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Originall Article
Original Arrticle Ind
Indian
dian Journal
Jo
ournal of
of Burns

A study of prognostic factors for prediction of

complications and outcomes in burn patients
Rahul Dalal, Col Alok Sharma, Brig B. Chakravarty, Col M. Alam Parwaz, Col Anil Malik
Department of Plastic and Reconstructive Surgery, Armed Forces Medical College, Pune, Maharashtra, India

Correspondence to:
Dr. Rahul Dalal,
Flat No. K-302, Queen’s Tower, New D.P. Road, Aundh, Pune, Maharashtra - 411 007, India. E-mail: dr.rahul.dalal@gmail.com

Abstract
Aim: The aim of the present study is to evaluate various prognostic factors in burn patients and predict
prognosis and mortality of patients on the basis of prognostic factors. Materials and Methods: A study was
conducted on 10 adults, total body surface area burns of >40% (40-90%) sequential thermal burn admissions at
Burns Center. Blood samples were drawn from day of admission to discharge. Results and Statistics: (1) Fatal
outcome in four patients, persistent serum cholesterol <100 mg%. (2) The difference in cholesterol values
in patients with fatal outcome and survivors was significant. On comparing median cholesterol values for
non-survivors and survivors on post-burn day-7, there was statistically significant difference (P = 0.039)
by Mann-Whitney U-test. Serum cholesterol was significantly lower in fatal cases. (3) Infection or sepsis
in patients correlated with the presence of toxic granules, toxic vacuoles on peripheral smear, raised total
leukocyte count and low values of serum cholesterol. (4) Echinocytes (spiculated red blood cells [RBC])
were seen in all patients. In four patients, they persisted from post-burn day 4 until death. Progressive
decrease in echinocytes, which correlated with rising cholesterol values was seen in survivors. Conclusion:
Poor outcome in burn patients is related to persistently low serum cholesterol, high serum triglyceride and
presence of echinocytes, toxic granules, toxic vacuoles and high white blood cell counts or vice-versa.

Key words:
Cholesterol, echinocytes, total leukocyte count, toxic granules, toxic vacuoles, triglyceride

AIM order to determine the statistical significance of these

biochemical and hematological indicators for early
The aim of the present study was to evaluate the behavior prediction of post-burn complications or recovery.
of serum cholesterol and triglyceride levels, echinocytes,
toxic granules, toxic vacuoles and total leukocyte count INTRODUCTION
(TLC) in the early and late phases of severe burns, in
Thermal injury is caused by overheating of body tissues
above the critical temperature, leading to tissue damage.
Access this article online
An improved understanding of burn pathophysiology
Quick Response Code:
Website: has contributed to improvement in fluid resuscitation,
www.ijburns.com infection control, support of hypermetabolic response to
trauma, nutritional support and early closure of the burn
DOI: wound and burn outcome in general.[1] Thermal injury can
10.4103/0971-653X.147007 cause many changes in the skin i.e., local response and in
the body in general i.e., systemic response. The metabolic
56 Indian Journal of Burns || December 2014 || Vol 22 || Issue 1
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Dalal, et al.: Burn prognostic factors

changes are important among systemic response.[2] The
pathophysiology of the burn syndrome is characterized
by the burn wound infection and the host’s impaired
defense to it, hypermetabolism and increased energy
demand. Ominous post-burn complications are pulmonary
insufficiency, renal insufficiency and complications
involving the gastrointestinal tract.[1] Any biochemical or
hematological markers which can predict poor outcome or
complications will open a new vista to modify treatment
strategies in order to improve outcome and decrease
morbidity and mortality in major burn injury.
MATERIALS AND METHODS
Feeds were started with water, then diluted milk and then
upgraded to burns high protein diet as tolerated by the
patient, depending on condition of the patient [Table 1].
Antibiotic protocol
In the first 48 h no antibiotic was given for small area
burns (<10% TBSA)
For large area burns with inhalation burns-on admission
intravenous antibiotics were given
a. Cefotaxim/amoxicillin-clavulanic acid
b. Amikacin
Later antibiotics were given as per culture and sensitivity.

Totally 10 consecutive thermal burn patients with 40- Exclusion criteria

90% of total body surface area (TBSA) involvement were
admitted to our burns center at a tertiary teaching
hospital. Out of a total of 10 patients, five male and
five female patients were studied with age range of 21-
55 years and mean age of 31.8 years. Written/informed
consent was taken from each patient or their relatives.
The study was conducted as per ethical guidelines.
All patients received a uniform regime of treatment
consisting of standard fluid resuscitation, nutritional
support, plasma expanders, fresh frozen plasma and
prophylactic antibiotic therapy. Wounds were dressed
with topical silver sulfadiazine.
Blood samples were collected from all subjects by
venepuncture on admission to burn center and after 24 h.
Samples were collected daily for 1st week and for patients
developing complications and twice weekly thereafter
until discharge from burn unit.
Diet protocol
Diet consisted of high protein with balanced carbohydrate
and fat diet to provide high calorie diet.
Energy requirement was calculated as per Curreri formula:
Age 16-59 years: (25) W + (40) TBSA
Age ≥60 years: (20) W + (65) TBSA
Enteral feeding was started within 24-48 h, and was given
orally or through ryles tube.
Patients referred >24 h post-burn injury, burns <40% or
>90%, electrical and chemical burn injury patients and
patients with pre-existing co-morbid conditions.
Parameters studied
1. Serum cholesterol levels.
2. Serum triglyceride levels.
3. Presence of echinocytes, toxic granules and toxic vacuoles
in peripheral smear.
4. TLC.
Lab methods
1. In-vitro diagnosis of total cholesterol in serum and plasma
by — cholesterol oxidase-peroxidase method with Enzo
Kit-liquid cholesterol reagents obtained from RFCL
Limited, Dehradun, Uttarakhand, India.
2. Low-density lipoprotein (LDL)-cholesterol assay by LDL-
cholesterol reagent obtained from ERBA diagnostics
Mannheim GmbH, Germany.
3. High density lipoprotein (HDL)-cholesterol assay by HDL-
cholesterol reagent obtained from ERBA diagnostics
Mannheim GmbH, Germany.
4. Trigycerides assay by — GPO-Trinder method end
point, based on the method of Wako and modifications
of McGowan et al. and Fossati et al., obtained from
Transasia Bio Medicals Ltd., Baddi, Solan, H.P, India in
Tech association with ERBA diagnostics Mannheim GmbH,
Germany.

Table 1: Diet protocol schedule

Feed time (h) Milk (ml) Eggs (quantity) Butter (g) KabiproTM (g) Sugar (g)
0500 100 4 20 24 15
0700 100 4 20 24 15
1000 100 4 20 24 15
1200 100 4 20 24 15
1500 100 4 20 24 15
1700 100 4 20 24 15
2000 100 4 20 24 15
2200 100 4 20 24 15
Total 800 32 160 192 120
4887 Cal 496 Cal 2080 Cal 1147 Cal 699 Cal 465 Cal

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Dalal, et al.: Burn prognostic factors

5. Total leucocyte count study by Auto analyzer machine 5. Poor signs observed were:
(SysMex KX-21, Kobe, Japan). a. Decreasing serum cholesterol levels or failure to
increase by 10% (a 10% figure used for statistical
Laboratory data analysis and data assessment).
Expected cholesterol values, normal range 150-250 mg% b. Increased serum triglyceride levels which fail to
(average 200 mg%) were based on the comprehensive age decrease progressively.
and sex-specific data from the general population. c. Presence of echinocytes, toxic granules and toxic
White blood cell (WBC) response, presence of echinocytes, vacuoles on peripheral smear.
toxic granules, vacuoles, [Figures 1 and 2] cholesterol d. TLC counts increased by 20% or >16000 and <4000.
and triglyceride levels at the time of a culture-positive
infection were recorded. The antimicrobial therapy was
modified when there was clinical evidence of a new
infection.
Statistical analysis
Data were analyzed with Statistical Package for the
Social Science (SPSS Inc., Chicago, Illinois) for Windows
(version 17) for quantitative data analysis. Data are
expressed as means ± standard deviation to test changes
in dependence on time after thermal injury, comparisons
were performed using the Mann-Whitney U-test and
P < 0.05 were considered to be significant. The unpaired
t-test was used for correlation analysis. In all tests,
P < 0.05 was considered as significant.
Figure 1: Toxic granules
RESULTS AND STATISTICS

Fatal outcome was seen in four patients, with persistent

serum cholesterol <100 mg%. The difference in
cholesterol values in patients with fatal outcome and
those who survived was significant. On comparing
median cholesterol values for non-survivors and
survivors on post-burn day-7, there was statistically
significant difference (P = 0.039) noted (by Mann-
Whitney U-test). Cholesterol was significantly lower in
fatal cases [Figure 3 and Table 2].
1. TLC was significantly higher in non-survivors than in
survivors at the time of admission but not subsequently.
No significant difference in values was noted for
triglycerides (TG), echinocytes, toxic granules and toxic
vacuoles [Figures 4 and 5]. Figure 2: Toxic vacuoles
2. Infection or sepsis in patients correlated with presence of
toxic granules, toxic vacuoles on peripheral smear, raised
TLC and low values of cholesterol.
3. Echinocytes (spiculated RBC) were seen in all patients.
In four patients they persisted from post-burn day 4
unil death. Progressive decrease in echinocytes which
correlated with rising cholesterol values was seen in
survivors.
4. Mortality was seen in a case of TBSA 40% (lowest burn %
death) while the highest burn percentage associated with
survival was 63%. Fatal outcome in 04 cases: I = Post-
burn day 7, II = Post-burn day 8, III = Post-burn day
10, IV = Post-burn day 24. Figure 3: Cholesterol levels

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Dalal, et al.: Burn prognostic factors

Table 2: Cholesterol levels statistical analysis

Unpaired t-test

Cholesterol values Status N Mean Standard deviation P value

Cholesterol on admission 1 4 148.2500 50.55937 0.857
2 6 155.3333 63.44657
Cholesterol 24 h 1 4 116.5000 35.36948 0.396
2 6 145.6667 57.47231
Cholesterol 48 h 1 4 104.7500 35.28338 0.277
2 6 141.3333 55.02969
Cholesterol 5 day 1 4 77.0000 15.53491 0.130
2 6 109.1667 35.38597
Cholesterol 7 day 1 3 63.0000 6.55744 0.041
2 6 115.6667 35.04664
Mann-Whitney U-test
Values Cholesterol on admission Cholesterol 24 h Cholesterol 48 h Cholesterol 5 day Cholesterol 7 day
Mann-Whitney U 11.000 7.000 6.500 5.000 1.000
P value 0.831 0.285 0.240 0.136 0.039

1: Death, 2: Survived

Figure 5: Triglyceride levels

Figure 4: Total leukocytes count levels

DISCUSSION Cholesterol is an inevitable component of almost all

The degree of metabolic changes experienced by burn
patients is directly related to the extent of injury. In
large burn injuries, cortisol, glucagon and catecholamines
are markedly elevated.[3] Cortisol is strongly catabolic
and is associated with negative nitrogen and calcium
balance, loss of tissue protein and bone mineral. It also
stimulates gluconeogenesis, increases proteolysis and
sensitizes adipocytes to the action of lipolytic hormones.
Catecholamines increase the rate of glycogenolysis, hepatic
gluconeogenesis, promote lipolysis and peripheral insulin
resistance.[4] These changes lead to release of amino acids
from muscles and lipolysis of adipose TG leading to the
release of fatty acids into the plasma. The free fatty acids
can be used directly by most peripheral tissues for their
energy requirements.[5] In burn patients, fat oxidation is
increased to obtain endogenous energy substrates. In
addition to that, there is increased recycling of fatty acids
that leads to increase in triglyceride plasma level.
Indian Journal of Burns || December 2014 || Vol 22 || Issue 1
phospholipid membranes in the human organism. It
occurs in both the free and ester form of cholesterol and
fatty acids.
Free cholesterol is a component of cell membranes.
Cholesterol in the organism originates both from the
external environment by absorption from the digestive
tract and by synthesis de novo from acetyl-CoA. Under
normal circumstances, a significant portion of the
required amount of cholesterol is obtained from food.
Absorbed cholesterol from the diet is a component of
chylomicrons and is directed as chylomicron remnants
toward the liver. The hepatic cholesterol pools originating
from chylomicron remnants (dietary cholesterol) and de
novo synthesized cholesterol are combined and excreted
as very low density lipoprotein (VLDL) lipoproteins.
Intravascularly, VLDL converts to LDL lipoprotein and this
particle is a major source of cholesterol for many tissues,
specifically those undergoing frequent cell divisions. The
maximal synthesis of cholesterol in a healthy human
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Dalal, et al.: Burn prognostic factors
being varies in the range of 500-1000 mg a day. About
1 g of cholesterol is eliminated from the body per day.
Approximately half of this is excreted in faeces after
conversion to bile acids. The remainder is excreted as
cholesterol.[6]
Dunham et al. in their study demonstrated that patients
with severe trauma had a sudden reduction in total serum
cholesterol concentration.[7] Hypocholesterolemia has been
found in patients undergoing surgical interventions,[8] and
in those with multiple organ dysfunction syndrome[9-11] and
burns.[12,13] Fraunberger et al. demonstrated a relationship
between hypocholesterolemia and several disease states,
as well as organ dysfunction. In patients with multiple
organ dysfunction syndromes plasma cholesterol below
100 mg/dl was associated with increased mortality
(P < 0.05). A decrease in plasma cholesterol was also
associated with increased circulating levels of tumor
necrosis factor.[14]
Other authors have associated hypocholesterolemia with
inflammatory states.[15,16]
Nearly 30% or greater reduction in lipid and lipoprotein
concentrations is known to occur in a variety of
inflammatory states.[16] Interleukin-6 and tumor necrosis
factor- have been implicated as potent negative regulators
of lipoprotein metabolism in-vitro[14,17] and in-vivo.[18,19]
Coombes et al. documented an increase in triglyceride
level and a fall of serum cholesterol level following
severe burn injury.[12] Birke et al. demonstrated that the
cholesterol level fell gradually after thermal injury and
that these changes were proportional to the extent of
burn trauma.[20] It is also seen that serum cholesterol
correlates with organ failure and sepsis.[7] Proposed
explanations for the development of hypocholesterolemia
include down regulation of hepatic synthesis,[11] dilutional
effects with resuscitation,[21] loss of apoproteins in burns
after blister formation,[12] and metabolic utilization.[11,22]
Hypocholesterolemia occurring with the development of
infection was demonstrated during the 15-year period of
the Kaiser Permanente study, conducted in 15,000 healthy
men and women.[23]
In our study, we found similar reduction in cholesterol
and increase in triglyceride levels, which can be attributed
to increased energy demands, increased recycling of
fatty acids, hyper metabolism due to release of cortisol,
glucagon and catecholamines.
Ahmed SS[13] has done his study of comparison of three
parameters i.e., difference in cholesterol, TG and HDL
levels on burn patients in Iraq. In our study, the subjects
studied are of Indian ethnic origin with different food
habits compared with Middle Eastern population. Our
study has five different parameters of serum cholesterol,
TG, echinocytes, TLC, toxic granules and vacuoles. All
60
these parameters were studied simultaneously in all
patients. These parameters were selected on the basis
of ease of availability of simple tests for detection and
affordability. No previous study has been done on burned
Indian patients regarding these parameters. Our study
doesn’t concentrate only on cholesterol but on all five
parameters. The study was carried out with the basic idea
that “Results of original research are not always consistent;
studies of similar therapies may reach contradictory
conclusions, especially in different populations.”[24]
Infection or sepsis in burn patients in our study correlated
with low cholesterol, raised triglyceride levels, presence
of toxic granules and vacuoles and raised TLC.
Morphologic changes can be seen on the blood smear of a
patient with severe thermal burn injury. Acute hemolysis,
leukocytosis and thrombocytopenia are the most common
abnormal hematologic findings. The severity of the
hematologic abnormalities is most closely related to
the extent and severity of the burn. Involvement of at
least 15-20% of the body surface by third degree burns
is typically associated with a severe acute hemolytic
anemia. This hemolytic anemia is initially due to acute
intravascular hemolysis followed by extravascular
hemolysis and is associated with a wide range of abnormal
red cell morphology. The most common abnormalities are
the presence of spherocytes, schistocytes and echinocytes
i.e., spiculated RBCs [Figure 6].
These abnormalities are due to the increased osmotic and
mechanical fragility of erythrocytes following exposure
to increased temperatures. The hemolysis is most severe
within the first 24-48 h following exposure. Up to 30%
of the red cell mass may be destroyed during this time
period. Simultaneous with the insult to the red cells
is increased vascular leakage due to changes in the
endothelium. This results in decreased plasma volume
secondary to an increase in fluid sequestration within the
tissues and extracellular spaces. Patients are at high risk
for intravascular shock and renal failure during this time.
Figure 6: Echinocytes
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Dalal, et al.: Burn prognostic factors
Initially a stress leukocytosis with a neutrophilia may be
present due to the tissue damage associated with thermal
burn injury.
Erythrocytes exposed to temperatures of greater than
47°C, undergo a variety of structural and functional
changes. Changes to spectrin, one of the main proteins
that make up the red cell cytoskeleton, results in
intravascular globular fragmentation of the red cell
membrane and the formation of membrane buds. These
pieces and fragments produce schistocytes, with the
largest fragment resealing its damaged cytoskeleton with
resultant spherocyte formation. The shed buds become
microspherules or tiny spheroidal red cell fragments.
These changes result in increased osmotic and mechanical
fragility and decreased cellular flexibility and elasticity.[25-28]
In our study, echinocytes were seen in all burn patients.
They gradually disappeared in survivor group but
persisted in non-survivor group.
CONCLUSION
Poor outcome in burn patients was seen to be related
to persistently low serum cholesterol, high serum
triglyceride and presence of echinocytes, toxic granules,
toxic vacuoles and high WBC counts in this study. A larger
study may be of value perhaps to validate these findings
and point the direction for modulation or intervention for
improving survival in burns.
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How to cite this article: Dalal R, Sharma CA, Chakravarty BB, Alam
Parwaz CM, Malik CA. A study of prognostic factors for prediction
of complications and outcomes in burn patients. Indian J Burns
2014;22:56-61.
Source of Support: Nil, Conflict of Interest: None declared.
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