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

Abstract

Severe burn injuries result in a massive systemic inflammatory and hypermetabolic response, often disrupting multiple organ systems, including the cardiovascular system. Cardiac troponins are frequently elevated in burn patients, but the interpretation of these elevations is hardly straightforward. Sometimes, elevated troponin means type 1 myocardial infarction (MI) due to an acute coronary event, but it might also reflect type 2 MI due to an imbalance between body oxygen demand and supply, or even non-ischemic myocardial injury from things like overwhelming inflammation, sepsis, or direct thermal effects on the heart itself. This narrative review explores the prevalence, underlying pathophysiological mechanisms, diagnostic challenges, and prognostic implications of troponin elevation in burn patients. We discussed the limitations of applying conventional MI diagnostic criteria in this unique population. The role of electrocardiographic and echocardiographic assessment, as well as the potential utility of high-sensitivity troponin assays, is also discussed. Understanding of how burn pathophysiology relates to myocardial injury is essential for accurate diagnosis, improved management, and better outcomes in this highly vulnerable group of patients.

Plain language summary

Detecting heart attacks in burn patients using different tools

Burn injuries affect different organs in the body due to inflammation, and one of them is the heart. When the heart is injured, a protein called troponin increases, which could indicate a heart attack. In this review, we learn about using troponins and another machine called echocardiogram to detect if a burn patient is suffering from a heart injury or possibly a heart attack. We learn the mechanism behind the increase of troponins, how often the increase occurs, what does it mean if troponins increase, and problems we face trying to detect if an increase has occurred. Understanding this is important as it we are able to find gaps in our knowledge and create better tools to diagnose them to help burn patients.

Keywords

burn cardiomyopathy burn injury cardiac dysfunction cardiac troponin echocardiography fluid resuscitation global longitudinal strain high-sensitivity troponin myocardial injury

Introduction

Severe burn injury precipitates a whole-body pathophysiologic response characterized by hyperinflammation, hypermetabolism, and neurohormonal activation that extends well beyond the skin and drives multi-organ dysfunction, including clinically important cardiovascular (CV) involvement. The systemic stress response after major burns involves a sustained surge of catecholamines and glucocorticoids with mitochondrial dysfunction across organs, providing a mechanistic bridge between cutaneous injury and downstream cardiac derangements.¹ Contemporary burn physiology reviews emphasize that tachycardia, increased myocardial oxygen demand, and a high-output circulatory state often coexist with intrinsic myocardial depression, underscoring the complexity of hemodynamics in this population.^2,3

The CV stress response following severe burns is multifactorial: catecholamine excess, cytokine signaling, and nitric oxide (NO) pathways converge to impair contractility and diastolic relaxation, while fluid shifts and capillary leak compound preload–afterload abnormalities.^3,4 Experimental and translational data show that tumor necrosis factor-α (TNF-α) and inducible NO synthase can depress myocardial mechanics through NO-dependent and NO-independent mechanisms, linking the inflammatory milieu of burns and sepsis with burn-related myocardial dysfunction.^5,6 In human studies, echocardiographic indices demonstrate early reductions in systolic performance and restrictive diastolic filling patterns after burns, aligning with biochemical evidence of myocardial injury.^7,8

Early detection of myocardial injury is clinically important because cardiac dysfunction (CD) after burns correlates with longer intensive care stays and worse outcomes, and may not be apparent from vital signs or global ejection fraction (EF) alone.⁹ High-sensitivity cardiac troponins (cTn) provide a specific biochemical signal of myocardial injury in critical illness and, in burn cohorts, elevated troponin I within the first 72 h identifies patients at higher risk of adverse events.^10,11 Large critical-care studies further show that troponin elevation, irrespective of primary admission diagnosis, is associated with increased mortality, supporting its use as a prognostic biomarker when interpreted in a clinical context.¹² Because nonischemic myocardial injury is common in systemic inflammation, contemporary consensus recommends using assay-specific thresholds and dynamic changes to attribute acuity, which is particularly relevant in burn patients with overlapping etiologies of injury.¹³ Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) complement biomarkers by repeatedly and noninvasively characterizing systolic and diastolic function at the bedside; in burns, echocardiography detects both global and regional dysfunction and can reveal diastolic abnormalities that portend worse outcomes.^3,14 Advanced deformation imaging with speckle-tracking enhances sensitivity to subclinical injury and better tracks loading-independent myocardial performance, which may be advantageous when fluid resuscitation and vasopressors confound conventional metrics.¹⁵

The purpose of this narrative review is to synthesize the most up-to-date evidence on troponin assays and echocardiographic modalities, conventional and strain-based, for detecting and monitoring myocardial injury in adults with burn injury, with attention to assay interpretation, imaging protocols, and the hemodynamic context unique to burn resuscitation. We aim to integrate mechanistic insights from burn pathophysiology with clinical data on biomarker, imaging concordance, highlight knowledge gaps, and outline pragmatic approaches that leverage serial high-sensitivity troponin testing alongside targeted echocardiography to improve risk stratification and guide therapy.

Pathophysiology of myocardial injury in burn patients

Through a combination of direct myocardial injury, metabolic stress, and hemodynamic instability, severe burn injuries can have a significant impact on heart function (Figure 1). Massive fluid changes, capillary leaks, and decreased myocardial perfusion characterize the initial shock phase. A hypermetabolic condition that significantly raises cardiac workload follows. Oxidative stress and inflammatory mediators also reduce contractility, which leads to early and persistent cardiac depression. In addition to affecting acute outcomes, these pathophysiologic alterations may cause long-term heart dysfunction, underscoring the necessity of close observation and focused treatments for burn patients.

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.

As illustrated in Figure 1, a major burn injury initiates a storm of changes, including hemodynamic, metabolic, and inflammatory changes that collectively contribute to the myocardial injury. The diagram brings together what we know about the early burn-shock phase, when capillaries leak and reduced myocardial perfusion, followed by the hypermetabolic phase, where catecholamine surge occurs and the heart’s demand for oxygen increases. These mechanisms appear clearly in both lab and clinical research, and they form the backbone for the pathophysiologic model discussed in section “Pathophysiology of myocardial injury in burn patients.”

Burn shock, fluid shifts, and impaired myocardial perfusion

Major burn injuries trigger an acute phase, commonly referred to as burn shock, characterized by systemic capillary leak, massive interstitial edema, and intravascular volume depletion.¹⁶ Following a major burn (including >40% total body surface area (TBSA)), there is a massive inflammatory response caused by a peak in circulating inflammatory mediators that include histamine, kinins, TNF-α, serotonin, prostaglandins, interleukins (e.g., IL-1β, IL-6, and IL-8), leukotrienes, and thromboxane A2.^17,18

Moreover, activation of inflammatory, complement cascades, and coagulation establishes a positive feedback loop that leads to microvascular dysfunction, the opening of junctions between adjacent endothelial cells, and the shedding of the endothelial glycocalyx allowing up to 50% of plasma water to extravasate within hours of a ⩾20% TBSA burn, resulting in hemoconcentration and hypovolemia despite aggressive crystalloid resuscitation.^2,17

Hemodynamically, this manifests as a 40%–60% decline in the cardiac output (CO), reduced stroke work, and diminished coronary blood flow, even when central venous and wedge pressures suggest adequate filling.^18,19

Restoration of tissue and myocardial perfusion relies on carefully titrated fluid replacement. Most centers employ the Parkland formula, but “fluid creep” frequently leads to over-resuscitation, pulmonary edema, and abdominal or extremity compartment syndromes.²⁰ Continuous hemodynamic monitoring (using clinical and laboratory parameters) is therefore essential to balance volume repletion against the risk of edema-related organ dysfunction.^2,20

Hypermetabolic state and increased cardiac demand

Within 24–72 h of injury, patients enter a sustained hyperdynamic, hypermetabolic phase that is mediated by up to 50-fold elevations in plasma catecholamines, cortisol, and inflammatory cells that lead to whole-body catabolism, elevated resting energy expenditures, and multiorgan dysfunction.^21,22 Resting energy expenditure often doubles, and myocardial oxygen consumption rises sharply as heart rate (HR) and contractility remain elevated.²² By day 3–4 postburn, CO can exceed 150% of normal, and metabolic rate may approach 200% of basal levels.²³

This demand is driven by mitochondrial uncoupling and futile substrate cycling, which increase cellular oxygen utilization without proportional ATP generation.²³ The persistent tachycardia and elevated rate-pressure product during this phase exacerbate myocardial work and predispose to oxygen-supply–demand mismatches, particularly in patients with underlying coronary disease.²² Therefore, β-adrenergic blockade and anabolic agents (e.g., propranolol, oxandrolone) have demonstrated efficacy in attenuating these responses, reducing HR and oxygen demand, decreasing resting energy expenditure and muscle catabolism in patients with severe burns, ultimately improving lean-body mass and overall outcomes.^24,25

Inflammatory mediators (e.g., cytokines, ROS) affecting the myocardium

Burn injury causes significant hemodynamic stress through a profound cytokine- and oxidant-mediated insult to cardiomyocytes. As burn injury elicits rapid release of TNF-α, IL-1β, and IL-6, which impair contractility by dysregulating calcium handling, upregulating NO synthase, in addition to promoting mitochondrial dysfunction and apoptosis.²⁶

Moreover, reactive oxygen species generated by activated neutrophils and endothelial cells induce lipid peroxidation of cardiomyocyte membranes, which further disrupts excitation–contraction coupling.²⁶ Experimental models demonstrate that neutralization of macrophage migration inhibitory factor, which is another pro-inflammatory mediator elevated postburn, restores contractile function within 24 h. This emphasizes the direct cardiotoxicity of burn-induced inflammatory cascades.²

Burn-induced myocardial depression: Prevalence and clinical consequences

Burn injury results in intrinsic myocardial depression, which is evident within minutes of injury and is not fully reversible by volume resuscitation alone. CO and stroke work decreased by 40%–60%, and contractility is detectably impaired as early as 15 min postburn, implicating direct myocyte injury and cytokine-mediated dysfunction.¹⁹

Although EF often normalizes or even becomes supranormal during the flow phase, advanced echocardiographic and hemodynamic studies reveal persistent abnormalities in myocardial strain and elevated rate-pressure product for up to 2 years postburn in pediatric cohorts. HR, CO, cardiac index, as well as rate-pressure product, remained significantly increased in burned children for up to 2 years when compared with normal ranges (p < 0.05), which indicates chronic cardiac stress and remodeling.²⁷

Taken together, these data support a three-phase model of burn-related myocardial injury that has practical implications for cardiac assessment.^16–23 In the early burn-shock phase, capillary leak and hypovolemia dominate, so reduced CO and troponin release are most likely to reflect supply–demand mismatch and transient membrane injury rather than primary coronary occlusion.^16–20 During the hypermetabolic phase, sustained tachycardia, catecholamine excess, and mitochondrial inefficiency generate chronic myocardial stress, so modest troponin elevations accompanied by preserved or supranormal EF may still indicate biologically relevant subclinical injury.^21–23 Finally, in the chronic remodeling phase, persistent strain abnormalities or diastolic dysfunction on echocardiography point toward structural remodeling and long-term risk, even if troponin has normalized.^27,28 Framing the burn response in this way helps clinicians interpret biomarker and imaging changes in temporal context instead of treating each abnormal value as an isolated event.

Troponins as biomarkers in burn-associated myocardial injury

cTn, comprising troponin C (calcium-binding), troponin I (actomyosin ATPase inhibitor), and troponin T (tropomyosin-binding), is a key component of the cardiac muscle contractile apparatus. Among them, cardiac-specific troponin I (cTnI) and troponin T (cTnT) are highly specific markers of myocardial injury, occurring exclusively in heart tissue. cTnI is more specific to the myocardium and less likely to cross-react with skeletal muscle isoforms than cTnT, which may be elevated in skeletal muscle disease. The molecular weight of cTnI is approximately 24 kDa, and its unique phosphorylation sites regulate its activity and may influence detection by immunoassays, contributing to its high clinical specificity.^11,29,30

Figure 2 demonstrates how troponin gets released during burn-related heart injury, with evidence pulled from both animal models and studies on people. It separates two main processes: sometimes troponin leaks out when the cell membrane is damaged, but the cell survives; other times it escapes because heart muscle cells have died. Both pathways show up in burns. The figure also points out other medical issues, such as kidney problems or sepsis, that can interfere with troponin levels. These confounders matter when doctors try to interpret test results, backing up the diagnostic points covered earlier in this section.

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.

According to recent studies, cTn is not only a marker for acute myocardial injury. It also reflects chronic or subclinical cardiovascular problems. If someone’s troponin levels are elevated, even when they feel stable, that usually reflects structural heart disease, more stress on the heart muscle, and a higher long-term risk of CV disease. Elevated baseline cTn has been shown to identify individuals with subclinical myocardial remodeling, diastolic dysfunction, and who face a higher chance of developing heart failure and mortality, even if they never show signs of an acute ischemic event.³¹

In major burn injuries, troponin elevations may result from both irreversible and reversible cardiac insults. Severe burns can cause systemic hypoperfusion, hypovolemia, and catecholamine surges, placing significant stress on the myocardium and leading to necrosis or transient membrane permeability changes that allow troponin leakage. Even in the absence of coronary artery disease, myocardial dysfunction may result from oxidative stress and inflammatory responses. Studies have shown that troponin levels may increase within hours after thermal injury and remain elevated for several days, particularly in patients with >20% TBSA burns.^11,30,32

Elevated troponin levels in burn patients have been increasingly recognized for their diagnostic and prognostic value. Increased cTnI has been associated with worse outcomes, including sepsis, myocardial infarction (MI), and multiorgan dysfunction. For instance, a large retrospective study of over 5000 burn patients found that early troponin elevation (within 72 h) was significantly linked to higher 30-day mortality, more in-hospital cardiac complications, and increased intensive care unit (ICU) interventions. These findings support troponin’s role as a risk stratification tool that may enable earlier and more focused interventions.^29,33

However, despite their utility, troponin levels in burn patients are subject to several confounders. Even without acute cardiac injury, troponins, particularly cTnT, may remain elevated due to renal dysfunction, which is common in severe burns. Sepsis, a frequent complication, is also associated with myocardial damage through inflammatory rather than ischemic mechanisms.³² Some cTnT assays may cross-react in the context of extensive muscle breakdown seen in large burns, whereas cTnI is less affected by skeletal muscle injury. Moreover, interpreting serial measurements can be challenging in the setting of hemodynamic instability, frequent fluid resuscitation, and vasopressor use.²⁸

When viewed across studies, burn patients with elevated troponin appear to fall into at least three overlapping phenotypes.^10–12 First, patients with isolated low-grade troponin elevation and normal imaging likely represent reversible membrane leak in the setting of burn shock, sepsis, or hypermetabolic stress; these patients still have higher mortality than troponin-negative peers but may not benefit from invasive coronary evaluation.^34,35 Second, patients with marked troponin rise and classical ischemic features (typical symptoms, ischemic ECG changes, or regional wall-motion abnormalities) behave more like type 1 or type 2 MI and warrant standard cardiology pathways.^32,33 Third, patients with persistent troponin elevation and nonischemic imaging abnormalities (reduced strain, diastolic dysfunction, right-ventricular strain) may represent burn-specific cardiomyopathy and are candidates for long-term cardiac follow-up.^11,36 Explicitly recognizing these patterns moves troponin interpretation beyond a binary “positive/negative” threshold and supports more tailored decision-making in burn ICUs.

Role of echocardiography in burn injury

Echocardiography is crucial for burn patients because it enables the assessment of heart function, fluid status, and the detection of complications such as cardiac stress or pericardial effusion. This supports better management during critical care.

Figure 3 demonstrates echocardiographic patterns that appear in burn patients, findings extracted from both adult and pediatric studies. Normal systolic and diastolic parameters stack up against the abnormalities reported after major burns, such as regional wall-motion abnormalities, reduced systolic function, and decreased global longitudinal strain. These patterns match what the literature shows: after a major burn, both overt and subclinical cardiac involvement following thermal injury.

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.

A cross-sectional observational study evaluated left ventricular diastolic function in well-healed adult burn survivors using TTE. Despite prior concerns about long-term cardiac impairment after major burn injuries, no significant differences were found in key diastolic parameters between moderately burned, severely burned, and nonburned control groups. All measurements remained within normal physiological ranges, indicating preserved diastolic function regardless of burn severity. These findings suggest that chronic burn injury does not lead to diastolic dysfunction and that reduced aerobic fitness, rather than structural cardiac abnormalities, may account for observed cardiovascular limitations in this population.³⁷

Another study examines the effect of nonsevere burn injuries on cardiac structure and function, utilizing echocardiography in both animal models and human patients. In mice, echocardiographic measurements revealed a transient increase in left ventricular posterior wall and interventricular septum thickness at 1 week postburn, suggesting early cardiac remodeling. In a clinical setting, echocardiographic assessment of burn patients at baseline and 3 months postinjury showed subtle but significant alterations in cardiac dimensions, including an increase in left ventricular end-systolic diameter and a decrease in posterior wall thickness. Despite these structural changes, key functional parameters such as fractional shortening and EF remained within normal ranges, indicating preserved overall cardiac function.³⁸

These findings highlight that even nonsevere burns can induce measurable changes in cardiac morphology, detectable by echocardiography, which may predispose patients to long-term cardiac complications. The study demonstrates the importance of cardiac monitoring in burn patients and suggests potential benefits of early therapeutic interventions.³⁶

Also in this study, which highlights persistent cardiac abnormalities in young adults after severe burns, was revealed by echocardiography. Demonstrate significantly reduced systolic function, with a mean EF of 52% compared to 61% in healthy controls, and 28% having an EF below 50%. Diastolic dysfunction was evident, indicating increased left ventricular filling pressure. These echocardiographic findings underscore long-term cardiac remodeling and dysfunction in burn survivors.³⁶

This study compared CO measurements in severely burned children using TTE and the transpulmonary thermodilution method. Results from 105 paired measurements showed that Pulse Index Contour Cardiac Output (PiCCO)—an advanced monitoring technique that measures heart function and fluid status in critically ill patients using thermodilution and pulse contour analysis. Consistently reported higher CO and cardiac values than TTE, which means that TTE tends to underestimate CO. The study recommends using the PiCCO system for hemodynamic monitoring and guiding fluid resuscitation in critically ill pediatric burn patients.³⁹

Across these studies, a common theme emerges: echocardiography in burn patients is most informative when it is serial and question-driven rather than a one-time screening test.^36–39 Early in resuscitation, TTE or TEE helps distinguish hypovolemia from primary myocardial depression and can prevent “fluid creep” by demonstrating when further volume no longer improves stroke volume.⁴⁰ Later in the course, advanced techniques such as tissue Doppler and speckle-tracking strain can uncover subclinical myocardial impairment in patients whose EF appears normal, identifying survivors at risk for long-term cardiac sequelae.^3,41 Rather than serving as a generic monitoring tool, echocardiography in burn care should be viewed as a dynamic test that answers specific hemodynamic questions at each stage of the burn response (Figure 3).

Clinical evidence supporting troponin and echo use

The past two decades have transformed the notion of “burn‑related cardiomyopathy” from anecdote to a measurable entity. Contemporary cohorts show that cardiac‑specific troponins rise early after thermal injury, track with burn size, and predict downstream events such as MI and death. In a 2024 single‑center analysis of 138 adults, serum cTnI became detectable (⩾0.04 ng mL^-¹) in one‑third of all burn admissions and in more than half of those whose TBSA exceeded 15 %. Troponin‑positive patients had a fourfold adjusted rise in cardiac complications and mortality and spent, on average, three additional days in intensive care. The prognostic gradient sharpened in a federated TriNetX study of 5388 adults: cTnI >0.30 ng mL^-¹ within 72 h carried odds ratios of 9.8 for AMI and 2.6 for 30‑day death across both “mild” (<20% TBSA) and “severe” burns, even after propensity matching for age, comorbidity, and inhalation injury.¹¹

Beyond absolute values, kinetics matter. High‑sensitivity assays detect cTnI within 3 h of injury, and values typically peak by 12–18 h before declining over the next 48–72 h, thus mirroring transient membrane leak rather than frank necrosis. This time course was first detailed in survivors of high‑voltage electrical burns, where cTnI normalized within 3 days, yet every transient surge coincided with electrocardiographic or echocardiographic abnormalities.⁴² Although renal dysfunction and rhabdomyolysis can confound interpretation, high‑sensitivity cut‑offs retain prognostic value in mixed‑ICU meta‑analyses, doubling the risk of early mortality even when acute coronary syndrome is excluded.³⁴

Echocardiography provides the functional corollary to biochemical leak. In peri‑operative pediatric burns (mean TBSA 64%), TEE documented systolic dysfunction in 62% of children, reduced EF doubled ventilator days, and almost doubled ICU length of stay (67 vs 34 d).⁹ Adult data, though numerically smaller, are remarkably concordant. A 2025 prospective trial in 78 children extended these findings, showing that TTE-guided fluid titration reduced crystalloid volumes by 18% and shortened lactate normalization time without compromising urine output.⁴³

Systematic evidence synthesis reinforces the bedside observations. A 2014 Burns systematic review pooled 11 TEE studies and estimated a 50%–60% prevalence of either systolic or diastolic impairment in moderate‑to‑severe burns, with right‑heart strain and pericardial effusion as recurring themes; real‑time imaging prompted a change in resuscitation or inotrope strategy in one‑third of cases.⁴⁴ The broader critical‑care literature is equally compelling: a landmark meta‑analysis of 4492 mixed‑ICU patients confirmed that any troponin elevation nearly doubled adjusted mortality, signaling that burn physiology merely amplifies an already robust biomarker‑outcome.³⁴ More recently, a 2025 high‑sensitivity troponin synthesis in sepsis reported an odds ratio of 1.78 for short‑term death, underscoring the incremental prognostic reach of modern assays even when confounding inflammation is present.³⁵

Advanced echo technologies promise further refinement. Two‑dimensional speckle‑tracking imaging, applied in survivors of high‑voltage electrical injury, detected subclinical strain abnormalities that paralleled cTnI kinetics and persisted despite normal EF, suggesting early myocardial fiber dysfunction.⁴¹ Three‑dimensional echocardiography and contrast‑enhanced studies are technically feasible in patients with chest eschar or dressings, offering volumetric accuracy when acoustic windows are poor, though these modalities remain under‑studied in burns.³

Taken together, these data suggest that troponin and echocardiography interrogate complementary dimensions of burn cardiomyopathy rather than duplicating each other.^{9,34,35,41,43,44} Troponin elevation captures the biochemical footprint of membrane injury and necrosis, while echocardiography reveals mechanical consequences, including subtle diastolic dysfunction and strain impairment that may precede overt pump failure.^3,41 Observational cohorts consistently show that patients who are dual-positive (elevated troponin and abnormal echo) occupy the highest-risk stratum, with more vasopressor use, longer ventilation, and higher mortality, whereas those who are dual-negative generally follow an uncomplicated course despite the systemic stress of major burns.^34,35,44 The most ambiguous group is the discordant phenotype (troponin-positive with normal echo or vice versa), in whom burn-related systemic factors, preexisting cardiac disease, and measurement timing become crucial to interpretation.^10–12 By explicitly framing burn-related myocardial injury in this three-tiered structure, our review integrates heterogeneous burn and critical-care data into a pragmatic risk-stratification framework that can be prospectively tested.

Table 1 summarizes the main studies on troponin levels, echo results, and outcomes in burn patients. It figures out each study’s design, sample size, which biomarkers or imaging tools they used, and what they actually found, in addition to what it means for patient care. When data are compared side by side, some clear patterns are seen, including: prognostic significance of elevated troponin and the prevalence of burn-associated CD.

Table 1.

Diagnostic and prognostic roles of troponins and echocardiography in burn-related myocardial injury.

Tool	Key findings	Advantages	Limitations	Prognostic value	References
cTnI	Elevated in 30%–50% of burn patients, especially >15% TBSA	High myocardial specificity; early detection within 3–6 h	Affected by renal dysfunction, hemodynamic instability	Strong predictor of mortality, MI, ICU stay	28, 39, 41
cTnT	Elevated in burn patients, sometimes without MI	Widely available assays	Cross-reacts with skeletal muscle injury; less specific than cTnI	Prognostic but confounded in muscle breakdown	32, 33
High-sensitivity troponins	Detect minor injuries, dynamic changes within hours	Sensitive to subclinical injury	Interpretation difficult in systemic inflammation	Independent predictor of death and complications in ICU patients	41, 47, 51
TTE	Detects systolic and diastolic dysfunction, remodeling	Bedside, repeatable, noninvasive	Limited accuracy in critically ill (dressings, edema)	Identifies patients at risk of long-term dysfunction	35, 36, 37
TEE	Detects subtle wall-motion changes, preload abnormalities	High resolution, useful intraoperatively	Semi-invasive, not always feasible	Guides fluid resuscitation and inotrope use	42, 43, 45
Advanced Echo (Speckle Tracking, 3D Echo)	Detects subclinical strain abnormalities	More sensitive than EF	Limited availability in burn ICUs	Potential role in early detection, long-term monitoring	15, 48, 49

cTnI, cardiac Troponin I; cTnT, cardiac Troponin T; EF, ejection fraction; ICU, intensive care unit; MI, myocardial infarction; TBSA, total body surface area; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Figure 4 demonstrates how troponin and echocardiography work together to assess heart injury after burns. Evidence across multiple studies supports that biochemical markers and imaging capture distinct but overlapping dimensions of myocardial stress. In the figure, a high-risk group of people with both raised troponin and abnormal echo findings is shown. Observational studies link this combination to worse outcomes (Figure 4).

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.

Gaps in current evidence and practice

Burn patients, particularly those with large TBSA injuries, are at a high risk for myocardial injury, but current clinical practice does not adequately carry out early detection and management of such complications. A major limitation in the topic area is the lack of universalized screening guidelines for identifying cardiac involvement. Unlike practices established in cardiology or general trauma medicine, no specific, evidence-based standards exist in burn medicine for the use of cardiac biomarkers such as troponins. As a result, clinicians are likely to turn to site-specific clinical discretion when making decisions to test cardiac enzymes, leading to pronounced variability between both the time and the interval of testing. Such variability is then further compounded by disagreement regarding which type of troponin assay, conventional as opposed to high-sensitivity, best lends itself to being administered among burn patients. High-sensitivity troponin assays are superior to traditional troponin assays at early detection amongst noncardiac ICU patients; their utility in burn care has not been well studied or widely implemented.^45,46

In addition to laboratory testing, another critical gap lies in the underutilization of cardiac monitoring tools in burn ICUs. Despite growing recognition that burn injuries can cause systemic inflammation, fluid shifts, and myocardial stress, all of which increase cardiac risk, most burn ICUs do not routinely employ advanced imaging techniques like TTE or tissue Doppler imaging unless overt cardiac symptoms are present. Several studies have noted elevated troponin levels in burn patients with no obvious clinical signs of CD, suggesting that subclinical myocardial injury may be more common than previously recognized. Without routine imaging, these subtle changes often go unnoticed, delaying intervention and potentially compromising outcomes.^11,47

Following this is the nonuniform application of high-sensitivity troponin assays and the underemployment of advanced imaging modalities, even as both are ubiquitous within most other ICU settings. Measurement of high-sensitivity troponin has improved early detection and prognostication within a variety of critically ill patients, such as those undergoing high-risk surgery or sepsis therapy. Nevertheless, within burn care, such tests are not standard of care and not sufficiently investigated. Similarly, advanced echocardiographic modalities such as tissue Doppler or strain imaging, capable of detecting early diastolic dysfunction, remain sporadic within burn ICUs despite clinical usefulness as evidenced by trauma and critical care publications. Limited integration of such diagnostic modalities results in late cardiac involvement detection and fails to allow for proper risk stratification.^46,48,49

Finally, the small scale and low quality of the current studies on cardiac injury in burn victims are a major restriction in the literature. Small cohorts, typically fewer than 30 patients, and retrospective designs are common in the majority of studies that have been reported to far. This raises questions regarding bias and reproducibility in addition to limiting statistical power. Furthermore, it is challenging to combine data or reach definitive conclusions because of the significant variation in outcome measures throughout research, which ranges from biomarker elevation to modifications in EF or overall survival. There aren’t many big, prospective, multicenter trials in the field that particularly address cardiac injury in burn populations and have uniform endpoints. To improve patient outcomes and provide evidence-based regimens, these research gaps must be filled.^11,47

Clinical implications

The available evidence supports a more structured approach to myocardial assessment in burn patients than is currently practiced.^28,32,33 Small but consistent cohorts indicate that even modest cTnI elevations in patients with ⩾15%–20% TBSA burns identify a group at substantially higher risk of MI, arrhythmia, and early death, regardless of whether they have typical chest pain or known coronary disease.^34,35 When these biomarker changes are combined with echocardiographic evidence of systolic or diastolic dysfunction, risk appears to rise further, supporting the use of combined troponin–echo evaluation rather than relying on either modality alone.^11,36,39

Soejima et al.⁶’s data present how elevated cTnI levels in both mild and severe burns are associated with a 10-fold risk of MI within a month, and more than 2-fold risk of mortality. Bak et al.⁷’s study presented the value of combining TTE and cTnI in risk stratification, and not depending on only one, as their model that combined both was able to detect more high-risk individuals, and thus allowed doctors to monitor them more closely for better results. These results present the importance of screening for cTnI and echocardiographic assessment of patients with burn injury, even if no signs of cardiac distress are present. However, it is important to note that these studies involved 12 participants at most, which limits generalizability. The combination of both assessment tools will allow earlier detection of myocardial injury and thus better outcomes.

The use of echocardiography and testing of troponin levels can also be used for guiding treatments and fluid administration. Burn resuscitation, which involves fluid administration to counteract the effects of shock, is one type of treatment used.⁸ Additionally, the use of TEE to guide resuscitation was used in a retrospective analysis of 21 burn patients, where hemodynamic parameters using Doppler were measured hourly. This approach was able to provide information to physicians on when to avoid over-resuscitation in patients with impaired contractility.⁹ This is very important to monitor, as over-resuscitation could impair wound healing and result in compartment syndrome.¹⁰

Cardiology consultation should be incorporated in the management of burn patients’ care from the beginning, especially if troponin elevation or any echocardiographic abnormalities are detected. The 10-fold risk of MI within a month mentioned previously by Soejima et al.⁶ emphasizes the importance of involving cardiologists early on. This will allow better diagnosis and treatment management for the patient. Cardiac risk should be assessed using valid tools such as the Revised Cardiac Risk Index. Screening for myocardial injury, using troponins and echocardiography, should be integrated as routine for patients with burns exceeding 20%, who have pre-existing cardiovascular diseases, edema, or those who present with hypovolemia. Earlier detection of myocardial injury and more strict guidelines for routine monitoring could influence long-term outcomes.

Figure 5 shows a diagnostic and management algorithm for myocardial evaluation in burn patients. The algorithm pulls together what critical-care and burn-care studies suggest: start with early troponin tests, use echocardiography, keep an eye on hemodynamics, and consider indications for cardiology consultation.

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.

This review integrates burn physiology, troponin kinetics, and echocardiographic findings into a unified approach for evaluating myocardial injury in burn patients, which have not been synthesized in prior literature. By combining biomarker and imaging evidence, we highlight clinically meaningful diagnostic patterns and propose a practical framework for risk stratification. However, as a narrative review, our work is limited by the heterogeneity and small size of available studies, variation in troponin assays and imaging protocols, and the lack of large prospective trials. These factors underscore the need for standardized multicenter research to validate the strategies discussed.

Future directions

To translate current insights into clinical practice, future studies must systematically test standardized troponin and echocardiography protocols in well-designed multicenter cohorts. Future research should move beyond descriptive studies and toward prospectively testing integrated troponin–echocardiography strategies in burn populations.^45,46 Large multicenter cohorts with standardized time-points for high-sensitivity troponin (admission, 6, 12, 24, and 48 h) and protocolized echocardiographic assessments would allow the development and validation of a burn-specific myocardial risk score incorporating TBSA, inhalation injury, troponin kinetics, ventricular strain, and diastolic indices.^10,11 Such harmonized datasets would help distinguish transient biomarker elevations from clinically meaningful myocardial injury that requires cardiology intervention or structured long-term monitoring.

Beyond traditional imaging, more evidence is needed regarding the utility of point-of-care ultrasound (PoCUS) for rapid myocardial assessment in burn patients, especially in settings with limited resources. If validated, PoCUS could provide a practical alternative to full echocardiography and enable early hemodynamic evaluation at the bedside.⁴⁰

Emerging technologies may further refine cardiac risk stratification. AI-driven tools, such as models capable of detecting structural heart disease from ECG or echocardiographic data, hold promise for real-time interpretation and automated risk prediction, potentially enhancing early detection of burn-related myocardial injury.⁵⁰

The research efforts outlined above may ultimately clarify how burn injury affects myocardial function and how serial biomarker patterns can be applied for diagnosis and prognostication. Integrating these datasets into AI algorithms could enable automated risk assessment and individualized prognostic insights for each patient. As AI continues to advance, models such as EchoNext, which uses electrocardiograms to identify structural heart disease, illustrate the potential for automated cardiac interpretation.⁵⁰ Ultimately, combining serial biomarkers, advanced imaging, PoCUS, and AI-driven prediction tools offers the possibility of developing personalized myocardial surveillance strategies for burn patients.

Conclusion

Burn-related myocardial injury remains a clinically significant yet under-recognized complication. There’s no clear approach for diagnosing it; doctors don’t have a single strategy that brings together both lab results and imaging findings. Troponins and echocardiography are standard in heart care, but in people with burns, doctors don’t always use them together, and even when they do, it is often limited by specific confounders such as fluid shifts, systemic inflammation, and hypermetabolic stress. This review highlights the need for better, standardized ways to diagnose heart injury in burn patients. The field needs a pathway that actually takes these burn-specific challenges into account, ideally by coordinating serial troponin tests with targeted cardiac imaging. The literature demonstrates a wide variation; different study designs, assay selection, and imaging protocols make it hard to compare results. There’s no agreement on the best approach yet. This review highlights some major gaps; we still don’t know what troponin kinetics really mean for burn patients, the role of advanced echocardiographic modalities such as strain imaging, or whether combining biomarkers with imaging actually helps guide resuscitation or long-term care. We need large, prospective studies across multiple centers to build solid, evidence-based guidelines.

Footnotes

Acknowledgements

All authors confirm that no AI tools were used to generate, analyze, or edit any scientific data, results, or conclusions. All figures, tables, and scientific interpretations come directly from the authors, who verified and created them independently. We take full responsibility for everything in this manuscript and take full responsibility for its accuracy, originality, and integrity.

Declarations

ORCID iDs

Samia Aldwaik

Ameer Awashra

Anwar Zahran

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