Severe burns cause unique and serious physiological changes, i.e. burn shock. Appropriate early resuscitation in burn shock decreases mortality and morbidity but it now seems that the use of clinical criteria (vital signs, urine output) to assess the adequacy of fluid therapy is not sufficient.13
Several studies have shown that despite normal blood pressure and adequate urine output, tissue hypoperfusion may occur, leading to plasma base deficit decreases and plasma lactate increases.6,7,14,15
The literature contains various studies on the use of plasma base deficit and plasma lactate to predict mortality or morbidity in trauma patients. Some articles report that reducing the plasma base deficit from the start of admission was the main prognostic factor for mortality in multiple trauma patients;5,16
in such cases the reduced plasma base deficit was of course not due to hypercholoraemic acidosis.17
A base deficit of < or = -6 is a marker of severe injury and significant mortality in all trauma patients,18
for which reason the value -6 of BD was set as the limit for evaluating the role of BD in the prognosis of burn patient injuries.7,14
This cohort study attempted to eliminate interventional factors. All patients with chemical or electrical burns, inhalation injury, and carbon monoxide poisoning were excluded. There was no significant difference between the groups with regard to the frequency of escharotomy, and consequently the reduction of local tissue perfusion (e.g. impaired circulation in the limbs) did not cause significant plasma base deficit reduction. While the number of patients in the two groups was similar (38 patients per group), the mean TBSA, age, and the percentage of the two genders in the groups was not significantly different.
In this study, only patients who were admitted to the hospital within 6 h of injury were enrolled. Therefore, there was no delayed resuscitation in any patients.
In both groups, standard fluid therapy was performed according to the same protocols in the first 24 h after injury (without the use of saline solutions). This study used urine output to gauge burn resuscitation (30-50 ml/h in adults and 1-1.5 ml/h in children). There were no significant differences between the two groups in the urine output in the first 24 h after injury (p > 0.05) (). The mean urine output in both groups of patients was over 1.5 ml/kg/h in the first 24 h after injury, which according to reliable sources is adequate.1
Thus, considering the clinical criteria involved, it would appear that an adequate volume was administered to all patients. In view of the aim of the study we did not use BD as a guideline for burn resuscitation. One question that arises is why there were significant differences in the mean plasma base deficit in the first 24 h, the SIRS score in the first ten days of hospitalization, the MODS score, and the mortality rate between the two groups despite the fact that there were no significant differences between the two groups in the mean volume of fluid administered, urine output in the first 24 h after injury, and the removal of interfering factors.
The results of our study are similar to those of Cartotto and Choi,7,14
except that in our study the number of patients in the two groups was equal and the sample size was larger. In this study, interfering factors - including chemical burns, electrical injuries, inhalation burns, and CO poisoning, were excluded. Additionally, the mean age and burn percentage in the two groups were not significantly different.
Some studies have confirmed that inadequate resuscitation in the first 24 h after burn injury decreases the plasma base deficit.7,14,15
Tissue ischaemia has an important role in creating systemic inflammation and organ failure.19
The mean total body surface area burned in the two groups did not significantly differ, but the mean difference in the plasma base deficit between the two groups was significant. Our study and similar reports have proved that, contrary to previous thinking, the burns percentage is not the only cause of the plasma base deficit decrease in burn injury. According to Cartotto's report, decreased tissue perfusion due to inadequate resuscitation was the most important factor in reducing the plasma base deficit.7,12
Several hypotheses consider why there is a further reduction of the plasma base deficit in some patients but not in others in almost the same conditions:
- it is probably due to unknown reasons - presentday fluid therapy formulae are inadequate in some patients;
- in some patients, despite sufficient resuscitation, other factors such as abdominal compartment syndrome reduce the plasma base deficit.
In some studies, the predictive power of the ABSI in the establishment of the prognosis of burn patients has been demonstrated.12
In this study, ABSI was calculated for both groups: there was no significant difference between the two groups, but the mean MODS and SIRS scores, as also the incidence of sepsis and mortality, were significantly higher in group A (BD ≤ -6).
Our results and those of other studies20
showed that physiological indicators (e.g. burn percentage, degree of burn, mucosa burn, age) were not sufficient for predicting mortality and morbidity in burn patients and that it was also necessary to use biochemical parameters (lactate or plasma base deficit). The value of the plasma base deficit in predicting the prognosis of burn injury patients is controversial. According to Husain's study, plasma lactate is more valuable as a marker of shock and resuscitation than the plasma base deficit, and the predictive power of plasma lactate is not limited to trauma patients, as non-trauma patients were admitted to the ICU.8
The main finding of Andel et al.21
was that plasma base deficit and plasma lactate were both very reliable predictors of outcome in burn patients in the first 24 h after injury. When the plasma base deficit returned to a normal range within 24 h, mortality was reduced.21
In 2007, a retrospective study by Cochran et al. evaluated the correlation of plasma lactate and plasma base deficit with mortality in burn patients.9
The study was unable to confirm a relationship between an extremely negative base deficit and increased complications, including ARDS or SIRS/sepsis.9
In the same study, the plasma base deficit at 24 h after admission in patients who died was significantly lower than it was in survivors. These findings are limited for several reasons. As the research was conducted retrospectively, serial data were not collected for the plasma base deficit during the first 48 h after admission. The study's retrospective nature also did not permit the matching of patients by age and TBSA. Additionally, the delay in resuscitation due to the patients' prolonged transport time was a problem for the study. As noted, the "conclusion generated by this study may not be appropriate in other geographic setting."9
Our study was prospective and we were therefore able to collect serial data for the plasma base deficit during the first 24 h after injury in all patients, and we were able to match patients for age and TBSA. Additionally, in our research, there was no delay in resuscitating patients and as far as possible we eliminated interventional factors.
As limb ischaemia, chemical burns, inhalation burns, the administration of saline solution, and abdominal compartment syndrome also reduce BD, these factors must be considered when using BD to monitor the resuscitation status of burn patients.
One of the limitations of our study was that abdominal pressure was not routinely measured in all patients in both groups, and the association between the development of the abdominal compartment syndrome and the more negative BD was therefore not clear.