Principles and Practice of Burn Care

Fluid, Electrolyte and
Acid-base Disturbances in Burns
12
Sujata Sarabahi
Chapter
Electrolyte and acid-base disturbances can occur in a burn
patient from immediately post burn till any time during the
convalescent period and the severity of these disturbances
are directly related to the initial resuscitation therapy given
to the patient. Timely resuscitation has reduced the incidence
of oliguria leading to acute renal failure even in the most
extensive burns and thus, hypovolemic shock is not the
most common cause of death in burns any longer.
HYPOVOLEMIA AND OLIGURIA
Hypovolemia following burns usually responds to increasing
fluid therapy. However, hypovolemia leading to oliguria may
be seen in two instances following burns, namely a) High
voltage electrical injury or associated crush injury leading
to myoglobinuria which blocks renal tubules and b)
Extensive burns patient whose initial resuscitation has been
delayed. In these cases, the oliguria does not respond to
fluid load alone and require addition of an osmotic diuretic
(mannitol).
An osmotic diuretic is indicated for electrical injury for
flushing the renal tubules and avoiding precipitation of
hemochromogens in the tubules. An initial loading dose of
25 gm of mannitol followed by 12.5 gm of mannitol with
each 1 liter of fluid is given till urinary output is adequate.
After administering a diuretic, the urinary output can no
longer be used as an indicator for adequacy of fluid
resuscitation.
Apart from the initial fluid loss following burns which is
easily correctable, there is a continuous loss of watery
exudates from the burnt surface even in the convalescent
period which needs to be replaced in order to prevent
dehydration. The exact volume of fluid lost from the wounds
which is to be replaced is difficult to estimate. By and large,
in burns treated by exposure method at normal room
temperature, the daily evaporative and respiratory losses
are calculated as 0.3 ml/cm2 of body surface area burned
(Davies, Lawke and Lilejedahl, (1974). The total body surface
area is calculated from the formula of Du Bois and Du Bois,
1916 as follows:
Area in cm 2 = W 0.425 × H 0.725 × 71.84
(W= weight in kg and H= height in cm)
(The Du Bois nomogram is given in the appendix for easy
calculations.)
Another formula given by Scott McDougall et al (1978) is
as follows:
Evaporative water loss in ml/hour is = (25+ % BSA burn) ×
Total Body Surface Area in m2.
These formulae are only very general guidelines and
depend on various factors. When using them to estimate
daily fluid requirements, one has to consider the following
factors as well: whether patient is having high temperature
or tachypnea, the environmental temperature (controlled and
optimum or uncontrolled and same as outside), urinary
output and whether closed or exposed technique for dressing
wounds is used. Practically, if the wounds are dressed, the
normal daily requirement (an average of 2.5-3.0 liters/day
for an adult) is added to the amount calculated by these
formulae. Last but not the least, monitoring of the burn
patient, clinical and by laboratory investigations, is essential
for individual modifications.

138
Principles and Practice of Burn Care
OVERHYDRATION
In the initial resuscitation phase, infusing large amounts of
fluid also does not lead to fluid overload as majority is lost
in extravascular space due to the increased capillary
permeability. After 48-72 hours postburn, the capillary
permeability is restored to normal and diuretic phase begins
because of reabsorption of large amounts of this leaked out
fluid. There is a possibility of fluid overload leading to
pulmonary edema especially at the extremes of age and in
patients with cardiac disease. Thus, the patient’s chest should
be auscultated frequently during the first postburn week.
Later, in the recovery period, pulmonary edema may be
seen if patient has a cardiac malfunction. The treatment for
this condition is restriction of fluid, use of a diuretic and
rarely intubation and mechanical ventilation.
HYPONATREMIA
The normal serum sodium level is 135-147 mEq/L and levels
less than 130 mEq/L are considered to be hyponatremia.
This is the commonest electrolyte imbalance seen in a burn
patient and can present at any stage. Early hyponatremia is
seen following infusion of large amounts of ringer lactate
(sodium concentration of 130 mEq/L) in initial phase, which
reduces level of sodium in blood or when resuscitation is
done orally with salt free fluids in small burns. This can be
managed simply by restricting fluid administration. More
severe hyponatremia is seen in pediatric burn patients
resuscitated with hypotonic solutions or if overhydrated.
The child may become apathetic or may show signs of
cerebral irritation, convulsions and hyperpyrexia. This can
be corrected by withholding sodium free fluids and giving
sodium containing fluids (hypertonic saline) and
anticonvulsant medication. Dose of hypertonic saline can
be calculated by the following formula:
Sodium needed (mEq) = (140 – patient’s sodium in mEq/L)
× 60% body weight in kg
Half of this dose is given initially and response observed
followed by slow correction with the remaining amount.
Serum electrolytes have to be repeated every 4-6 hours to
guide the further therapy with sodium. A further
improvement can be done by promoting diuresis if the renal
function is normal by giving small dose of furosemide ( the
renal sodium loss may increase with this but it will be lesser
than the gain from the intravenous correction and plasma
sodium loss will gradually increase).
The use of 0.5% silver nitrate as a topical antimicrobial
agent can also increase sodium loss through eschar leading
to hyponatremia. Burn patients can develop hyponatremia
as a manifestation of SIADH (syndrome of inappropriate
anti-diuretic hormone secretion) if all other causes have
been excluded. Treatment of SIADH includes restriction of
fluids and diuretics.
Another treatable cause of hyponatremia in burn patients
is the ‘Sick cell syndrome’ resulting from inability of the
red blood cells to exclude sodium because of receiving
inadequate energy following an insufficient calorie intake
by the burn patient. This leads to increased sodium
concentration in the cells as well as increased hydrogen ion
and water entering the cells whereas potassium is released
from the cells into the extracellular space thus, resulting in
intracellular edema and intracellular acidosis. This is
manifested clinically by non-pitting edema, tachypnea,
confusion, low serum sodium and reversal of sodium/
potassium ratio in urine. However, this is a correctable
situation by infusion of intravenous hypertonic Glucose,
Potassium, Insulin or ‘GKI drip’. This allows sodium and
water to be released from the cells and potassium to enter
the cells thus restoring the homeostasis. Because of high
incidence of insulin resistance, very high doses of soluble
insulin (as high as 600 units of soluble insulin) may be
required per day. On an average, approximately 150 units
insulin and 600 g of glucose is needed in 24 hours. This can
be given in the following manner:
25% glucose –500 ml
Potassium chloride –10 mEq
Plain insulin –30 units
100 ml of this is given hourly in adults. In children the dose
is as follows:
9-10 years
approx adult dose
5-9 years
½ to ¾ adult dose
2-5 years
¼ to ½ adult dose
<2 years
1/8 to ¼ adult dose
(As quoted in Treatment of Burns –JS Cason, Chapman
and Hall, 1981)
This is usually administered by an infusion pump. With
this treatment, the serum sodium levels return to normal
with increased excretion of sodium and water in urine with
normal level of nitrogen and potassium in urine.

Fluid, Electrolyte and Acid-base Disturbances in Burns
139
HYPERNATREMIA
Following burns, hypernatremia (serum sodium > 150
mEq/L) occurs if patient is dehydrated (if evaporative losses
are not corrected), if Monafo’s hypertonic saline therapy is
given (irrelevant in present scenario), if an osmotic diuretic
is given (in the form of mannitol or low molecular weight
dextran), sepsis or rarely diabetes insipidus like syndrome
is produced (by excretion of large volumes of dilute urine).
The reasons for dehydration can be increased water
losses during burn sepsis by hyperventilation, hyperthermia,
and increased renal blood flow causing increased urinary
water loss. This results in increased serum sodium levels.
The management for this condition includes infusing
sufficient fluids to replace water loss in the form of 5%
dextrose over 48 hours.
HYPOKALEMIA
Hypokalemia can occur in burns due to increased potassium
losses(amounting to 100-200 mEq/L/day) following
resuscitation with inadequate potassium replacement, with
Sulfamylon dressings which causes kaliuresis, topical
treatment with 0.5% silver nitrate soaks (which promotes
trans-eschar potassium losses) or because of diarrhea
(during burn sepsis or due to hyperosmolar feeding). Serum
potassium level less than 3 mEq/L is life threatening as it
produces cardiac arrest. It is difficult to calculate accurately
the degree of hypokalemia in relation to the extent of total
body deficit. A fall in serum potassium from 4 to 3 mEq/L is
usually associated with a total body deficit of 100-400 mEq;
a larger deficit is required to lower the plasma potassium
from 3 to 2 mEq/L. Therefore, although many rough
guidelines exist for relating the deficit of potassium to the
degree of hypokalemia, these are unreliable in an individual
patient. Correction of the potassium deficit is mandatory.
Therefore, daily serum potassium has to be measured. In
general, oral route is the safest and intravenous route should
be used when gastrointestinal problems limit the intake or
absorption in the presence of severe degree (< 2.5 mEq/L)
of hypokalemia with either respiratory muscle weakness or
cardiac arrhythmias or when there is an anticipated shift of
potassium into the intracellular fluid (recovery from diabetic
ketoacidosis).
The most common replacement fluid is KCl, which is
available as a concentrated solution (2 mEq/L) with an
osmolality of 4000 mOsmol/kg water. It must be diluted
before infusion. When correcting hypokalemia, potassium
should not be diluted in glucose containing solutions as the
glucose (via insulin) can lead to an initial lowering of the
plasma potassium. Preferably a large central vein should be
used for infusion because of the irritant properties of
hyperosmotic potassium solutions. When serum potassium
is > 2 mEq/L and no ECG abnormalities are present,
potassium chloride is given as infusion at a rate of 10 mEq/
hour. When serum potassium is < 2 mEq/L, ECG abnormality
is present or in the presence of muscle weakness or
paralysis, potassium chloride is infused at a rate of 40 mEq/
hour in saline. Offending drugs, e.g., diuretics, steroids,
beta agonists, gentamicin, ampicillin, penicillin, carbenicillin,
ticarcillin, etc. should be discontinued.
HYPERKALEMIA
Hyperkalemia is seen when acute renal failure occurs due
to hemolysis and tissue destruction due to either extensive
thermal injury (when inadequate resuscitation leads to
acidosis) or high voltage electrical injury. This is seen in the
immediate postburn period. Later, if the patient goes into
septicemia, the serum potassium levels may again be elevated
following renal failure. Cardiac arrest may occur if serum
potassium is more than 6 mEq/L.
Hyperkalemia results in ECG abnormalities which
includes elevation of T waves, ST segment depression and
lengthening of QRS segment. It is well known that
administration of succinylcholine in a burn patient may cause
sudden hyperkalemia which may be life threatening and this
can happen any time in acute period till months after
sustaining burns. It is, therefore, essential to get serum
potassium levels checked prior to getting any surgery done
in a burn patient and use succinylcholine judiciously.
The standard treatment for correction of hyperkalemia
is as follows:
•
Calcium gluconate 10%, 10 ml over 2-5 min I/V. The
onset of its action is in 1-3 min and duration of action is
30-60 min. It may be repeated once if there is no response
to the first dose.
•
10 units of regular insulin diluted in 500 ml of 10%
dextrose at the rate of 150-200 ml/hour. Its onset of
action is within 20 minutes and duration of action is
4-6 hours.
•
I/V salbutamol (4 µg /kg in 5 ml water) or nebulizer
salbutamol (2.5-5.0 ml) given over 15-20 minutes also
lowers potassium levels.
•
Avoid drugs that predispose to hyperkalemia, e.g. ACE
inhibitors, beta-blockers, NSAIDS, potassium sparing
diuretics and heparin, etc.

140
Principles and Practice of Burn Care
•
Promote urinary potassium loss by loop diuretics.
•
Potassium exchange resins.
•
Hemodialysis.
HYPOCALCEMIA
Mild hypocalcemia (6-7 mg/dl) due to hypoalbuminemia
and calcium sequestration in burned tissue may be seen in
moderate burns (> 30%TBSA). However, this may not
manifest clinically. Depression of serum albumin by 1g/dl
lowers the total serum calcium concentration by
approximately 1mg/dl, though the ionized calcium is usually
normal. Marked alkalosis also lowers the serum calcium by
increasing the protein binding. Severe hypocalcemia may
result from either alkalosis in shock stage or following use
of 0.5% silver nitrate soaks which may manifest clinically
with cramps, facial nerve twitching, carpopedal spasms,
tetany, Chvostek’s sign, etc. This requires correction by
intravenous calcium gluconate.
There is evidence that calcium administration in the
critically ill may cause hypoxic cell damage, so calcium
should be corrected in this setting only if the patient is
symptomatic. Ionized calcium also should be determined to
ascertain whether or not true hypocalcemia exists. When
indicated, treatment of symptomatic hypocalcemia consists
of 100-200 mg of elemental calcium (as 10% calcium
gluconate) intravenously followed by a slow infusion of
0.5-2.0 mg/kg /hour with frequent determination of total
and ionized calcium levels as well as correction of underlying
cause. It is crucial to ensure that hypomagnesemia is
corrected as this may potentiate the tendency to tetani and
arrhythmias.
HYPERCALCEMIA
It is a rare problem in burn patients.
HYPOMAGNESEMIA
It is rarely seen in burn patients if adequate nutrition is
ensured. If the patient is on prolonged Total Parenteral
Nutrition (TPN) with inadequate magnesium supplements
or if there is excess gastrointestinal and wound fluid losses,
hypomagnesemia may manifest clinically with neurological
signs, disorientation, neuromuscular irritability, seizures and
tetany. This can be corrected by intravenous magnesium
chloride or magnesium sulfate. Magnesium is best retained
when given slowly over several hours.
HYPOPHOSPHATEMIA
Hypophosphatemia with serum phosphorus levels less than
1 mg/dl is observed in extensive burns that require large
amount of fluid for resuscitation leading to dilutional effect
and also receiving large volumes of intravenous glucose
solutions and antacid therapy. Therefore, it may be safer to
monitor serum phosphorus levels as well. Phosphorus plays
an important role in oxygen unloading from red cells,
muscular activity and neutrophil function. Enteral
replacement of phosphorus is usually sufficient, although if
levels are really low, intravenous sodium or potassium
phosphate (0.08-0.16 mmol/kg of sodium phosphate in 500
ml 0.45 normal saline over 6 hours) may be administered
with caution only if phosphate is below 1.0 mg/dl.
ACID-BASE BALANCE
A burn patient may have metabolic or respiratory acidosis
or metabolic alkalosis.
Metabolic Acidosis
It is usually seen in early phase of extensive burns or in
case the patient develops sick cell syndrome. It may even
be seen on admission in pediatric age group in less than 2
years of age since their buffering capacity is less. Oliguria
due to insufficient or delayed fluid resuscitation may elevate
blood lactate levels to 2 mEq/L or more due to anaerobic
metabolism. This condition is diagnosed by low arterial pH,
in combination with low arterial PCO2. It can be corrected
by increasing fluid infusion and oxygen therapy for
hypoxemia. If blood pH falls to below 7.1, it should be
corrected by sodabicarb intravenously. However, in general,
the underlying cause of the acidosis should be determined
and appropriate treatment undertaken. Empirical bicarbonate
therapy can be complicated by intracellular acidosis. The
formula used for calculating the dose of sodabicarb is as
follows:
Base deficit × 0.3 × body weight (in kg) = 8.4% NaHCO3
(in ml)
Half of this dose is given immediately and one hour
after this correction, ABG is repeated and further correction
is done according to the new pH value in order to keep the
pH above 7.1.
It has been noticed that if plasma is used for treating
burn shock, no early acidosis is seen because of alkalization

Fluid, Electrolyte and Acid-base Disturbances in Burns
141
produced by the citrate in the transfused plasma. If saline
or dextran alone is used for resuscitation, the acidosis may
occur and may require addition of bicarbonate. It is essential
to check this early metabolic acidosis as it predisposes to
acute renal failure.
Respiratory Acidosis
It is rarely seen in initial post burn period except in patients
who have inhalational Injury which leads to pulmonary
insufficiency or pulmonary edema or atelactasis,
bronchopneumonia, pulmonary thromboembolism with or
without sepsis. It is characterized by low pH, high pCO2
and hypoxemia. The treatment includes attempt to identify
and correct the underlying cause of the respiratory acidosis
and in very severe cases by intubation and mechanical
ventilation and antibiotics for treating sepsis.
Metabolic Alkalosis
It can occur following extensive burns and is attributed
to the increased adrenocortical activity and also in response
to respiratory alkalosis due to high excretion of
catecholamines. It also follows prolonged hypokalemia,
hyperaldosteronism and prolonged nasogastric suction due
to paralytic ileus. This usually requires correction of
hypokalemia and fluid replacement. Treatment consists of
removal of the precipitating factors and correction of
electrolyte deficits to restore acid-base balance. Adequate
chloride must be provided in those cases associated with
volume and chloride deficit. Continued diuresis in the face
of a metabolic alkalosis can be helped by acetazolamide
which is a carbonic anhydrase inhibitor with potassium
supplement to increase urinary bicarbonate excretion. Infact,
acetazolamide is frequently used in chloride resistant
metabolic alkalosis.
BIBLIOGRAPHY
1. Androgue HJ, Madias NE. Management of life threatening acid
base disorders. The New Eng J of medicine, 1998;338(2)107-11.
2. Androgue HJ, Madias NE.Management of life threatening acid base
disorders. The New Eng J of medicine 1998;338(1):26-34.
3. Cason JS. Treatment of Burns. Chapman and Hall, London, 1981.
4. Davies JWL, Lamke LO, Liljedahl SO. A guide to the rate of non-
renal water loss from patients with burns. Br J Plast Surg
1974;27:325-9.
5. Du Bois D, Du Bois E. Clinical calorimetry: A formula to estimate
the approximate surface area if height and weight be known. Arch
Intern Med 1916;17:863.
6. Hood V L,Tannen RL. Protection of acid base balance by pH
regulation of acid production; New Eng J of Med, 1998;339(12):
819-26.
7. Halperil ML, Goldstein MB. Fluid, Electrolyte and acid base
physiology—a problem based approach. WB Saunders Company
3rd edition,1999.
8. Lanken P N. Intensive care unit manual,W. B Saunders Company,
Philadelphia 2001;425-40.
9. Mark HB, Robert P, Thomas VJ, Justin LK, Michael B. The Merck
Manual of diagnosis and therapy, 18th edition 2006;1233-1263.
10. Rose B D, Post T W. Clinical physiology of acid base and electrolyte
disorder, Mc Grawhill publication,5th edition.
11. Schwartz. Principles of Surgery, Bruni cardi, 8th edition, McGraw
Hill publication, 2005;189-221.
12. Scott McDougall W, Slade CL, Pruitt BA Manual of Burns. Springer-
Verlag, New York, 1978.
13. Vladimir Fencl, Antonin Jabor, Antonin Kalzda, James Figgi.
Diagnosis of metabolic acid base disturbances in critically ill patients.
Am J of Respiratory Critical Medicine, 2000;162:2246-51.

142
Principles and Practice of Burn Care
Acute Renal Failure in
Burns and its Management
13
Rajiv Kohli, Arun Goel
Chapter
The initial effects of a burn injury on kidney and its functions
are in response to circulatory and metabolic consequences
followed later by effects of treatment and complications.
After an extensive burn injury, there occurs a marked shift
of intravascular fluid into the interstitial spaces all over the
body including the non-burnt sites resulting in hypovolemia
and decreased circulation. This in turn, decreases renal
perfusion and urine output. Urinary specific gravity and
osmolality increases. With timely and appropriate fluid and
electrolyte replacement therapy, the hypovolemia is corrected
and normal circulation is restored. Once the capillary
permeability gets restored, the fluid is withdrawn from the
interstitial spaces back into the intravascular compartment
and diuresis occurs to remove this excess fluid. Additionally,
the renal function is also altered as a direct effect of the
stress of burn trauma in response to which the posterior
pituitary releases antidiuretic hormone (ADH) and maximum
reabsorption of water occurs. In addition to ADH,
aldosterone is released from adrenal cortex and maximum
sodium is absorbed. Thus, under the influence of ADH and
aldosterone, the kidney excretes an amount of urine just
sufficient to handle the normal solute load, largely represented
by urea.
If the resuscitation is delayed and/or inadequate, renal
blood flow and glomerular filtration rate decrease and may
ultimately lead to prerenal form of acute renal failure. This
may progress to intrinsic renal failure which is usually caused
by septicemia and nephrotoxic drugs. Renal failure may
become part of multi-organ dysfunction syndrome (MODS).
In extensive thermal burns, damage to red cells and in
contact electrical burns, necrosis of muscles may release
hemoglobin and myoglobin pigments respectively into
circulation leading to blockage of renal tubules, again leading
to renal failure.
Acute renal failure (ARF) or Acute kidney injury (AKI),
as it is known these days, is one of the most devastating
complication of burns with a high mortality rate. It has
been said to affect from 0.5 to 30% of the patients admitted
to a burn unit. The incidence depends not only on the severity
of burn injury but also on the definition of acute renal failure
used. Once the acute renal failure develops in a burn patient,
the prognosis becomes remarkably unfavorable. This fact
has been recognized for over 50 years now and most studies
have reported a mortality rate of around 80% in those patients
who require dialytic support. However, the prognostic
importance of less severe forms of acute kidney injury, not
requiring dialysis, is not well documented.
ETIOLOGICAL FACTORS IN ACUTE RENAL
FAILURE IN BURNS
Depending upon the interval between the time of burn injury
and the onset of acute renal failure, two different forms of
ARF have been described in burn patients. Burns affecting
more than 20% of skin surface are likely to cause enough
loss of extracellular fluid and albumin from plasma volume
to produce shock and hypoalbuminemia. The ARF occurring
in the first few days (within 5 days) after thermal injury is
related to a decrease in renal perfusion resulting from
hypovolemia (due to fluid shifts from the intravascular
compartment into the interstitial space and extensive fluid
losses from the burnt areas which may get accentuated by
a delay in fluid resuscitation), low cardiac output and

Acute Renal Failure in Burns and its Management
143
systemic vasoconstriction during the resuscitation period
or to myoglobinuria with damage to tubular cells. Elevated
levels of stress related hormones, such as catecholamines,
angiotensin, aldosterone and vasopressin have been
implicated in the pathogenesis of this form of ARF. This
form of ARF occurs less frequently than before because of
the widespread availability of cheap intravenous electrolyte
solutions and the aggressive fluid resuscitation performed
nowadays in most burn units. However, this is still a life
threatening complication in patients with extensive deep
burns and those with electrical burns.
The other form of ARF developing at a later date (after
5 days) has more complex pathogenesis. This form has
been reported to be related to the sepsis and multi-organ
dysfunction syndrome (MODS) and very often proves fatal.
It occurs more commonly in patients with inhalational injury
and is presently the most frequent cause of renal insufficiency
in burned patients. Administration of nephrotoxic drugs like
aminoglycosides, vancomycin and amphotericin B etc. are
also contributing factors in the development of ARF.
Various studies done have shown significant correlation
between total body surface area burnt and presence of
inhalation injury and development of ARF. Parameters like
age, third degree burns or electrical injury were not significant.
DEFINING, QUANTIFYING AND CLASSIFYING
ACUTE RENAL FAILURE
Acute renal failure is characterized by an abrupt and
sustained fall in glomerular filtration rate (GFR) leading to
accumulation of nitrogenous (clinically manifesting as a rise
in urea and creatinine) and non-nitrogenous waste products.
This potentially reversible condition is accompanied by
metabolic disturbances such as metabolic acidosis and
hyperkalemia, changes in the body fluid balance and effects
on many other organ systems.
The two major functions of a healthy kidney are
excretion of nitrogenous wastes and formation of urine.
Creatinine is more specific in assessing renal function than
blood urea nitrogen (BUN), but it corresponds only loosely
to GFR. Same value of serum creatinine may correspond
to different GFRs in two individuals with different body
masses. However, rise in serum creatinine values
corresponds to similar decline in GFR.
There is no universal definition of ARF. Common criteria
are either biochemical (rise in serum creatinine of 0.5 mg/dl
or 50% from baseline) or clinical (oliguria, urine output <
400 ml/day) or a combination of both. The acute dialysis
quality initiative (ADQI) group proposed the RIFLE
SYSTEM classifying acute renal failure into 3 severity
categories (Risk of renal dysfunction, Injury to the kidney
and Failure of renal function) and 2 clinical outcome
categories (Loss of renal function and End stage renal
disease) (Table 13.1). Loss (Persistent AKI) denotes the
need for renal replacement therapy for more than 4 weeks
whereas in ESRD, the need is for longer than 3 months.
CAUSES OF ACUTE RENAL FAILURE
The causes of ARF can be broadly grouped into three major
categories. These are decreased renal blood flow (Prerenal
causes), direct renal parenchymal damage (Intrinsic renal
causes) and obstructed urine flow (Post renal or Obstructed
cause). In burned patients, it is mainly the prerenal and the
intrinsic renal failure that occur unless a patient of renal calculi
gets burnt to have an additional postobstructive failure.
Prerenal Failure
In the prerenal form, there is a reversible increase in serum
creatinine and BUN. It results from decreased renal
perfusion, which leads to reduction in GFR. The main cause
in burned patients is acute hypovolemia and hypotension.
Table 13.1: RIFLE classification (Adapted from Bellomo et al, 2004)
GFR Criteria
Urine Output Criteria
Risk
Serum creatinine increased 1.5 times
< 0.5 ml/kg body weight/hour for 6 hours
Injury
Serum creatinine increased 2 times
< 0.5 ml/kg body weight/hour for 12 hours
Failure
Serum creatinine increased 3 times or creatinine
< 0.3ml/kg body weight/hour for 24 hours or anuria
= 4 mg%, when there was an acute rise of > 0.5 mg
for 12 hours
Loss
Persistent acute renal failure, complete loss of kidney function
for longer than 4 weeks
End stage renal
End stage renal disease for longer than 3 months
disease(ESRD)

144
Principles and Practice of Burn Care
This activates a number of neurohumoral vasoconstrictive
systems to maintain them. Changes in preglomerular and
postglomerular arteriolar resistance, mediated by
prostaglandins and nitric oxide and activation of angiotensin
II, enables renal blood flow and glomerular filtration rate to
remain roughly constant across a wide range of mean arterial
pressures. However, below a mean arterial pressure of 70
mmHg, this autoregulation is impaired and glomerular
filtration rate falls proportionately. Administration of drugs
that interfere with autoregulation, like non-steroidal anti-
inflammatory drugs (NSAIDs) and ACE inhibitors,
precipitate the prerenal failure.
Intrinsic Renal Failure
The cause of intrinsic renal failure is acute tubular necrosis
(ATN), resulting from continuation of the same
pathophysiological processes that lead to prerenal
hypoperfusion (ischemic ATN). Drugs may also cause a
direct damage to the renal tubules (nephrotoxic ATN).
Intrinsic renal failure is often multifactorial. The most
common cause in burned patients is sepsis and use of
nephrotoxic drugs may also be a contributing factor. It is
often accompanied by multi-organ failure.
DIAGNOSTIC APPROACH TO RENAL FAILURE
Serum Creatinine
In acute renal failure, renal function is commonly monitored
by daily estimations of serum creatinine. However, it has
limitations as a marker of GFR in patients with acute renal
failure because its concentration depends not only on urinary
clearance of creatinine but also on the rate of production
and the volume of distribution. Serum creatinine levels do
not reflect the GFR accurately in the non-steady-state
condition of ARF.
Serum Cystatin C
Serum cystatin C, excreted by the glomerulus, is one of the
newer markers. It is a cysteine proteinase inhibitor having a
low molecular weight and is produced by nucleated cells
independent of their pathologic status. Although some studies
have found it to be an early and reliable marker, it has not
yet been well validated as an indicator of GFR in acute renal
failure as standardised assays are not available.
Urine Volume
Acute anuria or severe oliguria are quite specific clinical
indicators of acute renal failure. While prerenal forms of
ARF nearly always present with oliguria (< 400 ml/day in
an adult), the renal and postrenal forms can be associated
with any amount of urinary output from almost nil to normal
to polyuria. A severe ARF can coexist with a normal urinary
output. The change in the amount of urine excreted precedes
the biochemical alterations.
Urinary Indices
If the renal tubular function is intact, renal vasoconstriction
during the initiation phase of acute tubular necrosis is
associated with increased tubular reabsorption and the
fractional excretion of sodium (FE Na), i.e.
Urinary sodium × plasma creatinine
100
Plasma sodium × urinary creatinine
should be less than 1%. This physiological response is altered
when the patient is administered diuretics in the form of
furosemide or mannitol or has glucosuria. To differentiate
between prerenal and renal forms of ARF, especially when
the patient has received a diuretic, fractional excretion of
urea is more specific and sensitive than that of sodium.
Other urinary indices are shown in Table 13.2.
Biomarkers
A number of biomarkers have been proposed and are being
studied for the early diagnosis of acute renal failure, for
example, urinary interleukin 18 (IL-18) and tubular enzymes
such as intestinal form of alkaline phosphatase, N acetyl-β
glucosaminidase and alanine amino peptidase etc. However,
more validation is required before their routine use.
PREVENTION OF ACUTE RENAL FAILURE
As is true for the burn injury itself, prevention of acute
kidney injury is the desired goal of every clinician. There is
clear evidence that a burn complicated by renal failure has a
greater overall mortality. While prevention is in every
clinician’s domain, once the failure sets in, a nephrologist
must be called upon by the burn surgeon for appropriate
and specialized management. Various pharmacological and
non-pharmacological strategies have been devised and used
apart from some novel therapies.
Non-pharmacological Strategies
Fluids
An early and adequate fluid therapy is crucial in maintaining
renal function in extensively burnt patients. Even a general
practitioner who sees the patient first should be able to start
an intravenous drip and infuse fluids before the patient is

Acute Renal Failure in Burns and its Management
145
Table 13.2: The most important urinary variables in the differential diagnosis between prerenal and renal acute renal failure
(Adapted and modified from: Lameire et al, 2005)
Urine analysis
Prerenal
Renal
Specific gravity of urine
>1020
1010 approx.
Osmolality(mOsm/kg H2O) of urine
>500
<350
Urinary sodium concentration (mmol/l)
<20
>40
Fractional excretion of sodium %
<1
>2
Fractional excretion of urea %
<35
>35
Fractional excretion of uric acid %
<7
>15
Fractional excretion of lithium %
<7
>20
Low molecular weight proteins
Low
High
Brush border enzymes
Low
High
Ratio of urinary to plasma creatinine
>40
<20
Ratio of urinary to plasma osmolality
>1.5
<1.1
Urinary sediment
Hyaline and fine granular casts
Coarsely granular and cellular casts
transported to an appropriate burn care facility. Intravascular
volume correction is the single most important factor in
preventing renal failure. With the widespread availability of
cheap intravenous fluids, the incidence of renal failure in
burns due to hypovolemic causes has certainly come down
over the years. Various fluid formulae, such as Parkland or
Brooks, are just general guidelines. Which is the optimal
resuscitation fluid is still debated. Normal saline and 4 %
albumin have clinical equivalence, shown by SAFE study
of patients admitted in ICU’S in Australia and New Zealand.
Once the patient is considered euvolemic (normotensive,
no postural drop, JVP and/or CVP normal), care should be
taken to avoid fluid overload and a maintenance regime
started, which takes account of renal and insensible losses
accounting for a positive balance of 500 ml/day. Hourly
input should equal previous hour’s output plus 25 ml. This
requires accurate observation and record keeping by the
nursing staff and reassessment by the doctors.
Nephrotoxin Exposure
Minimal nephrotoxin exposure is an important strategy to
prevent ARF. Antibiotics like aminoglycosides, amphotericin
B and vancomycin, etc. should be used carefully with
regular monitoring of renal function and if possible, serum
levels of these drugs should also be monitored. It is important
to avoid drugs like NSAIDs and ACE inhibitors during pre-
renal phase of ARF.
Pharmacological Strategies for Prevention of
Acute Renal Failure
Dopamine
The use of low dose (1-3 μgm/kg/minute) dopamine has
been advocated to increase renal perfusion in critically ill
patients. Recent studies including a large randomized
controlled trial have shown it to lack efficacy on renal
outcome or overall mortality. Use of dopamine may also
reduce splanchnic perfusion, depress respiration, suppress
anterior pituitary hormone release and function and worsen
renal function in hypovolemic or normovolemic patients.
Its routine use in ARF is not currently justified.
Diuretics
There is a theoretical rationale for the use of loop diuretics
in ARF – inhibition of Na+/ K+/Cl– pump in the thick
ascending limb of loop of Henle, with subsequent decrease
in Na+/K+—ATPase activity, should reduce the oxygen
requirement of these cells and thus, their susceptibility to
ischemic damage. However, there are scarce clinical data
to support this and recent studies have either correlated the
use of diuretics with increased mortality or shown no benefit.
It seems reasonable to use diuretics only in adequately
resuscitated oliguric patients at a dose suitable to the degree
of renal impairment (250 mg furosemide intravenous over
one hour is a standard regimen) and to stop diuretics if oliguria
persists. Converting oliguric to non-oliguric renal failure may
help with fluid and electrolyte management but does not seem
to affect eventual need for dialysis or overall mortality and
should not delay the start of renal replacement therapy.
Other Therapeutic Measures and Novel
Therapies
Various other agents have been studied for potential use in
prevention of acute tubular necrosis, e.g. Fenoldopam, atrial
natriuretic peptide (ANP), theophylline, N-acetylcysteine,
calcium-channel blockers, epidermal and insulin-like growth

146
Principles and Practice of Burn Care
factors, scavengers of oxygen free radicals and prostag-
landins, erythropoietin, etc. None of these novel therapies
have been proven to be effective or safe in human acute
renal failure.
MANAGEMENT OF ACUTE RENAL FAILURE
When a burn patient goes into acute renal failure, the
management is based on supportive care as there is no
definitive pharmacological treatment. Once the supportive
treatment fails, initiation of renal replacement therapy is
desired before uremic complications emerge.
Supportive Treatment of ARF
The aim of treatment of ARF in burns is to prevent further
fall in renal function. Supportive treatment mainly consists
of maintaining metabolism, taking care of life threatening
complications like hyperkalemia, pulmonary edema,
metabolic acidosis and taking care of nutrition of the patient
and treatment of infections.
Fluid Balance
An accurate fluid balance should be maintained by daily
measurements of body weight and Input/Output. In oliguric
patients, daily fluid intake should be limited to 500 ml plus
the previous day’s urinary output unless there are signs of
volume depletion/overload. Dietary sodium is restricted to
2 gm/day. In the absence of hyperalimentation, an individual
with acute tubular necrosis is expected to lose 0.3-0.5 kg
body weight daily. If this expected weight loss does not
occur or there is weight gain, fluid therapy must be
reassessed. Hyponatremia might necessitate stringent free
water restriction.
Acidosis
Severe metabolic acidosis (pH < 7.2) often occurs once
ARF develops and arises through a variety of mechanisms
related both to reduced renal function and the underlying
cause of illness. Systemic acidosis impairs cardiac
contractility, induces bradycardia, produces vasodilatation
and augments hyperkalemia. Reversing acidosis through
administration of sodium bicarbonate solution seems sensible
although there is very little evidence to show that it provides
benefit. It can cause volume overload by increasing the
sodium load. Hemodialysis or hemofiltration is usually
required to treat severe acidosis in oligoanuric patients.
Hyperkalemia
Hyperkalemia is defined as serum potassium levels of more
than 5.5 mmol/l. Severe hyperkalemia (i.e., plasma potassium
> 6.5 mmol/l) is a medical emergency because of risk of
cardiac arrhythmias. Emergency treatment of hyperkalemia
primarily dictated by changes in ECG includes the use of
intravenous calcium, driving potassium into the cells with
glucose and insulin or nebulization with salbutamol. If these
measures fail, emergency dialysis is indicated to save the
patient’s life. The treatment of hyperkalemia is summarized
in Table 13.3.
Pulmonary Edema
Oligoanuric patient with pulmonary edema resulting from
fluid overload represents a clinical challenge. If significant
ventilatory failure is present, supplementary oxygen, non-
invasive ventilation or intubation and ventilation are to be
started. Pharmacological treatment to offload the
decompensated heart can be started in the form of
intravenous opioids (diamorphine 2.5mg) and intravenous
infusion of nitrate (glyceryl trinitrate 50 mg in 50 ml of
0.9% saline at a rate of 2- 20 ml/hour, keeping the systolic
blood pressure >95 mm Hg) and attempts to provoke diuresis
by furosemide 250 mg in 100 ml saline over 1 hour. If these
measures fail, immediate hemodialysis or hemofiltration is
to be done.
Table 13.3: Summary of treatment strategies in hyperkalemia
Treatment
Immediacy of action
Reduction in K+
Duration of action
10% calcium gluconate –10-20 ml I/V over
1 -3 minutes
Nil
30-60 min
2-5 min
Insulin/glucose 10 units plain insulin in 50 ml of 50%
15 -30 minutes
0.65 -1.0 mmol/l
4-6 hours
dextrose infused over 10-20 min
Salbutamol (nebulized/intravenous) 10-20 mg via
30 minutes
0.6-1.0 mmol/l
2-4 hours
nebulizer or 0.5 mg I/V
Ion exchange resin 15 gm three times a day orally
2-3 hours
0.5 -1.0 mmol/gm resin
4-6 hours
Hemodialysis
immediate
< 1.5 mmol/l
when dialysis is ongoing

Acute Renal Failure in Burns and its Management
147
Nutritional Support
The goal of nutritional support is to preserve lean body
mass, maintain immunocompetence, offer substrate for the
acute inflammatory state and help promote wound healing.
It is an important part of the treatment of the burnt patient
as a whole, with or without renal failure. As these patients
are in a hypercatabolic state due to both burn as well as
ARF, they are to be given hypercaloric diet. This intake
must be without excessive volume. Carbohydrate intake
should be sufficient (> 100 gm/day) to avoid breakdown of
endogenous proteins for glucose. Combination of
carbohydrates and lipids should be used. These patients
also require enough protein of high quality. As far as possible,
enteral feeding should be preferred over parenteral feeds.
Fulfilling the nutritional requirement may not be possible
without the dialytic support.
Renal Replacement Therapy
In the last 15 years a number of advances have been made
in the renal replacement therapy in the management of acute
renal failure. However, as there are several techniques
available, there is controversy about selection of the best
modality for a given patient. Also, there are no absolute
rules as to when renal replacement therapy should begin
but too soon is better than too late and the treatment should
be started before complications occur. In general, the
indications for dialysis fall into three broad categories, viz.,
solute indications, e.g. marked azotemia, volume indications,
e.g. fluid overload, or both.
The following are the criteria for starting renal
replacement therapy:
1. Oliguria, with urine output less than 200 ml/12 hours.
2. Anuria, with urine output less than 50 ml/12hours.
3. Hyperkalemia, serum potassium > 6.5 mmol/l
4. Severe acidosis, pH < 7
5. Azotemia, blood urea > 200 mg/dl
6. Complication of severe uremia viz., encephalopathy,
pericarditis, neuropathy/myopathy, etc.
7. Plasma sodium > 155 mmol/l or < 120 mmol/l.
MODE OF RENAL REPLACEMENT
THERAPY (DIALYSIS)
Dialysis is a process in which molecules from one solution
(i.e., blood) diffuse across a semi-permeable membrane into
another solution (i.e., dialysate). This transfer of solute across
the membrane is determined by the characteristics of the
membrane and the solute concentration on its the two sides.
The movement of small molecular weight solutes from the
blood to dialysate under the driving force of an
electrochemical gradient is called diffusive clearance.
Convective clearance (Ultrafiltration), on the other hand,
occurs when water is driven across the membrane by
hydrostatic/osmotic forces. Solutes that can pass through
the membrane pores move along with water (solute drag).
Vascular Access
For hemodialysis, a good vascular access is required to
withdraw the blood from the patient, to be passed through
dialyser and then returned back. Effective vascular access
can be in the form of placing one catheter in an artery and
another in a vein. A double lumen catheter can be placed in
a central vein like femoral, internal jugular or subclavian
and blood can be withdrawn through one lumen and returned
back through the other with the help of a pump.
Anticoagulation
To avoid clotting in a dialysis membrane or circuit tubing or
at the vascular access, anticoagulants are generally required
in patients undergoing dialysis. These are generally in the
form of unfractionated heparin or low molecular weight
heparins. Regional citrate anticoagulation or frequent saline
flushing of the system is also used in patients in whom
heparin cannot be used.
Types of Dialysis Modalities
Two types of dialysis modalities are available:
1. Intermittent therapy, an extracorporeal dialysis, where
the patient is treated for less than 24 hours.
2. Continuous therapy [(Continuous Renal Replacement
Therapy, (CRRT)], again an extracorporeal dialysis,
where the patient is treated for 24 hours or more.
These modalities are detailed in Table 13.4.
Which Modality to be Used?
Both the modalities have their advantages and disadvantages
as shown in Table 13.5. Various studies done have proved
that both the modalities are equally effective in treating such
patients. Mortality rates are also similar for both the
modalities. The use of a particular modality depends upon
the patient’s condition, availability of infrastructure at a
particular center, availability of trained manpower and
experience of physicians and nurses in handling such
patients.

148
Principles and Practice of Burn Care
Peritoneal dialysis may not be possible in burn patients
as the area may be burnt and chances of infections are also
more. Intermittent therapies may be useful if more solute is
to be removed as in patients with sepsis. Intermittent therapy
also leaves time for any surgical procedure(s) which might
be required in such patients.
If fluid removal is a major concern, continuous therapies
are more useful and a lot of fluid can be removed to help
give the drugs and nutritional support to such patients. In
hemodynamically unstable patients who have low blood
pressure, continuous therapy is more useful. For burn
patients CVVHD or CVVH is the therapy of choice in most
of the patients.
Dose of Dialysis
It is how much dialysis has to be given to the patient. In
End Stage Renal Disease (ESRD) the KT/V of 1.2 per
treatment is the acceptable minimum dose. Here K represents
urea clearance, T is the time of dialysis and V is the volume
of urea distribution. Patients with ESRD have a relatively
constant urea generation rate and are in a steady state.
Patients of ARF tend to have a fluctuating body fluid
composition and varying urea generation rates. These
formulae may not always be correct. Nonetheless three
treatments per week with KT/V of 1.2 seems good enough
for ARF patients. Some studies have suggested that daily
dialysis may be more useful for early recovery of these
patients.
In CRRT, the dose of therapy is correlated with effluent
flow rate. There are studies comparing higher ultrafiltration
with low ultrafiltration rates but the results are conflicting.
There is some consensus that ultrafiltration rates of 35 ml/
kg/hour show better results.
THE OUTCOME AND PROGNOSIS
Outcome of burn patients with Acute Kidney Injury (AKI)
is poor. These patients require prolonged hospital stay,
prolonged ICU treatment, greater need for ventilator and
Table 13.4: Dialysis modalities for acute renal failure (Adapted and modified from: Abdeen et al, 2002)
Intermittent therapies
Continuous therapies (CRRT)
Hemodialysis
Peritoneal dialysis
Hemofiltration
Ultrafiltration ( SCUF)
Ultrafiltration
Hemofiltration ( CAVH , CVVH)
Extended daily dialysis (EDD)
Hemodialysis ( CAVHD ,CVVHD)
hemodiafiltration ( CAVHDF , CVVHDF)
Slow low efficiency dialysis( SLED)
SCUF, Slow Continuous Ultra Filtration; CAVH, Continuous Arterio Venous Hemofiltration; CVVH, Continuous Veno Venous Hemofiltration;
CAVHD, Continuous Arterio Venous Hemo Dialysis; CVVHD, Continuous Veno Venous Hemo Dialysis; CAVHDF, Continuous ArterioVenous Hemo
Dia Filtration; CVVHDF, Continuous VenoVenous Hemo Dia Filtration; SLED, Slow Low Efficiency Dialysis
Table 13.5: Advantages and Disadvantages of Intermittent versus continuous renal replacement therapy
(Adapted and modified from: Fry et al, 2006)
Intermittent hemodialysis
Continuous renal replacement therapy
ADVANTAGES
•
Lower risk of systemic bleeding
•
Better hemodynamic stability
•
More time available for diagnostic and
•
Fewer cardiac arrhythmias
therapeutic interventions
•
Better pulmonary gas exchange
•
More suitable in severe hyperkalemia
•
Better fluid control
•
Low cost
•
Better biochemical control
•
Shorter stay in ICU
•
Good removal of inflammatory mediators
•
Can be done at bed side
DISADVANTAGES
•
Availability of dialysis staff
•
Greater vascular access problem
•
More difficult hemodynamic control
•
Higher risk of systemic bleeding
•
Inadequate dialysis dose
•
Long term immobilization of patient
•
Inadequate fluid control
•
More filter problem
•
Inadequate nutritional support
•
Higher cost
•
Poor removal of inflammatory mediators

Acute Renal Failure in Burns and its Management
149
The prognosis of severely burned patients with ARF
has not improved for the last 50 years. It may be because
of the fact that the burn patients developing ARF generally
have multi-organ failure resulting in high mortality.
SUMMARY AND CONCLUSION
Acute renal failure is fairly common in burn patients. Patients
with high total body surface area (TBSA) burns have higher
chances of developing acute renal failure (ARF). With better
fluid resuscitation, majority of these patients develop acute
renal failure later in the course of their illness due to sepsis
and associated multi-organ failure. Management of ARF
should include early diagnosis and renal replacement therapy,
which ideally should be performed as a continuous veno-
venous hemofiltration. The modern approach with
aggressive fluid resuscitation which is now practiced in
most burn centers should be continued as this seems to
effectively prevent early prerenal failure.
BIBLIOGRAPHY
1. Abdeen O, Mehta RL. Dialysis modalities in the intensive care
unit. Crit Care Clin 2002;18:223-47.
2. Aikawa N, Wakabayashi G, Masakazu U, Shinozowa Y. Regulation
of renal function in thermal injury. J Trauma 1990;30:S174-78.
3. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute
renal failure—Definition, outcome measures, animal models, fluid
therapy and information technology needs: The Second
International Consensus Conference of the Acute Dialysis Quality
Initiative (ADQI) Group. Crit Care 2004;8:R204-12.
4. Bellomo R. Defining, quantifying and classifying acute renal failure.
Crit Care Clin 2005;21:223-37.
5. Chrysopoulo MT, Jeschke MG, Dziewulski P, Barrow RE, Herndon
DN. Acute renal dysfunction in severely burned adults. J Trauma
1999;46:141-44.
6. Coca SG, Bauling P, Schifftner MS, Howard CS, Teitebaum I, Parikh
CR. Contributions of acute kidney injury towards morbidity and
mortality in burns: A contemporary analysis Am. J. Kidney Dis.
2007;49(4): 517-23.
7. Cone JB. What’s new in general surgery: Burns and metabolism J
Am Coll Surg 2005;200:607-15.
8. Fry AC, Farrington K. Management of acute renal failure Postgrad
Med J 2006;82:106-16.
9. Hilton R. Acute renal failure. Br Med J 2006;333:786-90.
10. Holm C, Horbrand F, von Donnersmarck GH, Muhlbauer W. Acute
renal failure in severely burned patients. Burns 1999;25:171-78.
11. Jeschke MG, Barrow RE, Wolf SE Herndon DN. Mortality in burned
children with acute renal failure. Arch Surg 1998;133:752-56.
12. Kim GH, Oh KH, Yoon JW et al. Impact of burn size and initial
serum albumin level on acute renal failure occurring in major burn
Am. J Nephrol 2003;23:55-60.
13. Klahr S, Miller SB. Acute oliguria N Eng J Med 1998;338:671-75.
14. Kuitunen A, Vento A, Suojaranta-Ylinen R, Pettila V. Acute renal
failure after cardiac surgery: Evaluation of the RIFLE classification
Ann Thorac Surg 2006;81:542-46.
15. Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet
2005;365:417-30.
16. Leblanc M, Thibeault Y, Querin S. Continuous hemofiltration and
hemodiafiltration for acute renal failure in severely burned patients
Burns 1997;23:160-65.
17. Lopes JA, Jorge S, Neves FC, et al. An assessment of the RIFLE
criteria for acute renal failure in severely burned patients Nephrol
Dial Transplant 2007;22:85.
18. Mustonen K, Vuola J. Acute renal failure in Intensive care burn
patients. J Burn Care Res 2008;29:227-37.
19. Planas M, Watchel T, Frank G, Henderson LW. Characterization of
acute renal failure in the burned patient. Arch.Intern Med
1982;142:2087-091.
20. Schiavon M,Dilandro D, Baldo M, et al. A study of renal damage in
seriously burned patients. Burns 1988;14:107-14.
21. Schrier RW, Wang W. Acute renal failure and sepsis N Eng J Med
2004;351:159-69.
22. Schrier RW, Wang W, Poole B, Mitra A. Acute renal failure:
definitions, diagnosis, pathogenesis and therapy J Clin Invest
2004;114:5-14.
23. Traynor J, Mactier R, Geddes CC, Fox JG. How to measure renal
function in clinical practice Br. Med. J 2006;333:733-37.
24. Tremblay R, Ethier J, Querin S, et al. Veno-venous continuous
replacement therapy for burned patients with acute renal failure.
Burns 2000;26:638-43.
25. Tonelli M, Manns B, Feller-Kopman D. Acute renal failure in
intensive care unit: a systematic review of the impact of dialytic
modality on mortality and renal recovery. Am. J Kidney Dis.
2002;40:875-85.
26. Uchino S, Bellomo R, Goldsmith D, Bates S, Ronco C. An assessment
of the RIFLE criteria for acute renal failure in hospitalized patients
Crit Care Med 2006;34:1913-17.
27. Van Biesen W, Vanholder R, Lameire N. Dialysis strategies in
critically ill acute renal failure patients.Curr Opin Crit Care
2003;9:491-95.
28. Venkataraman R. Prevention of acute renal failure. Crit Care Clin
2005;21:281-89.
prolonged stay on ventilators. Recent studies have shown
that progressive renal injury, as suggested by RIFLE criteria,
have poorer outcomes. Despite much progress in treatment
modalities, mortality in a burn patient with ARF requiring
renal replacement remains high and in various studies it is
around 80% as shown in Table 13.6.
Table 13.6: Mortality rates in severely burned patients with
acute renal failure requiring renal replacement therapy
(Adapted and modified from: Holm et al, 2000)
Author
No. of patients
Mortality ( No.
with ARF
of patients)
Cason (1953-1956)
49
100%(49)
Vertel et al (1960-1966)
24
88% (21)
Cameron et al (1967)
22
96% (21)
Davies et al (1958-1979)
28
86% ( 24)
Davies et al (1990-1991)
15
80% (12)
Leslanc et al (1987-1994)
16
82%(13)
Holm et al(1994-1998)
48
85%(41)
Kim et al (2000)
28
100%(28)
Coca et al (1998-2003)
73%

(Trang không có chữ)

Section Local Care of Burn Wound

(Trang không có chữ)

Burn Wound Management
14
Sujata Sarabahi
Chapter
EVALUATION OF BURN WOUND
Introduction
The survival of a moderate to extensively burnt patient
depends on the successful management of the burn wound.
A burn patient is always at risk as long as his/her wounds
persist. There is a general consensus that burn wound
infection is the primary cause of morbidity and mortality
following an extensive burn injury. Hence, an early wound
closure can eliminate not only the risk of infection but also
the risk to life of the extensively burnt victim.
After the initial management and resuscitation of a burn
patient is complete, the focus shifts to the management of
the burn wound. This management requires a careful
evaluation of the burn wound.
Wound Evaluation
A burn wound is evaluated with respect to its site, extent
and depth in order to decide the appropriate method(s) of
treatment. The methods for assessment of the extent and
depth of burn wounds have been discussed in previous
chapters elsewhere in detail in this volume. For practical
purposes for patient management, the burn wounds can be
categorized into 3 groups when first seen by a burn specialist
in the casualty:
a. Partial thickness burns—They can heal on their own
with conservative treatment in the form of topical
antimicrobial treatment and dressings which facilitate
spontaneous healing from the remaining skin elements
over a period of upto 3 weeks (Figs 14.1A to 14.2C).
b. Full thickness burns –They require surgical intervention
as there are no chances of spontaneous healing because
Figs 14.1A to C: (A) Superficial partial thickness burn in a child. (B) closed dressing. (C) Complete healing in 9 days
A
B
C

154
Principles and Practice of Burn Care
of loss of all dermal elements. The type of surgical
intervention and timing of surgery eventually affect the
outcome of these wounds (Fig. 14.3).
c. Indeterminate depth burns—They cannot be clearly
allocated to either of above two groups in the first look.
Their potential for regeneration is doubtful. These areas
require initial conservative management followed by a
second look after 10-14 days when they may reveal
their true depth. A definitive plan is then formulated
(Fig. 14.4).
Partial thickness burns involving dermis may be
superficial dermal or deep dermal. The superficial dermal
Fig. 14.4: Mixed burns in a child –Reassessment of depth
done at 10 days
Fig. 14.3: Full thickness burns requiring surgical intervention
burns which involve the papillary layer of dermis are typically
pink and moist (Fig. 14.5), whereas, deep dermal burns
involve the reticular layer and are dry and pearly (waxy)
white in color (Fig. 14.6A). Full thickness burns (Fig.
14.6B), as the name indicates, involve the whole of epidermis
and dermis and appear parchment like with visible,
thrombosed subcutaneous veins. As the sensory end organs
are concentrated in the skin, the presence of sensation (tested
by pinprick) in the burnt area indicates that the skin is viable
and the burn is partial thickness whereas absence of
sensation indicates full thickness burns. Similarly, easy
removal of hair (by pulling) indicates deeper burns whereas
Figs 14.2A to C: Partial thickness burn, healing with conventional
dressings by day 13 post burn
A
B
C

Burn Wound Management
155
inability to pull out hairs indicates otherwise (Fig. 14.7A
and B). Deeper a burn injury, greater is the loss of hair
follicles, sebaceous and sweat glands. It is the epithelial
lining of these epidermal adnexal elements which re-
epithelializes the surface. In very deep dermal burns, their
number may be very small and any superimposed bacterial
infection can convert a partial thickness wound into a full
thickness wound hampering the process of spontaneous
healing. Thus, it is imperative to prevent this conversion by
appropriate wound care. The primary objective in treating a
partial thickness burn injury is to provide an environment
which inhibits microbial growth and at the same time
promotes wound healing. On the other hand, the aim while
Fig. 14.5: Superficial dermal or superficial partial thickness burns
with moist and red look
Fig. 14.6A: Deep dermal burns with pearly white look
Fig. 14.6B: Deep burns with charred look
Fig. 14.7B: Superficial partial thickness burn but deeper than Figure
14.7A, with loss of some hairs. Remaining hair allowing epithelialization–
Epithelial buds seen
Fig. 14.7A: Superficial partial thickness burns with almost all hair
intact–Heals very quickly

156
Principles and Practice of Burn Care
treating a full thickness burn is early removal of dead tissue,
preventing/minimizing and localizing infection to the burn
wound and closure of raw area at the earliest with skin grafts.
Aims of Local Burn Wound Care
The basic aims of local burn wound care are:
1. To clean debris and particles from the burn wound
2. To prevent damage to remaining viable epithelium
3. To produce an environment which inhibits microbial
growth
4. To encourage slough separation by natural means
5. To allow free drainage of exudates from the wound and
prevent them from coming in contact with the
environment
6. To immobilize the injured area in order to reduce pain
7. To prevent damage to regenerating, delicate neo-
epithelium, and
8. To prevent development of bacteremia and septicemia.
Since minor burns (<10% in children and <15 % in
adults) do not require intravenous fluid replacement, the
local wound care can be instituted as soon as the patient
arrives. However, in moderate to severe burns (> 10% TBSA
in children and > 15-20% TBSA in adults) where intravenous
fluid replacement and other emergency steps for
resuscitation are essential, the burn wound care has to be
delayed for sometime and till then, the wounds should be
covered with a sterile sheet to reduce the chances of wound
contamination.
Principles of Wound Management
The principles of wound management which should be
kept in mind while treating burn wounds are as follows1:
Debridement
Debridement involving removal of dead material within a
wound to improve normal healing is a very essential step
for burn wounds. Thermal injury involves necrosis of skin
and subcutaneous tissues to varying depths which results
in formation of eschar which releases chemical mediators
which damage local capillaries and epithelial elements though
they also stimulate leucocytes to digest debris. As a result,
if this necrotic tissue is not removed early, it prolongs
inflammation and retards epithelialization and hence healing
of wounds (Fig. 14.8).
During World War I, the battlefield surgeons realized
that regular excision of dead tissue from war wounds
reduced the incidence of infection and accelerated healing
process.2 This concept is now used as a fundamental
principle while managing burn wounds worldwide.
Debridement of burn wound is different from excisional
surgery. It involves washing and gradual removal of loose
debris and necrotic tissue and handling of blisters, which is
usually done bedside or in the dressing room without
anesthesia. Excisional surgery, on the other hand, is excision
of the burn wound (surgical removal of the eschar) carried
out in the operation theater in order to prepare the wound
for early skin grafting.
Oxygenation of Tissues
A continuous supply of oxygen is essential for all phases of
wound healing. Following burns, the blood supply to the
burn wound is reduced because of edema and impaired
circulation leading to poor oxygenation of tissues. This
reduced tissue oxygenation not only impairs wound healing
but also favors bacterial invasion of the wound. The result
is that the wound heals poorly and with excessive scarring.
To counter this, some burn centers have used hyperbaric
oxygen to assist wound healing. However, it has not been
used widely.3,4
Simpler measures can also be taken to ensure adequate
oxygenation of burn wounds (a) the burned extremities
should be elevated, (b) constricting dressings and casts
should be avoided, (c) early escharotomies/fasciotomies
should be done to avoid compartment syndrome in case of
circumferential full thickness burns (Figs 14.9A to C), (d)
early ambulation with full range of joint motions to be started
and e) removal of dead tissue.
Fig. 14.8: Debridement of dead skin

Burn Wound Management
157
Epithelialization
In all partial thickness burns (other than first degree
epidermal burns), the epidermis is completely destroyed.
However, the epidermal appendages, i.e. the hair follicles,
sweat glands and sebaceous glands are spared. It is from
these surviving epithelial structures that the epithelium
spreads rapidly to provide a new intact epithelial surface
which is elastic and supple. In case of deep dermal burns
the majority of the dermis and all sebaceous glands are
destroyed and only deeper parts of hair follicles or sweat
glands survive. As the eschar separates, epithelial buds
emerge from the site of these remaining epidermal
appendages and from these tiny islands the new epidermis
proliferates over the wound surface (Fig. 14.10). As this
re-epithelialization is very slow, the healed skin shows
hypertrophic scarring. Superficial dermal burn wounds
should be managed with moist protective dressings which
enhance epithelial growth. Exposure technique which
involves exposure of burns to air leads to formation of a
scab which retards epithelial migration and hence healing.
In recent years, a number of synthetic, occlusive and semi-
occlusive dressings have been developed and used for
superficial burns and donor areas.5,6 These have been found
to protect the fragile new epithelium during early phase of
healing and thus hasten wound healing. Burn wounds should
be closely watched for development of infection because
the latter can increase the depth of wounds.
Formation of Granulation Tissue
In case of very deep dermal and full thickness burns, in the
absence of infection, the dead tissues become dry, firm and
Fig. 14.9C: Tissues underneath the eschar bleed once
escharotomy is done
Fig. 14.9A: Circumferential full thickness burns in an infant,
compromising circulation to the hand
Fig. 14.9B: Incision through the eschar—Escharotomy
Fig. 14.10: Epithelialization occurring underneath the eschar–Seen
once the slough is removed

158
Principles and Practice of Burn Care
black called eschar. Beneath this eschar, cellular and capillary
activity in the underlying viable tissues produces a layer of
red granulation tissue which is exposed when the eschar
separates. The granulation tissue is totally devoid of epithelial
cells so that the healing of a burn raw area can take place
only by epithelial migration from the normal surrounding
epithelial edge and wound contraction. Initially this ingrowth
is rapid but only for a certain distance after which the cells
stop growing. Over flexor aspects of joints or in areas where
the skin is loose and contraction is possible, the wound
closes of its own with development of contractures. In
areas where the underlying bone(s) prevent contraction,
the granulation tissue remains as a non-healing wound till it
is covered with a skin graft/flap (Fig. 14.11).
to severe contractures causing severe deformities in burns
which will then require correction by release and grafting
(Figs 14.12A and B) which will then require correction
release and grafting. To avoid this, a burn surgeon covers
them with skin grafts as soon as the patient is fit for surgery
and the area is fit for an optimal graft ‘take’, thus limiting
the formation of scar.
Fig. 14.11: Granulating wound, shows that epithelialization from the
margins stops after a certain distance
Wound Contraction
In case of untreated/conservatively treated deep burn
wounds, the granulation tissue forms on the raw areas and
epithelialization begins from the margin of the raw areas. At
the same time, there is laying down of collagen fibers under
the granulation tissue. These areas, if not grafted at the
earliest, go on to develop chronic granulation tissue. Their
vascularity reduces, the superficial layers of granulation
tissue ooze serum which clots and this is again invaded by
inflammatory cells and capillaries to form fresh granulation
tissue. As time passes, the deeper layers progressively
mature into fibrous scar tissue with overlying thin
granulations. This begins to contract in an effort to close
the raw areas. It is this contraction of the bed which leads
Fig. 14.12A: Wound contraction —If surgical intervention is not done
the wound bed contracts leading to contracture of neck
Fig. 14.12B: In same patient —Surgically released neck
with split skin grafting

Burn Wound Management
159
INITIAL CARE OF BURN WOUND
Once the resuscitation procedures have been initiated, the
burnt area has to be evaluated in detail for its extent and
depth. It is preferable to shift the patient to the specified
dressing room where the wound can be managed with all
aseptic precautions. This is important because immediately
following burns the skin surface is sterile as all surface
bacteria are killed by the heat. One should avoid introducing
exogenous bacteria to the wound by all means in order to
avoid burn wound infection. All the loose nonviable tissues
should be removed with minimum trauma. The area should
be thoroughly washed with Savlon® and then normal saline
to remove all the debris. Only after thorough debridement,
a proper appraisal of depth of burns can be done and it
should be properly charted in the “Burn Chart” for future
reference (Fig. 14.13). This chart contains detailed
observations of the wound along with any surgical procedure
performed. Any change in burn wound depth can also be
charted in the same form at a later date to follow the progress
of the burn wound. All encircling bracelets, rings and other
jewellery on the person of the burn victim should be removed
because they can act as tourniquet once edema sets in,
causing distal ischemia.
Management of Blisters
Management of blisters is very controversial. Theoretically,
the fluid in an intact blister is sterile. However, it is rich in
proteins which cause it to set into a gelatinous form which
is an ideal culture medium for bacterial growth if the fluid
happens to get contaminated. This fluid retards the local
immunity by impairing the normal function of inflammatory
cells and also retards the fibrinolytic process thus, delaying
the wound healing.7 The controversy about blisters is (a)
whether they should be ruptured and deroofed or else kept
intact, and (b) whether the blister skin acts as a skin
substitute or not. While very small blisters(< 5 cm) may be
allowed to be kept intact, the larger blisters (> 5 cm)run the
risk of rupture at the time of initial dressing or else may get
ruptured in odd situations and the burn wound gets
contaminated. It is very difficult to keep blister fluid sterile
for a long time and so it has been advocated to at least
aspirate them with a needle to allow the blister membrane
to stick to the wound. Other workers consider the blister
skin as dead and necrotic tissue and hence deroof the blister
and dress the wound (Figs 14.14A and B). In children, it is
preferable to rupture the blisters because they are bound to
get ruptured soon due to their uncontrolled activity.
After cleansing, the wounds are dabbed dry with sterile
gauze and then the appropriate method of further wound
management is selected, i.e. exposure method (open method)
or closed method (occlusive method) of dressing. In most
patients, neither of these methods used alone is ideal for
local care and frequently both methods are used in different
areas of the body in the same patient for best results.
Exposure or Open Technique
The open method of burn treatment has been used since
eternity but was reintroduced by Wallace in 1948.8 It is
especially useful for burns of face and perineum which
cannot be adequately dressed. Extensive non-salvageable
burns more than 90 % TBSA may also be managed by this
method decreasing the requirement for manpower, material
and cost. This technique consists of placing the patient on
a clean, dry, sterile sheet after cleaning and debriding the
wounds. The wounds are left exposed to air without any
topical agents or any covering agents. The exudate from
the wounds dries up and along with the layers of destroyed
skin forms a scab or an eschar. The latter acts as a ‘dressing’
protecting the underlying tissues from bacterial colonization
(Fig. 14.15A). Although the dry cool air inhibits bacterial
growth, pathogenic organisms can grow from the deep
surface of the crust. Under these circumstances, the activity
of the organisms is usually low and the body is able to fight
them and hence, healing can take place. The drying process,
however, may retard the spread of epithelium which is faster
under moist conditions.
For deeper wounds, open treatment may be less
satisfactory as the dry eschar takes a long time to separate.
The patient and his attendants also may find the exposed
wounds unsightly and uncomfortable. This method is not
very suitable for wounds over joints as the scabs over a
joint surface may crack repeatedly and bleed. In case of
hands, exposure method allows full range of movements at
all joints which avoids deformities of the hand.
A modification of the open technique is to apply a thin
layer of antibiotic ointment over the wounds after cleansing
and drying them daily, especially on the face. Sometimes an
antimicrobial impregnated gauze is used on exposed wounds
and this gauze acts as a wick to transport the exudates to
the gauze surface where it dries up forming a scab. The
advantage with this technique is that the scab does not
adhere to the wound and the gauze can be removed easily

160
Principles and Practice of Burn Care
Fig. 14.13: Burn chart used in the author’s unit–Depth of burns in different areas can be charted

Burn Wound Management
161
without the risk of bleeding from the wound or else damage
to the newly formed epithelium (Fig. 14.15B).
If the burned area is superficial partial thickness, the
whole scab/gauze begins to separate after a week or so and
this is trimmed gently and repeatedly with scissors and
finally comes out in 15-21 days to leave a well healed skin
surface. If the scab does not separate by 3 weeks, the burn
is treated as a full thickness burn and the management is
changed to the technique of occlusive dressings which
hasten separation of eschar so that the raw area can be split
skin grafted. For patients treated by exposure method,
appropriate maintenance of the environmental temperature
and humidity is very important. This is because leaving the
wounds exposed increases the evaporative losses as well as
substantial body heat loss. To compensate for this, the ambient
Fig. 14.15A: Facial wounds treated by exposure technique –Exudates
from the wound dries up and forms a scab which acts as an external
dressing to protect underlying tissues from infection
Fig. 14.14B: Deroofing of blister done surgically—Underlying
coagulum seen
Fig. 14.14A: Blister being incised
Fig. 14.15B: Exposure technique but with application of antibiotic
impregnated paraffin gauze—Transports exudates to the surface of
the gauze so that the scab does not adhere to wound surface and
gauze can be removed easily without causing pain or bleeding from
wound surface
temperature must be maintained in the range of 28-32 °C
and humidity at about 40 %.
The advantages of open method are:
•
Wound examination is easier
•
Earlier detection of wound infection
•
Early physiotherapy
•
Easier control of hyperpyrexia, and
•
Wound environment is not conducive for bacterial
colonization.

162
Principles and Practice of Burn Care
The disadvantages of open method are:
•
Delay in eschar separation
•
Evaporative losses increase
•
Chances of hypothermia are more because of loss of
body heat, and
•
Not possible where isolation is not available.
Occlusive Dressing or Closed Technique
This method is most useful for patients who are treated on
outpatient basis, patients who need to be transported from
one center to another, circumferential burns of extremities
and torso, in infants and children and uncooperative adults
(Fig. 14.16). Occlusive dressings are avoided in burns of
face and neck and perineal burns.
The advantages of occlusive dressings are:
•
It reduces evaporative losses
•
Provides a mechanical barrier to prevent bacteria from
contaminating the wounds
•
Absorbs exudates from the wound surface
•
Assures maintenance of functional position in burned
extremities
•
Maintains moist environment which encourages
epithelialization
•
Patient is more comfortable
•
Provides splintage to joints thus preventing contractures.
Dressing Technique
The technique of dressing a burn wound is very important
for the final outcome of burn wound treatment program.
All burn dressings should be done with proper aseptic
precautions to prevent wound contamination. All doctors
and nursing staff should be properly gowned and gloved.
Majority of the dressings can be performed without general
anesthesia. Usually sedation with opioid analgesics (e.g.
morphine) is adequate.
A satisfactory burn dressing is one which can absorb all
the fluid exuded from the burn wound and distributed evenly
throughout so that there is no collection of the exudate on
the wound surface. The material which fulfills these
requirements is the Gamgee pads which consists of cotton
wool sandwiched between two layers of absorbent gauze.
These are easy to prepare and can be made in assorted
sizes suitable for small as well as extensive areas. These are
prepared, sterilized and kept ready to use so that they are
available at all times.
The innermost layer of occlusive dressing consists of a
layer of an antimicrobial agent over which a wide mesh
gauze impregnated with paraffin or petroleum jelly is applied.
This tulle grass is non-adherent so that pain and trauma to
the regenerating neoepithelium can be minimized at the time
of change of dressing. After the non-adherent gauze and
antimicrobial agent is applied, multiple layers of Gamgee
pads, depending on the expected amount of exudate, are
applied and kept in place with gentle compression bandage.
This dressing prevents edema formation, splints the wound
and facilitates absorption of discharge. However, it should
not be constricting in any way. This outer layer of the
dressing should be porous to allow evaporation of water
and prevent inner layers from becoming soggy as that
encourages microbial growth (Figs 14.17A to D).
The frequency of dressing change depends upon depth
of burns and degree of infection in burn wound. In case of
partial thickness burns when there are no signs of infection,
the first dressing can be left intact for 5 days. In case of
full thickness burns, the dressing should be changed every
3 days. Earlier change of dressing in either case is indicated
if there is soakage in dressing or any sign of infection of
burn wound which includes local pain, unexplained fever,
foul smell from dressing and increased purulent discharge
from wound. In these cases frequency of dressing change
can vary from daily dressing to alternate day dressing till
infection is controlled. The topical agent being used on
wound should also be changed if discharge increases. There
Fig. 14.16: Closed dressing technique

Burn Wound Management
163
beneficial effects of biological dressings in superficial burns
even though the final outcome is the same. Pain is absent or
reduced significantly, patient is more comfortable and
discharged from the hospital sooner. Hence, the overall
morbidity is reduced. The most commonly used temporary
skin substitutes are collagen dressings, Biobrane®, Integra®
etc. Their use and application are described in detail in the
chapter on Biological dressings.
Escharotomy/Fasciotomy
In full thickness circumferential burns of limbs, neck and
chest, the tight dry eschar with underlying edema may
produce a tourniquet effect. This has to be diagnosed early
in order to avoid vascular compromise to distal extremities
and respiratory impairment. To diagnose distal vascular
compromise, the following clinical signs and symptoms are
looked for: cyanosis of distal unburned skin, delayed capillary
filling in nails of fingers or toes distal to circumferential
are various antimicrobial agents used for burn dressings
which are discussed later in this chapter.
Biological Dressings
The use of topical antimicrobial creams for burn wound
dressing has been in vogue for about half a century. Their
use for treatment of partial thickness burns was favored by
all surgeons as they allowed better control of burn wound
sepsis. However, the application of topical creams requires
frequent dressing change which causes pain and anxiety to
the patient. These drawbacks instigated the research for
alternative treatment with temporary skin substitutes or
biological dressing materials. The application of biological
dressings is a good alternative to daily change of
conventional dressing with antimicrobial agents for
superficial burns. Though their use improves the quality of
care given to burn patients, they are expensive and their use
should be rationalized. Prospective studies have shown
Figs 14.17A to D: (A) Removal of loose dead skin. (B) Application of silver sulfadiazine over paraffin gauze.
(C) Application of gauze and Gamgee. (D) Light compressive bandage of the limb
A
B
C
D

164
Principles and Practice of Burn Care
burns in limbs, paresthesias or deep tissue pain. All these
signs warrant a second look at the burn wound and diagnosis
can be confirmed by a color Doppler to look for arterial
flow in distal palmar arch for upper limb and posterior tibial
artery in lower limb. These circumferential burns are treated
by performing an escharotomy (Fig. 14.18) wherein an
incision is made through the full thickness of the eschar
releasing the constricting effect and thus, decompressing
the underlying structures and improving the distal blood
supply. In case escharotomy does not give adequate
decompression, as in case of high voltage electrical injury
where the muscles are also involved leading to edema under
the deep fascia and raising the compartment pressure, the
incision has to be extended till the underlying deep fascia
(fasciotomy) in order to release the compartment pressure
(Fig. 14.18B).
Technique: The procedure is done bedside using sterile
technique (Fig. 14.18B). Anesthesia is not required as the
eschar is dead tissue and hence painless. Sites for incisions
for escharotomy are given in Figures 14.19A and B, taking
care to avoid injury to major peripheral nerves. The incision
has to be first given in the midlateral line across involved
joints and throughout the length and thickness of the eschar.
If perfusion does not improve, midmedial incision is given
to increase the decompression. Blood loss is usually minimal
because incision goes through the avascular eschar only.
In case of electrical burns when there is edema of the
muscles which increases the compartment pressures,
fasciotomy is required (Figs 14.20A to D). In these cases,
the skin of the limb may be unburnt and requires local
anesthesia before giving the fasciotomy incisions in different
compartments. At times, the carpal tunnel has to be opened
in the hand to release the pressure on the nerves (Figs 14.21A
and B). In that case, the incision can be extended over the
forearm as an S-shaped incision over the flexor aspect of
the forearm and hand. Fasciotomy incisions should be given
from proximal to distal direction so that the pressure is
released gradually and immediate profuse bleeding does not
occur interfering with the incisions. If there is significant
bleeding during fasciotomy, it can be controlled by pressure
dressing for a brief duration or by using electrocautery.
Since the incisions expose the underlying healthy tissues
to a risk of infection by bacteria colonizing the burn wound,
it is important to give cover by topical antimicrobial agent
during dressing.
Fig. 14.18A: Escharotomy incisions for full thickness circumferential
burns of chest restricting chest expansion
Fig. 14.18B: Fasciotomy incision over arm in electrical contact burn
Figs 14.19A and B: (A) Line diagram showing escharotomy incision
lines. (B) Line diagram showing escharotomy incisions for hand
A
B

Burn Wound Management
165
Fig. 14.20B: Incisions given till deep fascia, releasing the
compartment pressure
Fig. 14.20C: Fasciotomy incisions over dorsum of hand
Fig. 14.20A: Electrical contact burn in arm causing gross edema of
limb and distal circulation compromised due to compartment syndrome,
demanding urgent fasciotomy
Fig. 14.20D: Following fasciotomy, the underlying muscles bulge out
and bleeding on surface is seen
Hydrotherapy
Hydrotherapy involves washing the burn wound or giving a
bath to the entire patient prior to dressing change. This can
be given in the form of a shower or immersion in saline
bath (Arzo bath tub) or Hubbard tank (Figs 14.22A and B).
The advantages of hydrotherapy are:
•
It improves general hygiene and decreases the number
of bacteria
•
Patient has a feeling of well-being
•
Dressings can be removed easily and wounds cleaned
painlessly
•
Active exercises can be performed during hydrotherapy
which prevents stiffness of joints
Ambulatory patients are managed by using shower bath
whereas non-ambulatory patients or those with extensive
burns are best managed in a saline bath or Hubbard tank.
Minor debridements can also be carried out during this
procedure. The main disadvantage of using bath tubs or
tanks is the risk of cross contamination amongst the patients.
Additionally, this is a cumbersome procedure involving a
team of doctors, nurses and therapists.
Fig. 14.21A: Incision for opening carpal tunnel to decompress
nerves
Fig. 14.21B: Incision extended into forearm—Circulation to hand
restored and hand saved by timely intervention

166
Principles and Practice of Burn Care
TOPICAL ANTIMICROBIAL THERAPY IN
THE TREATMENT OF BURN WOUND
A variety of local medicaments have been used on burn
wounds since eternity,which ranged from tinctures (600
BC), vinegar soaked dressing (430 BC), greasy dressing
(1596), tannic acid by Edward Clark Davidson (1894-1933)
to Gentian violet by Aldridge in 1933 to Petroleum gauze by
Harvey Allen in 1942. All these methods, however, fell into
disrepute because of local and systemic toxicity or
ineffectiveness of these substances. This initiated a research
into finding newer topical agents which are more effective
and have fewer side effects.
History of Topical Antimicrobial Agents
The topical therapy of burn wounds dates back to the
beginnings of civilization. Throughout history, a number of
famous philosophers, physicians and scientists have
contributed to the knowledge of burn wound management,
including such notables as Hippocrates, Celsus, Pliny the
Elder, Galen, Aristotle, Rhases, Clowes, Paré, Hildanus,
Marjolin, Dupuytren and Syme. A diverse variety of
substances have been advocated as effective topical burn
treatments including various plants, gums, milk (goat milk
and milk from “a women who has given birth to a son”),
tea leaves, roasted angle worms, oak bark extract, honey,
cork, bear fat, bran, ashes, vinegar, wine, fat from “very
old wild hogs,” calcium chloride soaks, moss “from the
skull of a person hung,” red sandalwood, cold water, saline
baths, lemon strips soaked in oily dressings, soot, spider
webs, linseed oil mixed with lime water, picric acid,
medicated paraffin, carbolic acid, cod liver oil and “portions
of a genuine mummy.” Over the years, the goals of topical
burn treatment have changed. By the beginning of the 20th
century, it was believed that the systemic derangements
seen in burn patients resulted from a release of ‘toxins’
from the burn wound and thus, the goal of topical therapy
would be to bind or leach toxins before they can be
absorbed.11 A secondary goal was to dry out the burn wound
or to create a hard coagulum to minimize exudate, drainage
or fluid loss. A number of “escharotics”, including 5% or
10% silver nitrate solution, gentian violet, 12, 13 “triple” dyes,
trinitrophenol and tannic acid were employed, either alone
or in combination.
There was a drastic change in the treatment of burn
wound with dressings along with an antiseptic agent in 1868
following discovery of the concept of antiseptics by Lister.
Carbolic acid, mercurial compounds and aniline dyes were
used as inner layer of burn dressing. Unfortunately, they
were unselective in their action and damaged normal tissues
along with bacteria colonizing the wound surface. Hence,
their use was discontinued. In the mid-twentieth century
phenol containing dressings were highly recommended.
Davidson at the Henry Ford Hospital first described the
use of tannic acid spray in 1925,12,14 and believed that this
modality reduced pain and produced a cleaner wound bed.12
In 1935, Bettman added 10% silver nitrate to a 2.5% tannic
acid solution, which allowed wound tanning to occur in
seconds.11 Reports of liver necrosis in patients treated with
tannic acid began to appear in the 1930s, although the liver
necrosis was often ascribed to the burn injury itself.
Additionally, pus tended to accumulate under the coagulum
formed by tannic acid application. McClure (1944) 12, also
from Henry Ford Hospital, reported that tannic acid was a
hepatotoxin and the use of this agent was discontinued.
Fig. 14.22A: Shower bath on a shower trolley
Fig. 14.22B: Saline bath tub used in the author’s unit

Burn Wound Management
167
Work by Aldrich, Teplitz, Lindberg and others established
that septicemia in burn patients, a major cause of mortality,
frequently originated in the burn wound.13 Attention now
turned to the application of various topical antimicrobials to
the burn surface and the development of mafenide
(Sulfamylon®), silver nitrate, silver sulfadiazine and others
revolutionized burn care.
In early part of World War II, Marfanil which was later
called Mafenide was used by German army and was found
to reduce the incidence of gas gangrene. Subsequently, it
was used by US Army for traumatic wounds as it was
found to be effective against clostridial and enteric organisms.
Its efficacy in controlling burn wound sepsis was discovered
by Moncrief in 1964. Although it was found to be very
effective against Pseudomonas especially in treatment of
established infections, it was relatively inactive against gram-
positive organisms, especially streptococci which was the
main cause of burn wound infection at that time.
In 1965, Moyer and colleagues showed excellent
prophylactic use of 0.5% Silver nitrate against
Psuedomonas. But it had no role in established infections
and also caused dys-electrolytemia and the patient was
uncomfortable because of the black staining and continuously
wet feeling. So its use fell into disrepute.
In 1968, a new antimicrobial, namely silver Sulfadiazine,
was discovered by Fox for use in burns. Even after half a
century later, no serious side effects have been reported
despite its widespread use.
Many other antibiotics and antiseptics have been used
singly and in various combinations for burn dressing, namely,
gentamicin, neomycin, bacitracin, polymyxin, framycetin,
nitrofurazone and chlorhexidine, etc. Many of these have
proved useful under certain circumstances. However, they
have all failed to prevent serious systemic infections in
extensive burns, especially Pseudomonas infection, which
is now the most common organism responsible for burn
wound sepsis worldwide.
Basis for Topical Therapy
Immediately following burns, the surface of the burnt skin
is sterile and the only organisms present are those present
deep in the skin appendages and these are not very
pathogenic. Some of these organisms come to the surface
following burn but a sterile dressing and use of an
antimicrobial agent can kill these organisms. In case of closed
dressings, presence of exudates in the dressings, warmth
and lack of light under the dressing are ideal conditions for
proliferation of organisms after they gain entry to the skin
surface through exogenous or endogenous routes, resulting
in infection. This can be avoided by using a broad spectrum
antimicrobial agent which has action against both gram-
positive and gram-negative organisms. The topical agents
used for burn wound dressing have a dual purpose –first to
control any organisms on the surface of the burn wound
and secondly to prevent entry of new organisms from the
exterior.
By the end of first week post burn, the deeper surface
of eschar especially around the hair follicles shows active
proliferation of organisms which can penetrate into deeper
tissues and adjacent viable tissue as well, if not controlled.
This can again be checked by the application of topical
antimicrobial agents which have a good eschar penetration.
The deeply burned areas are avascular10 which not only
provide a favorable environment for bacterial proliferation
but also prevent penetration of antibiotics administered
systemically and thus, ineffective delivery of antimicrobial
to the burn wound surface to fight the surface
contamination. This is better tackled by topical antimicrobial
agents and obviates the need for systemic antibiotics. It is
very important to understand that topical therapy does not
sterilize the burn wound. It only controls the bacterial
proliferation and confines it within the limits of the burn
wound. Topical agents are also no substitute for meticulous
wound care which includes proper debridement of
devitalized tissues which favors bacterial proliferation and
prompt de-roofing of sub-escharotic abscesses. On the other
hand, proper and judicious use of topical agents can prevent
conversion of superficial burns into deeper wounds and also
result in spontaneous healing of wounds which appeared to
be deep initially and decrease the incidence of systemic
sepsis.
Criteria for a Good Antimicrobial Agent
1. It should have a broad spectrum of activity which
includes organisms which are most commonly isolated
from the burn wound, e.g. Pseudomonas aeruginosa,
Staphylococcus aureus, Klebsiella and Enterococci etc.
2. Ideally the topical agent should penetrate the eschar and
yet not be significantly absorbed systemically.
3. There should be minimal emergence of resistance
amongst organisms against the agent. If there is high
frequency of acquired resistance against the substance
being used, the efficacy of the agent decreases and
resistant strains produced are also more virulent.

168
Principles and Practice of Burn Care
4. It should cause minimum or no discomfort to the patient.
5. It should be economical and easily available.
6. It should have minimal side effects. Though majority of
the agents do get absorbed systemically, their use has to
be restricted for only certain specific established
infections and on the smallest possible wound areas.
7. It should be economical as in many areas of the world,
cost is the primary factor which affects selection of the
agent.
8. Application should be simple and easy.
Topical Agents
The topical antimicrobial agents, most frequently used for
burn wound dressings, are discussed below. As any one
agent is not uniformly efficacious in all the cases, it may be
necessary to substitute it with a different agent on all or
part of the wounds during the course of treatment at
different times.
Silver Sulfadiazine (SSD)10,12,15-17
It is a white crystalline, highly insoluble compound
synthesized by Fox 15 in 1968 by reacting silver nitrate with
sodium sulfadiazine. It is the most frequently used topical
agent in the form of a water soluble cream base at 1 %
concentration, which provides the same amount of elemental
silver as 0.5 % silver nitrate solution (30 m Eq /L).12 At this
concentration, the amount of agent at the surface is more
than that necessary in vitro to inhibit the growth of sensitive
organisms.
Mode of Action
The mechanism of action is supposedly due to both silver
ion and sulfadiazine moiety which are released at the wound
surface by gradual dissociation. Sulfadiazine is a competitive
inhibitor of para-aminobenzoic acid (PABA) which is a
metabolic precursor. The ionic silver acts primarily on
bacterial cell walls where it induces ultrastructural changes
and also reacts with the DNA of the bacteria impairing its
replication.12 It is, therefore, primarily bacteriostatic. It is
active in vitro against a wide range of organisms which
include Staphylococcus aureus, Escherichia coli, Proteus,
Enterobacteriaceae and Herpes virus. Clinical trials have
shown that it has reasonable prophylactic effect against
gram-negative bacteria. It delays wound colonization by gram-
negative bacteria from 10-14 days in extensive burns.
In spite of the dissociation of the compound there is no
absorption of the silver from the wound. On the other hand
Sulfadiazine levels of 1.5-4 mg/100 ml have been reported
in the blood. There is also some grayish silver discoloration
of the wound because of minimal precipitation of silver
chloride or silver sulfide following oxidation of silver by
exposure to sunlight.
Mode of application: It is applied as 1% cream to the
burn wound in a thickness of approximately 0.5 -1 cm either
twice a day in case of exposed treatment or once a day in
closed method. The substance has to be washed off between
applications in order to debride the wounds properly.
Advantages
It is an odorless cream, easy to apply and causes minimal
to no pain on application. It does not stain the skin or linen
unlike silver nitrate.
It has intermediate penetration capacity into the burn
eschar between that of readily absorbable Mafenide and
minimally absorbable silver nitrate.
Bacterial resistance to silver sulfadiazine, even after
prolonged therapy, has not been reported.
Disadvantages
•
Crystalluria has been occasionally reported though not
of much clinical significance.
•
Methemoglobinemia is a well known side effect of
sulfonamide, although seen very rarely.
•
Transient leucopenia occurs in many patients treated
with SSD and it occurs 2-3 days after starting treatment.
This resolves spontaneously within a few days despite
continued use of the agent.
•
A macular rash is seen in <5 % patients and is a cutaneous
sensitivity reaction to SSD.
•
A thin proteinaceous gel called’ Pseudoeschar’ forms
on the wound surface after topical application of SSD.
This can confuse an inexperienced observer during
assessment of the depth of burn. However, this can be
removed easily in sheets.
•
With prolonged use of topical SSD, there is a risk of
sulfadiazine resistant gram-negative bacilli, especially
Enterobacteriaceae group, developing plasmid mediated
resistance.16
•
Inhibition of epithelial regeneration with the
use of 1% SSD has been demonstrated experimentally.12

Burn Wound Management
169
Silver Nitrate Solution (0.5%)
Silver nitrate has been used for the treatment of burn wounds
for over a century but fell into disrepute because of side
effects since it was used in higher concentrations. Five and
10% silver nitrate solution was used as a caustic and
escharotic for burn care in the early 20th century, but was
largely abandoned by the time of World War II because
infections tended to become trapped under the hard eschar
produced. It was reintroduced by Moyer in 1965 as 0.5%
solution and later popularized by Monafo as a topical agent
for burn wound treatment. Though in 95% strength silver
nitrate is still used to cauterize hypertrophic granulation
tissues, in a 0.5% concentration it has antimicrobial effect
without being histotoxic. 0.5% silver nitrate remains the
first-line topical agent in many burn centers. For many years,
0.5% silver nitrate has also been used as a topical agent for
patients with toxic epidermal necrolysis (TEN).
Mode of Action
Mode of action is apparently due to the free silver ion which
is effective against the common microbial flora seen in the
burn wound especially gram-negative bacteria. It is mainly
bacteriostatic. There is no known resistance seen to this
agent and if properly used, it is very effective as a
prophylactic agent. There is minimal absorption of silver
through the open wounds into systemic circulation because
its salts are insoluble. Instead, there is precipitation of its
salts, i.e. silver chloride and silver sulfide which cause the
characteristic black discoloration of the burn wounds.
Mode of application: The technique of application of
silver nitrate solution as described by Monafo and Moyer 11
remains unchanged even today. After cleaning and debriding
the loose tissues in the wound, it is covered with a 8-10
layer thickness of gauze dressing which is then soaked with
warm 0.5% silver nitrate solution. The dressings have to be
wetted every 2 hours so as to ensure that the concentration
does not become caustic (> 2-3 %). The advantage of this
bulky wet dressing is that it minimizes evaporative loss.
The dressings are changed twice daily and their removal
achieves significant debridement of the wound also.
Advantages13
•
Application of silver nitrate is painless.
•
No patient hypersensitivity has been reported to it.
•
No resistant organisms have been isolated after its use.
•
Its use helps in rapid debridement of the eschar because
of twice daily change of the bulky gauze dressing and
wound becomes ready for grafting 7-10 days earlier
than with other methods.
•
Its continuous use decreases evaporative water loss
which further helps in decreasing metabolic rate and
improves nutritional status of the patient.
Disadvantages
•
0.5% silver nitrate has been found to be ineffective in
established burn wound infections and over dead
epidermis because of its inability to penetrate the eschar.
•
It stains all the linen and floor brown or black which are
difficult to remove. Thus, its use necessitates use of
disposable linens and stain-resistant floor and wall
coverings which can increase the cost of treatment.
•
There are severe electrolyte derangements noticed with
its use. Use of distilled water as a vehicle for application
of silver nitrate leads to a markedly hypotonic solution
and it causes absorption of large volumes of distilled
water into the tissues and eventually into the blood
stream. There is leaching of sodium by reverse
mechanism which results in hyponatremia which can
lead to convulsions, if very severe. This can be prevented
by administering large quantities of sodium chloride orally
or intravenously. The precipitation of silver as silver
chloride and silver sulfide salt results in hypochloremia
which can also be corrected by infusing saline.
There is leaching of potassium and calcium also resulting
in hypokalemia and hypocalcemia. Hence, careful monitoring
of electrolyte levels is required in order to assess the
replacement therapy accurately. Ideally 40-120 mEq of
potassium and 4-8 gm calcium along with vitamin
supplements are necessary either orally or intravenously. It
is also recommended to replace about 350 mEq of sodium
per square meter of wound surface in order to maintain the
adequate serum levels. If replacement is inadequate not only
serum sodium levels fall, even the urinary sodium
concentration falls below 40 mEq/l. Once the replacement
therapy has been decided upon, the electrolytes have to be
checked on a regular basis. The electrolyte imbalance with
the use of silver nitrate is noticed mainly in infants and children
and in patients with larger burns particularly > 20% TBSA,
unless the replacement therapy is maintained. In extremes
of age dys-electrolytemia can occur within 6-8 hours of its
use and therefore, less frequent saturation of wound
dressings is recommended in these age groups.

170
Principles and Practice of Burn Care
•
The black discoloration of the burn wound surface
interferes with further assessment of the wound depth
and changes in the burn wound condition.
•
Some of the gram-negative bacteria especially
Enterobacter cloacae metabolize nitrate ion to nitrite
which when absorbed through the wound results in
methemoglobinemia. Though it is a rare complication, it
has to be suspected if there is cyanosis or slate gray
discoloration of skin without any pulmonary injury and
arterial blood is brown in color even though PaO2 is
normal. Diagnosis can be confirmed by estimating
methemoglobin levels in the blood. Management of this
condition includes withdrawal of silver nitrate dressing
and intravenous administration of reducing agents like
methylene blue or ascorbic acid.2
The best use of silver nitrate, therefore, is in case the
patient is seen within a few hours of burns and silver nitrate
therapy is started immediately. If there is a delay of several
days and the burn wound has deteriorated because bacterial
sepsis has supervened or is impending, silver nitrate will
not be effective as it does not penetrate tissues effectively.
It can only act on the surface flora. In these cases, other
agents with better penetrating ability should be used. Silver
nitrate dressings are used in treatment of toxic epidermal
necrolysis syndrome and in rare patients allergic to silver
sulfadiazine or mafenide.
Mafenide (11.1%)
It is a methylated sulfonamide which was introduced for
clinical use as a topical agent for burn wounds in 1964 by
Moncrief. It is presently used as a cream with 11.1%
concentration of drug in a water miscible base.
Mechanism of action: It is active against most gram-
positive organisms and wide spectrum of gram-negative
organisms including Pseudomonas. It is particularly effective
against Clostridial species. It has minimal antifungal action.
Its mechanism of action is not known but it is primarily
bactericidal only in higher concentrations.
It actively penetrates the burn wound and minimal
amount is left on wound surface after 3 hours.14 After 10
hours, the tissue level is below the concentration required
to inhibit bacterial growth. Therefore, to maintain therapeutic
levels of the agent in the wound, it has to be reapplied after
12 hours.
After getting absorbed from the wound and entering the
circulation, the drug is broken down into its active acid salt
which is excreted in the urine. The resultant large osmotic
load along with its carbonic anhydrase inhibiting effect results
in significant alkaline diuresis. The combined effect of the
acid load and drug induced renal bicarbonate excretion
(because of carbonic anhydrase inhibition) leads to
hyperchloremic metabolic acidosis. This is compensated
by hyperventilation (to a maximum of 50 L per minute).
This can result in pulmonary complications including
respiratory failure and pneumonia. These side effects are
reversible if the drug is discontinued within 24-36 hours.
Mode of Application
Mafenide is used as a 11.1% water miscible cream which is
applied to wound with a gloved hand in a thickness of 3-5
mm usually without dressings. As patient is free to move
about in bed, the joint activity is maintained. Usually, twice
a day application suffices as a means for controlling burn
wound sepsis but reapplication may be required in some
areas where the drug gets wiped off the wounds due to
patient’s shifting position. More frequent application is
unnecessary and may also lead to sulfonamide toxicity which
can be fatal. During reapplication, the remaining cream on
the wound surface has to be wiped off with wet gauze.
Occlusive dressings are not advocated with the use of
mafenide because the effective antibacterial action of the
drug exists for less than 10 hours only and dressing change
every 12 hours is very cumbersome. Hence, twice a day
application by open technique is usually followed.
Advantages
Mafenide is the most useful topical antibacterial agent for
control of established or incipient burn wound sepsis where
the bacterial invasion has started or extensive colonization
is present. This is mainly because it has the best eschar
penetration ability. An overall reduction in mortality of 50 %
was noticed with the use of mafenide in a number of
studies.13,17
Disadvantages
•
Application of mafenide is associated with significant
pain which is probably because of its high osmolarity
and hygroscopic effect of the sulfonamide suspension.
The painful sensation persists for several minutes,
thereby earning its nickname of ‘white lightning’.
Alternately, applications of mafenide cream can be limited
to no more than 20% of the BSA at any one time. The
sites of mafenide applications can then be rotated every
2 hours until the entire burn has been treated. It is also
advisable to alternate mafenide and silver sulfadiazine

Burn Wound Management
171
creams on badly contaminated wounds as a form of
‘pulse therapy’.
•
5% of the patients develop maculopapular rash which is
characteristic of sulfa sensitivity. It can be easily
controlled by oral antihistamines.
•
Experiments have shown that its use leads to inhibition
of epithelial regeneration also.
•
The most significant complication of the use of topical
mafenide is the compensated metabolic acidosis which
results from its carbonic anhydrase inhibiting effect
which decreases the reabsorption of bicarbonate from
the renal tubule. The acidic breakdown product of
mafenide adds to the acid load. In addition, the
bicarbonate is converted to carbon dioxide in the lung
and excreted during hyperventilation which is a
compensatory mechanism. This is usually seen in
patients with > 40 % TBSA burns being treated with
mafenide. If the patient is only hyperventilating it may
not be a big problem. However, if the patient shows
signs of respiratory distress in the form of use of
accessory muscles, the drug has to be immediately
removed from the burn wound surface and some other
topical antimicrobial agent has to be applied. Additionally,
ventilatory support and metabolic support in the form
of sodium bicarbonate as per the laboratory
test reports is also to be provided in these circumstances.
•
Patients treated with mafenide also exhibit inappropriate
polyuria which results from significant reduction in
evaporative water loss from the burn wound (because
of 95% water content of the cream base) as well as the
osmotic load on the kidney due to the breakdown
product of mafenide.
•
Hemolytic anemia is a rare complication seen with the
use of mafenide.
Despite its disadvantages, mafenide is still the best topical
agent for control of established burn wound infection.18, 19
Its use should be reserved for short duration of time and
withdrawn before significant side effects become evident.
Gentamicin13,20,21
It is an aminoglycoside used as a 0.1% ointment or cream
in burn wound dressing. It is a relatively safe broad spectrum
antibiotic.
Mode of Action
It is primarily bactericidal. It is not effective against viruses
or fungi. It is effective against both gram-positive and gram-
negative organisms particularly Pseudomonas aeruginosa.
It acts by inducing defective protein synthesis.
Indiscriminate use of gentamicin for serious systemic
infections has shown development of resistant strains.
Mode of application: It is applied as 0.1% ointment or
cream 11as a thin layer to the wound surface twice a day
without dressing or with a light dressing. The application is
painless and absorption rate from wound is low. Therefore,
the incidence of ototoxicity and nephrotoxicity with topical
application is negligible.
It has good eschar penetration but its absorption
decreases as the water content of the eschar decreases.
Later, as the eschar separates and granulation tissue appears,
the rate of absorption of drug again increases. The absorption
of the drug is faster if applied as cream base than from
ointment base. Therefore, if an occlusive dressing is used,
it should be applied as ointment rather than as cream.
Advantages
•
Painless and easy application
•
Active penetration of eschar
•
Low incidence of toxicity when used topically
•
Good antipseudomonal action
Disadvantages
•
If used indiscriminately, there are high chances of
developing resistant strains especially Pseudomonas.
•
There are chances of ototoxicity and nephrotoxicity with
prolonged use.
Although gentamicin gives good results as a topical agent
on the burn wound, its use should be reserved exclusively
for systemic use.
Bacitracin
Despite lack of efficacy against common gram-negative
burn pathogens, bacitracin remains popular in burn care,
particularly on partial-thickness face burns. Whether this
beneficial effect is due to the antibiotic itself or simply to
the bland petroleum base remains controversial.
Less Commonly used Topical Agents
Chlorhexidine Gluconate
Chlorhexidine gluconate has been used in moderate burn
injuries either as such or in combination with 0.5% silver
nitrate as a prophylactic agent. Its absorption and toxicity
are not documented fully and hence, it is not used routinely.

172
Principles and Practice of Burn Care
Povidone Iodine
Povidone iodine (Betadine®) has been used as a water
miscible base (10%) for burn wound dressing. Though it is
found to be effective against gram-negative, gram-positive
organisms, fungi, viruses and protozoa, it has little effect
on Staphylococcus strains. Its use is restricted because of
certain disadvantages like its painful application. If used in
large quantities in extensive burns, there can be absorption
of large quantities of iodine leading to high iodine levels in
the blood.
Soframycin, Polymyxin B, Bacitracin
Soframycin, Polymyxin B, Bacitracin have been used only
for dressing of small burn wounds and are not indicated for
extensive burns because of systemic toxicity resulting from
absorption of these drugs from the extensive wounds.
Nanocrystalline Silver
(Figs 14.23A to E)
In the traditional silver containing antimicrobial agents, such
as Silver nitrate and Silver sulfadiazine, most of the silver
Fig. 14.23D: Wound almost healed after three dressings with
ACTICOAT® i.e. after 12 days showing gray staining because of metallic
silver
Fig. 14.23C: Wound in healing phase
after first dressing with ACTICOAT®
Fig. 14.23A: Superficial to deep dermal
burns of the back
Fig. 14.23B: Nanocrystalline silver dressing
(ACTICOAT)® applied to the burns on the back
Fig. 14.23E: Same patient
after 1 month with well
settled scars

Burn Wound Management
173
carries a strong positive electrical charge which makes it
highly soluble, but it also reacts readily with substances
such as chloride from the salt in the wound forming silver
chloride which is ineffective. As a result most of these
compounds allow initial release of silver ions and then most
are rapidly inactivated. Therefore it is necessary to apply
these agents frequently.
Recently newer products have been launched in the
market like ACTICOAT® (Smith and Nephew/Silicryst)
which have revolutionized the antimicrobial barrier dressing
because they contain nanocrystalline Silver which delivers
silver rapidly to the wounds for rapid onset of antimicrobial
action to control infection and then gradually over a sustained
period of time usually 3 days. As a result the dressing
changes are reduced to every 3-4 days. The decreased
frequency of dressing also decreases the chances of
exposing burn wound to infection from the external
environment which is critical to the survival of burn patients.
Another advantage of nanocrystalline silver is that it
releases both silver ions and metallic silver. The metallic
silver does not react with chloride as quickly as the ionic
silver and is therefore not inactivated quickly by wound
fluids. Therefore its effect lasts longer without the need for
repeated applications.
Summary
Use of topical antimicrobial agents in burn wound care can
prevent or minimize burn wound infections and sepsis. In
minor and superficial burns, there is no risk for burn wound
sepsis and patient may not benefit from the use of topical
antimicrobial agents. However, as these cases are treated
on an outpatient basis, they are used empirically to prevent
conversion of superficial wounds to deep wounds. It is
important to understand that any one single topical agent
cannot be used in all patients in all circumstances to the
exclusion of others. All agents are effective if used in the
right circumstances and at the same time, indiscriminate
use of any one single agent can be more harmful in the long
run. It is therefore imperative to use the topical antimicrobial
agents judiciously, selecting the right agent for the right
patient at the right time. At times, the drugs can be used in
combination in order to reduce their toxicities and overcome
their shortcomings.
Thus, the main aim of topical therapy is to control burn
wound sepsis and improve the condition of the deep wounds
so that they can be closed as early as possible by skin
grafting.
FURTHER BURN WOUND CARE
After the initial resuscitative measures and acute burn wound
management, the patient comes out of the shock phase and
general condition stabilizes. This usually takes about a week
in moderate to extensive burns. Now all the attention is paid
towards the burn wound as that would then be the greatest
threat to the survival of the patient. Apart from the supportive
care, the proper wound management per se will help in the
spontaneous healing of the partial thickness burn wounds
and successful resurfacing of the full thickness wounds.
Modes of Management
After initial dressing, the further wound care varies according
to the depth of burn wound. There are various modes of
managing burn wounds:
Conservative Treatment
Conservative treatment involves dressings with topical
antimicrobial agents only, allowing wounds to heal
spontaneously or else reveal granulating wounds which can
be split skin grafted. This is mainly indicated for the
superficial dermal burns. It may also be indicated in deep
dermal and full thickness burns where immediate excision
and grafting is not possible. This is usually seen in developing
countries where early excision and grafting is not routinely
done for all such cases because of paucity of technical
support, manpower, postoperative monitoring and overload
of burn patients. In these situations, majority of the patients
are managed by conservative treatment.
Surgical Management
Surgical management can be:
a. Early excision and grafting
b. Late excision and grafting
c. Progressive debridement and grafting
This is indicated for full thickness or deep dermal burns
where the wounds either cannot heal of their own or where
they heal with severe hypertrophic scarring or with
development of contracture. These surgical techniques are
used in different patients or different areas in the same
patient. The main aim of treatment is to close the burn
wound as soon as possible by the most appropriate method
available depending on the specific wounds.
Further care of the burn wound, according to the depth
of burns, is as follows:

174
Principles and Practice of Burn Care
Superficial Dermal Burns
All partial thickness burns which are superficial dermal heal
by proliferation of skin appendages in less than 3 weeks.
Therefore, conservative management as described above
by either conventional dressings with topical antibacterial
creams or biological dressings is normally the rule. The aim
of this local treatment is to prevent their conversion into
deeper burns by avoiding infection and provide optimal
conditions for healing.
Deep Dermal and Full Thickness Burns
In partial thickness burns which are deep dermal, most of
the dermis and hence majority of the epidermal appendages
have been destroyed. These wounds usually heal after a
long time (3-6 weeks) by proliferation of the sparse residual
skin appendages residing deep in the dermis after the dead
and necrotic tissues come out with conservative treatment.
This prolonged period of inflammation and healing leads to
hypertrophic scar formation which gives poor aesthetic and
functional results. In full thickness burns on the other hand,
spontaneous healing of burn wounds is just not possible
because of total loss of skin. If left alone, in both these
conditions, there are very high chances of septic
complications and the surviving patients are left with multiple
and severe sequelae as discussed elsewhere in this volume.
To overcome these problems, early excision of dead tissue
and coverage with split skin autografts should be the standard
treatment of choice (Figs 14.24A to 14.25B). A temporary
dressing with a good antimicrobial cream needs to be applied
while the patient is awaiting surgery. The excisional surgical
procedures are described elsewhere in this volume.
In patients with very extensive deep dermal burns who
may not be fit for early excisional surgery, the routine
conventional dressings are continued with intermittent
debridement of the eschar till healthy granulation tissue grows
and autografting is done. Meanwhile during this waiting
period, the general condition of these patients has to be
built up continuously as they tend to be in a catabolic phase
with negative nitrogen balance till the raw areas are covered.
At the same time, one has to be vigilant about patient landing
into septic complications during this intervening period. In
such circumstances appropriate systemic antibiotics and
change of topical antimicrobial agent can save the life of
the patient.
Fig. 14.24A: Early tangential excision of arm
Fig. 14.24C: 7 days postoperative picture of same patient showing
good hand movements
Fig. 14.24B: Split skin grafting of same limb
Indeterminate Depth of Burns
There are situations where the burn wounds are a mixture
of superficial dermal and deep dermal burns presenting as a
geographical pattern with some areas showing blanching
together with white non-blanching areas. It is difficult to
definitely diagnose these areas as superficial or deep partial
thickness. Hence, early surgical excision of doubtful areas
may not be justified as some areas of superficial dermal
burns may be unnecessarily sacrificed during excision,
extending the area of grafting and scarring further to areas
which would have otherwise healed spontaneously. This
may worsen the final outcome of the healed wounds.

Burn Wound Management
175
•
Isolate the burn wound from the other sources of
contamination
•
Maintain an environment which promotes epithelialization
of the partial thickness wounds.
The superficial dermal burns usually heal within 3 weeks
with this type of dressing. The first dressing can be left on
for 3-5 days provided there is no soakage and smell in the
dressing and subsequently at 3 days interval. If there is any
soakage, pain, fever and smell, the dressing should be
changed immediately and more frequently till the wound
condition improves. By three weeks post burn most of the
superficial dermal burns heal. It is also easy at this time to
identify wounds which are full thickness. For superficial
dermal burns, similar dressings can be continued at infrequent
intervals till healing is complete. It is the deep dermal and
full thickness burns in which there is a lot of slough and the
type of dressing needs to be changed as per the requirements
of the wound to assist in removal of slough. The non-
adherent dressing with silver sulfadiazine or mafenide is
continued till loosening of the eschar although separation of
slough is slow with use of these antimicrobials. If the eschar
is still adherent at 21 days, late surgical excision of eschar
can be considered as an option (Figs 14.26A to 14.27B).
Another option is Grid Escharotomy. In this incisions are
given in a grid fashion so as to allow introduction of surface
bacteria underneath the adherent eschar and the subsequent
pus formation allows the eschar to be lifted off the surface.
Once the eschar is loosened, it is debrided mechanically
and the remaining nonviable tissue is best removed by
repeated dressings with eusol. This is a wet to dry type of
dressing which involves direct application of eusol soaked
gauze followed by dry gauze and bandage. Eusol is a good
desloughing agent. Eusol (Edinburgh University solution)
contains the following:
•
Calcium hypochlorite 1 part by weight
•
Boric acid
1 part by weight
•
Water
80 parts by weight
If patient complains of pain, it can be diluted with normal
saline to half or quarter strength. Gauze well soaked in eusol
and lightly squeezed out is directly applied to the wound
without any paraffin gauze or any other nonadherent layer
and covered further by Gamgee pads and bandage. Since
this is an adherent dressing, it has to be soaked well with
normal saline on removal during dressing change to avoid
pain. Ideally eusol dressings should not be allowed to dry
for greater efficacy. The action of hypochlorite is transient
Fig. 14.25B: Split thickness skin graft after excision
of dry eschar
Fig. 14.25A: Dry eschar of full thickness burn on post burn day 10
These burns have to be treated with an initial conservative
approach with conventional dressings for 10-14 days after
which reassessment of the area is made. If the wounds
appear to be healing and complete wound closure is expected
within 21 days, the conservative treatment is continued.
Areas which do not appear to be healing are treated as deep
dermal wounds and are prepared for delayed excision or
debridement and autografting.
Conservative Management
There are different types of dressings used at different stages
in conservative burn wound management in order to achieve
different goals. The primary dressing in all acute burn
wounds have already been described above. This includes
open or closed method using topical antimicrobial agent,
usually 1% Silver sulfadiazine.
The main aim of dressing is to:
•
Decrease evaporative losses
•
Prevent and control colonization of wounds by bacteria

176
Principles and Practice of Burn Care
dead tissue and help in earlier removal of eschar.
Unfortunately, it does not prepare the bed to accept graft as
it does not stimulate granulation tissue formation and may
even form a neoeschar. As the wounds are not protected by
granulation tissue there are higher chances of invasive
infection. In fact reports suggest that patients, whose burn
wounds are subjected to enzymatic debridement, are at a
higher risk of sepsis than those treated with topical
antimicrobial agents only. Till date none of the enzymatic
preparations have been found to have much practical value.22
Once the slough is cleared off the wound surface, another
change in the type of dressing which promotes granulation
tissue formation is required. For this simple wet dressing in
Fig. 14.26A: Traditional wound management—Eschar
separation by autolysis
Fig. 14.26B: Granulating burn wound following
separation of eschar
so it is advised to repeat the dressing 3-4 times a day. As
this is not practicable, the dressing is changed on daily basis.
Although the action of eusol has not been studied by any
clinical trial, it has been used by surgeons for decades and
found to be very effective.
Enzymatic Debridement
Enzymatic debridement using various enzyme preparations
(e.g., collagenase –Salutyl®) has been tried from time to
time with the assumption that the enzyme can digest the
Fig. 14.27A: Preparing wound bed by surgical removal of eschar
Fig. 14.27B: After eschar separation—The granulation tissue is still
not healthy – needs further dressing with eusol. Followed by Povidone
iodine saline dressing

Burn Wound Management
177
the form of saline or Povidone iodine lotion gauze is helpful.
This includes a layer of paraffin gauze over which saline or
Povidone iodine soaked gauze is applied followed by Gamgee
and bandage. These gauze compresses have to be in
continuous contact with the burn wound and should be
wet at all times and replaced preferably twice or thrice a
day. As this is not practically feasible, at least once daily
dressing is essential. These wet dressings help in
development of healthy granulating wounds ready for skin
grafting. Wet dressings provide continuous drainage and
thus prevent pocketing and abscess formation. These are
continued till the patient is fit to be taken up for grafting.
Various growth factors are now being used in clinical
trials to hasten wound healing though their efficacy has not
yet been fully established. Epidermal growth factor (EGF)
23,24 is one of the recombinant cytokine growth factor which
has been successfully used in treating burn wounds. There
have been trials of using EGF alone or in combination with
silver sulfadiazine cream. Their use has shown marginal
improvement in burn wound healing when compared to
silver sulfadiazine alone.
SKIN GRAFTING OF BURN WOUND
Skin grafting is the ultimate procedure undertaken during
the care of a burn patient and it achieves the final goal of
wound closure. The grafts used are split skin grafts taken
from unburnt areas of the body. Full thickness grafts have
no role to play in post burn raw areas.
History
The history of skin graft dates back to 1869 when Reverdin
published his method of skin grafting. He took 1-2 mm
diameter skin pieces from a donor area of the patient and
transferred it to granulation tissue of skin defect.25-27 This
method was soon introduced throughout Europe despite
French surgeons objecting that this method of producing
new wounds encourages the risk of erysipelas. Reverdin
believed in the principle that the advancing edge of
epithelialization makes the wound heal faster. This was also
the basis for meshing of the graft. Pollock 28 at St. George’s
hospital started performing skin grafting in Great Britain in
1870. Reverdin’s discovery led to many more clinical
experiments which explained the type of granulation tissue
best suited for grafting and how the thickness of the skin
graft affected the speed of epithelialization.
In 1870, Ash29 concluded that thinner the graft, the
quicker the spread of epithelium around it. With the
discovery of the fact that complete coverage of wounds
with grafts produced better scars, arose the need for larger
grafts. In 1872, Ollier30, a Frenchman, used grafts as big
as 8 cm square.
Gradually surgeons performing eyelid surgery succeeded
in covering a wound surface with full thickness skin graft.
In 1870, Lawson 31, a British surgeon had applied this
technique for upper eyelid reconstruction. In 1875, Wolfe32
pioneered the full thickness grafts which were then called
‘Wolfe grafts’ or ‘Wolfe Krause ‘ grafts after Krause gave
his experiences with large size full thickness skin grafts in
Germany in 1893.33
Till this time no importance was given to the wound
bed and apart from the patient’s own skin, other humans as
well as animals were used as donors which led to a lot of
disappointing results. The next important criteria for skin
grafting were laid down by Thiersch, a German surgeon 34
who on the basis of years of his experience, concluded that
grafting should always be done from patient’s own skin
and grafts should be placed on fresh wound bed and if
granulation tissue was present on wound bed it should be
excised to improve graft ‘take’ and lastly, split skin grafts
and not the full thickness grafts should be used to cover
wound surface.
Thiersch procured grafts using a razor and they were
thicker in the middle than at the edges. Therefore, for many
years efforts were made to find new ways of improving
harvesting techniques in order to get thin grafts of uniform
thickness.
Skin grafts were applied only after granulation tissue
had appeared, although graft application after excision in
case of burns on eyelids on 6th post burn day were also
reported.35,36
Methods of skin grafting fell into disrepute at the end of
the 19th century because of the technique and the
disappointing results. Interest in Reverdin’s technique was
reinvoked at the beginning of the 20th century with
modifications. Davis referred to the modified version of
Reverdin grafts as ‘Small deep grafts’37 which were later
renamed as ‘Pinch Grafts’ by Gatch.38 Douglas et al called
them ‘Steele grafts’ after Steele, one of the first British
surgeons to apply the skin grafting techniques.
It was in 1929 that Blair and Brown described their
successful technique of split skin grafting. They
differentiated and elaborated the advantages and

178
Principles and Practice of Burn Care
disadvantages of thin, intermediate and full thickness grafts.
Split skin grafting for burn wounds with their technique
became an accepted procedure from 1930 to 1950.The
techniques were improved and more importance was given
to the preoperative, peroperative and postoperative care. In
1934 Humby formulated various criteria for graft cutting
instruments and though his first device did not function too
well, he introduced the ‘Humby’s’ knife in 1936 which was
a greatly simplified version.39,40 The original Humby’s knife
was a razor with a guard which did not allow precise control
over the thickness of the grafts. Further modifications were
made to increase its reliability.
Another instrument which could be adjusted to procure
grafts of a uniform width with varying thickness was the
‘dermatome’. In 1924, Hagen developed a mechanical
dermatome which was driven with a flywheel. In 1939,
Earl Padgett, a surgeon and Hood, a mechanical engineer,
designed the Padgett-Hood dermatome in USA 41 which
could be set at a specific thickness. Brown, another surgeon,
developed the ‘Brown dermatome’ with the help of Barron,
a mechanical engineer.42 This had a rapidly vibrating knife
driven by an electric motor.
Preparation of Wound for Grafting
A couple of days prior to grafting, the paraffin gauze is
omitted from the dressing so as to make the raw surface
non-greasy for better adherence of skin graft.
The condition of the granulation tissue is quite suggestive
of the wound preparation for grafting. A healthy bed which
is ready for grafting shows clean red granulations devoid
of any necrotic areas and does not bleed readily on touch(Fig.
14.28). If the wound looks angry red and granulation tissue
is very fragile and bleeds readily on touch with unhealthy
copious discharge, it is suggestive of beta-hemolytic
Streptococcus infection (Fig. 14.29). This is the only true
contraindication for skin grafting of wound. Since
Streptococcus is still found to be sensitive to penicillin and
other antibiotics, systemic penicillin should be started
immediately and continued till swab culture is negative for
this bacterium. If the granulation tissue appears slimy it is
suggestive of Staphylococcus infection (Fig. 14.30). In these
cases, systemic antibiotics, based on wound swab culture-
sensitivity data are administered and local dressings are done
with anti-staphylococcal agents like fucidin, mupirocin, etc.
Skin grafting is done only after Staph.aureus is cleared.
If there is edematous, hypertrophic granulation tissue,
gentle compressive dressings using crepe bandages should
be done to reduce edema. Local steroid cream is also
effective (Fig. 14.31). Bluish green pus discharge from the
wound suggests Pseudomonas growth (Fig. 14.32). In these
cases, dressing with 1% acetic acid solution is very effective
or else mafenide can be used (Fig. 14.33). Pale granulation
Figs 14.28A to C: Healthy granulating wounds covered with split skin graft
A
B
C

Burn Wound Management
179
Fig. 14.30: Slimy dirty granulation tissue with copious discharge
Indicating Staphylococcus infection
Fig. 14.29: Fragile Granulation tissue bleeding profusely on touch –
Indicating streptococcal infection
tissue suggests anemia which should be corrected by blood
transfusions (Figs 14.34 and 35).
Once granulation tissue appears, swab cultures are
always taken to look for microbial growth and its sensitivity
pattern to various antibiotics before taking up the patient
for skin grafting. Growth of beta-hemolytic Streptococcus
is an absolute contraindication for grafting. Initial ‘take’ of
graft followed by loss after a few days with an eaten up
appearance is typically indicative of Staphylococcus aureus
infection (Fig. 14.36).To prevent further loss of graft, action
has to be taken immediately as advised above. Sometimes
the burn wounds are neglected and they turn into chronic
Fig. 14.33: Dressing with mafenide or sulfamylon cream to counter
Pseudomonas growth
Fig. 14.31: Edematous hypertrophic granulation unfit
for grafting
Fig. 14.32: Greenish discoloration of wound indicative
of Pseudomonas infection

180
Principles and Practice of Burn Care
heal. Wound swabs can be repeated more often to know
the change in bacterial flora of the wound and its sensitivity
pattern if any unexpected worsening in condition of the
patient and/or wound occurs. When the patient is taken up
for grafting, wound swab is sent 3 days prior to surgery
for culture and sensitivity examination.
Local antibiotic agents have a poor effect in controlling
local burn wound colonization. At the same time, if dead
tissue is present both local and systemic antibiotics are not
very effective because they cannot enter the dead tissue. In
such circumstances, the dead tissue or slough has to be
debrided rapidly and then both local and systemic antibiotics,
as per the sensitivity report, are started.
For cases where the burn wound sepsis is caused by
Pseudomonas aeruginosa, frequent dressings with mafenide
is very effective as it penetrates eschar very well and clears
the organism within a week. Since the separation of slough
may be delayed by the use of mafenide, surgical excision of
dead tissue may be required.
Usually when the slough separates there is a layer of
granulation tissue already forming under it, though it may
not be very healthy. Slough separation can be hastened by
using wet to dry dressings which help to soften the eschar
and since they are adherent to the eschar when the dressing
begins to dry, they help in removal of slough from the wound
surface during change of dressings.
In case of deep dermal or deep partial thickness burns,
the wounds are inspected at regular intervals to look for
surviving epithelial elements which can produce islands of
regenerating epithelium which spread and then coalesce to
heal the wound completely. A smooth white bed of dermal
Fig. 14.35: Old burn raw area with fibrosis occurring in the bed
with pale and very thin granulation tissue
Fig. 14.34: Severely pale wound with scarce granulation, at places
underlying fat is also visible
fibrosed wounds.These wounds cannot be prepared by
dressing alone and require excision of the fibrotic bed till
healthy soft and supple vascular bed is reached before
application of split skin graft (Figs 14.37A and C).
Wound Swabs
Wound swabs are taken on admission to know the state of
wound at start of treatment and then on first dressing, i.e.
third or fourth day and thereafter once a week till wounds
Fig. 14.36: Loss of skin grafts with MRSA infection

Burn Wound Management
181
collagen intermixed with red islands of granulation tissue
usually indicates a deep dermal burn with enough epithelial
elements which can heal the wounds although very slowly
and hence with a lot of hypertrophy.
Types of Skin Grafts
There are different criteria for classifying skin grafts.
Based on the Anatomy
Based on the anatomy skin grafts can be classified as follows:
(a) Partial thickness or Split thickness skin graft (SSG) – It
includes epidermis and part of dermis. Though they can
survive on less vascularity from the bed, they have greater
tendency for contraction. These are most effective for post
burn raw area coverage. Donor sites of split thickness grafts
heal spontaneously by re-epithelialization from epithelial cells
lining the hair follicles and sweat glands within 10-21 days.
These can be reharvested once the wound epithelializes.
(b) Full thickness grafts (FTG) –Include epidermis with
entire dermis and are approximately 0.035 to 0.045 inch
thick. They require better vascular bed for survival as well
as good vascularity from the margins. They undergo
minimal contraction. Their sensory recovery is better than
that of split skin graft. They have no role to play in post
burn raw areas but have an important role to play in covering
areas following post burn contracture release. The donor
areas for full thickness grafts cannot resurface spontaneously
because of lack of epithelial elements. The defect needs to
be closed primarily. Therefore, they are not used for large
defects.
The post graft contracture is actually due to contraction
of the wound bed. It is widely believed that thicker the
graft, greater will be the inhibition of contraction. This holds
good only if the grafts are harvested from a given site. The
fact is that when split-skin grafts are harvested from
different sites it is the total percentage of dermal thickness
grafted, which determines how much contraction will be
inhibited. Delayed application of skin graft does not inhibit
contraction as effectively as immediate grafting.
Based on Thickness
Based on thickness the split thickness grafts can be further
categorized into 3 types:
a. Thin split thickness graft—which has a thickness of
0.006 to 0.012 inch.
Fig. 14.37C: 10 days after application of skin graft which is fully
taken up on the healthy bed post excision
Fig. 14.37A: Old neglected post burn raw area with fibrosed bed with
slough and no granulation. This wound needs to be excised to remove
the unhealthy tissue
Fig. 14.37B: Excision of the same wound

182
Principles and Practice of Burn Care
b. Intermediate thickness graft—which has a thickness of
0.012 to 0.018 inch
c. Thick split thickness graft—has a thickness of 0.018 to
0.030 inch.
Post burn raw areas should be covered by thin and
intermediate thickness split skin grafts.
For treating burn patients with skin grafts, apart from
the age and sex there are many more factors to be considered
when deciding the thickness of the graft to be harvested.
By and large, for all burn wounds, grafts should be thin
because their ‘take’ is better. However, because they undergo
greater contraction, thicker grafts (intermediate thickness)
are preferred for regions like face especially eyelids and lips
so that they contract less postoperatively. In children and
elderly, usually thin grafts are harvested as the dermis is
thin. If a donor site is to be reused more than once for
procuring grafts as in patients with extensive burns, thin
grafts should be harvested. This is because the donor sites
may not heal due to loss of dermis if thick split thickness
grafts are harvested repeatedly.
Based on Size and Technique
Based on size and technique of harvesting split skin grafts
they are classified into following types;
(a) Pinch grafts—These are ‘small deep ‘grafts’ which are
not used at present because of the extremely ugly scarring
of the donor site. The donor area chosen, therefore, is a
hidden area usually the thigh or groin. The procedure involves
lifting the skin with a needle and a 0.5 cm fragment is cut to
obtain a graft which is thicker in the center and tapering
towards the edges. The resulting wounds can even be closed
primarily. The grafts are transferred to the wound at regular
intervals, distance between them being about 5 mm. This
method is now of historical importance only.
(b) Stamp grafts – These are split thickness grafts which,
after harvesting, are cut as square or rectangular pieces of
skin of different sizes. They are applied to the wound and
held in place with occlusive dressings. The intervening areas
between the stamps heal by epithelialization from the margins
of the graft. As a result, these areas tend to hypertrophy
and give unsightly scars. This method may be of use in
case of very extensive raw areas.
(c) Sheet grafting – It is the most widely used at present as
the grafts can now be easily harvested with the help of the
latest modified Humby skin grafting knife or dermatome.
Large sheets about 10 cm wide or more can be procured
easily and they can cover large raw areas. This gives good
aesthetic results especially on the face. These sheets can be
meshed to increase their size to cover larger areas.
(d) Meek grafting– It is being used lately. This was described
in 1958 by an American surgeon, CP Meek. It involved the
use of a ‘Meek-Wall ’ dermatome to obtain postage stamp
autografts which are expanded using double pleated
gauzes.This produced a regular distribution of autograft
islands with a ninefold expansion but required donor areas
of suitable size and shape.It was discontinued for a while
after the introduction of Mesh grafts in 1964, because of
problems encountered with the old technique of meek
grafting. The meek grafting technique was redesigned to
overcome the imperfections of the original method. A special
spray called ‘meek adhesive’ was developed and the
prefolded gauzes were manufactured with expansion ratios
of 1:3, 1:4, 1:6 and 1:9. This required very small donor
areas and the graft islands were evenly placed in a regular
pattern. The epithelialization and hospitalization time is
reported to be shorter with this technique, compared to the
mesh graft method. This method is preferred in extensive
burns where the donor areas are very limited.52,53
Indications for Skin Grafting
Skin grafting is indicated in the following situations in burns:
1. Following excisional surgery of burn wounds
2. Post burn raw areas following full thickness burns
3. Following release of post burn contractures
4. Following excision of post burn scars like hypertrophic
or hypopigmented scars, etc.
Essential Criteria for Skin Grafting
1. Grafting of post burn raw areas should be done as soon
as the granulation tissue is healthy. If delayed for long,
the granulating areas become fibrotic and graft ‘take’ is
less than satisfactory.
2. The granulation tissue should have healthy red
appearance i.e. it should be a well vascularized bed.
3. The wound bed should be free from infection. Wound
cultures should always be done prior to grafting. The
presence of beta–hemolytic Streptococcus pyogenes is
an absolute contraindication for grafting as it does not
allow the graft to ‘take’ at all as it eats the fibrinogen
which is responsible for graft adhesion to the bed.
Presence of other bacteria like Pseudomonas aeruginosa,
E. coli, Klebsiella is not a contraindication for grafting
if present in < 105 organisms/gm of tissue. They may
hinder graft ‘take’, yet not to the extent as to delay

Burn Wound Management
183
grafting. Although Staphylococcus aureus allows graft
to ‘take’ initially, it eats away the graft progressively to
unacceptable degree and it is not advisable to graft a
wound until it has been eradicated. In extensive raw
areas it is not possible to have bacteria-free surface.
4. The general condition of the patient should be stable.
Anemia should have been corrected by blood
transfusion(s). Hemoglobin should be a minimum of 10
gm%. The patient should be built up nutritionally (both
enteral and parenteral). By and large, the patient should
be stable enough to bear the stress of surgery.
5. Quantitative culture of the wound should be sent if
infection is suspected. Counts of >105 organisms /gm
of tissue should be first treated using systemic and topical
antimicrobial therapy and frequent change of dressing
till the colony count decreases.
6. Complete hemostasis should be achieved in the wound
bed prior to graft application especially if the granulations
have been scraped. This can be achieved by pressure
dressing with adrenaline soaked gauze or spray of fibrin
glue (Tissel®). However, if there are many areas of
adherent slough in the granulation tissue which cannot
be rubbed off using dry gauze, they should be tangentially
excised with a scalpel or skin grafting knife followed by
pressure dressing with adrenaline packs.
7. Granulation tissue, if unhealthy, can be removed or
scraped from the wound bed. However, it causes more
bleeding which impairs graft ‘take’ if applied immediately.
8. Immobilization of the part without shearing between the
graft and bed is very essential.
Donor Areas
Skin grafts can be harvested from any area of the body
including scalp and feet if there is scarcity of donor areas.
The most common sites whenever available are the lower
limbs and upper limbs.The thigh is the most commonly
used in lower limb especially the anteromedial and
anterolateral thigh. (Fig. 14.38) The back and buttocks are
useful sites if thighs are also burned. If the limbs and back
is burnt, the chest, abdomen or scalp can be used as donor
areas. In these areas, adrenaline saline (1 in 2,00,000) can
be injected subcutaneously to eliminate the depressions of
the intercostal areas or the curvatures of the abdominal wall
or bony prominences in order to form a flat base from
which it becomes easier to harvest a good sheet of graft. It
also reduces blood loss from donor site.
Similarly, scalp is shaved and infiltrated with adrenaline
saline solution before harvesting the graft. The advantage
with scalp is that grafts can be harvested repeatedly, every
10 days, as epithelialization is very fast from the epidermal
lining of the large number of hair follicles (Figs 14.39A
and B).
While harvesting grafts from a hairy region, it is
important to take thin grafts as thicker grafts contain
undesirable hair follicles which lead to hair growth in the
recipient area.
The donor areas of split skin graft heal in 10-21 days.
The donor areas are dressed by application of paraffin gauze
which may or may not be antibiotic impregnated followed
by gauze and then Gamgee pads and a compressive bandage.
This bandage usually gets loosened up in 2 weeks and gauze
falls off when opened in 3 weeks as majority of the
superficial donor area re-epithelializes by 12 days. The other
dressings which have been used for donor areas include
collagen dressings, Biobrane and Opsite. All these have been
found to reduce pain, act as a barrier to bacteria, fasten
healing and reduce the bulk of dressing. However, they are
very costly.
Instruments for Grafting
There are various skin grafting knives available and they
have been modified from time to time to improve the quality
of graft which can be harvested with their help. The earliest
free-hand instrument to be used for grafting was the Blair
knife which required manual sharpening regularly. Then
came the Humby knife which had a fixed blade but an
adjustable roller guard which adjusted the thickness of graft
harvested. The amount of pressure applied to the instrument
on the surface of the skin also altered the thickness of the
graft, i.e. the greater the pressure applied, the thicker the
Fig. 14.38: Anterolateral and anteromedial aspect of thigh–
Commonest site for harvesting graft

184
Principles and Practice of Burn Care
graft and lesser the pressure, thinner the graft. There were
various modifications to the Humby knife with disposable
blade, e.g. Braithwaite knife–in which the roller guard moved
longitudinally as well as rotated on its axis so that the graft
tends to roll on to the rod and its edges were ragged. Then
came another modification—Bodenheim knife– in which
the roller guard moved only to and fro but did not rotate on
its axis.The latest is the Watson’s modification of Humby
Skin Grafting Knife (Fig. 14.40A) in which the guard is
fixed and immobilized so that the edges of the graft are
clean cut rather than ragged and the graft does not roll on
to the rod as the knife proceeds forward. This is the most
commonly used manual skin grafting knife at present. For
procuring smaller sized grafts, ‘Silver’ knife has been used
for many years (Fig. 14.40B).
Fig. 14.39B: Graft being harvested from scalp
Fig. 14.39A: Scalp as donor area – Saline infiltration being done
Fig. 14.40B: Silver knife—Used for harvesting small grafts
Fig. 14.40A: Watson’s modification of Humby’s knife—Most
commonly used manual skin grafting knife
The adjustment of the guard for varying the thickness
of the graft in Watson’s skin grafting knife is done by the
screws present at both ends of the roller guard according
to the calibrations present on proximal screw and then
tightening the distal one. Another method for assessing then
required gap between the blade and the guard is by holding
the knife against the light so that the gap between roller
guard and the disposable blade can be seen and the screws
tightened. Increasing or decreasing the distance between
guard and the blade produces thicker or thinner grafts
respectively. Even increasing the angle at which the knife is
kept on the surface of skin and the pressure exerted varies
the thickness of graft harvested.
The free hand knives have been replaced by dermatomes
(Figs 14.41A to D). Padgett-Hood dermatome was a
mechanical drum dermatome in which the depth of cut could
not be modified. After this the Brown dermatome was
introduced which was driven by an electric motor. The
advantage with these motorized dermatomes was that they
produced uniform long grafts with predetermined width
and depth. The air Zimmer dermatome powered by
compressed, water pumped, nitrogen was introduced and
was easier to use. Dermatomes may not be useful when the
donor areas are narrow.

Burn Wound Management
185
Technique of Harvesting Split Skin Graft
(Figs 14.42A to D)
Once the donor site has been selected, the graft can be
harvested under general anesthesia, regional nerve blocks
or even local anesthesia. Infiltration of local anesthesia with
adrenaline reduces the amount of blood loss from the donor
area apart from prolonging the duration of the effect of the
local anesthesia. The area is lubricated with Vaseline or
paraffin and saline. An assistant gives traction to the skin
from one end of the donor site while the operating surgeon
gives traction from the opposite side. Wooden / metallic
Gabbroo graft boards are frequently used for applying the
traction and counter traction. The knife is placed parallel to
the surface of skin and then moved ‘to and fro’ with
moderate pressure and gradually moved ahead with moderate
speed till a long sheet is removed. The width of the graft
harvested can be adjusted according to the area available.
In case of dermatome, it is kept on the skin surface at
an angle of 30-45° and the throttle is pressed and the
dermatome advanced flat to the skin with gentle downward
pressure. Once the sheet of graft is harvested, the
dermatome is angled upwards and lifted off the donor site
cutting the graft.
Thin grafts can also be taken from areas adjacent to
burn if other donor sites are not available. There is no risk
of infecting the donor areas. Whenever the raw areas are
extensive and donor areas limited, the split skin graft can be
meshed to expand the graft to cover the whole defect.
Meshing of Graft (Figs 14.43A to 14.44C)
Meshing of a skin graft is an old technique first described
by Lanz of Amsterdam in 190746 when it was done manually.
It was re-introduced by Tanner, Vandeput and Olley(1964)
with a new instrument.43 They used a device that made
slits in the graft at regular intervals producing a net like
structure when the graft is stretched. Tanner et al were
inspired by Dragstedt and Wilson (1937)44 who used the
same technique in full thickness graft for drainage of fluid
from wound bed.They, in turn, were impressed with the
‘seive’ graft developed by Douglas (1930)45 in which circular
holes were cut in a full thickness graft by leaving small islands
of skin on the donor site for re-epithelialization.
The principle behind meshing a graft is to gain expansion
by making incisions parallel to the longitudinal axis of the
graft and the maximum advantage of meshing is gained
when the long axis of the meshes parallel the stress lines of
the area to be grafted.
Fig. 14.41B: Same dermatome showing the surface of the drum on
which the glue is applied when placed in contact with the skin
Fig. 14.41C: Electric dermatome
Fig. 14.41D: Electric dermatome–Another view
Fig. 14.41A: Padgett’s drum dermatome