MANAGEMENT OF BURN INJURIES

Dr. LAWAL G.D

Registrar, dept. of Surgery, NHA
OUTLINE
• INTRODUCTION
• EPIDERMIOLOGY
• AETIOPATHOGENESIS
• MANAGEMENT - Initial Assessment and Resuscitation
-Management of Inhalational injury
-Wound Care
-Nutritional Support
-Pharmacological Support
-Rehabilitation and Re-integration
• COMPLICATIONS
• PROGNOSIS
• EMERGING TRENDS
• CONCLUSION
INTRODUCTION
• Burns are one of the most devastating conditions
encountered in medicine.

• The injury represents an assault on all aspects of the

patient, from the physical to the psychological

• >90% of burns are caused by carelessness or

ignorance and are completely preventable.
INTRODUCTION (contd)
• Burns patient often require years of supervised
rehabilitation, reconstruction and psychosocial support.
The quality of burn care is no longer measured by only
survival but also by long-term function and appearance.

• The goal for any burn management is a well healed

durable skin with a normal function and near normal
appearance.
DEFINITION:
• A burn is tissue injury from thermal (heat or cold)
application or from the absorption of physical energy
or chemical contact. More than 90% of burn injury is
from thermal application

• It can also be defined as the coagulative necrosis of

skin ( and sometimes deeper tissues ) following
contact with injurious agents
EPIDEMIOLOGY
• Varying incidence worldwide

• Incidence Increasing in the last 3 decades- a major cause being

terrorists activities in recent times .

• In the United Kingdom about 250 000 people are burnt each year.
Of these, 175 000 attend accident and emergency departments,
and 13 000 of these are admitted to hospital.

• Mortality and Morbidity: Reducing in developing countries. This is

due to reduction in poverty, ignorance, illiteracy, and the advances
in technology; No real change in sub-Saharan Africa and other
poor nations
EPIDEMIOLOGY (contd)

PREDISPOSING FACTORS:
• Extremes of age (<3yrs, >60yrs)
• Male sex/adolescence
• Compromising factors such as alcoholism, epilepsy,
chronic psychiatric or medical illness/disability
AETIOPATHGENESIS
The common burns are :
• scald- hot water, hot soup, hot oil, hot tar/asphalt etc.

• flame/dry heat- house fire, petroleum product

explosion, road traffic accident, bomb blasts etc

• contact with-hot metals, hot plastic, hot objects, caustic

chemicals, electricity etc
AETIOPATHGENESIS (contd)
MEDIATORS OF THE BURN RESPONSE INCLUDES:
• Cytokines
• Oxygen radicals
• Arachidonic acid metabolites
• Endotoxins
• Others- Cathecholamines, Aldosterone, Growth hormone, 5HT,
Histamine, Thyroxin, Cortisol, Glucagon, Insulin
EFFECTS OF THESE MEDIATORS
• Alter vascular permeability
• Catabolism of muscle
• Production of anaemia
• Initiate wound healing
• Produce fever
• Cause RBC haemolysis
• Disrupt interstitial matrix
THE BODY’S RESPONSE TO A BURN
Extent of initial burn injury is determined by ;
• The temperature of the burning agent
• The duration of contact with agent
• The consequent inflammatory reaction

Effect on the skin (Local Injury):

Coagulative necrosis, Disruption of basement membrane,
Blistering, Vascular changes, 3 zones (Jacksons burn zones of
injury)- coagulation, stasis, hyperaemia
JACKSONS BURN ZONES OF INJURY
REGIONAL INJURY
• Usually seen in circumferential burns (eschars)
• Mainly vascular (direct vascular injury is rare)
• Venous obstruction due to gross oedema
• Poor regional circulation may lead to ischaemia
SYSTEMIC INJURY
A. Fluid loss
• Initial vasoconstriction followed by vasodilation and increased
capillary leakage.
• Mediated by vasoactive agents and oxygen radicals

• There is extravasation of fluids, electrolytes and plasma to the

interstitial space- hypovolemia, (shock if severe),
Haemoconcentration-sluggish blood flow (stasis) may predispose to
thrombosis

• Fluid loss is fastest in the first 8 hours and tapers off within 24 -48
hours
• Without infection the reabsorption of oedema fluid is complete in 5-7
days
B. Renal dysfunction
• This is secondary to hypovolaemia- reduction in renal
perfusion → ↓GFR →acute tubular necrosis
• In deep burns haemoglobinuria and myoglobinuria may occur
leading to damage of the distal convoluted tubules

C. Gastrointestinal
• Mucosal damage – due to hypoperfusion →Loss of mucosal
integrity (Curling’s ulceration, GI bleeding), Ileus, Gastric
dilatation
• Translocation of gut bacteria via the portal system and
lymphatics- risk of sepsis
D. Anaemia
• Early anaemia is usually due to direct destruction
of red blood cells by heat

• Sludging from haemoconcentration or red cell

trapping following vessel thrombosis may also
contribute.

• Red cell loss is also noted following wound

dressing or bone marrow depression due to
infection
E. Inhalational injury
• Due to inhalation of noxious , irritant fumes (e.g. CO, hydrogen
cyanide )
• Acute inflammatory reaction → vasodilation, exudation and
oedema → separation of cilia from the basement membrane
→ ulceration
• Protein in the exudate form fibrin casts which adhere to the
bronchi and prevent expiration
• Release of oxygen free radicals TNF and interleukins also
damage the lung tissue
• During healing there may be loss of pseudostratified ciliated
epithelium
F. Adrenal changes
• Increased catecholamine release which helps with the
cardiovascular response to burns . They also cause
increased gluconeogenesis, glycolysis and lipolysis

G. Other systemic effects

• Increased production of ACTH and glucagon
• Negative nitrogen balance
H. Increased susceptibility to infections
• Presence of reactive free oxygen radicals destabilizes cell
membranes including the leucocytes

• Destruction of mechanical barrier

• Reduced peripheral lymphocytes

• Reduced NK cell activity

CLASSIFICATION
According to depth -based on Appearance, Blanching/Capillary refill,
Pain sensation (needle prick)
• SUPERFICIAL (EPIDERMAL)- erythema

• PARTIAL THICKNESS-
1.superficial partial thickness-blisters, pink, moist, good capillary
refill and blanches,
2.deep dermal partial thickness-dry, poor/absent capillary refill,
impaired sensation

• FULL THICKNESS- charred, densed white or brown leathery,

absent capillary refill, absent sensation
TREATMENT

Principles: Resuscitation, Repair, Rehabilitation, Re-

integration

CRITERIA FOR ADMISSION

• Burns >10% TBSA in children and >15% in adults
• Full thickness burns >5% in children and 7.5% in adult
• Inhalation injury
CRITERIA FOR ADMISSION (contd)
• Burns affecting hands, feet, face, perineum, joint surfaces
• Electrical burn
• Chemical burns
• Infected burn wounds
• Any suspected case of abuse or neglect
• Burns with other diseases
• People of extremes of life-young children and the aged
INITIAL ASSESSMENT AND RESUSCITATION
A. Manage according to ATLS protocol

ESCHAROTOMY
INITIAL ASSESSMENT AND RESUSCITATION (contd)

B. Assess the % Burnt area (helps to estimate the severity of

burn and in calculating the fliud requirement)- commonly used
method:
-Patient’s palm which is 1% of his or her body
-Wallace’s rule of 9
-Lund & Browder chart

C. Assess burn depth as discussed above

WALLACE’S RULE OF 9
LUND & BROWDER CHART
D. Fluid therapy
• Amount required in the resuscitative process estimated using
formulae.
• Various formulae available.
• Based on use of crystalloids or colloid in the resuscitative
process.
• The time-dependent variables for all of these formulas begin
from the moment of injury, not from the time the patient is
seen in the emergency department.
• Calculations for the rate of fluid resuscitation should take this
into account and reflect the decreased or increased starting
IV fluid rate.
Ringers Lactate solution
• Ideal crystalloid solution

• Preferable to normal saline for large-volume

resuscitations because its lower sodium
concentration (130 mEq/L vs 154 mEq/L) and higher
pH concentration (6.5 vs 5.0) are closer to
physiologic levels

• Has buffering effect of metabolized lactate on the

associated metabolic acidosis seen in burn injury.
Parkland formula
• commonly used
• fluid requirements estimated at approximately 4 mL/kg body weight ×
percentage burnt TBSA

• half the calculated volume given in first 8 hours post burn, with the
remaining delivered over 16 hours

• Next 24hrs: Colloids given as 20-60% of calculated plasma volume.

Dextrose in water is added and titrated in amount require to maintain a
hourly urine output of 0.5-1ml/kg/hr in adult and 1-2ml/kg/hr in children

NB: daily maintenance fluild in the form of 4.3% D/S is added in children-
they have a large surface area to body mass ratio and low glycogen store
Patients in need of higher fluid calculated from Parkland formula:
• electrical burns
• inhalational injury
• those on home diuretics
• presence of escharotomy or fasciotomy

Other formulae: Muir and Barclay ‘s, Modified Brookes; Evans;

Monafo; Shriner’s Cincinnati and Galveston (latter two formulae
being developed especially for children)
Antioxidant therapy: use of Zinc, Selenium, Vit. E and Vit. C etc have
been shown to help recovery in burn patients by stabilizing cell
membranes

E. Monitoring
-Hourly urinary output- aim for output of 1-2ml/kg/hr[n children and
0.5-1ml/kg/hr (or ≈30-50mls/hr) for adult
-vital signs temperature, pulse rate, blood pressure
-pulse oximeter
-continuous ECG monitoring in major burns
-serial determination of haematocrit, Serum electrolytes, glucose and
albumin
-doppler monitoring for compartment syndrome
MANAGEMENT OF INHALATIONAL INJURIES
Best managed in an ICU under the care of the anaesthesiologist,
burn surgeon and the chest physician

CLINICAL INDICATION FOR INTUBATION

ABSOLUTE:
-Burn of the palate, tongue and pharynx,
-Oedema of the posterior pharynx and upper glottis
- Burn of vocal cords.

RELATIVE:
- Hoarseness
- Facial burn
- Sooty sputum
MANAGEMENT OF INHALATIONAL INJURIES (contd)

• Escharotomy
• Bronchoscopy ± intubation
• Monitor arterial blood gases
• 100% Oxygen
• Nebulized adrenalin(5mg) and salbutamol (2.5-5mg)
• Positive pressure ventilation
• Repeated bronchoscopic lavage
• Incentive spirometry and Chest physiotherapy
WOUND CARE:
• Determination of depth of burns is critical
• Dressing could be by exposure or occlusive .
• Superficial partial thickness burn usually heals in 14-21 days
• Deep partial thickness burns heals in 2-6 weeks with some
scarring
• Full thickness burns takes longer to heal- complications
• Initial wound care aims to reduce bacterial load, remove dead
tissue, and prevent wound infection

• Topical antibiotic agents (Silver sulphadiazine, 0.5% silver

nitrate, povidone iodine, honey etc) are useful in preventing
wound sepsis
BURN WOUND / DONOR SITE DISCREPANCY
• Temporary skin graft- human allograft, xenograph (porcine
skin) , Biobrane etc
• Permanent skingraft- Integra, alloderm,
• Staged skin grafting

• Meshed skin grafting- allows for larger surface area to be

covered, allows for escape of bllod/plasma from beneath the
grafted skill thus reducing chances of graft uptake failure

• Biologic membranes such as amniotic membranes

• Cultured keratinocytes (skin culture)
MESHED SKIN
Treatment by exposure
• Areas that are difficult to dress: face, genitalia and perineum

• Minimally discharging wound

• To allow for frequent monitoring: finger tips

• To allow for joint movement (polythene bag on the hand)

TREATMENT BY EXPOSURE
NUTRITIONAL SUPPORT
• Patient is in a catabolic state with negative nitrogen balance.
• Necessary to enable the body to repair the damaged tissue and to combat
infection.
• This is only feasible when the patients are stabilized
• Immediate commencement of oral feeding in the absence of ileus
• TPN only when enteral route impracticable

• Daily energy requirement may be calculated using the Curreri formula- 25 ×

wgt(kg) + 40 × TBSA
(Other formulae includes: Harris-Benedict, the Toronto formula, the Davies etc)

• The protein intake should be approximately 2-3g/kg/day

• Trace elements, vitamins and essential proteins are also given
• ANTI TETANUS
• ANTI ULCER
• ANTICOAGULATION
• ANTIBIOTICS
• ANALGESICS
REHABILITATION AND RE-INTEGRATION
• Physiotherapy- Very aggressive therapy sessions; Full ROM early-
Elevation hands and lower extremity
• Prophylactic splinting
• Occupational therapy
• Psychotherapy
• Early wound closure
• Early institution of pressure therapy
• Silicone gel therapy
• Anti itch therapy
• Management of abnormal scarring, and contractures
PROPHYLACTIC SPLINTING
COMPLICATIONS
EARLY • GI haemorrhage
• Shock • Thrombophlebitis/DVT
• Respiratory • Paralytic ileus
depression • Infective endocarditis
• Wound infection • UTI
• Sepsis
• Acute renal failure
COMPLICATIONS (contd)
LATE

• Psychiatric disturbances
• Hypertrophic scarring
• Keloids
• Dyschromic scars
• Contractures/Deformities
• Marjolin’s ulcers
NEW AND EVOLVING MEANS OF MANAGEMENT
• Skin culture (Cultured Epidermal Autograft [CEA]) i.e growing
sheets of epithelium and applying it to the burn wound.
• Orcel temporary dressing- a marterial made up of layers of human
skin cells (from someone other than the donor0 and collagen from
cows. Use to dress burn wound and graft donor site for 2-3 weeks
then removed
• Tissue expanders made up of specialized balloon and inflated with
normal saline – use to cover areas burns injury
• Polychromatic light emiitting diodes use to stimulate healing of
burn wound in diabetics
PROGNOSIS
• age <3yrs, >60yrs
• TBSA >60%

• Inhalational injury

• % of full thickness burns

• Prognostic burns Index (PBI) = (age + %TBSA +

Grade of inhalational injury)- >140 unsurvivable
CONCLUSION
• A burn is the coagulative necrosis of tissue

• Proper rehydration in the first 24 hrs is important in the

management of this patient as this affects treatment
outcome and limits complications

• Good nutrition and proper wound care are essential

• The patient should be rehabilitated post burns treatment

• Giant strides being made in the search for treatment options

that will improve outcome
REFERENCES
• Grabb and Smith’s Plastic surgery 6th ed.
• Barret JP; Burns resuscitation BMJ; 392; 246-7
• Heimbach DM; Early burn excision and skin grafting
• Principles and Practise of surgery including pathology in the tropics by Badoe et al. 4th ed.
• Schwartz’s principle of surgery; 9th ed.
• emedicine.medscape.com/article/1277360/
• ncbi.nlm.nih.gov/pmc/articles/pmc30384061
• ncbi.nlm.nih.gov/pmc/articles/PMC31882641