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. 2020 Sep 30;33(3):209–215.

Base Deficit, Serum Albumin Level And Blood Haemoglobin Concentration Can Be Used As Predictor Factors For Mortality In Major Burn Patients

MA Megahed 1,∗, RH El-Helbawy 1, SS Gad 1, MM Mansour 1, KA Elkandary 1
PMCID: PMC7680201  PMID: 33304211

Summary

Hypoalbuminemia as seen in major burn injury results in widespread endothelial dysfunction. Base deficit provides the best estimate for degree of tissue anoxia. Acute blood loss describes anemia present in burn patients. Controversy focuses on the administration of protein-based colloids: whether to provide them, which solutions to use, and when to begin? The aim of this study was to determine whether alteration of gas exchange, excess base deficit, hypoalbuminemia and anemia could predict mortality in major burn patients, whether to provide protein-based colloids, and when to begin fluid resuscitation. The prospective study included 42 major burn patients. All the patients were admitted to the burn intensive care unit at Menoufia University Hospital. Serum albumin level, hemoglobin concentration, arterial blood gases and base deficit were measured at admission, third day and after one week. Average serum albumin on admission was 3.33 ± 0.44, after 3 days 2.85 ± 0.54 and after 1 week 2.46 ± 0.67 gm./dL, while hemoglobin concentration was 14.79 ± 2.13, 12.25 ± 1.99, and 10.24 ± 2.47 gm./dl respectively. However, base deficit was 5.75 ± 2.40, 5.24 ± 2.05 and 5.45 ± 2.76 respectively, with significant statistical difference (p<0.001) between the death and survivor groups. Binary logistic regression analysis for independent predictors of mortality declared that base deficit, albumin and hemoglobin serum levels were independent predictors for mortality with an odds ratio of 2.23, 95% CI, 1.66-16.75 for base deficit, 3.56, 95% CI, 1.88-12.59 for albumin and 2.21, 95% CI, 1.56-13.54 for hemoglobin. Hypoalbuminemia, anemia and excess base deficit can be used as prognostic factors for mortality in major burn patients.

Keywords: albumin, anemia, base deficit, burns, mortality

Introduction

Major burns are characterized by total body surface area (TBSA) burned of more than (>) 25% in adults or 20% at extremes of age, deep burns >10%, inhalation injury and burns associated with critical medical disorders.1 Major burns destruct tissues and activate local inflammatory response.2 The death rate from burns remains a major problem. There are important risk factors for mortality that impact prognosis: the type, site and depth of burn, associated injuries, as well as treatment strategy.3

Burn provokes metabolic and catabolic reactions, which are correlated to the depth and TBSA of injuries. 4 Two distinct phases are distinguished: the shock phase and the hyper-metabolic phase.5,6

Major burn results in extracellular fluid excess: increasing vascular permeability and serum albumin loss due to wound exudations together prompt shock stage. Low serum albumin level has a sequel of complications including edema, abnormalities in healing, and increased liability to sepsis.7,8

Acute blood loss takes place over the first and second weeks post burn injury, blood is lost promptly due to synchronized traumatic injury, red blood cell (RBC) sequestration, and direct erythrocyte leakage. Anemia is in charge of minimized hemoglobin serum level operatively, over healing of the wounds and during resolving of the acute phase of burn injury.9,10

In major burn patients, tissue hypoxemia occurs when the supply of oxygen is inadequate for the needs of aerobic metabolism. Lactic acid is the end product of anaerobic glycolysis and the accumulation of lactate in blood is widely used as a marker for tissue hypoxemia. Metabolic acid base disorder is a change in hydrogen ions that is a direct result of change in HCO3; a decrease in HCO3 will increase the hydrogen ions and produce metabolic acidosis. In burn injury, an elevated base deficit is a marker of global tissue acidosis resulting from impaired oxygenation. Most blood gas analyzers determine base deficit routinely using a PCO2/HCO3 monogram: the normal range is +2 to -2 mmol/L. Correction of the base deficit is associated with favorable outcomes.11,12,13 Base deficit is corrected by treatment of underlying cause and giving sodium bicarbonate (NaHCO3) only if pH <7.30 and with base deficit >7, where dose of bicarbonate (mEq) = base deficit × 0.2 × body weight (Kg).13

Fluid resuscitation is one of the gold standards for burn management. Colloids given as 20-60% of calculated plasma volume after 24 hours according to Parkland approaches in fluid management for major burn patients, infusion of 5% albumin 0.3–1 ml/kg / % burn/16 per hour was recommended according to modified Parkland formula. Controversy focuses on the administration of protein-based colloids.14

The aim of this study was to determine if low serum albumin, anemia, gas exchange alteration, and excess base deficit can predict mortality in major burn patients.

Patients and methods

This was a prospective cohort study involving 42 burned patients admitted to the burn intensive care unit at Menoufia University Hospital. The patients had major burns with the following criteria: total body surface area burned >25% in adults or >20% at extremes of age, full thickness burns >10%, burns involving face and neck, inhalation injury, associated trauma, and pre-existing serious medical disorders. Patient consent and approval of the medical Ethics Committee of Menoufia University Hospital were obtained. Each patient was subjected to history taking, general and local examination, laboratory investigations, and medical and surgical treatment.

Demographic and anthropometric data, history of comorbid diseases as well as burn causation (direct flame, scald, electrical or chemical agents) were registered. History of being trapped in a closed space, production of carbonaceous sputum, peri-oral burns, altered level of consciousness, respiratory distress, change or loss of voice were encountered criteria suggestive of inhalation injury. Presence of two or more criteria was considered to represent unequivocal smoke inhalation.

Local burn examination

TBSA burned was estimated according to the rule of nines. Abbreviated burn severity index (ABSI) and scoring of each patient was calculated according to gender, age, TBSA%, burn thickness and presence of inhalation injury. With an increasing ABSI score, there is an increase in mortality probability (Figs. 1 and 2).

Fig. 1. 34-year-old male patient presented with major burn (23% TBSA burn).

Fig. 1

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Fig. 2. 41-year-old male patient with inhalation injury and 20% TBSA burn.

Fig. 2

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Admission of burned patients

The patients were admitted to the burn unit according to the policy of admission, however decisions for each patient were made according to monitoring parameters such as blood pressure, pulse rate, oxygen saturation, temperature, urine output and central venous pressure.

Laboratory investigations

Routine laboratory investigations - CBC (complete blood count), liver function test (liver enzymes and serum albumin), kidney function test (urea and creatinine), serum electrolyte (Na+, K+ and Ca++) levels, arterial blood gases (ABGs) and base deficit (BD) - were estimated at the time of admission, 3 days later and after one week. Wound swab as well as blood culture and sensitivity test were done in patients with continuous fever.

Statistical analysis

Continuous variables were presented as mean and standard deviation; categorical variables were presented as counts and percentages. Differences of categorical variables were assessed by the twotailed Fisher exact test (t-test). Differences between continuous variables were assessed by two-tailed unpaired t-test. The statistical analyses were used to assess the relative predictive power of TBSA% of burn, age, sex, inhalation injury, pregnancy, cause of burn, Hb%, serum albumin and ABGs (PH, PO2, and base deficit) as predictors for patient mortality. P-value <0.05 was considered statistically significant. Microsoft Excel 2007 (Redmond, WA, USA) and SPSS for Windows (version 17) were used for data processing and statistical analysis (Tables I to VI).

Results

The prospective cohort study involved 42 patients with major burn, admitted to the burn intensive care unit at Menoufia University Hospital. Patients were divided into 2 groups according to outcome (died or survived). There were 21 females (50%), and 21 males (50%), 19 patients were <15 years old (45.2%), 16 were aged from 15 to 45 years (38.1%) and 7 were >45 years old (16.7%). The major burn causes were direct flame in 20/42 (47.6%) patients, 19/42 (45.2%) patients presented with scald and 3/42 (7.1%) with electrical burn. Abbreviated Burn Severity Index (ABSI) varied in patients from 3 to 11 with mean 7.33/42 (78.6%), 5/33 (15%) patients healed spontaneously without deformity (such as keloids, erythema, contracture in skin), 9/33 (27%) patients healed with minimal deformity, 9/33 (27%) patients healed with skin graft one setting, but 5/33 (15%) patients healed with 2 skin graft settings and another 5/33 (15%) patients after 3 settings, while mortality rate was 21.4% (Tables I and II).

Table I. Outcomes of studied group.

Table I

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Table II. Comparison between the two studied groups according to albumin & haemoglobin levels (initial, after 3 days, and after 1 week).

Table II

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Age, as well as TBSA burn, ABSI, existence of inhalation injury, Hb%, serum albumin level and ABGs (PH, PO2 and base deficit) were all significant predictors for mortality, as shown in Tables III and VI. Binary logistic regression analysis for independent predictors for mortality among the 42 patients declared that serum albumin level, hemoglobin concentration and base deficit (BD) were independent predictors for mortality with an odds ratio of 2.23, 95% CI, 1.66-16.75 for BD, 3.56, 95% CI, 1.88-12.59 for albumin, and 2.21, 95% CI, 1.56-13.54 for hemoglobin (Tables III to VI).

Table III. Comparison between the two studied groups according to albumin & haemoglobin levels (initial, after 3 days, and after 1 week).

Table III

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Table IV. Arterial blood gases of studied group according to patient's outcomes.

Table IV

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Table V. Comparison between the two studied groups according to base deficit (BD).

Table V

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Table VI. Multivariate regression analysis regarding the risk factors for mortality among the studied patients.

Table VI

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Discussion

Burn injury is a disastrous trauma, which may range from a minor to a life threatening injury. Several factors influence the outcome of patients, including age, TBSA, depth of the burnt area, presence of inhalation injury, previous medical conditions, infection and septicemia.15

Colloidal substances are commonly used among major burn patients under the justification that it is necessary to correct the oncotic pressure of the plasma resulting in reducing edema of the burnt area and hypotension. ABG measurements are nonetheless useful to assess the adequacy of pulmonary gas exchange; the presence of PaO2 level within the reference range may not exclude significant tissue hypoxia due to the effects of CO. The presence of low PaO2 (<60 mm Hg in room air) or hypercarbia (alveolar [arterial] carbon dioxide pressure [PaCO2] level of 55 mm Hg) indicates significant respiratory insufficiency, and metabolic acidosis suggests inadequate oxygen delivery to the tissues.

Studies on critically ill burned patients have found that 77% of patients are anemic at the time of hospital admission.16 A multicenter retrospective review of 666 burned patients shows that 13.7 ± 1.1 units of blood were transfused per patient during their hospital stay. Acute onset of declines in hemoglobin concentration promptly occurs after burn injury directly due to thermal injury, erythrocyte damage, red blood cells (RBCs) sequestrations, concurrent trauma and operative intervention during wound debridement. Mechanism for thermal anemia is still ambiguous, but imbalance between production and destruction of RBCs was declared.17-18

Olivia et al. studied 486 burned victims and declared that serum albumin levels <2 g/dL had >80%, 84% and 83% risk of mortality sensitivity and specificity respectively. Initial serum albumin level was a reliable biochemical marker for mortality as well as a prognostic indicator of burn severity. Nevertheless hypoalbuminemia exacerbates the patient’s liability to malnutrition, immune response suppression, septicemia and toxemia.19

Ramos et al. declared that there were highly significant negative correlations between hypoalbuminemia (<2 g/dL), which was observed in 15/73 (20%) burn patients, and %TBSA burn (p<0.001), abbreviated burn severity index (ABSI) (p<0.001), as well as mortality rate (33% vs. 0%).20

On the contrary, in a cross-sectional study Miquet-Romero et al. announced a mortality rate of <10% in major burn victims in whom hypoalbuminemia was commonly spotted, with a significant correlation between %TBSA burned and serum albumin level.21 Despite the incompatible opinion of the preceding works, Kim et al.’s cross-sectional study of 147 burn victims revealed that albumin level was an indicator of outcome as well as renal failure, which ultimately caused mortality in 28 patients.22

Eljaiek and Dubois executed one more cross-sectional study of 56 major burn patients with %TBSA burn of 30.3±10.9%: hypoalbuminemia (<30 g/L) was recorded in 36 (64.3%) patients, however 20 (35.7%) had albumin levels of >30g/L.23 The authors elucidated that hypoalbuminemia on the first day post injury was an independent risk factor of organ malfunction. Survival was observed in patients with normal albumin levels, but 16.7% mortality was seen in hypoalbuminemic patients. However, the difference was not statistically significant due to the small sample size.

Base deficit

The results of this study indicate that initial base deficit level at day 0, after 3 days, and after 1 week are useful parameters to separate survivors from non-survivors.

Ibrahim et al.24, in a published systematic review of studies over the past 25 years, found that BD values >6 mmol/L are associated with severe injuries and increased mortality.

Mutschler et al. identified that BD −6 mmol/L on admission is an adequate cutoff point for mortality.25

In the Pediatric Trauma Center of the University of Florida, U.S.A., 118 children were admitted to the level 1 Pediatric Trauma Center. The patients were divided into two groups based on initial base deficit (group I defined as BD <8; group 2 defined >8). They conclude that a high initial base deficit in injured children predicts a higher incidence of complications and a less favorable outcome.26

In another unique study in the Department of Surgery, Division of Burn, Trauma and Critical Care, University of Texas, U.S.A, arterial base deficit (BD) of 165 burned patients was analyzed as a marker for shock at each of the 24-hour (n = 81) and 48-hour (n = 75) time points after injury. The median base deficit (BD) was 1.1 mEq/L (0.8-4.7 mEq/L) at the 24-hour time point and 1.1 mEq/L (2.9-1.1 mEq/L) after 48 hours. Few patients had evidence of shock (BD ≥6 mEq/L) at the 24 hours (12/81, 15%) or 48-hours (2/75, 3%) time point.

Patients who died (22%) had a greater base deficit at both the 24-hours and 48-hours time point. After controlling for the effects of inhalation injury, full thickness burn size and age, a base deficit of ≥6mEq/ L at 24 hours was associated with death. However, Fitzwater et al. declared that base deficit (BD) of ≥6mEq/L at 48 hours was not associated with mortality.27

Effective fluid resuscitation

Controversy focuses on the administration of protein-based colloids: whether to provide them or not, which solutions to use and when to begin?

Several studies have revealed that colloids provide few clinical advantages when supplied on the first day post burn, and may have some detrimental effects on lung mechanics.28 Although leakages of plasma proteins at extravascular compartment potentiate edema formation, the time of protein leakage cessation is variable according to different authors. Baxter’s data showed that capillary leak may last for 24 hours post burn.29 Regarding Demling’s result, capillary leakage of protein stops approximately 12 hours after burn.30

Vlachou et al. declared that endothelial malfunction and capillary leakage existed within 2 hours post burn insult and for a median of 5 hours duration, less than previously announced.31

A lot of burn centers avoid colloid administration in the early burn period. However, Cohrane et al. illustrated declined mortality in burned patients who supplied albumin. Moreover, few burn clinicians had effective resuscitation including albumin in the early period with minimized volume needs and reduced weight gain compared to crystalloid resuscitation.32,33

O’Mara et al. declared minimized fluid requirements and less intra-abdominal pressures with administration of fresh frozen plasma in the first 2 days following extensive major burns (>50%),34 in accordance with Lawrence et al. who announced that early colloid uptake declined hourly fluid needs and improved fluid leakage.35

In burn centers located in Turkey, human albumin solution was forbidden unless blood albumin levels were below 2 g/dl. Initial albumin administration started at least 5 hours after the injury. Albumin after the first day is preferred in a dose of 0.5–1 g/kg/% burn. In the following days, albumin support is continued until the blood level of albumin is 3 g/dl.36

Conclusion

Serum albumin level, haemoglobin concentration (Hb%), arterial blood gases (ABGs) including PH, PO2 and base deficit were all significant predictor factors for mortality in major burn patients. Major burn resulting in increased vascular permeability and serum albumin loss had a series of complications including edema, abnormalities in healing, and increased liability to sepsis.

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