demand. Pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and reactive oxygen species directly impair cardiomyocyte contractility and promote apoptosis.

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  Figure 2.. Mechanism of troponin release in burn-related myocardial injury. Schematic representation of cardiomyocyte injury following major burns. In the normal state, cTnI and cTnT are bound to the actin–tropomyosin complex within the sarcomere. Burn-induced hypoperfusion, catecholamine surges, oxidative stress, and inflammatory cytokines cause reversible membrane leakage or irreversible myocyte necrosis, releasing troponins into the circulation. Factors influencing measured troponin levels include renal dysfunction, sepsis, and skeletal muscle injury (more pronounced for cTnT), with cTnI offering higher myocardial specificity. cTnI, cardiac troponin I; cTnT cardiac troponin T.

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  Figure 3.. Echocardiographic findings in burn patients. (a) Normal TTE showing preserved LV size and function. (b) Acute burn effects include reduced ejection fraction, regional wall-motion abnormalities, LV wall thickening (remodeling), and diastolic filling impairment. (c) Advanced imaging, including strain analysis, can detect reduced global longitudinal strain despite preserved ejection fraction. Comparison of TTE and PiCCO demonstrates that TTE may underestimate cardiac output in critically ill burn patients. LV, left ventricular; PiCCO, Pulse Index Contour Cardiac Output; TTE, transthoracic echocardiogram.

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  Figure 4.. Dual-diagnostic approach for burn-related myocardial injury. Venn diagram illustrating the complementary roles of troponin measurement (biochemical evidence) and echocardiography (mechanical dysfunction) in identifying high-risk burn cardiomyopathy. Patients with both troponin elevation and echo abnormalities represent a high-risk group warranting early cardiology consultation, fluid resuscitation adjustment, β-blockade or anabolic therapy, and long-term cardiac monitoring.

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  Figure 5.. Proposed screening and management algorithm for myocardial injury in burn patients. Flowchart outlining a practical protocol for patients with burns exceeding 20% TBSA. Initial assessment includes vitals, TBSA calculation, and laboratory testing. Troponin and TTE should be performed within 24 h. If both are normal, reassess every 48–72 h; if one is abnormal, repeat daily and consult cardiology. When both are abnormal, escalate therapy with tailored fluid titration and inotrope adjustment, and arrange long-term follow-up for persistent abnormalities. TBSA, total body surface area; TTE, transthoracic echocardiogram.