Principles and Practice of Burn Care

Microbiology in Burns
87
accurate result. Infection control practices should be at their
apex in burn units. The following of strict infection control
practices of physical isolation in separate room, use of gowns
and gloves during patient contact, hand washing before and
after each patient visit and appropriate empirical antimicrobial
therapy are the critical needs. These greatly aid in reducing
the incidence of infections due to antibiotic resistant
organisms. An institutional policy guiding appropriate
selection and use of antimicrobials for the treatment of
infections in burn patients further support efforts to reduce
the burden of illness due to antibiotic resistant organisms
while potentially reducing hospital costs, length of hospital
stay, and adverse effects due to these agents.
Reporting of Microbiological Results
The laboratory has a key role to play in providing information
about wounds that are deteriorating or failing to heal. From
a microbiological perspective, the main pathogens or groups
of microorganisms that the microbiology laboratory should
routinely detect and report (with antibiograms being provided
when appropriate) are as follows: S. aureus, P. aeruginosa,
beta-hemolytic streptococci, coliform bacteria, pigmented
gram-negative anaerobes (Prevotella andPorphyromonas
spp.), non-pigmented gram-negative anaerobes(primarily
Bacteroides, Prevotella, and Fusobacterium spp.),
Peptostreptococcus spp., and Clostridium spp. Fungal
species like Candida spp, Aspergillus, Mucor, Penicillium
etc. must be sought in patients with long standing burns
having broad spectrum antimicrobial therapy. In order that
the microbiology laboratory can provide the wound care
practitioner with clinically relevant information, it is essential
that the microbiology results (e.g., Gram stain, culture, and
antibiograms) be interpreted in association with clinical
information provided by the practitioner (e.g., wound type,
location, condition, signs of infection, and sampling method).
In this respect, the medical microbiologist may need to
interpret the significance of a particular wound pathogen in
the light of the clinical presentation.
In summary, a continuous dialogue between the
microbiology department and the clinician is essential to
ensure that:
i. Only those burn wounds that are likely to benefit from
a microbiological investigation are sampled (i.e., those
with clinical signs of infection or those that are failing
to heal);
ii. The microbiologist has a thorough understanding of
the clinical presentation of the wound which is possible
when the laboratory forms are filled with adequate
clinical information;
iii. The microbiologist must know the method used for
wound sampling;
iv. The microbiologist is aware of the requirements of
the practitioner and the urgency of the results and
v. The practitioner understands the rationale for advice
given by the microbiologist, e.g. the reporting of a
mixed culture and an antibiogram for a bacterium
isolated from a mixed culture may not be provided if
clinical signs of infection are not evident and if no
inflammatory cells are seen in the Gram stain.
This interaction between clinician and microbiologist in
the management of burn wound complications definitely
results in significant savings in cost and time (medical,
nursing and microbiological) along with an appropriate
treatment for the patient.
OTHER MICROBIOLOGICAL METHODS
Blood Cultures—Blood cultures are essential in determining
septic episodes. The best time to collect the specimen is
before the temperature spikes. A temperature above 39.5°C
is the body’s method for cleansing the blood stream of
bacteria. Most bacteria do not survive at prolonged
temperature above 39.5°C. Care must be taken not to
contaminate the blood culture bottle. Site selection for
collecting the specimen must be meticulously and aseptically
cleansed prior to specimen collection. If the site is through
a contaminated area, appropriate comments should be made
on the request slip. These considerations are somewhat
aberrant in the burn patients as the body temperature may
not represent sepsis and even acquiring samples for blood
culture is difficult in extensively burned patients.
Diagnosis of sepsis in burn patients can be difficult to
distinguish from the usual hyperdynamic, hyperthermic,
hypermetabolic post-burn state. Blood cultures are
commonly negative. Fever spikes are not proportional to
degree of infection.
Clinical diagnosis of sepsis is made by meeting of at
least 3 of the following criteria:
1. Burn wound infection (>105 organisms/gm tissue) with
histologic or clinical evidence of invasion
2. Thrombocytopenia (<50,000) or falling rapidly
3. Leukocytosis or -penia (>20,000 or <3,000)
4. Unexplained hypoxia, acidosis or hyper/hypoglycemia
5. Prolonged paralytic ileus
6. Hyper/hypothermia (>39°C or <36.5°C),

88
Principles and Practice of Burn Care
7. Positive blood cultures
8. Documented catheter or pulmonary infection
9. Altered mental status
10. Progressive renal failure or pulmonary dysfunction
Urinary Tract Infection (UTI)—If a UTI is suspected
as the cause of sepsis, urine must be collected
aseptically. Appropriate comments should be made on the
request slip (e.g. Temp. 39.8°C, clean catch, catheterized,
suprapubic, etc.)
Respiratory Infection—If a respiratory infection is
suspected or evident from clinical signs or an X-ray,
bronchial washings are essential in order to identify the
etiologic agent or infection. However, based on recent
mortality studies, the organism isolated from lung abscesses
are most closely correlated with organisms from the wound,
rather than the organisms isolated from sputum specimens.
AUTOMATION IN CULTURE AND SENSITIVITY
Cultivation of the fluid or macerated tissue sample using
rapid systems of isolation such as BacT Alert 3D, BACTEC
(for pyogenic bacteria), TREK/ESP systems, etc. can greatly
hasten (6-24 hours) the isolation of pathogens but have a
limited role to play in mixed flora. However, quantifying the
samples has not been standardized using these systems.
They also are unable to process swabs, velvet pads, filter
paper, etc. Fluid, pus or homogenized tissue is an appropriate
sample for these systems. Their prohibitive cost precludes
their use in routine and also in surveillance. These automated
machines have a critical role to play in blood cultures in
burn wound septicemias.7
Most laboratories now routinely use an automated
system for identification and susceptibility testing of the
bacteria. These are like the VITEK from Bio-Me´rieux,
Durham, NC; Phoenix from Becton Dickinson, Franklin
Lakes, NJ; or Microscan from Dade-Behring, Deerfield,
IL, etc. These must be in combination with disk diffusion
for screening and E-test, and agar dilution for confirmation
of some of the automated system’s susceptibility results.
This is particularly true when unusual multiple drug resistant
organisms (MDRO) are observed like Vancomycin
intermediate or resistant Staph. aureus (VISA/VRSA),
Vancomycin resistant Enterococcus (VRE), MDR
Acinetobacter spp and MDR Pseudomonas spp.
Most antimicrobial agents have not been subjected to
controlled clinical efficacy trials in the treatment of burn
wound infections and there are limited data about the ability
of systemically administered antibiotics to penetrate the
devascularized burn eschar.59 Hence, burn patients infected
with bacterial strains that appear to be susceptible to a
particular antimicrobial agent in vitro may fail to respond
clinically. These apart, standard methods have not yet been
published to allow clinical microbiology laboratories to
routinely perform antibiotic susceptibility testing of burn
wound isolates against commonly used topical antimicrobial
agents.
Polymerase Chain Reaction
The role of molecular tests in rapid diagnosis of infective
conditions has been very well elucidated for slow growing
and difficult to grow pathogens. Its role in certain infective
diseases like tuberculosis and meningitis is noncontrovertial.
Detection of role of viral infections of burn wounds has
been possible with this technique. Using PCR based virus
detection and immunohistochemical staining, burn wound
infection with HSV - I could be identified.57
A real-time polymerase chain reaction to detect and
quantify Pseudomonas aeruginosa in wound biopsy samples
has been tried. This method produced a linear quantitative
detection range of 7 logs, with a lower detection limit of
103 colony-forming units (CFU)/g of tissue or a few copies
per reaction. The time from sample collection to result was
less than 1hour. This method has potential for rapid
quantitative detection of pathogens in burn patients, enabling
early and individualized treatment.58 Although molecular
methods allow rapid quantitation of individual organisms,
bacterial tissue biopsy culture is still necessary in order to
identify and perform antibiotic susceptibility testing on the
different types of bacteria present in a given sample. If a
predominant resistotype is expected then molecular tests to
detect the mutational type can greatly aid in the rapid
diagnosis of resistance. Emerging antimicrobial resistance
trends in burn wound bacterial pathogens represent a serious
therapeutic challenge for clinicians caring for burn patients.
Antibiotic-resistant organisms such as MRSA, vancomycin-
resistant enterococci, and multiple-resistant gram-negative
rods, including Pseudomonas aeruginosa, Acinetobacter spp.
and various members of the family Enterobacteriaceae have
been associated with infections of the burn wound and other
anatomic sites in patients with major thermal injury,
occasionally in the form of nosocomial outbreaks. Role of
molecular biology in rapidly identifying mutations leading
to resistance and epidemiological typing of isolates using
Restriction Fragment Length Polymorphisms (RFLP), Pulse
Field Gel Electrophoresis (PFGE), Multilocus Strain Typing

Microbiology in Burns
89
(MLST), etc. will definitely play an enormous role in the
future in burn microbiology.7
Gas Liquid Chromatography (GLC)
This is particularly of use in the presence of anaerobic
bacteria. Since these microorganisms can be characterized
on the basis of the fatty acids produced as end products of
metabolism, rapid determination of the presence of
potentially pathogenic anaerobic bacteria can be performed
by direct GLC analysis on the specimen. However,
specimens that can benefit from this type of analysis are
normally restricted to purulent drainage from enclosed
abscesses. Although GLC is a valuable method for rapidly
identifying anaerobic bacteria in clinical specimens, the
costs and expertise involved with such equipment have
prevented its use as a routine procedure in microbiology
laboratories.
ANTIBACTERIAL THERAPY
Burn wound progression is complex and caused by additive
effects of inadequate tissue perfusion, free radical damage,
and systemic alterations in the cytokine milieu of burn
patients, leading to protein denaturation and necrosis. The
current mainstays of treatment include adequate fluid
resuscitation, nutritional support and local wound care with
an emphasis on topical antimicrobial agents and biosynthetic
dressings.
For the Prevention of burn wound infection
•
Topical antimicrobials which should be used according
to the local recommendations.
•
Systemic antibiotics are not routinely indicated except
as prophylaxis before dressing changes and in order to
prevent septicemia related to manipulation/surgical
debridement/grafting, etc of the wound (choice of agents
being determined by results of previous surveillance
cultures).
•
Nasal mupirocin in some cases, at the time of presentation
has shown some evidence of benefit to prevent
staphylococcal infections.
Topical Therapy
Topical therapy is often applied to prevent infection and to
treat ongoing infections or used as an adjunct to surgical
treatment and systemic antibiotics. Systemic antimicrobial
agents should be directed at the underlying pathogen
recovered from culture or determined empirically from the
local burn unit’s antibiogram while culture results are
pending. Antifungal agents may also be used; however,
pathogen identification is necessary in order to determine
the ideal antifungal agent. Topical therapy is typically applied
to prevent infection and treat infection when adequate
surgical management is not possible. Wound care should
be directed at thoroughly removing devitalized tissue.
Currently, a number of topical agents are available to assist
in microbial control of the burn wound, including silver
sulfadiazine, mefenide acetate, 0.5% silver nitrate, bacitracin/
polymyxin B, mupirocin, and Mycostatin. No single agent
is totally effective and each has advantages and
disadvantages. Almost all agents affect wound healing and
increase metabolic rate. These various therapies differ in
their ability to penetrate eschars, antimicrobial activities and
adverse-event profiles. However, they may be associated
with drug pressure, resulting in infections with resistant
bacteria or fungus. A broad-spectrum surgical antimicrobial
topical scrub should be used along with adequate analgesia
and preemptive anxiolytic in order to permit adequate wound
care.
Silver sulfadiazine 1% cream is the most commonly used
topical antimicrobial agent in burns. Its antimicrobial
properties are derived from the dual mechanisms of its silver
and sulfa moieties (functional parts) and has a broad
spectrum of antimicrobial coverage including gram-positive
bacteria, most gram-negative bacteria, and some yeast
forms. Some gram-negative organisms (e.g. some
Pseudomonas species) do possess a plasmid mediated
resistance. Unlike mafenide or silver nitrate, silver
sulfadiazine does not hinder epithelialization, although it does
hamper contraction of fibroblasts. Mafenide acetate 11.1%
cream (e.g. Sulfamylon®) is one of the oldest effective
topical antimicrobial agents. Mafenide has a broad spectrum
of antimicrobial activity, including silver sulfadiazine-resistant
Pseudomonas and enterococci, but reduced antifungal
properties. Its exact mechanism of action is not clear, but
thought to be related to its water-soluble sulfa-
moiety. Mafenide cream is toxic to epithelial cells and
fibroblasts. Unlike other topical agents, mafenide has good
penetration through the eschar. For this reason mafenide is
commonly used on dirty or infected burn wounds, electrical
burns and on burned ears to prevent chondritis. Petroleum-
based antimicrobial ointments such as bacitracin and/or
polymyxin B are clear on application, painless and allow for
easy wound observation. These agents are commonly used
for treatment of facial burns, graft sites, healing donor sites
and small partial-thickness burns. Povidone iodine ointment
has a broad antimicrobial activity, including bacteria, fungi,

90
Principles and Practice of Burn Care
and some viral forms. Mupirocin (Bactroban) has improved
activity against gram-positive bacteria, especially methicillin
resistant Staph. aureus (MRSA) and selected enteric
bacteria. Mycostatin should not be combined with mafenide,
however, because both become inactivated. In addition,
Mycostatin 5-15 ml given orally 3 times daily reduces
alimentary fungal overgrowth. This regimen has markedly
decreased the incidence of Candida septicemia in our
patients. In severely burned patients (>40% BSA), the
combination of Mycostatin ointment or powder with other
topical agents reduces the incidence of fungal infections.61
Topical agents have been discussed at length in another
chapter of this textbook.
Systemic Antibiotic use and
its Guidelines
Antibiotics are indicated when there is evidence of pneumonia
(common in inhalational burn injuries) and when there is
evidence of sepsis. Large burn wounds also often warrant
the need for antibiotic use systemically. Specific choice of
antibiotics depends on the local surveillance information and
knowledge of antibiotic resistance pattern. Antibiotic
prophylaxis has also been studied in burn surgery at the
time of wound manipulation, but few studies have supported
the use of systemic antibiotics during acute burn surgery.
Antibiotics appear to be of no value in the prophylaxis of
wound infections accompanying surgery for small to
moderate burns. However, a few studies have recommended
surgical prophylaxis in patients with burns over more than
40% TBSA. In these circumstances, if an infection is
identified, antimicrobial therapy should be directed at the
pathogen recovered on culture. In the setting of invasive
infection or evidence of sepsis, empiric therapy is urgently
initiated. A local burn facility’s antibiogram must be
established to help direct empiric therapy.
There is currently no consensus on optimal empirical
treatment (Table 9.3) and recommendations for empirical
therapy are based on the following criteria:
•
Extent and depth of the burn wound
•
Age, state of hydration, creatinine clearance, serum
protein levels of patient
•
Presence of sepsis
•
Length of time since the burn was sustained
•
Prior administration of antibiotics
•
The likely pathogens encountered in the burn unit
(Pathogens vary somewhat from center to center but
useful information can be obtained from surveillance
cultures)
•
It is important to remember that in burn patients the
pharmacokinetics of many antibiotics are often altered
and some patients may experience periods during which
sub-therapeutic concentrations extend beyond the post-
antibiotic effect unless the dosing regimens are altered
appropriately.60
Local evidence of invasive wound infection includes:
•
Black or brown patches of wound discoloration
•
Rapid eschar separation
•
Conversion of wounds to full-thickness
•
Spreading peri-wound erythema
•
Punctuate hemorrhagic sub-eschar lesions
•
Violaceous or black lesions in unburned tissue (ecthyma
gangrenosum)
Initial empirical therapy can be modified subsequently
on the basis of the culture and sensitivity report. Prolonged
stay of these patients in the burn unit often leads to
colonization by nosocomial resident microflora which tends
to be multidrug resistant. It is unrealistic to expect to keep
a burn wound sterile. Bacterial counts of less than 103
organisms/gm are not usually invasive and allow skin graft
survival rates of >90%. Antimicrobial therapy is directed
Table 9.3: Empirical therapy as directed by the British Society of Chemotherapy, 2006
No. of days
Treatment
Organism
Antibiotic
after burns
history
likely advocated
none
Staph. Or Strept.
Penicillin & Flucloxacillin
yes
-do-
Cefuroxime
6-9
none
Staph or Strept
Cefuroxime
Coliforms
6-9
yes
Staph or Strept
Flucloxacillin + Gentamycin
> or =10
Coliforms
Pseudomonas
Flucloxacillin + Ceftazidime
Replace beta lactam antibiotic if allergy with clindamycin or macrolide antibiotic

Microbiology in Burns
91
by bacterial surveillance through routine tri-weekly sputum,
urine, and wound cultures. In addition, punch biopsies for
each 18% BSA of burn are obtained for wound monitoring
until the wound is closed. Organism identification and in
vitro sensitivities to antibiotics should be available in 48
hours. Agar diffusion assays can also be performed to test
susceptibilities to topical antimicrobials. If quantitative
biopsies reveal microbial density of >103 organisms/gm, a
change in topical therapy is indicated. If bacterial counts
are 105, worsening wound infection should be suspected
and rapid histological analysis and Gram stain should be
performed to confirm this. At this point, systemic antibiotics
must be instituted, and the wound excised.
Antibiotics for Deep Infections
Appropriate systemic antibiotics are administered as
indicated. The appropriate use of antibiotics should be based
on the following definitions:
Prophylaxis—A preventative or precautionary measure
designed to preserve health and prevent the spread of disease.
Perioperative—This may also be considered prophylaxis. It
is the administration of systemic antibiotics as a protective
measure for any type of surgical intervention. The time
frame for administration should be short-lived and is limited
to 1 to 3 doses, depending on the operative procedure.
Therapeutic—This is the administration of antibiotics for
the treatment of infection. Depending on the infection,
therapy may continue for several days.
Systemic antibiotic treatment for burn wound sepsis is
continued for at least 72 hours after evidence of sepsis has
resolved. If the wounds appear clean, other sources such
as the lungs, kidneys and peripheral veins should be
suspected as the primary source of infection. The commonly
used agents in several situations are Vancomycin, Imipenem,
Timentin or Ceftazidime for coverage against the usual strains
of Staph. aureus and Pseudomonas aeruginosa prevalent in
the burns unit. Routine perioperative antibiotics should also
take ward-endogenous organisms into account.
Postoperative antibiotics are continued until quantitative
excisional wound biopsies from surgery are identified.
Notes61, 62
1. For patients with burns of ≥ 2 weeks’ duration and/or
who are colonized with multidrug resistant gram-
negative bacilli, seek advice from a clinical
microbiologist.
2. Modify therapy, if appropriate, in the light of culture
and susceptibility test results (blood culture and burn
would surveillance cultures).
3. Duration of treatment: 5 days, if a significant pathogen
is isolated from blood cultures or the burn wound; 3
days, if a pathogen is not isolated from blood cultures
or the burn wound. As there is no or only limited
margin for error in patients who are severely ill with
suspected infection within five days of sustaining a
burn, broad-spectrum cover, with an agent such as
cefuroxime, should be administered if an aerobic
Gram-negative bacillus cannot be excluded.
4. It is important to remember that in burn patients, the
pharmacokinetics of many antibiotics are often altered
and some patients may experience periods during
which sub-therapeutic concentrations extend beyond
the post-antibiotic effect unless the dosing regimens
are altered appropriately.
5. Tetanus immunization is important (neonates, the
elderly or the debilitated may require immunoglobulin).
6. In case of multiple drug resistant organisms (MDRO),
immediate intimation should be given to the Infection
control personnel and advice from them may be
gathered. MDRO include Methicillin resistant
Staphylococcus aureus (MRSA), Vancomycin resistant
Enterococcus (VRE), Extended Spectrum beta
lactamase (ESBL) producing Gram-negative bacteria
(GNB), MDR. Pseudomonas and MDR Acinetobacter
and recently pan Drug resistant Pseudomonas and
Acinetobacter which are resistant to almost all the
known antibiotics.
7. Staph. aureus tends to remain localized to the wound,
if patient becomes toxic consider Toxic Shock
Syndrome (TSS).
8. Candida spp. remain localized but rarely do invade.
Always prove invasion with this pathogen.
9. Pneumonia is the most prevalent of complications with
high mortality. Staph. aureus is most commonly
implicated. Septic thrombophlebitis is also frequently
seen.
10. Daptomycin (4 mg/kg IV q24h) can be used instead
of Vancomycin.
Antibiotics for burn wound sepsis where MDRO are
seen.60,61
•
Vancomycin (1gm IV q12h) + Amikacin (10 mg/kg
loading then 7.5 mg/kg IV q12h) + Piperacillin 4 gm IV
q 4 h) (give ½ q 24 h Piperacillin dose in subeshcar
tissue and surgical removal of eschar in 12 hours).

92
Principles and Practice of Burn Care
•
If resistant bacteria, Piperacillin + Tazobactam may be
used instead of Piperacillin.
•
If ESBL producing GNB then Imipenem or Meropenem
can replace Piperacillin—Tazobactam combination).
Other suggested regimens63
•
Pseudomonas spp.—Tobramycin / Amikacin or
Aztreonam + Piperacillin/Ceftazidime/Cefoperazone or
Cefepime or Quinolones
•
Resistant GNB—Gentamicin or Aztreonam or Amikacin
+ Piperacillin or Mezlocillin or Third generation
Cephalosporin or Cefepime. Quinolones or Trimethoprim-
Sulphamethoxazole combination may be kept as reserve
in resistant but non ESBL GNB infections
•
In ESBL or AMP C producing GNB infections-
Metallobeta lactams—Imipenem, Meropenem MUST BE
USED. Other group of antimicrobials may be combined
if proven as sensitive and no deleterious effect of
combination is seen.
Suggested Groups of Antibiotics to be tested/applied
in the Microbiology Laboratory for Nosocomial isolates
as Primary, Primary but selective use and Supplemental or
reserved use for each major Group of bacteria64
I. Enterobacteriaceae (Klebsiella spp, E.coli, Proteus spp
etc.)
•
Primary—Ampicillin, Cefazolin, Caphalothin,
Gentamicin, Tobramycin.
•
Primary but selective use—Cefuroxime, Cefepime,
Cefotaxime, ceftriaxone, Cefoxitin, Piperacillin,
Amoxy-clav, Ampi-sulbactam, Piperacillin-
Tazobactam, Ticarcillin-clavulanate, Amikacin,
Ciprofloxacin, Meropenem, Imipenem.
•
Reserve—Aztreonam, Ceftazidime, Chloramphenicol,
Tetracycline, Newer agents and agents under trial.
II. Pseudomonas spp
•
Primary—Ceftazidime, Gentamicin, Tobramycin,
Piperacillin.
•
Primary but selective use—Amikacin, Aztreonam,
Cefepime, Piperacillin—Tazobactam, Ticarcillin,
Imipenem, Meropenem, Ciprofloxacin.
III. Staphylococcus spp.
•
Primary—Oxacillin ( group representative of beta
lactams drugs and resistance to this eliminates the
whole group including even metallobetalactams such
as imipenem and meropenem), Penicillin,
Erythromycin/Azithromycin/Clarithromycin,
Trimethoprim—Sulphamethoxazole.
•
Primary but selective use—Vancomycin, Teicoplanin,
Daptomycin, Linezolid, Doxycyclin/Tetracyclin,
Rifampicin( rifampicin should bever be used alone
in therapy).
•
Reserve—Ciprofloxacin or Ofloxacin or Levofloxacin,
Moxifloxacin, Synercid (Quinupristin and dalfopristin
combination), Gentamicin.
IV. Enterococcus spp.
•
Primary—Ampicillin, Penicillin.
•
Primary but selective use—Vancomycin, Daptomycin,
Linezolid, Synercid.
•
Reserve—High level Gentamicin and Streptomycin.
V. Acinetobacter spp.
•
Primary—Ceftazidime, Ampicillin-sulbactam,
Imipenem, Meropenem, Gentamicin, Tobramycin.
•
Primary but selective use—Cefepime Cefotaxime,
Ceftriaxone, Piperacillin, Piperacillin-tazobactam,
Ticarcillin-clavulanate, trimethoprim-sulphametho-
xazole.
•
Reserve—Colistin, Polymyxin B ( to be used in highly
resistant MDR Acinetobacter and Pseudomonas spp).
VI. Burkholderia spp.
•
Primary—Trimethoprim-sulphamethoxazole
•
Primary but selective use—Ceftazidime, Minocycline,
Meropenem.
VII. Stenotrophomonas spp.
•
Primary—Trimethoprim-sulphamethoxazole
•
Primary but selective use—Levofloxacin,
Minocycline.
The oral antibiotics (usually tested in the primary category
for each group of bacteria) included in the above list are
more for mild burn wounds and infections which do not
warrant parenteral antibiotics. This in the case of burn
wounds can be omitted altogether and topical agents can be
used instead of oral agents, the choice of which lies in the
clinician’s experience.
The selective use category of antibiotics is primarily
parenteral and is advocated for serious infections such as
the burn wound septicemias and other deep infections related
to burn wounds (Table 9.4). For polymicrobial infections
and infections in multiple sites also, a combination of
antimicrobials is advocated as has been suggested previously
in this chapter. Reserve drugs are used in special situations
where highly drug resistant pathogens are expected.
A brief mention of some of the newer agents available
for use, in the various sub-categories of bacteria observed
in the nosocomial setting is enlisted beneath. However, this

Microbiology in Burns
93
Table 9.4: New antibiotics and older antibiotics with new indications or treatment options 65
Antibiotic
Drug class
Initial development
Antibacterial
Limitations/adverse effects or
Current status
period
spectrum
new issues
New agents
Fluoroquinolone
Early 1960s
Variety of gram-positives (not
Resistance already established
Garenoxacin development
Gemifloxacin,
VRE, MRSA) and gram-
in some places, due to
halted
garenoxacin,
negatives
widespread ciprofloxacin use.
sitafloxacin
Role uncertain, given
availability of older agents
Ramoplanin
Glycolipodepsi-peptide
Early 1980s
Gram-positives, including VRE
Not absorbed orally — used
Not US FDA-approved.
for temporary suppression of
In Phase III trials
faecal VRE colonisation
Daptomycin
Lipopeptide
Late 1980s
Gram-positives: VRE, MRSA,
Myalgia at high doses
US FDA-approved
SA-RVS
Linezolid
Oxazolidinone
Late 1980s
Gram-positives: VRE, MRSA,
Haematological toxicity,
US FDA approved
SA-RVS, some Mycobacteria
especially thrombocytopenia;
spp., Nocardia spp.
peripheral neuropathy (rare)
Quinupristin,
Streptogramin
Early 1990s
Gram-positives: VRE (not
Infusion site pain, arthralgia,
US FDA approved
dalfopristin
Enterococcus faecalis), MRSA,
myalgia
SA-RVS
Oritavancin,
Novel glycopeptides
Late 1990s
Gram-positives: VRE
Toxicity uncertain
Not US FDA-approved.
dalbavancin
(oritavancin only), MRSA,
In Phase III trials
SA-RVS
Telithromycin,
Ketolide (related to
Late 1990s
Typical and atypical
Hepatotoxicity, blurred vision,
US FDA approed
cethromycin
macrolides)
respiratory pathogens,
QT changes on ECG
including Mycoplasma,
Chlamydia spp.
Tigecycline
Glycylcycline
Late 1990s
Gram-positives: VRE, MRSA,
Nausea, vomiting, headaches
US FDA approved
(semisynthetic
SA-RVS; some gram-negatives
derivative of
minocycline)
Contd.

94
Principles and Practice of Burn Care
Antibiotic
Drug class
Initial development
Antibacterial
Limitations/adverse effects or
Current status
period
spectrum
new issues
Older agents
Penicillin G
β-Lactam
Late 1930s
Gram-positives: streptococci,
Continuous infusion provides
enterococci, Clostridium,
high serum levels for
Listeria spp.
intermediate-resistant strains
(e.g., some VRE). Suitable for
hospital-in-the-home treatment
in some cases
Colistin,
Cationic peptides
1950s
Gram-negatives, including
Renal toxicity, neurotoxicity
polymyxin B
Pseudomonas aeruginosa,
Acinetobacter baumannii,
Klebsiella pneumoniae
Amphotericin B
Polyene
Late 1950s
Most fungi
Preliminary data suggest that
continuous infusion may reduce
renal toxicity and hence reduce
the need to switch to newer,
more expensive liposomal
analogues
Gentamicin
Aminoglycoside
Early 1960s
Many gram-negatives
Meta-analyses suggest a once-
daily dose of 4–6 mg/kg daily †
is associated with reduced renal
and ototoxicity, but efficacy is
similar to multidose regimens
ECG = electrocardiogram. FDA = Food and Drug Administration. MRSA = methicillin-resistant Staphylococcus aureus. SA-RVS = Staphylococcus aureus with reduced
vancomycin susceptibility. VRE = vancomycin-resistant enterococci.† Recommended dose for an adult with normal renal function.
Contd.

Microbiology in Burns
95
is an ever expanding field and even at the time of publication
of this document several more agents will have been tried
and tested for human use.
Multidrug resistant bacteria for which there are currently
few available treatment options.
Gram-negatives
•
Acinetobacter baumannii
•
Pseudomonas aeruginosa
•
Stenotrophomonas maltophilia
•
ESBL and very rare MBL Klebsiella pneumoniae
Gram-positives
•
Methicillin-resistant Staphylococcus aureus
•
Vancomycin intermediate or resistant Staph.aureus
•
S. aureus with reduced susceptibility to vancomycin and/
or linezolid
•
Methicillin-resistant coagulase-negative staphylococci
•
Vancomycin-resistant enterococci.
FUNGAL INFECTIONS
Invasive burn wound infections due to Candida spp.,
Aspergillus spp., and other opportunistic fungi (including
Alternaria spp. Fusarium spp., Rhizopus spp. and Mucor
spp.) are important emerging causes of late-onset morbidity
and mortality in patients with major burns and severely
perturbed immune systems.66 Thermally injured children
are at particular risk for fungal infections involving the burn
wound. Such infections usually occur after the second week
of thermal injury, usually following a period of burn wound
colonization with fungi found in the surrounding
environment and/or, in the case of Candida spp., from the
patient’s own gastrointestinal or upper respiratory tract
flora.67
Infections are most commonly due to Candida spp. and
Aspergillus spp. and generally appear as a darkening of the
burn wound area, with an appearance similar to that of
ecthyma gangrenosum.68 Burn wound infections due to
zygomycetes such as Rhizopus spp. and Mucor spp.,
although very rare, are important because of their remarkable
ability to spread rapidly across fascial tissue planes and to
invade the vasculature and are associated with a very high
mortality rate. Diagnosis of fungal infections of burn wounds
is most reliably made by histological examination of burn
wound tissue samples along with culture of the biopsy
sample. Aggressive wide surgical excision of the infected
areas of the burn wound before the development of deep
invasion, combined with systemic antifungal agents, may
lead to an improved chance of survival.68 The use of a
laminar-airflow isolation room, in conjunction with optimal
local wound care, appears to decrease the incidence of both
disseminated and local fungal infection. Topical prophylaxis
with an antifungal cream such as clotrimazole or nystatin
may lead to a reduced incidence of burn wound infections
and septicemia.67
If fungal etiology is detected on histopathology, culture
samples to detect the infecting genus and species are
necessary because the growing armamentarium of antifungal
agents have varying activity. Amphotericin B was once the
agent of choice, but some facilities have seen increased
rates of infections with Fusarium species and Aspergillus
terreus, which are innately resistant to amphotericin B. In
these cases, voriconazole is often used. A new agent,
posaconazole, may have broader antifungal activity but is
limited as it is available only in an oral formulation. In case
of proven Candida spp invasive disease Amphoteracin B or
Ketoconazoles may be initiated. Liposomal Amphoteracin B
has wider absorbance and efficacy, fewer side effects but
much more expensive. Caspofungin, an echinocandin, is
another new antifungal in the horizon which shows dramatic
results in therapy of resistant aspergillosis and candidiasis.
VIRAL INFECTIONS
Viruses of the herpes virus group, particularly herpes
simplex virus and varicella-zoster virus but less commonly
cytomegalovirus are rarely reported but increasingly
recognized causes of wound infections in thermally injured
patients. Such infections may be due to primary viral
infection, reactivation of latent virus, or exogenous reinfection
in previously infected patients. Burn wound infections due
to herpes simplex virus occur most commonly in healing or
recently healed partial-thickness burns particularly those in
the nasolabial area, or occasionally from skin graft donor
sites, while those due to cytomegalovirus typically involve
full-thickness burns. In the case of herpes simplex virus,
clusters of small vesicles or vesiculo-pustules may be found
within or around the margins of the burn wound, usually
occurring anywhere from 2 to 6 weeks following thermal
injury. Herpetic viral infections of the burn wound are usually
self-limiting, although systemic spread may occur. Diagnosis
is most reliably made by histological examination or culture
of burn wound biopsy specimens.

96
Principles and Practice of Burn Care
COMPLICATIONS
•
Burn wound infections are often the source of bacteria
responsible for other systemic infections including
bloodstream infections and pneumonia.
•
This can lead to Systemic Inflammatory Response
Syndrome (SIRS) and Multiple Organ Dysfunction
Syndrome (MODS) and death.
SUMMARY
Burn care involves a multisystem approach, requiring
numerous health care providers to be involved in the process.
The treatment of such infections is often prolonged and is
associated with an increased risk for complications, including
iatrogenic episodes. As such, continued diligence is needed.
Consultation with an infectious disease specialist is
suggested if multidrug-resistant bacteria are present. The
basal metabolic rate increases as the percentage of TBSA
burned increases. Early enteral feeds should be started.
Patients may be as active as they can tolerate. Aggressive
physical and occupational therapy of extremity injuries is
necessary to prevent long-term morbidity.
A primary focus during hospitalization is to prevent
nosocomial transmission of multidrug-resistant
pathogens, especially in patients with a greater percentage
of TBSA burn (approximately 30%) or who are known to
be colonized with multidrug-resistant bacteria such as
MRSA, vancomycin-resistant Enterococcus species, or
gram-negative bacteria known to develop resistance (e.g.,
Pseudomonas, Klebsiella, Acinetobacter species). Hand
hygiene should be aggressively implemented. Standard
precautions should be used in the care of all patients with
burn injuries. Patients should be managed in single rooms,
if possible, with use of contact precautions. Gowns and
gloves should be used when contact is expected with
infected material or open wounds. Masks and caps should
be implemented based on the presence of multidrug-resistant
bacteria. The use of individual-patient equipment should be
considered. Aggressive infection-control procedures should
be undertaken when transferring patients between facilities
because of the risk of transferring multidrug-resistant
bacteria. The prevention of burn wound infection is a team
approach that includes the support of surgeons, nurses,
infection-control providers and infectious disease
physicians. Emphasis on early wound care, infection-control
practices and long-term rehabilitative care is necessary to
improve the morbidity and mortality associated with burns.
Early removal of full-thickness burned tissue, as well as
early definitive wound closure and strict enforcement of
infection-control procedures, is necessary to mitigate poor
outcomes
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Initial Evaluation and Resuscitation of Burn Patient
99

(Trang không có chữ)

Initial Evaluation and
Resuscitation of Burn Patient
10
Madhuri A Gore
Chapter
INTRODUCTION
The goal of burn management is to achieve wound closure
at the earliest. The efforts in this direction must begin at the
first interaction between the victim and the health care
worker. The decision regarding the need for admission to
burn unit or management on outpatient basis should be
protocol based to minimize errors.
The plan of management of patients with large burns
that require inpatient care is usually determined by the
severity of the alterations in physiology due to the burn
injury. These patients require a coordinated approach that
involves a specialized team. Hospitalization is divided into 4
general phases:
1. Initial evaluation and resuscitation
2. Initial wound excision and biologic closure
3. Definitive wound closure
4. Rehabilitation and reconstruction.
An orderly and systematic initial evaluation is valuable
for delivery of comprehensive care. The early management
extends from first aid at site to complete resuscitation of
the patient and remains the chief determinant of final outcome
especially in a patient with major burn.
FIRST AID: THERMAL BURNS
First aid to a burn patient is generally provided by the
relatives, friends and other persons present at the site of
burn accident. A specialist burn surgeon is not present at
the site. However, the role of a burn specialist in carrying
out first aid in burns is to educate the masses about the
basics of burn injuries and do’s and don’ts. Media has a
great role to play in dissemination of this knowledge. This
information should also be given to school children in their
curriculum. All police and fire brigade personnel, etc. should
receive this training as part of their induction into service as
they may be required to provide first aid to victims of burn
disasters. Some of the points mentioned below may be
possible only in the nearest medical facility.
Management on Site
First make the scene safe for the rescuer.
1. If an individual is actually in flames, instruct the
victim to STOP – DROP – and ROLL. Douse the
fire with water or sand.
2. Switch off the mains in the event of electric burns.
3. Check for signs of circulation, breathing, coughing
or movement. If there is no breathing or other sign
of circulation, begin cardiopulmonary resuscitation
(CPR).
4. Cool the burn - Immerse affected extremity in bucket
full of tap water till burning sensation disappears OR
hold the burnt part under running tap water till the
burning pain disappears OR apply cold compresses
on the burnt area.
5. Do not use ice as this can cause cold injury and further
damage to skin.
6. Do not immerse severe large burns in cold water.
Doing so can lead to hypothermia.
7. Do not remove clothes that are adherent to wounds.
8. Do not apply any local agent on the wound (especially
colorful agents like gentian violet, mercurochrome)
as this interferes with the evaluation of burn depth
and extent.

102
Principles and Practice of Burn Care
FIRST AID: CHEMICAL BURNS
Chemical burn injuries are not hyperthermic, but are due to
tissue reactions to noxious substances, including oxidizing
agents, reducing agents, corrosives, protoplasmic poisons,
desiccants and vesicants (Fig. 10.1).
1. Remove the cause of the burn by flushing the
chemicals off the skin surface with cool, running water
for 15 minutes or more. Clothes soaked in chemical
should be removed. Deep alkali burns should be irrigated
for 24 hours. A balanced saline solution is preferable
for irrigation of mucosal surfaces or eyes. Dilution of
the chemical is of paramount importance and not
neutralization. Neutralization can produce exothermic
damage as well. If the burning chemical is a powder-
like substance such as lime, brush it off the skin before
flushing.
Initial copious hydrotherapy is indicated for all chemical
burns except those caused by dry-lime, phenol,
concentrated sulphuric acid, sodium metal and muriatic
acid; they are either not miscible with water or react
with water exothermically.
2. Antidotes are helpful for burns from hydrofluoric acid,
phenol and white phosphorous.1
Hydrofluoric acid (HFA) causes liquefaction necrosis
of the subcutaneous tissue and can penetrate to bone.
Systemic complications of HFA toxicity include
hypocalcemia and pulmonary edema. HFA wounds
should be covered with a 10% calcium gluconate solution
mixed to a slurry with a water soluble ointment or
infiltrated if the burn is excruciatingly painful.
Phenol is an acidic alcohol which produces local
coagulation and systemic toxicity in large doses,
including fatal arrhythmias. Acute phenol burns are
treated topically by irrigation with polyethylene glycol
solution.
White phosphorus is contained in grenades and anti-
personnel mines. Once particles are embedded in skin,
white phosphorus causes burn by both chemical and
thermal reactions, as particles are spontaneously ignited
with prolonged exposure to air. Patients should be
submersed in water until embedded particles can be
surgically debrided. The skin is washed with a solution
of 5% sodium bicarbonate, 3% copper sulfate and 1%
hydroxyl-cellulose to blacken the particles and aid earlier
identification. Prolonged exposure to copper sulphate
solution can induce coagulopathies.
3. Remove clothing or jewellery that has been
contaminated by the chemical.
4. Wrap the burned area loosely with a dry, sterile
dressing or a clean cloth.
5. Patient with even a minor chemical burn on the eye,
hands, feet, face, groin or buttocks or over a major
joint should be treated at a burn center.
9. Do not break the blisters. Broken blisters are more
vulnerable to infection.
10. Cover the area of the burn, this reduces the pain.
Use a sterile bandage or clean cloth. Sterile polyethylene
drape is very useful for covering the burnt area as it is
non-adherent and helps to avoid hypothermia. Do not
use fluffy cotton wool–it irritates the burn wound.
11. If the patient is conscious, give salt – sugar solution
to the patient orally.
12. Shift patient to appropriate facility for management
(Table 10.1).
Table 10.1: Key points in First Aid
1. Stop the burning process
2. Maintain airway.
3. If a burnt patient is unconscious, think of smoke inhalation and/
or of associated head injury.
4. If a burnt patient is breathless, think of inhalation injury, chest
trauma and / or aspiration.
5. If a burnt patient is in shock early after the incident, think of
associated chest or abdominal trauma causing blood loss or of
spinal trauma.
6. Shift the patient to appropriate burn care facility
Fig. 10.1: Chemical burns of face involving the eyes

Initial Evaluation and Resuscitation of Burn Patient
103
FIRST AID: ELECTRICAL BURNS
High-voltage electrical injuries are classified as major burns
due to associated massive tissue damage. On average, high-
voltage cutaneous involvement is only 10-15% BSA, but
this visible injury is only a small portion of the overall tissue
destruction (Fig. 10.2). The human body serves as a
volume conductor to electricity. Current flow is, therefore,
concentrated in the extremities by their narrowing. Since
bone has the highest resistance to electrical current,
conduction through bone produces the greatest amount of
heat. For this reason, damage to muscle by electricity is
greatest at tendinous attachments and periosteal regions.
Massive muscle destruction causes myoglobinemia.
Precipitation of myoglobin in the renal tubules can produce
acute tubular necrosis and acute renal failure. In addition,
high-voltage electrical burns are commonly associated with
dislocations, fractures, vertebral injuries, myocardial damage,
neurological sequel and intra-abdominal injuries due to
concomitant trauma. The most common cause of early
mortality is cardiopulmonary arrest due to induced fibrillation.
While helping someone with an electrical burn and
waiting for medical help, following steps are recommended:
1. Look first. Do not touch. The person may still be in
contact with the electrical source. Touching the person
may allow the current to pass through the rescuer.
2. Turn off the source of electricity if possible. If this
is not possible, move the source away from the injured
person using a non-conducting object made of
cardboard, plastic or wood.
3. Check for signs of circulation breathing, coughing
or movement. If absent, begin cardiopulmonary
resuscitation (CPR) immediately.
4. Prevent shock. Lay the person down with the head
slightly lower than the trunk and the legs elevated.
5. Cover the affected areas. If the person is breathing,
cover any burned areas with a sterile gauze bandage, if
available, or a clean cloth. Do not use a blanket or towel.
Loose fibers can stick to the burns.
TRANSPORTATION
Almost all burn patients in India are transported, at least
initially, by the relatives of the victim to the nearest medical
facility. Only an extremely small number of them have
inhalational injury significant enough so as to require
immediate control of airway and intubation or oxygen
therapy to avoid complications and death. The burn patients,
as opposed to the multiple trauma patients with active blood
loss, are unlikely to develop shock or airway obstruction in
the first one hour or so post burn. Commonly, it is only
during disasters with a number of casualties occurring
together that the ambulances are rushed to the site and/or the
police/fire brigade personnel transport the victims. In such
situations only, there is a possibility of intravenous fluid being
started or oxygen being administered to patients on site and
continued during transportation. In the large cities where
specialized burn centers are available, the patient may be
transported directly to it. Otherwise, they are transported
to the nearest medical facility. Here, the initial treatment is
started and then, transfer to a burn facility is considered.
The procedures that should be performed in the pre-
hospital setting (on site) by trained paramedics before and
during transportation to the initial medical facility or from
the latter by medical personnel before a long transportation
to a specialised burn care center are:
1. Stop the burning process: Use water for smouldering
clothes, chemicals, hot tar, etc.
2. Check airway: If deep facial burns are present and/or
there is a history of smoke exposure with obtundation
or stridor or other symptoms of impaired airway –
INTUBATE
3. Initiate high flow oxygen therapy if history of smoke
exposure is present, to treat carbon monoxide toxicity.
4. Check for other Injuries especially to chest (rib
fractures, pneumothorax, etc.) (Fig. 10.3) due to other
trauma suffered in the accident.
5. Assess hemodynamic stability and perfusion by looking
for evidence of impending burn shock.
Fig. 10.2: Electrical burns involving wrist – Even though external
injury appears to be a minor burn but the underlying tissue destruction
is extensive involving muscles, nerves, vessels and bone

104
Principles and Practice of Burn Care
6. Start I / V infusion if burn size is greater than 15% of
total body surface (or if there are other injuries) infuse
lactated Ringers
An estimate of fluid requirement is:
a. 15-25% BSA = 500 ml per hour
b. 25-50% BSA = 750 ml per hour
c. > 50% BSA = 1 Liter per hour
The transport vehicle should have adequate supply
of crystalloids as well as colloids needed for
resuscitation.
7. Assess depth and size of burn while keeping the patient
warm (remove wet clothes). Cover patient with clean
and dry dressing to conserve heat.
8. High tension (> 1000 Volts) injury—Look for cardiac
abnormalities, entrance and exit sites and other injuries.
9. Remove any constricting objects (Rings, Bangles, etc)
10. Information to receiving center should include:
a. Neurologic status at scene
b. Smoke exposure and airway status
c. Hemodynamic stability
d. Approximate size, depth and areas involved in burn
For transfer from the initial medical facility to a burn
unit or higher center, the ambulance used for transporting
the victim should have all the resuscitation equipment and a
competent team of qualified doctor and nurse/paramedic.
Safety during transfer is more important than speed. The
transport should be by the fastest mode available. It must
be remembered that initial treatment of an extensively burnt
patient has to do more with care of airway, breathing and
circulation and resuscitation with intravenous fluids which
ADMISSION CRITERIA
Burn Surface Area Assessment
An accurate estimate of the size of the burn is important for
treatment and transfer decisions. The size or extent of the
burn can be estimated in a number of ways. When calculating
burn area, erythema should not be included. This may take
a few hours to fade, so some overestimation is inevitable if
the burn is estimated acutely.
Wallace’s ‘Rule of 9’ is a quick and practical way of
estimating the surface area affected by burn. The adult body
configuration is divided into anatomic regions that represent
9% or multiples of 9% of the total body surface area (Fig.
10.4).
•
Head and neck, 9%
•
Front of trunk, 18%
•
Back of trunk, 18%
•
Upper limb each, 9%
•
Lower limb each, 18%
•
Perineum and external genitalia,1%
Body surface area proportions differ considerably for
children. Using ‘Rule of 9’ for a child can lead to wrong
estimation of the extent and hence improper fluid
resuscitation. For patients younger than 15 years, a more
precise method of burn size estimation must be used.2
Lund and Browder’s chart: Perhaps, the most accurate
method is the age-specific Lund-Browder’s chart (Table
10.3) that compensates for the changes in body proportions
Fig. 10.3: Chest tube drainage in situ for pneumothorax because of
fracture ribs following fall from height due to electric injury
comes in the domain of every qualified medical practitioner
than the wound itself which has to be simply protected
from further contamination. This much treatment is
presently available in almost all parts of the country. Hence,
the practice of transporting the patient in great hurry to a
higher center without providing simple care should be
discouraged (Table 10.2).
Table 10.2: Key points during transportation
•
Assess airway. Intubate if necessary.
•
Secure two large bore intravenous lines for > 20% burn extent.
•
Start intravenous Ringer’s Lactate infusion at desired rate.
•
Insert nasogastric tube.
•
Introduce per-urethral catheter to monitor urine output during
transport.
•
Apply topical agent. Wrap in sterile clean drape. Avoid
hypothermia.
•
Carry resuscitation equipment and develop competence to use it.
•
Intimate receiving center.
•
Provide information about patient’s condition, treatment given
and actual incident.

Initial Evaluation and Resuscitation of Burn Patient
105
Fig. 10.4: Wallace’s Rule of 9
Table 10.3: Lund and Browder’s chart for estimating area of burns
Area
Birth to1
1 to 4
5 to 9
10 to 14
15 years
Adult
2nd*
3rd*
TBSA
year
years
years
years
Head
19
17
13
11
9
7
Neck
2
2
2
2
2
2
Anterior trunk
13
13
13
13
13
13
Posterior trunk
13
13
13
13
13
13
Right buttock
2.5
2.5
2.5
2.5
2.5
2.5
Left buttock
2.5
2.5
2.5
2.5
2.5
2.5
Genitalia
1
1
1
1
1
1
Right upper arm
4
4
4
4
4
4
Left upper arm
4
4
4
4
4
4
Right lower arm
3
3
3
3
3
3
Left lower arm
3
3
3
3
3
3
Right hand
2.5
2.5
2.5
2.5
2.5
2.5
Left hand
2.5
2.5
2.5
2.5
2.5
2.5
Right thigh
5.5
6.5
8
8.5
9
9.5
Left thigh
5.5
6.5
8
8.5
9
9.5
Right leg
5
5
5.5
6
6.5
7
Left leg
5
5
5.5
6
6.5
7
Right foot
3.5
3.5
3.5
3.5
3.5
3.5
Left foot
3.5
3.5
3.5
3.5
3.5
3.5
Total:
100
100
100
100
100
100
The figures can be colored in red for full-thickness burns (3rd*) and blue for partial-thickness burns (2rd*). TBSA – Total body surface area.

106
Principles and Practice of Burn Care
with growth. The burn is drawn on a cartoon figure and an
associated age-specific table is used to calculate the body
surface area involved. This provides more accurate
distribution of body surface area and is especially valuable
for burnt children. For a burn unit, adoption of this burn
extent estimation chart is advisable. Its use also facilitates
comparison of data from different units.
Palmar surface: The surface area of an individual’s palm
(including fingers) is roughly 0.8% of total body surface
area 3, though it is taken as 1% for all practical purposes
(Fig. 10.5). Palmar surface area can be used to estimate
relatively small burns (< 15% of total surface area) or very
large burns (> 85%, when unburnt skin is counted) or areas
of irregular or non-confluent burns.
While assessing the extent of burn, it is important that
the entire body surface is exposed and assessed. The
environment should be kept warm and hypothermia should
be avoided. Burns of the pigmented skin can be difficult to
assess and it may be necessary to remove all the loose
epidermal layers to unveil the exact burn size.
Burn Unit Referral
To standardize the treatment categorization, American Burn
Association has identified three treatment categories for burn
patients: major, moderate and minor burn injuries4 (Table
10.4).
Major Burn Injuries: This group includes partial thickness
burns with a body surface area greater than 25% in adults
(20% in children); all full thickness burns with a body
surface area of 10% or greater; all burns involving hands,
face, eyes, ears, feet and perineum; all inhalation injuries;
electrical burns of any extent; complicated burn injuries
involving fractures or other major trauma; and all poor risk
patients (Fig. 10.6). Major burn patients should be
transported to a burn center. The choice of a hospital depends
on distance and time, the patient’s burn complications
(respiratory condition, shock) and availability of bed. The
American Burn Association emphasizes the importance of
direct communication and transfer agreements among
hospitals. This system is highly desirable though non-
existent in India at present. If the seriousness of the patient’s
injury dictates transportation to the closest emergency
department of a hospital, then subsequent transfer to a burn
Fig. 10.5: Palmar surface of hand with fingers closed representing
1% of body surface area in adult (Left) and child (Right)
Table 10.4: American Burn Association’s grading system for burn severity and disposition of patients
Type of burn
Minor
Moderate
Major
Criteria
<10 percent TBSA burn in adult
10 to 20 percent TBSA burn in adult
>20 percent TBSA burn in adult
<5 percent TBSA burn in young
5 to 10 percent TBSA burn in young
>10 percent TBSA burn in young
or old
or old 2 to 5 percent full-thickness
or old
burn
>5 percent full-thickness burn
<2 percent full-thickness burn
Excluding
High-voltage burn
High-voltage injury
Known inhalation injury
Suspected inhalation injury
Any significant burn to face,
Circumferential burn
eyes, ears, genitalia or joints
Concomitant medical problem
Significant associated injuries
predisposing the patient to infection
(e.g., fracture, other major
(e.g., diabetes, sickle cell disease)
trauma)
Disposition
Outpatient management
Hospital admission
Referral to burn center
Young = patient younger than 10 years of age; adult = patient 10 to 50 years of age; old = patient older than 50 years of age. Adapted from: Hospital
and prehospital resources for optimal care of patients with burn injury: guidelines for development and operation of burn centers. American Burn
Association. J Burn Care Rehabil 1990; 11:98-104, with additional information from Hartford CE. Care of outpatient burns. In: Herndon DN, ed.
Total burn care. Philadelphia: Saunders, 1996:71-80

Initial Evaluation and Resuscitation of Burn Patient
107
center should be arranged after cardiopulmonary stabilization
and intravenous fluid therapy for shock.
Moderate, Uncomplicated Burn Injuries: This second group
includes partial thickness burns with a body surface area of
15 to 25% in adults (10 to 20% in children), full thickness
burns with a body surface area of less than 10% and burns
that do not involve eyes, ears, face, hands, feet or perineum.
Excluded from the group are electrical injuries, complicated
injuries (fractures), inhalation injuries and all poor risk
patients (elderly patients and patients with an intercurrent
disease). Most of the patients in this group should receive
emergency care at the site of the injury and be transported
directly either to a hospital where burn care expertise is
available or to a hospital with a burn center.
Minor Burn Injuries: The third group includes partial
thickness burns with a body surface area of less than 15%
in adults (10% in children), full thickness burns with a body
surface area of less than 2% and burns not involving eyes,
ears, face, hands, feet or perineum. It excludes electrical
injuries, inhalation injuries, fractures and all poor risk patients.
The patients in this group may be transported to a hospital
emergency department where definitive care begins.
In Indian setting, it is highly desirable to provide
treatment to patients with moderate and minor burns in a
Level 2 hospital with support from burn unit at Level
1(tertiary care) hospital whenever necessary. This can
control the patient load in the few burn centers available
and hence help improve the quality of care.
Burn Unit Admission Criteria
A burn unit may treat adults or children or both.
Burn injuries that should be treated at a burn unit include
the following:
1. Partial thickness burns greater than 10% total body
surface area (TBSA)
2. Burns that involve the face, hands, feet, genitalia,
perineum or major joints
3. Full thickness burns in any age group
4. Electrical burns, including lightning injury
5. Chemical burns
6. Inhalation injury
7. Burn injury in patients with pre-existing medical
disorders that may complicate management, prolong
recovery or affect mortality
8. Any patient with burns and concomitant trauma (such
as fractures) (Fig. 10.7) in which the burn injury poses
the greatest risk of morbidity or mortality. In such
cases, if the trauma poses the greater immediate risk,
the patient may be initially stabilized in a trauma center
before being transferred to a burn unit. Physician
judgment is necessary in such situations and should
be in concert with the triage protocols.
9. Burned children in hospitals without qualified personnel
or equipment for the care of children.
10. Burn injury in patients who require special social,
emotional or long-term rehabilitative intervention.
Fig. 10.6: Major burn injury
Fig. 10.7: Fracture of lower end of radius, along with burns in the
forearm and hand, due to fall, after sustaining electric burns

108
Principles and Practice of Burn Care
Selection for outpatient care: Outpatient management is best
coordinated with the burn unit’s team of doctors, nurses
and therapists because their expertise may facilitate attaining
optimal outpatient results. Several factors are relevant to a
decision regarding the outpatient care. No question of airway
compromise should exist. The wound must be small enough
so that intravenous fluid resuscitation is not required. The
patient must be capable of oral intake of an adequate amount
of fluids. Generally, serious burns on the face, ears, hands,
genitals or feet should be initially managed in an inpatient
setting. The patient and his/her family must be able to
comply with an outpatient care plan. An adult caregiver
must be present with a child being managed in an outpatient
setting. A family member must be available to perform
necessary wound cleansing, inspection and dressing
applications because most patients cannot do these
themselves. The family must have adequate transportation
to return for follow-up visits and unexpected emergency
visits. Specific conditions that mandate an early return
should be detailed. Particularly important are pain and anxiety
associated with wound care to the degree that wound care
is compromised. This can be suspected if the wound shows
signs of infection or appears deeper than appreciated at the
time of the initial examination. In such a situation the patient
should be admitted. If abuse is suspected, outpatient
management is contraindicated. If on initial examination
surgery is clearly needed for a full-thickness burnt area, the
patient should be admitted. Despite all of these stipulations,
most patients with small burns can be successfully managed
in an outpatient setting.
OUTPATIENT WOUND CARE STRATEGIES 5
The components of outpatient burn care include:
1. Patient and family teaching,
2. Wound cleansing,
3. Choice of topical agent or membrane dressing,
4. Pain control,
5. Early return instructions,
6. Follow-up clinic visits,
7. Long-term follow-up.
Wound cleansing and dressing techniques must be taught
to whosoever will be doing the dressing changes.
Documenting this teaching is ideal.
INPATIENT MANAGEMENT
A major burn is defined as a burn covering 25% or more of
total body surface area (more than 20 % for children), but
any injury over more than 10% should be treated similarly.
Rapid assessment is vital. The general approach to a major
burn can be extrapolated to managing any burn.
Early Management of Major Burn
The burn wound should never take precedence over
potential life threatening conditions. As described by
the American College of Surgeons Committee on Trauma,
evaluation of the burn patient is organized into a primary
survey and a secondary survey using modification of the
methodology of Advanced Trauma Life Support Course.6
Primary survey: The emphasis is on detection and
treatment of life threatening conditions.
A – Airway patency - Heat affects primarily the oral
and nasal cavity, supraglottic area of the pharynx and causes
edema and mechanical upper airway obstruction. The gas,
particle and chemical components of the smoke affect
primarily the airway mucosa and cause the actual chemical
burn. The initial smoke injury occurs shortly after exposure
within 30 minutes to 1 hour, but the ensuing intense
inflammatory reaction evolves over a period of hours to
days resulting in lung damage. The initial edema usually wears
off within a day or two and is evident by air leak by the sides
of the endotracheal tube. Inhalation injury should be suspected
in all of the following situations (Fig. 10.8):
Fig. 10.8: Burn distribution suggestive of inhalation injury

Initial Evaluation and Resuscitation of Burn Patient
109
•
Individuals who sustained injury in a closed space,
•
Patients with extensive burns or with burns of the face,
•
Patients who were unconscious at the time of injury,
•
Patients with singed nasal and facial hair, hoarseness or
wheezing and
•
Patients who are coughing up carbonaceous sputum.
•
Explosions with burns to head and torso,
•
Carboxyhemoglobin level > 10%.
Pulmonary injury is known to result in substantially
increased burn mortality and morbidity. When indicated,
early intubation and positive pressure ventilation has been
shown to improve outcome (Flow chart 10.1).
A number of techniques have been used to assess the
degree of supraglottic and subglottic injury and to determine
the need for endotracheal intubation. Fiberoptic
bronchoscopy or laryngoscopy and virtual bronchoscopy
can reveal physical evidence of mucosal injury. In the
author’s experience, in patients with clinical suspicion of
inhalation injury, fiberoptic bronchoscopy confirmed the
suspicion in 93% of patients (unpublished data). Hence, in
the absence of diagnostic modalities, high index of suspicion
should guide the management.
As the injury process is progressive during the first 18
to 24 hours, initial appearance does not accurately predict
the severity of subsequent airway compromise. With increase
in edema, it becomes much more difficult to secure an
airway. This can be a particular problem in small children.
Endotracheal intubation is, thus, preferably performed on
admission, before severe edema develops. On the other hand,
unnecessary intubation and sedation can worsen a patient’s
condition. The decision to intubate should be made carefully
by an experienced clinician.6
Definite indications for endotracheal intubation are:
1. Deep facial burns - especially of the mouth and
oropharynx. Development of edema may impair patency
in the near future.
2. Massive body burns, especially in the presence of
circumferential chest burns, as ventilatory support is
needed.
3. Severe inhalation injury.
Flow chart 10.1: Algorithm for management of smoke inhalation

110
Principles and Practice of Burn Care
A patient with inhalation injury can be closely monitored
for upper airway obstruction without a tube, preferably with
the head elevated at 30°, only if intubation will be technically
possible later. However, if anatomic distortion from face
and neck burns is increasing to a point where safe intubation
might soon be precluded, the procedure is carried out
immediately. If edema distorts the anatomy, intubation using
fiberoptic bronchoscope should be resorted to by an
experienced clinician. Prolonged and multiple attempts
at intubation can further aggravate the hypoxia and
may precipitate cardiac arrest. So in the absence of
expertise, the option of a tracheostomy should be exercised
even if the incision has to be made through burnt skin (Fig.
10.9).
Once a definitive airway is secured, continuous
administration of humidified oxygen is indicated to maintain
adequate oxygenation as well as to assist clearing the airway
of inspissated products of combustion. If the patient’s
hemodynamic condition tolerates, elevation of the head
end of the bed by 30 degrees is helpful in reducing neck
and chest wall edema. The early addition of bronchodilators,
usually by aerosol, is especially advantageous in managing
the bronchospasm seen after chemical injury. Nebulisation
with Heparin + Saline helps in limiting the alveolar damage.
After a secure airway is established, the need for ventilatory
support is assessed. Blood gases are often misleading as far
as saturation is concerned as the carboxy-hemoglobin is
the confounding factor. The pH and bicarbonates can,
however, guide therapy.
B – Breathing is evaluated for depth of respiration and
effort. Detection of wheezing or rales suggests either
inhalation injury with bronchospasm or aspiration of gastric
contents. In a patient with burn, the respiratory effort and
hence the gas exchange may be inadequate due to:
1. Mechanical restriction of breathing—Deep dermal or
full thickness circumferential burns of the chest can
limit chest excursion and prevent adequate ventilation.
This may require escharotomies.
2. Blast injury—If there has been an explosion, blast lung
can complicate ventilation. Penetrating injuries can cause
tension pneumothorax and the blast itself can cause lung
contusions and alveolar trauma and lead to adult
respiratory distress syndrome.
3. Smoke inhalation—The products of combustion,
though cooled by the time they reach the lungs, act as
direct irritants to the lungs, leading to bronchospasm,
inflammation and bronchorrhea. Patients may need a
period of ventilation, as this allows adequate oxygenation
and permits regular lung toilet.
4. Carboxyhemoglobin—Carbon monoxide binds to
deoxyhemoglobin with 40 times the affinity of oxygen.
It also binds to intracellular proteins, particularly the
cytochrome oxidase pathway. These two effects lead
to intracellular and extracellular hypoxia. Pulse oximetry
cannot differentiate between oxyhemoglobin and
carboxyhemoglobin and may, therefore, give normal
results. However, blood gas analysis can reveal metabolic
acidosis and raised carboxyhemoglobin levels but may
not show hypoxia. Treatment is with 100% oxygen,
which displaces carbon monoxide from bound proteins
six times faster than does atmospheric oxygen. Patients
with carboxyhemoglobin levels greater than 25-30%
should be ventilated. It takes longer to shift the carbon
monoxide from the cytochrome oxidase pathway than
from hemoglobin. Hence, oxygen therapy should be
continued until the metabolic acidosis has been corrected.
C – Circulatory status is evaluated with pulse rate and
blood pressure and when indicated venous access is
established with two wide bore intravenous lines in upper
limbs in unburnt area. Initial fluid of choice is crystalloid.
Colloids should be considered in patients not responding to
Fig. 10.9: Tracheostomy for laryngeal edema due to
smoke inhalation

Initial Evaluation and Resuscitation of Burn Patient
111
crystalloids. Profound hypovolemia is not the normal
initial response to a burn. If a patient is hypotensive then
it may be due to delayed presentation, cardiogenic
dysfunction or an occult source of blood loss (chest,
abdomen or pelvis). In patients with circumferential deep
partial or full thickness burns of extremities and electrical
injury, assessment of distal circulation is mandatory for
detection of compartment syndrome. The circulatory
compromise can occur later as edema develops after
initiation of fluid resuscitation. On securing vascular access,
blood samples should be collected and sent for blood counts,
packed cell volume, estimating urea and electrolytes, blood
group and clotting profile.
Secondary Survey
The burn specific secondary survey should include (1)
determination of the mechanism of injury (2) evaluation for
the presence of inhalation injury and carbon monoxide
intoxication (3) examination for corneal burns (4)
consideration of the possibility of abuse and (5) detailed
assessment of the burn wound. Besides evaluation of A,B,C.
as detailed above, the secondary survey includes the
following.
D—Neurological disability—All patients should be
assessed for responsiveness with the Glasgow coma scale;
they may be confused because of hypoxia or hypovolemia.
E—Exposure with environment control—Whole of the
patient should be examined (including the back) to get an
accurate estimate of the burn area and to check for any
concomitant injuries. Burn patients, especially children, easily
become hypothermic. This may lead to hypoperfusion and
deepening of burn wounds. Patients should be covered and
warmed as soon as possible.
F—Fluid resuscitation—The resuscitation regimen should
be determined and begun. This is based on the estimation of
the burn area. A urinary catheter is mandatory to monitor
urine output in all adults with burns covering > 20% of
TBSA. Children’s urine output can be monitored with
external catchment devices or by weighing nappies provided
the injury is < 20% of total body area. In children the
interosseous route can be used for fluid administration if
intravenous access cannot be obtained, but should be replaced
by intravenous lines as soon as possible.
History: The history of a burn injury can give valuable
information about the nature and extent of the burn, the
likelihood of inhalational injury, the time of burn, the depth
of burn and probability of other injuries. The exact
mechanism of injury and any prehospital treatment must be
recorded. A brief medical history should be taken, outlining
previous medical problems, medications, allergies and
vaccinations. Patients’ smoking habits should be determined
as these may affect blood gas analysis. Development of
edema after initiation of fluid resuscitation may hamper the
patient’s ability to vocalise. Hence, detailed history should
be obtained from the patient at the initial assessment. After
completing initial assessment and initiation of resuscitation,
the complete extent and depth of burn wound should be
evaluated.
Fluid Therapy (See Appendix 1.1)
Fluid losses from the injury must be replaced to maintain
homeostasis. The main aim of resuscitation is to maintain
tissue perfusion to the zone of stasis and so prevent the
deepening of burn. This is not easy, as too little fluid can
cause hypoperfusion whereas too much may lead to edema
causing tissue hypoxia. Burns covering more than 15% of
TBSA in adults and more than 10% in children warrant
formal resuscitation as physiological compensatory
mechanisms may not be adequate to combat the fluid loss.
There is no ideal resuscitation regimen and many are in use.
All the fluid formulas are only guidelines and their success
depends on adjusting the amount of resuscitation fluid against
monitored physiological parameters. The greatest amount
of fluid loss in burn patients is in the first 24 hours after
injury. For the first eight to 12 hours, there is a general shift
of fluid from the intravascular to interstitial fluid
compartments.3 This means that any fluid given during this
time will rapidly leave the intravascular compartment.
Colloids have no advantage over crystalloids in maintaining
circulatory volume in this situation. Fast fluid boluses
probably have little benefit, as a rapid rise in intravascular
hydrostatic pressure will just drive more fluid out of the
circulation. However, much protein is lost through the burn
wound, so there is a need to replace this oncotic loss. Some
resuscitation regimens introduce colloid after the first eight
hours, when the loss of fluid from the intravascular space
is decreasing. The following facts need to be considered
while planning fluid resuscitation.
1. Burn patients may have substantially higher fluid
requirements than other trauma patients depending on
the surface area involved.
2. Fluid needs to be titrated to maintain adequate output
and special care needs to be taken when myoglobinuria
is present (Fig. 10.10).

112
Principles and Practice of Burn Care
3. The greatest loss of fluids occurs in first 48 hours.
4. The fluid should be administered at constant drip rate
and surges should be avoided. If indicated, aliquots of
250 ml of Lactated Ringer’s may be administered.
5. The fluid volume for each patient should be adjusted
according to urine output (30-35 ml per hour minimum)
and hematocrit (32%). Insert urinary catheter.
6. In children, provision for the daily maintenance
requirement (weight or surface area based formula)
on top of the calculated amount should be made if
Parkland formula is being used.
7. Sodium-salt solutions (crystalloids) are the essential
components of fluid resuscitation.
8. The most appropriate fluid is Ringer lactate because
its composition is the closest to that of extracellular
fluid. Also lactate is a source of base due to its
conversion to bicarbonate in the liver.
9. Fluids should be free of glucose (exception being small
children), since glucose intolerance is characteristically
present due to high circulating levels of stress
hormones.
10. The time frame of fluid resuscitation is to be calculated
from the time of burn and NOT from the time of
initiation of therapy.
The resuscitation formulae most commonly used for
fluid calculation are the Parkland formula, a pure crystalloid
formula (4 ml × % burnt area × body weight in kg.), modified
Parkland’s formula or modified Brooke’s formula (Table
10.5). The calculated volume is then given at different rates;
first 8 hours - half of total to be given;
next 16 hours -half of total to be given;
next 24 hours - half of total given on first day.
Any fluid already given should be deducted from the
calculated requirement.
Lactated Ringer’s solution without dextrose is the fluid
of choice except in children under 2 years, who should
receive 5% dextrose Ringer’s lactate.7 Early work by Baxter
and by Shire established the basis for modern protocols for
fluid resuscitation.8 They showed that edema fluid in burn
wounds is isotonic and contains same amount of protein as
plasma and the greatest loss of fluid is into the interstitial
fluid compartment. It led to successful clinical trial of
Parkland formula.
Colloid use is controversial. Some units introduce colloid
after 8 hours, as the capillary leak begins to shut down,
whereas others wait until 24 hours. Fresh frozen plasma is
often used in children and albumin or synthetic high
molecular weight starches are used in adults. Generally at
the end of 24 hours, colloid infusion is begun at a rate of
0.5 ml× total burn surface area (%) × body weight (kg)
besides maintenance crystalloid (usually dextrose-saline)
infusion. The end point to aim for is a urine output of 0.5-
1.0 ml/kg/hour in adults and 1.0-1.5 ml/kg/hour in children.
High tension electrical injuries require substantially more
fluid (up to 9 ml × % burn area × body weight) in the first
24 hours and a higher urine output (1.5-2 ml/kg/ hour).
Inhalational injuries also require more fluid.3
The above regimens are merely guidelines to the probable
amount of fluid required. This should be continuously
adjusted according to urine output and other physiological
parameters (pulse, blood pressure and respiratory rate).
Investigations at intervals of four to six hours are mandatory
for monitoring a patient’s resuscitation status. These include
packed cell volume, plasma sodium, base excess and lactate.
The debate on the choice of resuscitation fluid has been
on-going. Different fluids are expected to cause varying
degrees of plasma volume expansion (Table 10.6). But, it
was shown that changes in plasma volume were not related
to the type of resuscitation fluid in first 24 hours, concluding
that colloid solutions should not be used in first 24 hours
until capillary permeability returns to near normal. Others
have argued that normal capillary permeability is restored
somewhat earlier (6-8 hours after burn) and colloids could
Table 10.5: Resuscitation formulas (adult) for first 24 hours
Formula
Crystalloids
Colloids
Daily need
Parkland
4 ml/kg/% TBSA burn
None
None
Brooke
2 ml/kg/% TBSA burn
None
2.0 L
(modified)
Galveston
5 L/m2 burned area
None
1.5 L/m2 BSA
Fig. 10.10: Brownish urine suggestive of myoglobinuria

Initial Evaluation and Resuscitation of Burn Patient
113
be started earlier.9 Moncrief and Pruitt studied hemodynamic
effects of fluid resuscitation in burns culminating in Brooke
Formula which recommended use of 0.5 ml of colloid / %
of burn / Kg body weight and has now been modified to all
crystalloid resuscitation in first 24 hours. Efforts to avoid
wrong calculation of resuscitation fluid have led to usage
of Burns wheel10, Palm-top computer 11 and Resuscitation
Burn Card12 etc. at some burn centers. There is continuing
debate over the merits of colloid versus crystalloids for the
resuscitation of major burns.13 The crystalloid resuscitation
is widely accepted. Hypertonic saline solution has theoretical
advantage and has been shown to decrease net fluid intake14
and decrease edema.15 No significant difference was found
in volume requirement or weight gain in patients over 20%
TBSA burns, randomized on hypertonic saline or lactated
Ringer’s solution for resuscitation.16 Some have found an
increase in renal failure with hypertonic saline.17 According
to Berger et al, Hypertonic saline solutions, whether with
dextran or not, have shown no advantage over the classic
Ringer’s lactate solution.18 When using hypertonic saline,
care must be taken to avoid serum sodium concentration
greater than 160 mEq/dl.19 Some burns unit use a modified
hypertonic solution of sodium bicarbonate added to lactated
Ringer’s solution with success.20 Some studies favor
administration of protein-based colloids during the
resuscitation period for major burns, starting in the early
period after injury. These studies claim more beneficial effect
than potential side-effects.21 The results with albumin are
varied. Some studies show that use of albumin does not
reduce mortality when compared with crystalloids 22, 23,
while other claims higher mortality rate with liberal use of
albumin.18 According to Cochran et al, there was no increase
in mortality with albumin.24 There was no reduction in
multiple organ dysfunction score with albumin.25
According to Berger et al, artificial colloids, particularly
gelatine, remain a useful tool in patients with major burns
and hemodynamic instability and can be given as early as 6
hours after injury. 18 Chen et al studied utility of Hydroxy-
ethyl starch in burns resuscitation and claimed that it could
partially substitute plasma and be used in fluid resuscitation,
but plasma protein replenishment should be emphasized.26
The use of Composite Sodium Lactate and Sorbitol (CISS)
in resuscitation fluid during shock stage of the patients with
major burns can be beneficial to the replenishment of blood
volume, control of shock, promotion of diuresis and
subsidence of edema and can also provide electrolytes and
energy, without the influence on the level of blood glucose.27
Some found no added advantage with fresh frozen plasma
and recommended its use only for specific coagulation
disorders24 while according to others, it is useful for
resuscitation of burns. High dose (66 mg/kg/hour)
intravenous ascorbic acid (vitamin C) in early phase of fluid
resuscitation has been found to be advantageous.28,29 This
group showed reduced weight gain, wound edema,
improved oxygenation and reduced requirement of
resuscitation fluid volume.29
The ideal burn resuscitation formula does not exist.
Whichever formula is used, patients must be monitored
closely and the fluid resuscitation individualized according
to the response. Patients with delay in resuscitation,
associated trauma, inhalation injury or alcohol abuse may
require greater than predicted quantity of fluid. The goal is
to maintain urine output in the range of 0.5 to 1 ml/kg/hour
for adults and 1 to 1.5 ml/kg/hour in children. In patients
with fluid requirements greater than 150% of that predicted
by formula, the addition of colloid at 12 hours can reduce
total fluid requirements and burn edema. Early placement
of pulmonary artery catheters can be useful in patients with
Table 10.6: Preload expanding properties of standard fluids
Fluid
Osmolarity
Colloid
pH
Distribution Space
Ratio of fluid infused to
(mOms/L)
Osmotic
intravascular expansion
Pressure
5% dextrose
250
0
4
Total body water
8:1
Normal saline
308
0
5
Extracellular
3:1
Ringer’s lactate solution
270
0
6.5
Extracellular
3:1
Hypertonic lactated saline
450
0
6-7
Extracellular expansion by
<3:1*
(250 mEq Na+/L)
fluid shifts from cells
6% albumin
250
20-24
6-7
Intravascular
1:1
Dextran 70
300-303
20-40+
6-7
Intravascular expansion by
fluid shift
<1:1
* Depends on tonicity of fluid and plasma osmolarity

114
Principles and Practice of Burn Care
known myocardial dysfunction, age greater than 65 years,
severe inhalation injury or fluid requirements greater than
150% of that predicted by formula.30
Gastrointestinal fluid resuscitation31 by oral and rectal
route has been tried for burn patients in peripheral areas.
For burned children, the commonly used formulae are
modified to account for changes in surface area to mass
ratios. These changes are necessary because a child with a
burn requires more resuscitation fluid per kilogram as
compared to an adult (See Appendix 1.2).32
In Galveston formula the daily fluid requirement for a
child with burn is augmented to 2 L/ m2 of total body surface
area against 1.5 L/m2 for an adult.
Intravenous Access
A peripheral vein catheter through unburnt skin is the
preferred route for fluid administration. A central line or
pulmonary artery line is only occasionally required to monitor
the patient during the initial resuscitation period and is
removed as soon as possible. The possibilities for
intravenous access are:
Choices for Venous Access
•
First choice: Peripheral vein; unburnt area
•
Second choice: Central vein; unburnt area
•
Third choice: Peripheral vein; burnt area
•
Worst choice: Central vein; burnt area
Monitoring lines are required primarily for the elderly
patient or the patient with severe heart disease. A high
complication rate has been reported with central catheters
in burn patients as a result of infection.
Common Pitfalls in Initial Fluid Resuscitation
1. Initial Under Resuscitation: The largest fluid shifts
occur in the first several hours post burn. Initial
crystalloid infusion based on a formula will often be
inadequate if shock state is present due to delay in
initiation of resuscitation. More volume is needed. A
volume expander such as a non-protein colloid or protein
solution or hypertonic saline can be very useful along
with isotonic crystalloid for successful resuscitation.
2. Initial Over Resuscitation: Aggressive fluid infusion
is now frequently initiated in most emergency rooms
with placement of large bore lines. The practice of “wide
open” fluid infusion during early assessment and
transport regardless of hemodynamic response is to be
avoided. The excess fluid cannot be compensated for
by decreasing infusion rate in subsequent hours because
the extra fluid is already out of the vascular space.
3. Striving for Ideal Numbers: It is quite possible to
achieve ideal numbers (pulse less than 120, blood pressure
more than 100, urine output 0.5 to 1 ml/kg body weight/
hour) in a young patient with a moderate-sized
uncomplicated burn. In a massive burn (more than 60%
total body surface), especially in the presence of
inhalation injury or in the elderly, attempts at pushing
fluids beyond reasonable amounts to achieve “ideal
numbers” only accentuate edema-induced complications.
Adequate perfusion is not the same as “ideal numbers.”
While planning the treatment, possibility of pulmonary
and chest wall edema-induced complications need to be
considered.
4. Consideration of Fluid alone for Treatment of
Impaired Perfusion: Hypovolemia from burn-induced
fluid and protein shifts is the predominant cause of
hypoperfusion and fluid infusion is the treatment.
However, two other processes must be considered. The
first is impaired cardiac output due to an increasing mean
airway pressure, particularly from a noncompliant chest
wall burn. Ventilator adjustments, chest wall
escharotomy, elevation of the head of the bed to decrease
chest edema and the use of an agent, such as low-dose
dopamine, to assist fluids can be very helpful in
maintaining perfusion. Secondly, cardiac depression
from a deep body burn is well described, particularly in
the elderly. Supplementation of fluids, both crystalloid
and colloid, with a beta agonist can help reverse a
downward course reflected by continually increasing
fluid requirements and decreasing perfusion.
5. Use of Urine Output alone as Monitor for Volume
Restoration: Although usually a reliable indicator of
renal perfusion, factors such as high plasma alcohol or
glucose levels often lead to an inappropriately high urine
output relative to the status of tissue perfusion. The
value of the urine output must be considered to be
unreliable under these circumstances.
6. Failure to Secure Intravenous Lines: As edema
develops, the intravenous catheter may slip out of the
vein into the surrounding tissue. Not only does this lead
to transient hypovolemia, but finding a new site when
edema is present can be extremely difficult. A solution
is to secure the intravenous line with sutures.
Monitoring
In a burn patient no single monitor of perfusion can be
considered to be a completely reliable indicator of tissue

Initial Evaluation and Resuscitation of Burn Patient
115
oxygenation (perfusion). Therefore, several standard
hemodynamic monitors and laboratory tests should be
utilized.
Physiologic Measurements
Oxygenation: Use of pulse oximeter is standard for a major
burn.
Baseline Body Weight: The baseline weight is used to
estimate the initial fluid replacement and can be obtained by
history or be estimated.
Arterial Pressure: The increased sympathetic tone
characteristic of this early period makes arterial pressure
an insensitive measure of volume status. However, a minimal
level of perfusion pressure (more than 80 mm Hg) must be
maintained. Thus, blood pressure monitoring is necessary.
An arterial line may be required if:
1. Patient is hemodynamically unstable.
2. Extremities are burned and sphygmomanometric
pressure cannot be obtained manually.
3. If frequent blood gas analyses are required.
The arterial catheter should be placed through unburnt
skin and should be removed as soon as possible.
Pulse Rate: Tachycardia is inevitable in early post burn
period due to hypovolemia and catecholamine release from
tissue trauma and pain. The degree of tachycardia can be
very useful for determining adequacy of volume
replacement. The exception would be an elderly or the patient
with pre-existing heart disease in which the heart rate cannot
increase in proportion to the stimulus. In most patients: a
pulse rate of less than 120/minute usually indicates
adequate volume while more than 130/minute usually
indicates more fluid is needed.
Urine Output: The status of renal blood flow is usually an
accurate reflection of the adequacy of systemic perfusion
during this early phase of injury. A urine output of 0.5 to 1
ml/kg body weight/hour normally reflects adequate renal
blood flow, assuming there are no factors such as alcohol,
hyperglycemia or mannitol that alter the relationship between
renal blood flow and urine output.
Intake-Output: What goes in and what comes out should
be carefully tabulated. Intake may far exceed output during
this phase as edema develops.
Blood Gases: The monitoring of arterial oxygen and carbon
dioxide tension is required to judge the adequacy of
ventilation. The measurement of pH and acid-base balance
is extremely useful for the assessment of tissue oxygenation.
A base deficit during this phase usually reflects impaired
tissue oxygenation due to hypovolemia or carbon monoxide
toxicity (also cyanide).
Electrocardiographic Monitoring: Arrhythmias are not
common in the young patient as long as oxygenation is
adequate. They become a major concern in the patient older
than 45 years as a result of the response to burn stress. ECG
monitoring is also indicated in patients with electrical injury.
Body Temperature: The burn patient is very prone to
hypothermia during this early period, especially with infusion
of cold fluids. A decrease in temperature can lead to further
hemodynamic instability and impaired perfusion.
Central Venous Pressure (CVP): The central venous
pressure in a large burn at this stage is usually low, 0 to 5
cm H2O, even with adequate fluid resuscitation. Therefore,
it can be very dangerous to use an arbitrary value of central
venous pressure as an endpoint of resuscitation. Too much
or too little fluid can be infused based on an arbitrary value.
Pulmonary Artery Wedge Pressure: The majority of
young patients, even with massive burns, do not require
the use of these measurements for initial resuscitation. A
selected group of patients can benefit from this measurement.
These include: 1. Elderly or patients with pre-existent heart
disease with large burn or smoke inhalation. 2. Young patient
with massive burn who is not maintaining perfusion despite
fluid intake well in excess of predicted.
Cardiac Output, Mixed Venous Oxygen Tension: The
primary objective of fluid management is to maintain
adequate tissue oxygen delivery. The direct measurement
of cardiac output (cardiac index) can assist in the
determination of oxygen delivery. A cardiac index in excess
of 2.5 L/min/m2 is considered normal for an un-injured
person. The value for mixed venous oxygen tension (PvO2)
however, can greatly assist in this determination.
Association of mixed venous gas
•
PvO2 > 35 mmHg: oxygen delivery adequate
•
PvO2 > 30-35 mmHg: oxygen delivery marginal
•
PvO 2< 30 mmHg: oxygen delivery inadequate
Laboratory Measurements (See Appendices
1.3 to 1.7)
Hemoglobin and Hematocrit: Baseline hematocrit and
hemoglobin is useful for monitoring although changes in

116
Principles and Practice of Burn Care
their values may not accurately reflect changes in blood
volume due to the selective loss of the plasma component
of blood (Table 10.7).
White Blood Cell: Initial white blood cell counts may be
high, normal or low depending on the magnitude of the
stress response and white cell sequestration into the burn.
Low WBC count in association with inhalation injury is
indicative of poor prognosis.
Electrolytes: Since the initial losses are primarily plasma,
the Na+, Cl–, K+ values remain relatively constant despite
hypovolemia and vary mainly as a result of the type of
resuscitation fluid used. K+ increases in case of severe
hemolysis or renal impairment. The HCO 3 content varies
depending on the status of perfusion and acid-base balance.
Creatinine and Blood Urea Nitrogen: Baseline values are
helpful to define normal status.
Plasma Proteins: A marked decrease in plasma proteins
occurs early post burn.
Plasma Myoglobin: The plasma value of myoglobin is
obtained in very deep burns, especially electrical burns.
Myoglobin, released from deeply injured muscles, affects
renal function. A higher urine output should be maintained
(2-5 ml/kg/hour).
Prothrombin Time, Partial Thromboplastin Time and
Platelets: An initial value during this period is useful for
determining whether clotting factors may be needed. It is
not common to have the need for replacing clotting factors
and platelets during the first 36 hour period unless a prolonged
shock state has initiated disseminated intravascular
coagulation or pre-existing liver or hematologic disease is
present.
Chest radiograph: An initial chest radiograph should be
obtained in all patients with inhalation injury.
Initial Management of Burn Wound
After ensuring airway patency, adequacy of respiration and
initiation of fluid resuscitation, attention is directed to
complete evaluation of the extent and depth of the burn
wound. Till such time, care should be taken to avoid
hypothermia due to exposure. Based on the depth of
involvement, the burn wound is classified into Superficial,
Superficial partial thickness, Deep partial thickness
and Full thickness burn (Figs 10.11 to 10.15). Burn depth
has an impact on healing time, the need for hospitalization
and surgical intervention and the potential for scar
development. Although accurate classification is not always
possible initially, the causes and physical characteristics of
burns are helpful in categorizing their depth (Table 10.8).
Use of LASER, vital dye, ultrasound or thermography for
estimation of burn depth is expensive and cumbersome.2
Visual estimation by experienced eyes is the most practical
approach.
Wound care: For an acute burn which is to be transferred
to a burn center, cling film is an ideal dressing as it protects
the wound, reduces heat and evaporative losses, controls
pain and does not alter the wound appearance.6 This permits
accurate evaluation by the burn team later. The details of
burn wound care are discussed elsewhere in this volume.
Only an outline is given here for sake of completion.
Table 10.7: Hematocrit changes after large burn
Finding
Cause
Hematocrit increased
Plasma volume decreases while circulating red
blood cell volume remains relatively constant
Hematocrit normal
Normalization of blood volume has occurred.
Decrease in both plasma and red blood cell
volume, the latter from, e.g. hemolysis
Hematocrit decreased Hemolysis from prolonged heat exposure,
with only plasma volume replacement. Major
loss of blood from non-burn injury with only
plasma volume replacement. Pre-existing
anemia, hypervolemia (unlikely)
Fig. 10.11: Line diagram showing depth of burn injury

Initial Evaluation and Resuscitation of Burn Patient
117
Fig. 10.13: Superficial partial thickness burn after debridement of
dead skin
Fig. 10.14: Deep partial thickness burn
Fig. 10.15: Full thickness burn
Fig. 10.12: Superficial partial thickness burn with blister
Table 10.8: Classification of burns based on depth
Characteristics
Classification
Cause
Appearance
Sensation
Healing time
Scarring
Superficial burn
Ultraviolet light, very
Dry and red; blanches
Painful
3 to 6 days
None
short flash (flame
with pressure
exposure)
Superficial partial-
Scald (spill or splash),
Blisters; moist, red and
Painful to air and 7 to 20 days
Unusual; potential
thickness burn
short flash
weeping; blanches with
temperature
pigmentary changes
pressure
Deep partial-
Scald (spill), flame, oil,
Blisters (easily unroofed);
Perceptive of
More than 21 days
Severe (hypertrophic)
thickness burn
grease
wet or waxy dry; variable
pressure only
risk of contracture
color (patchy to cheesy
white to red); does not
blanch with pressure
Full-thickness burn Scald (immersion),
Waxy white to leathery
Deep pressure
Never (if the burn affects Very severe risk of
flame, steam, oil,
gray to charred and black; only
more than 2 percent of
contracture
grease, chemical, high-
dry and inelastic; does not
the total surface area of
voltage electricity
blanch with pressure
the body)

118
Principles and Practice of Burn Care
For in-patients, the protocol followed at the author’s
unit is as follows:
A. Partial thickness burn wound: Wounds are cleaned with
0.5% chlorhexidine solution and normal saline. Blisters
are deroofed and loose skin removed for ease of
dressing, except for palmar blisters (painful), unless these
are large enough to restrict movement. Wounds over
face and hands and all burns in children are covered
with collagen sheet if the patient is received within 6
hours of burn injury (Fig. 10.16). Once collagen is firmly
adherent, secondary dressings are not needed. The
author uses banana leaf dressing with 1% Silver-
sulfadiazine (SSD) for dressing of all other partial
thickness wounds.33 This is covered with sterile Gamgee
cotton pads and bandaged firmly (Fig. 10.17).
B. Full thickness burn wounds: In the author’s unit, if early
excision is planned, full thickness burn wounds receive
exposure treatment with application of povidine-iodine
ointment two or three times a day after cleaning of the
wound with 0.5% Chlorhexidine solution. If early
excision is not feasible, the wounds are dressed with
banana leaf dressing with povidine-iodine ointment as
the topical agent. At most other places the wounds are
dressed with 1% SSD.
C. Infected wounds: Exposure treatment with povidine-
iodine cream in the authors unit. Many other units prefer
closed dressing with antimiciobial agent as per organism
grown.
Early Surgical Management
Surgical procedures such as fasciotomy/escharotomy may
be needed early in patients with full thickness circumferential
burns of extremities or chest wall.
Impaired Chest Wall Compliance
Respiratory excursion can be markedly impaired by a
circumferential deep partial or full thickness burn of the
chest wall. The loss of elasticity in the burns of the chest
wall markedly increases the work of breathing. As more
subeschar edema develops, significant respiratory effort is
required just to maintain adequate gas exchange. Any process
that compromises the necessary increase in inspiratory force
and muscle activity, such as hypoxia, hypovolemia, pain or
sedation, accentuates the severity of lung dysfunction.
Symptoms may not be clearly evident until edema
development peaks at about 10 to 12 hours. The first clinical
evidence of the chest wall restrictive defect is often labored
breathing followed by a rapid respiratory deterioration,
particularly in the patient who is not receiving ventilatory
support. Clearance of secretions can be impaired due to the
inability to generate a hyperinflation. In the combined chest
burn and inhalation injury, it is very difficult to distinguish
the degree of impairment in total lung compliance due to
the increased airway edema and bronchospasm compared
with that due to the impaired chest wall movement. An
extremely deep burn results in tissue contraction due to
desiccation, making the chest wall tight even before edema
develops.
Patient with non-circumferential full thickness or
partial thickness burn is monitored closely for evidence of
respiratory restriction. Escharotomies are usually not
required in a partial thickness burn unless the edema is so
Fig. 10.16: Superficial partial thickness burn with
collagen application
Fig. 10.17: Autoclaved banana leaf dressing

Initial Evaluation and Resuscitation of Burn Patient
119
massive that the burned skin is tight. For circumferential
full thickness burn, chest wall escharotomy is performed
early. Even with an escharotomy, the restrictive process
can be of such magnitude that hypoventilation is clearly
evident. In these patients, endotracheal intubation and
positive-pressure ventilation should be initiated before
obvious pulmonary deterioration.
Impaired Distal Perfusion and Need for Escharotomy:
A full thickness burn tissue has complete loss of elasticity.
Hence, as subeschar edema develops under the burnt tissue,
the tissue pressure increases. Fluid resuscitation leads to
the development of burn wound edema and further swelling
of the tissue beneath this inelastic burnt tissue. With
circumferential full thickness burn of extremity, this increase
in tissue pressure initially decreases the venous return. This
further augments the tissue pressure and leads to impairment
of arterial flow causing ischemia (Fig. 10.18). Initially, limbs
at risk should be elevated and observed. Perfusion to the
distal extremity should be closely monitored. Pain and color
are unreliable indicators of perfusion in the presence of a
burn.3 A warm extremity invariably indicates good flow,
but a cool skin does not always indicate that the problem is
due to proximal constriction. Hypovolemia may well be the
cause. Use of simple hand held Doppler equipment provides
valuable information about perfusion. Evidence of ischemia
mandates escharotomy (Flow chart 10.2). Both of these
situations require escharotomy, division of the burn eschar.
Only the burnt tissue is divided, not any underlying fascia,
differentiating this procedure from a fasciotomy. Unless
decreased blood flow is evident in the accident and
emergency department, the escharotomy should be
performed in the burn center after expedious transfer. In
general, finger escharotomies should be performed in a burn
center only because of the associated potential morbidity.
Principles of Escharotomy
1. The escharotomy incisions should be located as shown
in (Fig. 10.19). Incisions are made along the midlateral
or medial aspects of the limbs, avoiding any underlying
structures. For the chest, longitudinal incisions are made
at each mid-axillary line to the sub costal region. The
lines are joined up by a chevron incision running parallel
to the sub costal margin.3 This creates a mobile breast
plate that moves with ventilation.
2. Anesthesia is not required as the full thickness burn is
insensate.
3. The procedure should preferably be performed in
operation theater, but can be performed bedside with all
aseptic precautions.
4. The incision should be deep enough to allow separation
of the edges permitting bulging of viable tissue.
5. Pain and significant bleeding is indicative of excessively
deep incision.
6. Escharotomy must extend completely through length
of burnt tissue crossing the joints till healthy skin is
reached.
7. Escharotomies are best done with electrocautery, as they
tend to bleed. Use of microcrystalline collagen to pack
the incision site can help control punctate bleeding. Larger
vessels usually require suture ligatures or cautery.
8. Dressing should be applied using a topical agent and
nonadherent wound cover.
9. Monitoring of distal perfusion should be continued after
escharotomy and if the impairment persists, existing
escharotomies should be extended or additional
escharotomies should be performed.
Fig. 10.18: Circumferential full thickness burn of forearm leading to
ischemic damage to hand
Fig. 10.19: Common sites for escharotomy

120
Principles and Practice of Burn Care
Table 10.10: Algorithm for management of circumferential extremity burn
Fasciotomy
Treatment of the high-voltage electrical burn victim should
include prompt initiation of aggressive fluid resuscitation
and serial assessment of distal vascular integrity.
Development of compartment syndromes should be
anticipated. Deeper muscle groups sustain the greatest
injury. Urgent surgical intervention for fasciotomies and
muscle compartment explorations under regional or general
anesthesia is often indicated. Intraoperative exploration,
decompression and debridement are an essential part of early
treatment. Serial technetium-99m stannous pyrophosphate
muscle scans has been shown to be useful in assisting
determination of progressive muscle damage.34 If
fasciotomies are delayed, development of compartment
syndrome and acute renal failure is imminent along with
development of gangrene of the affected extremity (Table
10.9).
Besides early fasciotomy, fluid resuscitation demands
attention. If the urine is rose-pigmented from
hemochromogens, the urine output should be maintained at
100-125 ml/hr (1-2 ml/kg/hour) in adults or twice the normal
hourly rate in infants and young children, until gross pigment
is cleared (Figs 10.20A and B). The urine can be alkalinized
by IV administration of sodium bicarbonate to prevent
myoglobin precipitation. In severe injuries, IV mannitol (12.5
gm in an adult) is given in addition to aggressive fluid
replacement to promote an osmotic diuresis.34 Early use
of other diuretics is contraindicated.

Initial Evaluation and Resuscitation of Burn Patient
121
INITIAL MANAGEMENT OF BURNS INVOLVING
SPECIAL AREAS
The face, ears, hands, genitals and the feet have functional
and cosmetic significance that far exceeds their size. Burns
of these areas need special attention and this should be
initiated early during the treatment.
Face Burns
•
Suspect inhalation injury in patient with burns of face.
•
After proper cleansing, apply collagen sheet in a patient
with superficial partial thickness burns, if seen within 6
hours of injury.
•
Deep partial or full thickness wounds may be treated by
exposure with silver sulfadiazine cream smear or may
be covered with face mask of nonadherent dressing and
Gamgee cotton pads.
•
30° propped up position. Insert Ryle’s tube for feeding.
Eye Burns
•
History of mode of burns and eye examination.
•
Observe for singed eyelashes, eyebrows, eyelid edema,
conjunctival lacerations, corneal opacity, any foreign
body, pupil size and reaction to light.
•
If chemical injury is suspected, irrigate the eye with
Normal Saline 0.9% for 15-20 minutes.
•
Application of ophthalmic antibiotic ointment 6-hourly
reduces risks of corneal drying and infection.
•
Cover the eye with eye shield and NOT with gauze and
cotton pad.
•
Repeat examination daily to look for corneal ulcer,
abscess or other complications
•
In the event of corneal injury or with severe burns of
the eyelids, an ophthalmologist’s consultation should be
obtained.
•
Early tarsorrhaphy should be avoided as it increases lid
deformity and prevents serial examinations of the corneal
surface.
Ear Burns
•
History of burn injury and examination of ear.
•
Examine the auricle for edema, tenderness and look for
discharge from canal.
•
If blisters are present, puncture them and expel the fluid
out but avoid removing any skin which is still firmly
attached
Table 10.9: Key points for escharotomy and fasciotomy
•
Remove constricting objects
•
Immediate elevation of burned extremities
•
Perform early escharotomies on circumferential full thickness
burn
•
Consider early fasciotomies for electrical burns involving
extremities.
•
Decreasing Doppler flow signal with adequate blood pressure or
tissue pressure more than 25 mmHg means escharotomy/
fasciotomy is needed.
•
Escharotomy is performed without anaesthesia while fasciotomy
requires regional anesthesia.
•
Escharotomy must extend completely through the burnt tissue.
•
Hemostasis is obtained with pressure, cautery or microcrystalline
collagen.
Fig. 10.20B: Rapid fluid infusion with I/V mannitol and sodium
bicarbonate till urine gradually clears to its normal color –This prevents
hemochromogens from blocking the renal tubules
Fig. 10.20A: Dark reddish black urine due to myoglobinuria suggestive
of renal insult, following electric burns with gangrenous changes in
hand

122
Principles and Practice of Burn Care
Hand Burns
•
Hand burns assume a high priority from the onset of
care.
•
During the first 24-48 hours, adequate blood flow must
be ensured. The consistency, the temperature and the
presence of pulsatile flow detectable by Doppler
ultrasonography monitoring of the digital pulp should
be regularly performed. If any doubt exists, escharotomy
or fasciotomy should be performed.
•
While dressing a hand burn, each finger should be
wrapped individually with nonadherent tulle grass and
web spaces should be separated.
•
The hands should be splinted in a position of function:
the metacarpophalangeal joints at 70-90°, the
interphalangeal joints in extension, the first web space
open and the wrist at 20° of extension.35
•
The hands should be elevated to minimize edema and a
therapist should perform range of motion exercises twice
daily.
•
Deep dermal and full-thickness burns should undergo
early excision and sheet autograft closure.
Feet Burns
•
They require specific care; so admit the patient with
burns to feet (especially circumferential burns).
•
Assess the depth of the burns (Fig. 10.22). Strict limb
elevation of the involved extremity.
•
Look for capillary refill to assess vascularity.
•
Do escharotomy early to avoid gangrene of the distal
part in patients with circumferential burns. Perform
primary excision with skin grafting whenever possible.
•
Apply antimicrobial cream and paraffin gauze in web
spaces.
•
Throughout the day encourage the patient for active as
well as passive physiotherapy of ankle joint to prevent
early contracture formation.
Perineal Burns
•
Admission of this patient is necessary for specific care.
•
Assess extent and depth of the burns. Look for the skin
loss and edema.
•
Per-urethral catheterization is essential to avoid
contamination by urine.
•
Apply a layer of Silverex ointment over burnt area and
cover it with double layer of paraffin gauze and Gamgee
or keep it exposed.
•
Avoidance of any pressure on the burned auricle is
essential (no pillows). Pressure is the biggest co-factor
in the production of chondritis35 (Fig. 10.21).
•
Apply paraffin gauze into the canal and apply povidone
iodine ointment on the burnt pinna. Wrap the ear with
nonadherent dressing and Gamgee cotton pad and apply
mastoid bandage gently.
•
Most ear burns respond well to conservative treatment,
although occasionally immediate coverage of exposed
cartilage with a temporoparietal facial flap and skin graft
may be required to salvage the pinna.
Fig. 10.21: Chondritis following ear burn
Fig. 10.22: Burns of foot

Initial Evaluation and Resuscitation of Burn Patient
123
Current research suggests that early vigorous analgesic
intervention is crucial to prevent the adverse consequences
of uncontrolled pain. For example, the burn patient who
associates dressing changes with agonizing pain is difficult
to treat, even with massive doses of opioids. Prompt,
aggressive analgesia is critical to avert the cycle of pain,
anxiety and more pain and to minimize adverse psychological
effects of pain commonly encountered in burn patients.
Acetaminophen (Paracetamol) or NSAIDs with opioids
can be a basic treatment for burn pain.36 Traditional analgesic
regimens usually neglect or ignore the inflammatory
component of burn pain, but it is extremely important,
especially during early treatment. Traditional NSAIDs are
not recommended in burn patients who are scheduled to
undergo extensive excision and grafting procedures because
their antiplatelet effects may increase blood loss. However,
this class of drugs may help patients who require minimal
skin grafts to reduce pain from superficial burn areas or at
donor sites (normal skin areas where skin is harvested for
grafting). Newer NSAIDs, the cyclooxygenase-2 (COX-2)
inhibitors, offer analgesia with few side effects, including
minimal inhibition of platelet function.36 Although the effects
of COX-2 inhibitors on wound healing remain to be
demonstrated, such medications may constitute a major
advance in the treatment of burn pain. These drugs can be
introduced early during treatment to reduce peripheral and
central sensitization, decrease opioid requirements and
reduce side effects.
Closed dressing over the partial thickness burn wounds
contribute significantly to pain relief as the exposed nerve
endings are protected from external stimuli. In patients with
major burns (i.e. with > 25 % TBSA burns) analgesics
should be administered by intravenous route during early
management (i.e. 48-72 hours after injury) as absorption
by intramuscular route is unpredictable and oral
administration may not be possible. For minor burns, the
pain medication may be administered by oral route.
The medications and their recommended dosages are
as follows:
1. Morphine: It should be administered only after
resuscitation has been initiated and following precautions
should be observed
a. Do not give if patient is asleep. Do not give for sleep,
give only for pain.
b. Do not give if patient is in shock or in sepsis.
c. Monitoring of ECG, pulse, respiration and oxygen
saturation is essential.
d. Do not give if respiratory rate is less than 20 or
oxygen saturation is less than 95 %.
In adults, patient controlled analgesia (PCA) probably
provides maximum pain relief. Morphine infusion is given
intravenously using PCA pump with total dose 15
microgram/kg/hour as continuous infusion and can be
combined with patient administered boluses.
Morphine can be administered 0.03 mg/kg every 4
hours intravenously after stabilizing the patient with
resuscitation.
Oral morphine (0.1 mg/kg every 4 hours) can be
given after 48 to 72 hours post burn. This can be used
to provide relief from both background as well as
procedural pain experienced during bath, dressing or
physiotherapy.
2. Buprenorphine: An alternative for Morphine,
Buprenorphine should be administered by observing same
precautions as morphine. The dose is 300-600
micrograms slowly intravenously over 10-15 minutes
every 6 hours for adults. It is not recommended for
children under 6 months of age. For children, the
•
Administer appropriate antibiotic cover including
anaerobic organisms, according to protocol.
PAIN MANAGEMENT
Burn injuries cause one of the most intense and prolonged
pain. Burn pain is difficult to control because of its unique
characteristics, its multiple components and its changing
patterns over time 36 (Table 10.10). Cleansing wounds,
changing dressings and providing physical therapy involve
repeated manipulations of painful sites. The sometimes
excruciating pain, along with extreme intra- and inter-
individual variability in severity, complicates the task of
providing analgesia to burn patients.
Table 10.10: Unique characteristics of burn pain
•
Three major components:
1. Background: At rest in burned areas and at skin graft donor
sites
2. Breakthrough: During simple activities such as changing
position, turning in bed, or walking
3. Procedural: During wound care procedures that must be
performed daily or even several times a day; can reach
excruciating levels
•
Is highly variable among patients and within each individual
•
Can last for weeks or months
•
Does not decline over time except toward the end of
hospitalization

124
Principles and Practice of Burn Care
recommended dose is 3-6 micrograms/kg of bodyweight,
6 hourly.
3. Butorphenol: 1-4 mg every 3-4 hours, slowly
intravenously.
4. Pentazocine: Pentazocine Lactate 30 mg intravenously
3-4 hourly is recommended for adults. It is not
recommended for children below 1 year of age. Above
1 year of age, the dose recommended is 0.5 mg/kg every
6 hours.
Besides the above mentioned opioids, the following
NSAIDs can be used to provide effective pain relief.
1. Diclofenac: 1mg/kg intravenously 6 hourly as slow
infusion.
2. Tramadol: 50-100 mg intravenously slowly or as
infusion every 4-6 hours upto a maximum dose of 600
mg/day.
3. Ibuprofen: Intravenous ibuprofen is under investigation.
The oral preparation can be used in children as well as
adults in minor or moderate burns on admission and in
major burns after the resuscitation is complete. The
recommended dose is 10 mg/kg 4 hourly.
4. Paracetamol: 15 mg/kg can be used orally for
procedural pain relief.
Orally administered Acetoaminophen (15 mg/ kg) and
Codeine can be combined along with opioids for effective
pain relief in major burns.
Agents such as Ketamine, Propofol, Fentanyl, Alfentanyl,
etc. should be used for controlling procedural pain under
supervision of an anesthetist and after complete resuscitation
in a patient with major burn.
Anxiolytics such as Lorazepam or Midazolam may be
combined with opioids or NSAIDs especially for relief of
procedural pain. The recommended dose is 0.03 mg/kg slow
intravenously.
Adequate pain relief is an important but often neglected
aspect of early management of burn. If attended to
appropriately in the initial period, it contributes significantly
to sustained compliance of the patient with various treatment
procedures.
EARLY REHABILITATIVE CARE
Once the patient’s survival has been assured, function and
cosmesis become the biggest factors for subsequent quality
of life. However, if efforts to achieve these goals are not
begun early in the initial management, the ultimate outcome
may be less than desirable despite successful resuscitation
and burn wound closure. Rehabilitation of the burn patient
should begin during the acute resuscitation period and
continue until the patient’s scars mature and occupation
resumes. Rehabilitation plans are carried out principally by
the Occupational and Physical Therapists.
There are principles which must be applied soon after
burn to ensure the earliest and optimal rehabilitation of the
patient. Rehabilitative care should commence on the day
of the injury and the goals of burn patients’ rehabilitation
are:
1. To limit or prevent loss of motion.
2. To prevent or minimize anatomic deformities.
3. To prevent loss of lean muscle mass.
4. To ensure return of the patient to work or normal activity
as soon and as completely as possible.
Much consideration must be given to a program of
rehabilitation for the burn patient and every patient needs an
individually tailored plan of care. There are four principles
for the rehabilitation of the burn patient:37
•
The program should start early, preferably on the day
of injury.
•
A program of care should avoid prolonged periods of
immobility and any body part that can move freely should
be moved frequently.
•
Range of motion exercises should be started on the day
of injury.
•
There should be a planned program of daily activity and
rehabilitative care. The plan should be reviewed daily
as rehabilitative needs change.
On admission, plans should consider the prevention of
skin and muscle contracture and anatomic deformity. The
institution of such plans should be individually tailored. Early
standing and ambulation and participation in daily living
activities are important and all extremities should be actively
moved frequently throughout the day. Proper positioning
is essential for the prevention of contractures. It has not
been uncommon in the past for burned patients to develop
contractures of both burned and non-burned joints. The
incidence of contractures in healing patients has been
significantly reduced through the use of frequent active or
appropriate passive motion exercises and proper positioning.
Burned patients and their families should be taught the
importance of early active exercise and proper positioning
during rest and sleep. Standing and ambulation should be
instituted as soon as possible. Such exercise can reduce
the loss of muscle mass and help stimulate the appetite.
Frequent standing and ambulation also reduces the risks of
pressure necrosis. Additionally, requiring the patient to get

Initial Evaluation and Resuscitation of Burn Patient
125
out of bed and sit in a chair for some part of the day increases
respiratory tidal volumes and the patient’s sense of normalcy.
This provides a great psychological boost to the patient.
Detailed account of rehabilitation activities is outside the
purview of this chapter and is discussed elsewhere in this
volume.
MEDICAL RECORDS
Most of the burn patients are medicolegal cases and are to
be informed to the law enforcement authorities and
meticulous medical records are of significant value in the
court of law. Besides the routine record of history and clinical
examination, the following information should be sought
and entered in the medical records of the patient.
1. Record the time of burn, exact incident and persons
present at the site.
2. Name and relation of person bringing the patient to
hospital and providing information.
3. Record details of pre-hospital treatment, co-morbid
conditions.
4. Record the actual incident in notes and not just–‘scalds
with hot tea’ or ‘flame burns with kerosene’.
5. If the patient wishes to change the statement, record
the new statement and place signature with name, date
and time. Inform the police constable on duty about the
patient’s wish to change statement.
6. Inform the expected prognosis and patient’s condition
to the close relatives and record it on the case paper
with the signature of the relative and name with date
and time.
7. The consultant should enter his/her observations and
treatment decisions in the record in his/her own writing
with signature, date and time.
8. Detailed orders including special instructions, wound
management plan and monitoring instructions should
be recorded.
9. Details of procedures performed during resuscitation
and reports of investigations should be recorded.
SUMMARY
1. The early management of seriously burnt patients is
similar to the management of other trauma victims. Life
threatening injuries must be treated first, followed by
secondary survey. Airway, breathing and circulation
should be attended to on priority. High index of suspicion
is required for inhalation injuries. Hypothermia should
be avoided.
2. If the burn surface area is greater than 15 % in an adult
and greater than 10% in a child, intravenous fluids should
be administered to restore the circulating blood volume
in order to maintain tissue perfusion and oxygenation.
3. Sodium containing crystalloid is the fluid of choice and
the most useful indicator of fluid resuscitation is hourly
monitoring of urine output.
4. Meticulous estimation of the extent and depth of burn is
necessary for planning the wound management. Burns
of special areas deserve attention. The rehabilitative
measures should be initiated early.
5. Completeness of medical records is highly desirable.
Systematic initial evaluation, methodical application of
basic surgical principles of resuscitation and vigilant
monitoring using simple clinical parameters leads to
successful initial management of a burn patient and also
lays the foundation for ultimate satisfactory outcome.
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34. Abston S, Blakeney P, Desai M, Edgar P, Heggers J, Herndon D,
Hildreth M, Marvin J, Nichols R Jr. Electrical injuries, Resident
Orientation Manual, Produced by Galveston Shriners Burn hospital
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and The University of Texas Medical Branch Blocker Burn Unit
Feb 2000.

Respiratory Tract Injury in Burns
11
JC Suri, MK Sen
Chapter
INTRODUCTION
Injury to respiratory tract due to burns was little appreciated
prior to 1940s. A pivotal point in the understanding of
pulmonary injury in burn patients happened to be the famous
“Boston night-club fire” in 1942. Between 1945 and 1975,
several innovations took place, which went a long way to
recognize the respiratory injuries and treat these patients in
a better and scientific way. In the last two decades,
management has changed greatly and survival has become
more likely.
Injury to the respiratory tract in a patient with burns
can occur in several ways. Firstly, there may be respiratory
tract involvement in pure thermal injuries. Second, there
can be non-thermal involvement of the respiratory tract due
to inhalation of either asphyxiant gases (like carbon monoxide
and cyanide) or irritant gases (like chlorine, ammonia, oxides
of sulfur and nitrogen). Anoxia is also another principal mode
of injury in respiratory tract involvement due to inhalation.
Inhalation injuries are reported in 19-28% of all burn patients.
On the other hand, the incidence may rise to 58 % in victims
who die.
PATHOGENESIS
The principal effects of inhalation injury include asphyxia
and direct respiratory tract injury. Asphyxia can result from
hypoxia or intoxication by carbon monoxide or cyanide.
These factors can affect the patient either alone or in
combination. Direct injury to the respiratory tract can involve
the airway or the alveolar-capillary membrane. Involvement
of the airway results in upper airway obstruction,
tracheobrochitis, bronchiolitis or atelectasis. On the other
hand, alveolar-capillary membrane injury can result in
pulmonary edema due to high permeability of the membrane.
Inhalation injury has now become one of the most important
cause of death in burn patients. The mortality from smoke
inhalation alone is low (0-11%). However, in combination
with cutaneous burns, it may be fatal in 30 to 90% of patients.
It has been recently reported that the presence of inhalation
injury increases burn mortality by 20% and that inhalation
injury predisposes to pneumonia. Pneumonia has been
shown to independently increase burn mortality by 40%
and the combination of inhalation injury and pneumonia leads
to a 60% increase in deaths.
Cutaneous burns can result in pulmonary dysfunction,
chest wall restriction (e.g. circumferential neck and chest
burns) or upper airway compression. Quite often, a
combination of smoke inhalation injury and cutaneous burns
co-exist in the same patient.
Other co-morbid respiratory complications in a patient
with burns include concomitant chest trauma and
exacerbations in a pre-existing cardiopulmonary disease like
cardiogenic pulmonary edema or chronic obstructive
pulmonary disease. There may be a variety of nosocomial /
iatrogenic problems in such patients. They include
hydrostatic pulmonary edema (due to over-enthusiastic fluid
resuscitation), pneumonia (aerogenous or hematogenous),
sepsis-related permeability edema (acute respiratory distress
syndrome), drug induced conditions (hypoventilation due
to morphine or hyperventilation due to mafenide), pulmonary
embolism and complications due to artificial airways and
aspiration.

128
Principles and Practice of Burn Care
Direct injury to respiratory epithelium and alveolar
macrophages by chemicals like aldehyde that are present in
smoke can trigger inflammation. This occurs due to release
of chemotactic factors as well as activation of
phospholipase. The various chemotactic factors lead to
priming of neutrophils; entrapment of these primed
neutrophils in the pulmonary vasculature, in turn, leads to
their activation and degranulation, resulting in release of
proteolytic enzymes and oxygen radicals which cause lung
edema. Activation of phospholipase, on the other hand,
results in formation of prostaglandins (thromboxane A2)
leading to bronchoconstriction, hypoxic pulmonary
vasoconstriction and lung damage. Airway obstruction and
ventilation-perfusion mismatch also occur.
The pathological alterations induced by inhalation injury
on lung host-defenses include mucosal burns, laryngeal
obstruction, tracheobronchitis, paralysis of mucociliary
apparatus, bronchorrhea, mucosal sloughing, bronchospasm,
airway edema, atelectasis, phagocyte dysfunction, alveolitis
and a decrease in pulmonary surfactant levels. The potential
immunosuppressive mediators following thermal burns
usually include bacterial endotoxin, prostaglandins (PGE2),
endogenous glucocorticoids, cytokines (Tumor Necrosis
Factor-alpha (TNF-α), interleukins, interferon), histamine,
immune complexes, neuropeptides, autoantibodies and
suppressor peptides.
Thus, a plethora of pathological effects of burn injury
occurs on the host defenses. They can result from depression
in cell-mediated immunity, activation (and subsequent
depletion) of the complement system, suppression of
phagocyte functions (macrophage and neutrophil), release
of immunosuppressive mediators, increased consumption
of immunoglobulins, depletion of fibronectin and serum
opsonic activity and an increase in T-suppressor cell activity.
Pathophysiology of Lung Parenchymal Damage
by Smoke Inhalation
Incomplete products of combustion present, for instance,
in burning cotton, aldehydes and oxides of sulfur and
nitrogen, hydrochloric acid and carbon monoxide, etc. are
all responsible for damage to lung parenchyma. Upper airway
damage, on the other hand, is mainly due to direct thermal
injury and chemical irritation.
A gradually progressive edema of the tracheobronchial
mucosa takes place over the initial 24 hours. In the
tracheobronchial mucosa, areas of de-epithelialization are
demonstrable; in the lower respiratory tract focal areas of
congestion and edema, alternating with areas of collapse
and pneumonia are seen. Lesions in the airway range from
superficial desquamation of epithelium to focal necrosis and
formation of pseudomembranes comprising mucus, cellular
debris, fibrinous exudates, polymorphonuclear leucocytes
and clumps of bacteria. Tracheobronchial casts can
ultimately lead to respiratory obstruction. A significant
decrease in pulmonary compliance takes place due to increase
in extravascular lung water and pulmonary lymph flow.
Inactivation of surfactant results from inhalation injury,
leading to extensive microatelectasis. Microvascular injury
with increased fluid flux to interstitium and alveolar space,
resulting in profound hypoxemia and acute respiratory
distress syndrome (ARDS) can also ensue.
CLINICAL FEATURES AND DIAGNOSIS
The general impact of respiratory complications of smoke
inhalation (airway injury, parenchymal injury and late onset
problems) is significantly higher in cases who have
concomitant cutaneous burns (Table 11.1).
Fiberoptic bronchoscopy helps to confirm the diagnosis
of inhalational injury. It can identify areas of airway oedema,
mucosal sloughing or charring or soot in the upper airways.
It is the current gold standard for diagnosis of inhalation
injury in major burn centers. Rigid laryngoscopy and flexible
nasopharyngoscopy are also helpful. In addition, repeated
bronchoscopies with lavage can also be done to help in
cleaning mucosal plugs. Chest skiagrams are of minimal
help in the initial period.
Xenon lung scans can evaluate alveolar air trapping.
Simultaneous thermal and dye dilution methods can be used
to assess extravascular lung water and determine parenchymal
fluid levels. Measurements of serum carboxyhemoglobin
levels are of immense importance.
Table 11.1: Presenting symptoms and signs of inhalation injury
Relative frequency (%)
Dyspnea
3-17
Hoarseness
13-61
Throat pain
10-13
Chest pain
32-41
Cough
9-76
Hemoptysis
6-18
Carbonaceous sputum
9-80
Cyanosis
6-15
Tachypnea
25-80
Stridor
5-33
Wheezing
13-47
Rhonchi
23-52
Crackles
23-35

Respiratory Tract Injury in Burns
129
A battery of diagnostic tests is judiciously utilized in the
management of patients with involvement of respiratory
system. They include objective measurement of asphyxiants
in the blood (carboxyhemoglobin, cyanide), arterial blood
gases, chest roentgenogram, endoscopic examination
(laryngoscopy, nasopharyngoscopy and bronchoscopy),
radio-nuclide scanning, and pulmonary function tests
(spirometry).
Respiratory Complications of Smoke
Inhalations
Common clinical presentations vary from patient to patient
and depend to a large extent on the degree of burns. At one
end of the spectrum are patients with smoke exposure
without overt respiratory dysfunction and no respiratory
injury with normal objective tests. There may be sub-clinical
injury with either normal/abnormal objective tests. Various
grades of clinically overt respiratory dysfunction can be
present. At the other end, there may be cardio-pulmonary
arrest or asphyxiant death at the scene of exposure. The
various symptoms and signs include dyspnea, hoarseness,
throat pain, chest pain, cough, hemoptysis, production of
carbonaceous sputum, cyanosis, tachypnea, stridor,
wheezing, rhonchi and crackles.
In less severe cases, there is an evidence of airway
obstruction and decreased pulmonary compliance on
pulmonary function testing. After several days of injury,
endobronchial debris can lead to small airway obstruction
and atelectasis.
Pulmonary edema is a sinister end result that can result
from multiple causes. Acute respiratory distress syndrome
(ARDS) is a common case scenario in a large majority of
burn-patients undergoing treatment in tertiary care hospitals
(Table 11.2). Common risk factors associated with the
occurrence of ARDS include sepsis syndrome with or without
shock, severe trauma (thoracic or extrathoracic), pneumonia
(bacterial, viral), aspiration of gastric contents, disseminated
intravascular coagulation (DIC) and near drowning.
Occasionally, it may be associated with fluid overload, smoke
or toxic gas inhalation, extensive surface burns, fat
embolization, anaphylactic reaction to drugs and blood,
neurogenic injury, toxic drugs and poisons. It is characterized
by tachypnea, refractory hypoxemia, diffuse pulmonary
infiltrates and reduced lung compliance. Over the last decade,
several studies have suggested that survival rates for patients
with acute lung injury (ALI) or ARDS may have improved.
The diagnosis of ARDS becomes highly probable in the
presence of the following features: tachypnea, PaO2/FiO2
< 200, presence of known common risk factors, diffuse
pulmonary infiltrates on chest X-ray and reduced lung
compliance. Hematological disturbances (like coagulopathy,
DIC and thrombocytopenia), multiorgan failure, ratio of
bronchoalveolar lavage fluid protein to serum protein being
more than 0.8 and a characteristic pathology are also typical
of ARDS.
Smoke inhalation injury has been clinically graded on
the basis of bronchoscopic criteria as follows:
Grade Features
0
No signs or symptoms referable to the respiratory tract.
Absence of carbonaceous deposits, erythema,
bronchorrhea or obstruction (No injury)
1
Signs and symptoms limited to the upper respiratory
passages, including mild laryngitis. Minor or patchy areas
of erythema, carbonaceous deposits in peripheral or
distal bronchi (Mild injury)
Table 11.2: Diagnosis of ARDS
High Probability
Moderate Probability
Tachypnea
Tachypnea
PaO2/FiO2 < 200
PaO2/FiO2 < 300-350
Known common risk factors
Uncommon risk factors
Diffuse pulmonary infiltrates
Patchy or multiple segmental infiltrates
Reduced compliance
Near – normal compliance
Pulmonary hypertension
Normal pulmonary resistance
Coagulopathy(Thrombocytopenia, DIC)
Normal coagulation or only thrombocytopenia
Multiorgan failure
Only pulmonary involvement
High bronchoalveolar lavage (BAL)/serum total
BAL/serum total protein < 0.6
Protein ratios >0.8
Large protein molecules found in BAL > 70A
BAL molecular protein radii < 70A
Characteristic pathology
No pathology specimen available

130
Principles and Practice of Burn Care
2
Evidence of involvement of the trachea and bronchi or
abnormal signs in the lungs other than those of frank
consolidation. Moderate degree of carbonaceous
deposits, erythema, bronchorrhea, with or without
compromise of bronchi (Moderate injury)
3
Dyspnea, cyanosis, wheezing or transient stridor or frank
signs of consolidation. Severe inflammation with friability,
copious carbonaceous deposits, bronchorrhea, bronchial
obstruction (Severe injury)
4
Evidence of extensive pulmonary involvement or of
obstruction to the airways necessitating tracheostomy
or resulting in severe asphyxia. Evidence of mucosal
sloughing, necrosis, endoluminal obstruction (Massive
injury)
Major risk factors include house fires, explosions and
other disasters. Direct thermal damage due to flame, liquid
or steam inhalation is rare. Thus, the spectrum and time
course of respiratory problems require special attention in
all patients. Classical clinical predictors should be watchfully
monitored and they include exposure characteristics (like
closed-space setting, entrapment, unconsciousness, known
inhaled toxin), respiratory signs and symptoms, presence
of facial and cervical burns and production of carbonaceous
sputum (Figs 11.1 and 11.2).
Asphyxia manifests as altered sensorium, coma, nausea,
vomiting; upper airway obstruction as stridor, hoarseness
dyspnea, sore throat, painful swallowing, respiratory area
burns, flash exposure, pharyngeal edema/erythema; lower
airway obstruction as dyspnea, tachypnea, wheezing,
carbonaceous sputum and parenchymal injury as dyspnea,
tachypnea, crackles. Resuscitative measures for cardio-
pulmonary arrest: successful cardiopulmonary resuscitation
(CPR) (grade V); supportive measures for clinically obvious
established respiratory dysfunction (grade II to IV) and
accurate triage for exposure history [possible delayed-onset
dysfunction (grade I)] should be promptly taken.
MANAGEMENT
Management of Inhalation Injury in Patients
without Cutaneous Burns
The management of inhalation injury in patients without
burns begins with a good history and examination of the
accident scene. Circumstances of inhalation should be
examined (history of suicidal attempt); closed spaces (e.g.
building, automobiles) result in more frequent and severe
respiratory abnormalities. The severity of inhalation injury
is also directly related to the duration of exposure. The lungs
can be an efficient means for the absorption of inhaled
toxicants, resulting in airway and pulmonary injury or
systemic toxicity. The type of smoke inhaled is also an
extremely important factor. Exposure to smoke from
polyurethane foam results in severe parenchymal injury.
Time elapsed between initial resuscitation and arrival at
hospital and presence of co-morbid disease(s) (chronic
obstructive pulmonary disease, COPD; coronary artery
disease, CAD etc.) are also important determinants of
severity of diseases. A history of closed space fire,
production of carbonaceous sputum, facial burn, singed
nasal hair, perioral burn, hoarseness, stridor or pharyngeal
edema are important pointers to upper airway injury
(Figs 11.1 and 11.2).
Fig. 11.1: Case with minimal burns of face but with signs of
inhalation injury
Fig. 11.2: A 3-year-old child with deep burns of entire face with
evidence of inhalational injury

Respiratory Tract Injury in Burns
131
Airway maintenance is of prime importance. Early
intubation is indicated in case upper airway burn is present.
Airway edema increases over 12-18 hours. Nebulization
with bronchodilators, heparin (10,000 units in 3 ml N-Saline
every 4 hours), N-acetylcysteine (3-5 ml of 20% solution
every 4 hours) are also very useful steps. Indications for
endotracheal intubation include inability to protect airway,
respiratory distress, hoarseness/stridor, dyspnea, 3rd degree
facial burns, carbon monoxide (CO) poisoning and edema
of supraglottic structures.
The management of respiratory burns has two primary
components, namely, bronchial hygiene therapy and
mechanical ventilation.
The thrust areas of bronchial-hygiene therapy are as
follows:
1. Oxygenation of the patient with humidified oxygen so
as to maintain SpO2 >90% (Fig 11.3).
2. Therapeutic coughing: either voluntary or induced by
placing index and middle fingers over sternal notch.
3. Deep breathing exercises every two hours.
4. Therapeutic posturing and chest physiotherapy every
4 hours.
5. Turning the patient side to side every two hours.
6. Aerosolization of 3 ml of 20% N-acetylcysteine every 4
hours with a bronchodilator.
7. Aerosolizing 5000 units of heparin with 3 ml of normal
saline every four hours.
8. Nasotracheal suctioning as and when required.
9. Encouragement of early ambulation by post burn day 5.
10. Culture of endotracheal secretions thrice a week.
Mechanical Ventilation
Mechanical ventilation is mainly initiated in the scenario of
acute refractory hypoxemia as seen in cases of acute
respiratory distress syndrome (ARDS) (Fig 11.4). Several
modes of ventilation are available to the clinician. The mode
used should be the one which is able to support oxygenation
and ventilation. Additionally, the clinician should also be
experienced in its use.
Fig. 11.3: Patient with facial burns with element of upper airway
injury requiring only oxygenation by nasal prongs
The ARDS Network study conducted by the National
Heart, Lung and Blood Institute of US (NHLBI) recommends
the use of low tidal volumes of 6 ml/kg of predicted
bodyweight and a plateau pressure of 30 cmH2O or less
while using the volume-assist mode. If the patient becomes
obstructed due to fibrin casts and develops an acute
hypercapnia and hypoxia, pulmonary toilet should be done
and change over to higher tidal volumes is considered. Initial
flow rates of 40-100 liters per minute, inspiratory /expiratory
(I: E) ratio of 1:1 to 1:3 and FiO2 (fraction of inspiratory
O2) of 1.0 may be sufficient. Positive end expiratory
pressure (PEEP) is applied to recruit lung units, elevate mean
airway pressure and improve oxygenation. The level of PEEP
varies with the disease process. Pressure-volume curves
help in determining the optimal level of PEEP. The optimal
level of PEEP is the one that results in the lowering of
pulmonary shunt, improvement in arterial oxygenation, only
a small change in cardiac output, A-V oxygen content
differences or mixed venous oxygen tension.
Fig. 11.4: X-ray chest showing ARDS

132
Principles and Practice of Burn Care
The various modes of ventilation available are as follows:
a. Control mode, where the ventilator cycles automatically
at a rate selected by the operator.
b. Assist-control mode, where the ventilator only assists
every spontaneous breathing effort of the patient; a
back-up control rate is set. Also set are tidal volume,
inspiratory flow rate, flow waveform, sensitivity and
control rate.
c. Synchronized intermittent mandatory ventilation
(SIMV), where a pre-set number of ventilator–delivered
mandatory breaths with pre-set tidal volume are delivered
along with the facility of intermittent spontaneous
breaths. It is usually a weaning mode.
d. Pressure control mode, where a ventilator breath of
constant pressure (pressure limited, time-cycled and
pressure triggered) is delivered. The inspiratory time,
pressure limit and back up rate are pre-set by the operator.
Tidal volume is dependent on compliance of chest and
airway resistance. This mode can be used in ARDS.
e. Pressure support mode, is a pressure targeted, flow-
cycled and patient triggered breath. The patient must have
an intact respiratory drive. It is a useful weaning mode.
Newer Modes of Mechanical Ventilation
a. High frequency percussive ventilation (HFPV): It
provides ventilation at low mean airway pressure and
supports the lung-protective strategy of ventilation to
reduce barotraumas. Sub-tidal volumes are delivered in
a progressive stepwise fashion until a preset oscillatory
equilibrium is reached and exhalation is passive. A high-
frequency time-cycled pressure ventilator (VDR
ventilator) is used. The pulsatile flow rate is set at 20
cm H2O peek inspiratory pressure (PIP); the pulse-
frequency (high rate) set at 500-600. The low respiratory
rate is set at 15-20 and demand PEEP on 3 cm H2O.
The I: E ratio is set at 2:1. Settings of the ventilator can
be adjusted later, based on clinical and arterial blood gas
(ABG) parameters.
b. Inverse ratio ventilation: It involves the setting up of I: E
ratio (inspiration to expiration ratio) greater than 1:1. It
maintains a high mean airway pressure and high peak
alveolar pressure; it prolongs inspiratory time to allow
for recruitment of lung units in dependent areas of chest.
Time-constant sedation and paralysis are always required
for this mode.
c. Airway pressure release ventilation (APRV): It is a
pressure-regulated mode of ventilatory support which
allows for time-cycled decreases in pressure to facilitate
elimination of CO2.
Weaning and Discontinuation of
Mechanical Ventilation
Attempts should be made to remove the patient from
mechanical ventilation as early as possible. The criteria that
should be followed before any such attempt is made are as
follows:
1. Reversal of underlying cause of respiratory failure,
namely improvement in respiratory burn/sepsis.
2. Adequate oxygenation as evidenced by PaO2/FiO2 > 200-
250, PEEP requirement < 5-8 cm H2O, FiO2 < 0.4-0.5
and pH > 7.25.
3. Hemodynamic stability or low-dose vasopressor
requirement.
4. Presence of spontaneous inspiratory effort.
A spontaneous breathing trial with T-tube breathing for
30 minutes or pressure-support/continuous positive airway
pressure (CPAP) of 1 hour should be administered.
Respiratory mechanics should be assessed.
1. Respiratory rate < 24 in adults
2. Spontaneous tidal volume > 4 ml/kg
3. Expired minute volume < 15 liters/minute
4. Negative inspiratory force > 30 cm H2O
5. Audible leak around endotracheal balloon cuff.
Racemic epinephrine aerosolization can help in alleviating
any inspiratory stridor that may be present following
extubation (due to mucosal edema).
Late Complications of Inhalational Injury
1. Tracheal stenosis due to tracheitis, tracheal ulceration
and tracheal granuloma formation. It occurs in the region
of the endotracheal cuff (sub-glottic region). It is best
prevented by paying attention to tracheal tube-cuff
pressure, particularly in the background of hypotension.
2. Obstructive/restrictive lung disease is occasionally
observed following inhalation injury.
Spirometry, cardiopulmonary exercise testing and
rehabilitation are important aspects in the after-care of these
patients.
Carbon Monoxide Poisoning
Carbon monoxide (CO) is the most common gas liberated
during fires. It is colorless, tasteless and has an affinity for
hemoglobin that is 200 times that of oxygen. It causes
reversible displacement of oxygen on the hemoglobin
molecule. It interacts with the myoglobin of cardiac muscle
and with mitochondrial cytochrome 3 oxidase complex
leading to additional effects on cellular oxygen metabolism

Respiratory Tract Injury in Burns
133
and organ function. When combined with hemoglobin
(carboxy hemoglobin-COHb), it results in impaired oxygen
delivery to the tissues and a decrease in mixed venous oxygen
content. Clinical features may result from mild headache
and confusion in lower degrees of exposure to coma,
seizures and death in severe cases (Table 11.3). In a case of
blood carboxy hemoglobin level of 5-10%, the symptoms
include mild headache and confusion. Throbbing headache,
blurred vision and flushing of the skin occur when it rises
to 11-20% while at a level of 21-30%, the clinical
manifestations include disorientation, nausea and impaired
manual dexterity. Irritability, dizziness, vomiting and syncope
occur when the levels rise to 31-40%. In case the levels go
to beyond 50%, coma, seizures, respiratory failure and death
may ensue.
associated problems (burns greater than 40% of body
surface area (BSA), other injuries or airway compromise)
should be considered for hyperbaric treatment only if there
is no risk to life endangered by the delay in treatment of the
other problems. Hyperbaric oxygen therapy can, at times,
be associated with several complications. They include
barotrauma to ears, aspiration, seizure, hypocalcemia,
oliguria, metabolic acidosis, respiratory acidosis,
dysarrhythmias and rarely cardiac arrest. Indications for
HBO include altered mental status, loss of consciousness/
cardiac arrest at scene, focal neurological deficits, seizures,
syncope, ischemic chest pain, ECG changes, new
dysarrhythmias, COHb>25%, COHb>15% with
cardiovascular/cerebrovascular disease, pregnancy with
COHb>10% or with signs of fetal distress.
Cyanide (CN) Poisoning
Cyanide poisoning is usually seen with burning of
polyurethane in the construction and furniture industries. It
acts by inhibiting the final step of oxidative phosphorylation
by binding the cytochrome AA3 complex resulting in lactic
acidosis and cellular asphyxia. Exposure to cyanide results
in altered level of consciousness, dizziness, headache,
tachycardia and tachypnea. Blood levels of CN should be
measured and lethal levels range between 1.0 to 3.0 mg/L.
Any patient with positive clinical criteria or blood CN levels
greater than 0.20 mg/L should be treated. Cyanide is
normally detoxified primarily by hepatic rhodonase and
requires sulfate as a substrate. Treatment includes the
following measures (3-step CN antidote package). Amyl
nitrite is given by inhalation for 15-30 seconds each minute.
Sodium nitrite (300 mg in 10 ml) is injected over 2-4 minutes
with careful monitoring of blood pressure. These two steps
produce methemoglobin (MetHb), which combines with
cytochrome-bound-CN to yield cyano-MetHb. Sodium nitrite
injection is given to keep MetHb levels below 40%. Finally,
sodium thiosulfate (12.5 gm in 50ml of 50% dextrose) is
injected over a 10-minute period. Vitamin B12
(hydroxycobalamine) 400 μg/Kg intravenously is given to
produce inactive cyanocobalamine. Cyanide shunted to these
minor pathways must eventually be detoxified by rhodonase.
Airway obstruction associated with inhalation injury
must be treated with inhaled β2-agonists (salbutamol,
terbutaline), racemic epinephrine, aminophylline (0.5-0.9 mg/
kg/hour as infusion), and anticholinergic drugs (ipratropium
bromide). The incidence of proximal airway edema on the
modern battlefield is likely to increase with the advent of
The elimination of CO is dependent on the level of oxygen
in blood (FiO2) and the law of mass action. It occurs in
two phases: (a) a rapid distribution to other tissues and (b)
a slower excretion phase. The elimination half-life of CO
while breathing room air is 250 minutes; at 100% oxygen,
it is 40 minutes while at 2 atmospheres hyperbaric oxygen
it is 30 minutes. At 2.5 atmospheres hyperbaric oxygen, the
dissolved oxygen content of plasma alone (>5 ml/100 ml)
is sufficient to meet the basal body oxygen requirements.
The various neuro-psychiatric sequelae of CO poisoning
include Parkinsonism, cortical blindness, temporospatial
disorientation, deafness, memory changes, mental
retardation and frank psychosis.
Patients with mild to moderate exposure (COHb < 30 %,
no coma, no neurologic findings) are probably treated
adequately with 100% oxygen. A patient who is comatose
on admission, has a COHb level of greater than 30% or has
an existing neurologic deficit, is at risk for permanent
damage and a hyperbaric oxygen (HBO) chamber, if readily
available, may benefit from a dive. The patient with
Table 11.3: Signs and symptoms of CO intoxication
Carboxy hemoglobin
Clinical manifestations
level (in percent)
5-10
Mild headache, confusion
11-20
Throbbing headache, blurred vision, flushing
of the skin
21-30
Disorientation, nausea, impaired manual
dexterity
31-40
Irritability, dizziness, vomiting, syncope
41-50
Tachypnea, tachycardia
50 and above
Coma, seizures, respiratory failure, death

134
Principles and Practice of Burn Care
enhanced blast and thermobaric weapons systems. Current
military medical doctrine suggests that soldiers who are at
risk of airway closure from edema should have a surgical
airway provided. Tracheal burns caused by thermal or
chemical injuries are uncommon. They can be difficult to
manage. Acutely, they are often life threatening unless
diagnosed quickly and managed properly. Tracheal burn
injuries can lead to long-term stenosis, which requires
specialized surgical techniques and chronic therapy, often
with Montgomery T-tubes, for their proper management.
Impaired oxygenation: Other problems like
(supplemental oxygen, mechanical ventilation with PEEP,
ventilatory strategies like high frequency oscillatory
ventilation (HFOV), airway control, hypoventilation, over-
hydration (limitation of fluid intake), airway secretions
(bronchoscopic removal of secretions) should also be
addressed simultaneously.
Management of Inhalation Injury in Patients
with Cutaneous Burns
Cutaneous burns affect pulmonary function by release of
circulatory factors and intravascular hypoproteinemia. The
degree of pulmonary dysfunction depends on effective care
of the burn site (wound-care). Basic principles of
management are similar to those outlined in the section on
care of inhalation injury without burns. Additional treatment
of burn area aimed at stopping burn process, dressings and
intravenous fluids are important measures. The presence
of facial and pharyngeal burns should raise the suspicion of
upper airway injury. Early endotracheal intubation in such
cases is desirable (Figs 11.5A and B). Tacheostomy can be
performed to avoid permanent damage to upper airway or
vocal cords (Figs 11.6A and B). Patient should be weaned
off the ventilator and tracheostomy tube as early as is
possible (Fig. 11.7). Depolarizing muscle relaxants should
be avoided. Stabilization of the endotracheal tube in patients
with facial burns requires specialized skill. Controlled fluid
management with close hemodynamic monitoring,
mechanical ventilation with PEEP and chest wall
escharotomies for full thickness thorax burns are other
measures that may be helpful (Fig. 11.8). Management of
delayed sequelae includes the treatment of pneumonia and
burn sepsis. A combination of inhalation and cutaneous burn
injury leads to increased incidence of pneumonia (46%)
due to local pulmonary changes and global immuno-
suppression. Enteral glutamine administration has been found
to be helpful in burn patients.
Fig. 11.5A: Patient with facial burns with endotracheal tube in situ
Fig. 11.6A: Severe facial burns with inhalation injury—
Tracheostomy was done for ventilation
Fig. 11.5B: Same patient after 4 days of mechanical ventilation:
Edema much reduced and patient extubated and then kept on nasal
prongs only

Respiratory Tract Injury in Burns
135
Preventive measures include meticulous wound care,
pulmonary toilet, early removal of central lines and early
extubation. Susceptible individuals (inhalation injury plus >
20% BSA burn) should undergo the following additional
measures: daily WBC count, X-ray chest, and Gram’s stain
of sputum, sputum culture (every 3 days), early and effective
treatment of burn wound (excision and grafting) etc.
Pneumonia usually develops during the second week
after burn. It is evidenced by fever, sepsis, leucocytosis
and abnormal X-ray chest. Antibiotic use should be
according to microbiological data. Pulmonary toilet and
possible ventilatory support may be required. Development
of ARDS is a sign of poor prognosis.
Basic therapeutic priorities in patients with inhalation
injury are as follows (Table 11.4):
Fig. 11.6B: Same patient on ventilator
Fig. 11.7: Patient with tracheostomy, improved after mechanical
ventilation and is being weaned off gradually
Respiratory problem
Response (s)
Asphyxia
Oxygenation, antidotes
Upper airway obstruction
Early, elective endotracheal intubation (rarely, tracheostomy)
Lower airway obstruction
Mild
Pulmonary toilet
Bronchodilators
Occasional therapeutic bronchoscopy
Severe (hypoventilatory failure)
Mechanical ventilation
Parenchymal injury
Mild
Supplemental oxygen (e.g. Low FiO2 achievable by nasal prongs/mask)
Severe (with hypoxemic respiratory failure)
Oxygenate (High FiO2 [O2 via ET tube])
Increase lung volume (CPAP, PEEP)
Minimize ongoing leak adjustments of resuscitative fluid volumes,
composition, and infusion rates.
Table 11.4: Basic therapeutic priorities in patients with inhalation injury
Fig. 11.8: Escharotomy incisions on chest in case of full thickness
circumferential chest burns