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Prediction of Mortality After Major Burn:


Physiological Versus Biochemical Measures

Article in Wounds: a compendium of clinical research and practice · April 2015

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ORIGINAL RESEARCH

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Prediction of Mortality After Major

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Burn: Physiological Versus
Biochemical Measures

SM Tahir, FCPS; Abdul Razak Memon, MCPS, MS; Mahesh


Kumar, FCPS; Syed Asad Ali, FCPS

OD
WOUNDS 2009;21(7):177–182 Abstract: Objective. To compare the predictive power of serum lactic
acid (LA) and physiological score (Tobiasen’s Abbreviated Burn
From the Department of Plastic & Severity Index [ABSI]) after a major burn. This prospective, analytical
Burn Surgery, Liaquat University of study was conducted at the Liaquat University of Medical and Health
Medical & Health Sciences, Sciences (LUMHS) Burn Unit (Jamshoro, Pakistan) from June 2007
Jamshoro, Sindh, Pakistan

Address correspondence to:


Dr. SM Tahir, FCPS
PR
to May 2008. Methods. Eighty adult patients presenting with burn
injuries of varying etiology with body surface area (BSA) of ≥ 20%
were enrolled in the study. The outcome measures included acute
phase death (≤ 3 days), and death within first week, second week, and
Department of Plastic & Burn fourth week of admission. The ABSI score and lactate values were
Surgery stratified into 4 groups to facilitate comparison. The correlation of out-
Liaquat University of Medical & come variables with independent variables was analyzed to measure
RE
Health Sciences linear association with Pearson’s correlation coefficient. The propor-
Jamshoro tionality of differences in hazard ratios was tested by the Cox propor-
35 Gulshan-e-Yasin, Unit No. 09 tional hazard method. The receiver-operator characteristics (ROC)
Latifabad, Hyderabad, Sindh curve analysis using the area under the curve (AUC) was determined
Pakistan using ABSI ≥ 12 and LA ≥ 4.0 mmol/L as a cutoff for a “positive test.”
Phone: 0300-3018532 Results. The mean age of patients (47 men and 33 women) was 31
E-mail: Syedsahib1@yahoo.com years. The mean body surface area affected was 42%. Mean BSA
affected for patients who died was 64.9%. A statistically significant
T

negative correlation of death during acute phase death and within the
first week of admission was observed for LA compared to ABSI. When
the Cox proportional hazard model was constructed, LA was found to
NO

be statistically significant (P = 0.001). The difference between areas


under receiver-operator characteristics (AUROC) was insignificant.
Considering ABSI and LA 4 mmol/L or greater as a “positive test,” LA
was found to have a sensitivity of 89.7% at 100% specificity, while
ABSI has a 79.3% sensitivity at 100% specificity. Conclusion. This
study has once again shown the clinical usefulness of ABSI.
Measurement of serum LA has emerged as a new promising approach
and a predictive tool for early death after major burn.
DO

lthough the chances of survival after burn injury have steadily

A increased over the last 3 decades, the prediction of mortality from


burn injury is still a subject of interest for burn surgeons. This is due
to the fact that an accurate method that quantitatively summarizes severity
of burn injuries has various practical applications. It provides clinicians not
Vol. 21, No. 7 July 2009 177
Tahir et al

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only a base for clinical decisions, but also assists in under-

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Table 1. Tobiasen’s Abbreviated Burn Severity Index
standing the relative contributions of different prognos-
(ABSI) score and prediction.
tic criteria. These estimates would also be useful to
patients’ families and medical professionals making med- Parameter Finding Points
ical and financial decisions regarding their care.1 The sim- Sex Female 1
plest formula for the prediction of mortality from burns Male 0
should be based on a minimal set of easily obtainable
Age (years) 0–20 1
variables. A classic example that calculates the percent 21–40 2

OD
likelihood of mortality is the patient’s age in years plus 41–60 3
the percentage of the body-surface area (BSA) that was 61–80 4
burned.2 This formula, while easy to remember, is only 81–100 5
useful for early outcomes assessment and has various lim-
Inhalation injury Yes 1
itations regarding long-term survival or mortality predic- No 0
tion. The Abbreviated Burn Severity Risk Index (ABSI)3
has been a more reliable and more frequently used for- Presence of Yes 1
mula in clinical practice for more than 15 years. full-thickness burn No 0

PR
Mortality prediction in individual patients by any scor-
ing system is limited and in general, no better than good
clinical judgment. Therefore, decisions for individual
patients should never be based solely on a statistically
BSA burn (%) 1–10
11–20
21–30
31–40
1
2
3
4
derived injury severity score. Conversely, it can be 41–50 5
assumed that biochemical analysis would have much bet- 51–60 6
61–70 7
ter practical implication when compared to the statisti-
RE
71–80 8
cally derived injury severity score since it eliminates the 81–90 9
human element. 91–100 10
The role of LA as a frequent cause of acute metabolic ABSI score and prediction.
acidosis is well established. It has recently been shown
that elevated serum LA is a predictor of mortality in burn ABSI Treat to Life Probability of
injuries.4,5 A raised serum LA level is associated with an survival (%)
increased risk of death in patients with infection6 and 2–3 Very low ≥ 99
sepsis7–11—a common complication in burn victims who 4–5 Moderate 98
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sustain acute phase burn shock. The Surviving Sepsis 6–7 Moderately severe 80–90
8–9 Serious 50–70
Campaign12,13 suggests that serum LA measurement can
10–11 Severe 20–40
help identify patients at high risk of death so that they ≥ 12 Maximum ≤ 10
NO

can be managed more aggressively.14 Therefore, measure-


ment of serum LA can be helpful not only to predict early adequacy of resuscitation was monitored with urine out-
mortality, but also to identify deaths as result of infection put and mean arterial pressure. The ABSI recorded and
and sepsis. the sample for LA was taken soon after admission. The
sample for LA measurement collected in a blood sample
Methods bottle containing a small amount of iodoacetate (0.5
This prospective case series was conducted at the g/L). The iodoacetate stabilizes LA by inhabiting the gly-
Burn Emergency Unit at Liaquat University of Medical colysis and lactic dehydrogenase activity without induc-
and Health Sciences (Jamshoro, Pakistan) from June ing pyruvate dehydrogenase. It also stabilizes the sample
DO

2007–May 2008. During the study period, adult patients at room temperature for 160 minutes.15 The test per-
presenting with major burn injury (N = 80) from differ- formed on a HITACHI automated analyzer using a sera kit
ent etiology having body surface area (BSA) affected 20% from ROCHE.
or greater were enrolled after obtaining written consent. The outcome measures considered included the acute
The BSA was calculated with Browder Charts. phase death (≤ 3 days) and death within the first, second,
Resuscitation was done with the Parkland formula; the and fourth week of admission.
178 WOUNDS www.woundsresearch.com
Tahir et al

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Statistics. The ABSI score and lactate values were Table 2. Total body surface area affected in different

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stratified into 4 groups to facilitate comparison. ABSI age groups.
score 2–7, 8–9, 10–11, ≥ 12 and lactate as low 0.0–2.0,
Age (years)
intermediate 2.1–3.0, high 3.0–4.0, and very high > 4 TBSA (%) Total
mmol/L. The correlation of outcome variable with inde- 15–30 31–45 46–60 61–85
pendent variables was analyzed to measure linear associ- 21–30 18 8 4 2 32
31–40 12 5 0 1 18
ation with Pearson’s correlation coefficient.The Cox pro- 41–50 5 5 0 0 10
portional hazard method was used to test proportionali- 51–60 3 0 1 0 4

OD
ty of differences in the hazard ratio. ABSI ≥ 12 and LA ≥ 61–70 2 0 1 0 3
4.0 mmol/L were used as the cutoffs for a “positive test” 71–80 4 2 0 0 6
81–90 4 0 0 0 4
to determine the sensitivity/specificity and ROC.
91–100 3 0 0 0 3
Total 51 20 6 3 80
Results
The mean age of
Table 3. Total BSA in relation to serum lactic acid.
patients in this series
was 31 years with a BSA (%)➞ 21–30 31–40 41–50 51–60 61–70 71–80 81–90 91–100 Total
minimum of 18 to a Lactic acid ↓
maximum of 71 years. Low
The male (47) to female Moderate
High
(33) ratio was 1.43:1. Very high
25
7
-
-
PR 5
12

1
-
-
5
3
2
-
-
-
4
-
-
1
2
-
-
6
-
-
-
4
-
3
-
-

-
30
24
17
9
The mean body surface 32 18 10 4 3 6 4 3 80
area affected was 42%
(range 21%–93%). In 30
RE
cases, BSA affected was Table 4. Total BSA in relation to ABSI.
more than 40%. The BSA (%)➞ 21–30 31–40 41–50 51–60 61–70 71–80 81–90 91–100 Total
most common cause of ABSI ↓
burns in this series was Low 28 8 - - - - - - 36
flame (58/80, 72.5%) Moderate 4 9 7 1 - - - - 21
followed by scald High - 1 3 2 2 8
(18/80; 22.5%), chemi- Very high - - - 1 1 6 4 3 15
32 18 10 4 3 6 4 3 80
cal (2/80; 2.5%), and
T

electrical (2/80; 2.5%).


The total BSA affected with respect to age, serum LA, Table 5. Overall mortality.
and ABSI are shown in Tables 2, 3, and 4, respectively.
Period No. % Cumulative
NO

The mean time elapsed between incidence and


deaths %
admission was 127.8 minutes (minimum 30, maxi-
Acute phase deaths 9 11.25 11.25
mum 240) while mean time to sample collection Death within first week 9 11.25 12.67
for analysis after admission was 24 minutes (mini- Death within second week 6 7.5 9.67
mum 10, maximum 45). Death between 16–30 days 5 6.25 8.92
During the study, 80 patients were admitted for Total 29 36.25 42.51
acute burn injuries resulting from various causes, of
whom 29 patients expired within 30 days of their admis- The data were analyzed with Pearson’s correlation
sion. The acute phase deaths (within 72 hours of inci- coefficient to measure the linear association between
DO

dence) accounted for 31.1% of all deaths; deaths within deaths with LA and ABSI.The outcome measures showed
first week (31.1%), second week (20.7%), at 30 days a negative linear relation with the independent variable.
(17.3%). Mean BSA for patients expired during the peri- A strong negative correlation of death during acute
od of study was 64.9%. The overall mortality was 36.3% phase and first week (-0.679, -0.762) was found for LA
(Table 5). Death within the first 7 days of admission when compared to ABSI (-0.270, -0.671; Table 6).
accounted for 62% of all deaths. However, for deaths between day 15 and day 30 from
Vol. 21, No. 7 July 2009 179
Tahir et al

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Table 6. Comparison of serum LA to ABSI. At 100% specificity,

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ABSI is 80% sensitive to
Acute phase death Death first week Death second week Death at 30 days predict death.
At 100% specificity,
Serum LA -0.679* -0.762* -0.791* 0.849*
ABSI -0.270* -0.671* -0.799* -0.850* serum LA is 90% sensi-
tive to predict death.
*Correlation is significant at P = 0.01 (2-tailed).
Discussion

OD
Table 7. Hazard ratio of mortality. Improvements in
B SE Wald df Sig Exp (B) intensive care over the
ABSI -0.007 0.296 .001 1 0.982 0.993 last 20 years have
Lactic acid 2.187 0.654 11.170 1 0.001 8.912 resulted in significant
reduction in mortality
2
B: estimated coefficient; SE: standard error; Wald: ratio of B to SE ;
(B): predicted change in the hazard for a unit increase in the predictor. from a major burn.
However, an extensive
burn still carries high

LA and ABSI was statistically insignificant.


PR
admission, the difference between correlation for both mortality. The overall mortality in this series was high in
contrast to other relevant studies.16–18 A simple explana-
When the Cox proportional hazard model was con- tion could be that this study was designed exclusively to
structed, LA was found to be statistically significant (P = assess the probability of death, and therefore, patients
0.001) with respect to the hazard ratio when compared who had major burns were recruited. The mean BSA
to the ABSI (P = 0.982).The Exp (B) in Table 7 shows that affected in this series of patients was 42% (50 cases with
the predicted change in the hazard is likely to increase 8- BSA between 21%–40% and 30 cases between 41%–93%
RE
fold with a unit increase in the serum LA as compared to BSA). This is in contrast to other studies16–18 and that of
ABSI where it is less then the double.The chance of mor- Ryan et al19 where 77.5% of patients had an affected BSA
tality increases 8-fold when serum LA increases from 3 of less than 20%. Inclusion of such low-risk cases yields
mmol/L to 4 mmol/L. However, with changes in ABSI no useful information regarding probability of death.
score the results are not expected to be as dramatic. The results of the present study have shown that the
Serum LA and ABSI are considered diagnostic tests. increasing body surface was associated with increased
The performance of these diagnostic variables was quan- risk of death (> 0.05). The results of this study show that
tified by calculating the area under the ROC curve LA, when compared to ABSI, is most sensitive to predict
T

(AUROC). The ideal test would have an AUROC of 1, acute phase death and deaths within the first week of
whereas, a random guess would have an AUROC of 0.5. hospitalization (62% of all deaths), a finding that is con-
Considering both as diagnostic tests, they were found to sistent with the results of Choi et al20 and Jeng et al.21
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be almost equally effective with respect to 30-day mor- When considering deaths between the second and fourth
tality (Table 5, Figure 1). weeks (38%), the difference between predictive powers
ABSI ≥ 12 and LA ≥ 4.0 mmol/L were used as the cut- of serum LA and ABSI were statistically insignificant.
offs for a “positive test” to determine the The finding that LA is a sensitive predictor of early
sensitivity/specificity and ROC. Lactic acid found 89.7% death will help redirect future management protocol in
sensitive while ABSI was 79.3% sensitive at 100% speci- individual cases at the very early stage with an overall
ficity (Table 8). improvement in burn mortality. Of the total patients who
died in the course of
Table 8. Area under curve for ABSI and lactic acid. the present study, 18
DO

(62%) died within the


Variable AUROC SE? P?? Test sensitivity
early period. In the
ABSI 0.970 0.016 0.000 0.793
Serum LA 0.979 0.015 0.000 0.897 future, a cohort of
patients with a higher
*Non-parametric assumption
level of serum LA will
**Null hypothesis: true area = 0.5
be given more atten-
180 WOUNDS www.woundsresearch.com
Tahir et al

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studies demonstrated and estab-

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lished that elevated LA is one of the
Serum LA on
most common metabolic abnormali-
admission
ties in critically ill patients. Soon LA
Threat to life (ABSI)

Reference line
was being used as a diagnostic, ther-
apeutic, and prognostic marker of
tissue hypoxia in circulatory
shock.23–25 In shock, anaerobic pro-

OD
Sensitivity

duction and impaired LA utilization


(or both) can be operative.26 Serum
LA has recently been associated
with an increased risk of death in
patients with infection6 and sep-
sis.7–11 The raised LA in body fluid is
also helpful in diagnosing infection.
Brook27 showed that raised LA in

1 - Specificity
PR
At 100% specificity, ABSI is 80% sensitive to predict death
At 100% specificity, serum LA is 90% sensitive to predict death
peritoneal fluid is the hallmark of
peritonitis. Soon Reynaert et al28
described that peritoneal fluid to
blood lactate gradient levels has a
better correlation for detection of
Figure 1. ROC curve.
peritoneal infections. The marked
rise in LA in cerebrospinal fluid is
RE
tion. Lactic acid was found to be more sensitive when indicative of meningitis, but also can help differentiate
compared to ABSI as a predictor of early burn mortality; bacterial from viral meningitis.29,30
however, as predictors of 30-day mortality, both LA and Early recognition of elevated blood lactate levels
ABSI had almost identical sensitivity (100% specificity). appears to be essential, as early interventions targeted on
The scoring systems to predict morbidity/mortality of hemodynamic endpoints can decrease mortality by strat-
patients with burns have received increasing acceptance ifying patients with major, extensive burns. It is not yet
in recent years. These scoring systems help in under- known whether interventions targeted specifically to
standing the relative influence of different prognostic normalize blood lactate concentrations can play any role
T

variables on disease processes, for stratification of patient in improving outcomes.


groups for various treatment modalities, and classifica-
tion of severity of injury with reduced reliance on clini- Conclusion
NO

cal suspicion. These play a vital role in the evaluation of This study confirms the clinical usefulness of ABSI.
economic burden of treatment and facilitate multicenter Measurement of serum LA has emerged as a promising
studies. It is important to recognize that for individual new predictive tool for early death after a major burn.We
patients, scoring systems can never be a replacement for believe that lactate should always be measured routinely
clinical decision-making. Any predictive scales for sur- after a major burn, as it may help to detect critically ill
vival should assist in redirecting appropriate levels of patients either for adequacy of treatment or selection of
care to maximize survival where feasible. other therapeutic options.
While the ABSI has been used in clinical burn practice
for only the last 15 years, Karl Wilhelm Scheele first iden- References
DO

tified LA in sour milk in 1780 and German physician- 1. Knaus WA, Wagner DP, Lynn J. Short-term mortality pre-
chemist Johann Joseph Scherer demonstrated LA in dictions for critically ill hospitalized adults: science and
human blood under pathological conditions in 1843 and ethics. Science. 1991;254(5030):389–394.
1851.22 Further investigations labeled LA simply as a 2. Zawacki BE, Azen SP, Imbus SH, Chang YT. Multifactorial
metabolic dead-end waste product of glycolysis due to probit analysis of mortality in burned patients. Ann Surg.
hypoxia. Resurgence of interest in LA arose when various 1979;189(1):1–5.

Vol. 21, No. 7 July 2009 181


Tahir et al

E
3. Tobiasen J, Hiebert JH, Edlich RF. Prediction of burn mor- 1957;145(2):210–222.

UC
tality. Surg Gynecol Obstet. 1982;154(5):711–714. 18. Tompkins RG, Burke JF, Schoenfeld DA, et al. Prompt
4. Cochran A, Edelman LS, Saffle JR, Morris SE. The relation- eschar excision: a treatment system contributing to
ship of serum lactate and base deficit in burn patients to reduced burn mortality. A statistical evaluation of burn
mortality. J Burn Care Res. 2007;28(2):231–240. care at the Massachusetts General Hospital (1974–1984).
5. Kamolz LP, Andel H, Schramm W, Meissl G, Herndon DN, Ann Surg. 1986;204(3):272–281.
Frey M. Lactate: early predictor of morbidity and mortali- 19. Ryan CM, Schoenfeld DA,Thorpe WP, Sheridan Rl, Cassem
ty in patients with severe burns. Burns. EH, Tompkins RG. Objective estimates of the probability

OD
2005;31(8):986–990. of death from burn injuries. N Engl J Med.
6. Shapiro NI, Howell MD,Talmor D, et al. Serum lactate as a 1998;338(6):362–366.
predictor of mortality in emergency department patients 20. Choi J, Cooper A, Gomez M, Fish J, Cartotto R. The 2000
with infection. Ann Emerg Med. 2005;45(5):524–528. Moyer Award. The relevance of base deficits after burn
7. Aduen J, Bernstein WK, Khastgir T, et al. The use and clin- injuries. J Burn Care Rehabil. 2000;21(6):499–505.
ical importance of a substrate-specific electrode for rapid 21. Jeng JC, Lee K, Jablonski K, Jordan MH. Serum lactate and
determination of blood lactate concentrations. JAMA. base deficit suggest inadequate resuscitation of patients
1994;272(21):1678–1685. with burn injuries: application of a point-of-care laborato-
8.

9.
Care Med. 2001;27(1):6–11.
PR
Bakker J. Lactate: may I have your votes please? Intensive

Bakker J, Coffernils M, Leon M, Gris P, Vincent JL. Blood


lactate levels are superior to oxygen-derived variables in
22.
ry instrument. J Burn Care Rehabil. 1997;18(5):402–405.
Kompanje EJ, Jansen TC, van der Hoven B, Bakker J. The
first demonstration of lactic acid in human blood in
shock by Johann Joseph Scherer (1814–1869) in January
predicting outcome in human septic shock. Chest. 1843. Intensive Care Med. 2007;33(11):1967–1971.
1991;99(4):956–962. 23. Varpula M, Tallgren M, Saukkonen K, Voipio-Pulkki LM,
10. Bakker J, Gris P, Coffernils M, Kahn RJ, Vincent JL. Serial Pettilä V. Hemodynamic variables related to outcome in
RE
blood lactate levels can predict the development of mul- septic shock. Intensive Care Med.
tiple organ failure following septic shock. Am J Surg. 2005;31(8):1066–1071.
1996;171(2):221–226. 24. Husain FA, Martin MJ, Mullenix PS, Steele SR, Elliott DC.
11. Varpula M, Tallgren M, Saukkonen K, Voipio-Pulkki LM, Serum lactate and base deficit as predictors of mortality
Pettilä V. Hemodynamic variables related to outcome in and morbidity. Am J Surg. 2003;185(5):485–491.
septic shock. Intensive Care Med. 25. Levraut J, Ichai C, Petit I, Ciebiera JP, Perus O, Grimaud D.
2005;31(8):1066–1071. Low exogenous lactate clearance as an early predictor of
12. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis mortality in normolactatemic critically ill septic patients.
T

Campaign: guidelines for management of severe sepsis Crit Care Med. 2003;31(3):705–710.
and septic shock. Crit Care Med. 2004;32(3):858–873. 26. De Backer D. Lactic acidosis. Intensive Care Med.
13. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis 2003;29(5):699–702.
NO

Campaign: guidelines for management of severe sepsis 27. Brook I. The importance of lactic acid levels in body flu-
and septic shock. Intensive Care Med. ids in detection of bacterial infection. Rev Infect Dis.
2004;30(4):536–555. 1981;3(3):470–478.
14. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed 28. Reynaert MS, Bshouty ZH, Bertrand C, et al. Early diagno-
therapy in the treatment of severe sepsis and septic sis of peritoneal infection by simultaneous measurement
shock. N Engl J Med. 2001;345(19):1368–1377. of lactate concentration in peritoneal fluid and blood.
15. Marbach EP, McLean M, Scharn M, Jones T. Sodium iodoac- Intensive Care Med. 1984;10(6):301–304.
etate as an antiglycolytic agent in blood samples. Clin 29. Genton B, Berger JP. Cerebrospinal fluid lactate in 78
Chem. 1975;21(12):1810–1812. cases of adult meningitis. Intensive Care Med.
DO

16. Saffle JR, Davis B, Williams P. Recent outcomes in the 1990;16(3):196–200.


treatment of burn injury in the United States: a report 30. Abro AH, Abdou AS, Ali H, Ustadi AM, Hasab AAH.
from the American Burn Association Patient Registry. J Cerebrospinal fluid analysis acute bacterial versus viral
Burn Care Rehabil. 1995;16(3 Pt 1):219–232. meningitis. Pak J Med Sci. 2008;24(5):645–650.
17. Barnes BA. Mortality of burns at the Massachusetts
General Hospital, 1939–1954. Ann Surg.

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