Burn injuries are a leading cause of morbidity and mortality in patients worldwide1. According to the World Health Organization, burn injuries attribute to more than 180,000 deaths annually worldwide1. Despite increased public awareness and prevention efforts, the American Burn Association (ABA) estimates that 450,000 patients per year require treatment for burn-related injuries with 30,000 requiring admission to burn centers2. Although 96.7% of patients treated in burn centers survive3, non-fatal burn injuries can result in decreased quality of life with devastating life-long sequela of emotional and physical disabilities1.
Burns are acute tissue injuries resulting from exposure to heat, electricity, chemicals, radiation or friction. The majority of injuries result from thermal burns4, however most burn fatalities result from smoke and toxic gas inhalation associated with thermal burns5. Thermal burns can cause both local injury to the skin from contact with hot surfaces, liquids, flame or steam and if severe, can also induce a systemic response4.
The local response in the skin results in three concentric zones of injury first described by Jackson in 1947 as the “zones of coagulation, stasis and hyperemia”6. The zone of coagulation is the inner-most region including the primary site of injury nearest to the heat source resulting in maximal damage and irreversible tissue necrosis6. Surrounding this area is the zone of stasis characterized by potentially viable tissue resulting from possible reversible hypoperfusion-inducing-ischemia6. The outermost zone of hyperemia is an area characterized by reversible vasodilatation resulting in increased tissue perfusion6.
Tissue injury from burn mediated damage immediately triggers the inflammatory cascade via the activation of a master transcription activator protein, nuclear factor kB required for wound repair and healing7. However, severe burn injury can lead to upregulation of the inflammatory cascade triggering an extensive systemic response which through various mechanisms ultimately induces an immunocompromised-like state in conjunction with a hypermetabolic state predisposing the burn victim to shock, sepsis, multiple organ failure and death7. During this initial phase of the burn injury, the interaction between pro-inflammatory and vasoactive mediators (including prostaglandins, IL-6 and TNF-a, histamine) in combination with stress-induced catecholamine release leads to increased capillary permeability, massive intravascular protein and fluid volume deficits and edema formation resulting in profound hemodynamic and cardiovascular dysfunction4,8,9 commonly known as burn shock8,10.
Burn shock is initially associated with decreased cardiac output as a consequence of decreased preload, with increased afterload and decreased myocardial contractility11. Early and effective fluid resuscitation with close monitoring is the cornerstone of preventing and treating shock in burn victims. The Parkland formula is commonly utilized to administer adequate amounts of fluid and prevent complications associated with overzealous administration of fluids in burn victims 11, 12. Although it is gold-standard for approximating early fluid needs in burn victims, it does not account for changes in hemodynamic status that may occur during the initial burn injury stage. Fluids must be adjusted accordingly with close monitoring. With early and appropriate treatment of burn shock, the survival rate in burn patients drastically improves 11, 13.
Shock index (SI) was first introduced in 1967 by Allgower and Buri as a simple and effective tool to predict hypovolemic shock severity 14. SI is calculated by dividing the heart rate (HR) by the systolic blood pressure (SBP), with a normal range currently accepted as 0.5–0.7 in healthy adults with evidence suggesting that values up to 0.9 are within the upper limit of normal; however, poorer outcomes associated with SI values ≥ 1.0 are indicative of worsening hemodynamic status and occult shock. Due to the nature of its linear inverse relationship with hemodynamic parameters including cardiac index, stroke volume, left ventricular stroke work and mean arterial pressure14, SI has been demonstrated to predict mortality and other severe outcomes including the necessity of intensive care unit admission and need for blood transfusion in trauma, postpartum hemorrhage, acute myocardial infarction, stroke and septic patients15; however, its role in predicting mortality outcomes in burn victims remains unknown.
Similarly, pulse pressure is another effective tool for approximating hemodynamic status. Pulse pressure is defined as the difference between the systolic and diastolic blood pressure, with normal values ranging from 40–60 mmHg in healthy adults. Low or narrow pulse pressures (< 40 mmHg) occur when the value is less than 25% of the systolic value and because systemic pulse pressure is proportional to the stroke volume16, a low or narrow pulse pressure indicates insufficient preload and reduced cardiac output suggestive of cardiogenic or hypovolemic shock from significant volume loss. Multiple studies have shown that narrow pulse pressure in seemingly hemodynamically stable patients is an independent early predictor of active hemorrhage and impending shock.
Pulse pressure and shock index have been extensively studied as prognostic tools that can help identify patients at risk for impending hemodynamic collapse and guide medical management in acute trauma, hemorrhage and septic settings; however, its application in acute burn settings has yet to be explored. The purpose of this study was to determine if hemodynamic physiological changes, such as shock index and pulse pressure, in response to significant thermal burn injuries, predict in-hospital mortality.