Burn injury induces complex physiological stress to the victim and untold anguish. Many determinants of burn mortality have been studied and include extremes of age, presence of comorbid conditions and inadequate or delayed resuscitation (8, 9). However, strong determinants of burn mortality are %TBSA, depth of the burn and presence of inhalational injury (3). The resulting burn pathophysiology lead to derangements in fluid metabolism, circulatory and respiratory perturbations, systemic inflammatory and metabolic responses. These alterations are worse in fire injuries due to greater thermal energy transfer and the potential for inhalational injury. These account for many deaths in fire victims which tend to occur at the scene of incident or in early course of hospitalization compared to deaths from other burn mechanisms (6, 10).
The burned skin loses its fluid conservation quality resulting in transdermal exudation of fluid and electrolytes (11). Moreover, blood vessels in the burned tissue suffer endothelial necrosis and breakdown causing further fluid and even blood loss (12). Thirdly, the burn injury initiates acute inflammatory process locally which is associated with vasodilation, increased vascular permeability and thereby third spacing of body fluids. The locally released cytokines may lead to systemic inflammatory response syndrome (SIRS). Furthermore, catecholamine surge due to the injury causes vasoconstriction that increases total peripheral resistance (13). These factors lead to contracted vascular volume and reduced perfusion resulting into hypovolemic and redistributive shock of various degrees. A reduction of oxygen tension in tissues and accumulation of metabolic waste in the interstitial fluid follows. If present, physicochemical inhalation injury to the respiratory epithelium leads to ventilation-perfusion mismatch which worsens hypoxemia. Besides, should there be asphyxiants such as carbon monoxide in the inhaled smoke, further hypoxemia results. These perfusion, inflammatory and respiratory disturbances lead to metabolic derangements including acidosis which was the target for this study.
The basic burns profile and mortality findings in this study were similar to prior studies carried out at the same institution involving the flame injured cohort. The mean %TBSA was 30.9%. Overall 28-day mortality was 38.8%. Sixty-one percent of the deaths occurred within the first five days and additional 7% occurring by day 7 of admission.
All the three acid base indices taken at admission were noted to worsen with increasing %TBSA indicating worsening pathophysiology. At derived cut offs, odds of early (5-day) mortality were significantly high.
Base deficit was found to be a good predictor of 5-day mortality at cut off value of -10.05 mmol/L (p < 0.001) with odds ratio of 11.4 (95% CI, 3.4–37.9). Choi et al reported that abnormal increase in BD (<-6 mmol/L) after a burn injury represents mal-perfusion state which may not be recognized by traditional parameters such as urine output (5). Similarly, Mutschler et al reported that BD increases with deepening degrees of hypovolemic shock in trauma patients. He noted that a BD of ≤ -10mmol/L represented Class IV hypovolemic shock (14). Furthermore, patients with high BD (< -6 mmol/L) measured within 24 hours of burn injury have more florid SIRS, more prevalent acute respiratory distress syndrome and experience more severe multiple organ dysfunction syndrome compared to those with BD of >-6 mmol/L. This translates to a higher mortality outcome (5). Our study echoes Choi and Mutschler’s finding such that a BD of -10.05mmol/L predicted mortality with a sensitivity of 73.7% and specificity of 80.3%.
Cochran et al reported that an early rise in serum lactate was an independent risk factor for death after a burn injury (15). This was demonstrable in our study where at 2.36 mmol/L or more, lactate showed an acceptable discrimination for 5-day mortality with 6.3 times more likelihood of death compared to patients with < 2.36 mmol/L (95% CI, 1.1–36.9). Therefore, just as BD, lactate elevations at day 0 is a useful parameter to separate survivors from non survivors of burns a position also observed by Andel et al (16).
The BD and lactate lower the blood pH. A pH of 7.344 or less predicted early mortality with a sensitivity of 94.7% and specificity of 67.2% (p < 0.001). The odds of burn patients dying at these levels was 36.9 times more than those with a higher pH (95% CI,4.6-296.4). A higher pH predicted 5-day survival of up to 97.6%.
From the foregoing, the three acid base parameters discussed can be utilized to identify burned patients at higher risk of death. Additionally, literature highlights importance of lactate and BD in particular, in estimating fluid requirement and adequacy of resuscitation in major burns. However, except for the work by Peaston, in 1968 there is paucity of information on utility of alkali therapy in treatment of acidosis in burns as applied to other causes of severe acidosis (14, 16, 17, 18). Therefore, whether or not alkali therapy can help better outcomes in severe acidosis associated with flame burns may be a potential area of study.