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Burn and its Management.

Dr.Barin Bose MS, FACRSI.
Consultant Surgeon.
Jabalpur Hospital and Research Centre.
JABALPUR. (M.P.)


The arrival of the victim of a burn accident at the emergency department is one of the most dramatic events in surgical practice. The suddenness of the accident, visibility of the damage, the pain, fear and the reaction of the patients relatives all combines to create an atmosphere of tension.

The immediate need of resuscitation and pain relief may interfere with assessment of the patient with history and examination. However the history of mechanism of burning is of major importance, in assessing its severity. The severity of the burn is estimated from the area of the burn surface and the depth of the burn wound.

On arrival a burn patient should be treated as other trauma case. ABC that is the airway, breathing and circulation applies as usual. If there is burn around the nose and mouth possibility of flame inhalation must be considered. Laryngeal edema can develop rapidly and lung function may dereriorate. Endotracheal intubation should be considered early, before laryageal edema sets in. If laryngeal edema develops endotracheal intubation is difficult and at times impossible. Then a surgical airway will be needed immediately.

Type of injury

The Primary Injury - It is the immediately damage caused by the burn. Little can be done to limit the primary injury in most cases of trauma. However a promt removal of the heat source and rapid cooling of the burn limits the extent of primary injury.
The Secondary Injury -It is the deleterious effect resulting from the primary injury. A major burn can result in loss of fluid, secondary infection , endogenous and exogenous release of toxins, powerful inflammatory response, fluid shift, coagulopathy, oedema, constriction caused by burn eschar.

Jackson's Burn Model - A burn wound is dynamic and subject to the effect of secondary injury. The burn may deepen if the blood supply of the wound is impared. Example by- hypovolaemia, hypotension or if infection occurs. Jackson's model describes the distinct areas within every burn wound.
(a) Centrally lies the zone of coagulation, which represents the zone of severe damage caused by primary injury, these tissue will not recover and will slough out in due course of time.
(b) Surrounding this lies the zone of stasis which comprises of less damaged tissue in which inflammation occurs and vascularity is impaired. Tissue in this zone have the potential to recover under correct conditions
(c) The outer layer the zone of hyperaemia is tissue with intense vasodilation and increased blood flow. The margins between the zone are not static they are influenced by local and systemic factors, reduced blood flow,excessive oedema tends to extend the zone of coagulation and hence the area of tissue necrosis. In favourable conditions the margin of the central zone remains static and the zone of stasis shrinks as it is replaced by the zone of hyperaemia.


Fig. 1. Jacksons Burn Model.


Assessment of the burn area - A widely used clinical rule- The rule of nine acts as a rough guide to the body surface involvement. As a general rule an adult with more than 20% of the burn surface area involvement, or a child with more than 10% of the body surface area involvement will require intravenous fluid replacement. However an intravenous line may be necessary to achieve adequate analgesia for much smaller burn and in children fluid replacement may be required because of vomiting.

The prognosis depends upon the percentage of body surface area burned. A rough guide is that, if the age and percentage of burned is added together and the score of 100 or above than the burn is likely to be fatal.

A child can survive a larger burn but a small burn in elderly patient is potentially fatal.

The rule of nine - May be used to estimate the total body surface area burnt. By adding together the affected area the percentage of the total body surface that is burnt can be calculated. This rule does not apply to infants and children. The patient own hand (fingers and palm) is 1 % body surface area.

Fig. 2.

Assessment of the depth of burn - The burn depth depends upon -
(a) The temperature of the burning agent.
(b) The mode of transmission of heat.
(c) The duration of contact.
Superficial Burn -
(1) Superficial epidermal burns look red are painful blisters are not present. They heal themselves by epithelisation.
(2) Superficial dermal burns - Are blistered painful and they heal by epithelisation without scarring.

Deep Burns - These have lost all adnexal structure and if left can only heal by secondary intention with scarring.
(a) deep dermal burn- May be blistered and have a blotchy red appearance with no capillary return on pressing and abscent sensation to pin prick.
(b) Full thickness burn - Have white or charred appearance called escar. Again with loss of sensation.

Depth of burn is important in the assessment of a burn injury to -
(1) It has important implications for the remaining blood supply.
(2) The remaning skin elements from which re epithelization can occur . (3) Tissue elasticity (particularly in circumferential burns).
These factors determine the healing time, management options and associatiated complications.



Deeper burns causes loss of tissue elasticity and their coagulated protein results in eschar contration. If deep burn cover a significant circumference of the neck, limb or thorax the resultant contriction has a dangerous result over airway , distal blood supply respectively.

To avoid secondary injury, escharotomy ( surgical incision extending through the full thickness of the burn eschar, often to deep fascia ) are done. The incision are made at conventional site as shown in the Fig 7 to release constrictions.

Fig. 7.

Mechanisms Of Injury - Burn is a tissue injury from thermal application or absorbtion of physical energy or chemical contacts.
Scald - Hot water produces a well defined type of skin damage. As the temperature of boiling water is constant (100o C) the determinant of severity of injury is the duration of its contact with the skin. In home spills from kettle or cooking pot are common injurys.
Spills - Cools rapidly, thus limiting the duration of damage.
Immersion - In boiling water or prolonged steam exposure are particularly dangerous and likely to cause deeper burns.
Fat Burns - Cooking fat or oil has much higher temperature (180o C) than boiling water and secondly hot fat cools slowly on the skin surface. Such spills therefore causes deep burns.
Flame Burns - They often occur in confined space and is often associated with inhalation injury When clothing ignites there is a prolonged flame contact with skin resulting in deep burns.
Electrical Burn - The passage of electric current through the tissue causes heating resulting in tissue damage. The amount of heat produced depends upon
(1) Resistance of the tissue.
(2) Duration of contact.
(3)Square of current.
Bones are poor conductor of electric current where as blood vessels, nerves and muscles are good conductors. Bones therefore become very hot on passage of current causing secondary damage to the surrounding tissue near to the bone . Low voltage current from domestic supply (240 V) causes significant contact wound and may induce cardiac arrest, but no deep tissue damage. High voltage current ( > 1000V) causes damage by two mechanisms- (1) Flash (2) Current transmission. Flash from an arc causes cutaneous burn but will not result in deep damage. High voltage current transmission result in cutaneous entrance and exit wounds which are deep burn. Lightening causes very high voltage for very short duration discharge. A direct strike has a high mortality but a side strike causes superficial burns to the skin and deep exit burn to the feet. Internal damage is not common but respiratory and cardiac arrest can occur.
Cold Burn - Tissue damage from cold can occur from spills of liquid nitrogen or cooking gas. The injuries cause acute cellular damage with either partial of full thickness burn. Frost bite is due to prolonged exposure to cold and there is often an element of ischaemic damage. Vasoconstriction reduces the resistance of the tissue to cold exposure as the warming effect of the circulation is reduced. There is combined tissue damage from freezing and from vasospasm.
Friction Burn - The tussue damage in friction burn is due to a combination of heat and abrasion.
Ionising Radiation - X irradiation may lead to tissue necrosis. The tissue necrosis may not develop immediately. Of grater significance is the long term cumulative affect of ionizing radiation in the induction of skin cancer.
Chemical Burns - Numerous chemical in industrial and domestic situations can cause burns. The tissue damage depends on the strength and quantity of the agent and the duration of contact with the skin. Chemicals causes local coagulation of protein and necrosis, but some chemical have systemic effect ( example liver and kidney damage). The harmful effect of chemicals will coutinue until chemical is diluted or neutralized with running water.

Effects Of Burn Injury - The effect of the burn injury on the patient can be considered as -
(a) Local.
(b) Regional.
(c) Systemic.

Local Effects -
(1) Tissue damage - Heating af tissue results in cell necrosis. In the peripheral cells may be viable but injured.There is damage to the peripheral microcirculation occurs. The capillaries are either thrombosed where the damage is severe or in less damaged area there is increased capillary permeability such that the tissue become oedematousand there is external leakage of serous fluid. The essential difference between a partial thickness and full thickness skin loss is the depth of injury.But it is possible that a partial thickness may progress to full thickness skin loss.
(2) Inflammation - There is a marked and immediate inflammatory response. In the area least damaged by burning is manifested by erythema . The precise cause of this vasodilatation is neurovascular response to trauma. Mild area of erythema resolves within a few hours. Severely damaged tissue develops a prolonged inflammatory response. Macrophages produce inflammatory mediators and cytokines and phagocytose necrotic cells. Neutrophils protects against infection. Damaged tissue separates by a process called desloughing which completes by 3 weeks.
(3) Infection - The damaged and dead tissue acts as a nidus for infection . Burn wounds will almost always be infected by micro-organisms within 24 to 48 hours.There may in addition be a bacteraemia and septicaemia. Bacteraemia is a common cause of fatality in severe burns.

Systemic Effect From Burning -
(1) Fluid loss - Fluid loss from the damaged capillaries either by visible external loss or internally into the tissue from oedema in the region of burn. In addition there may be more extensive oedema of the region or even of the entire body which is mediated by the cytokines acting on the microcirculation. Thus prevention of hypovolaemia is the most important function in early burn resuscitation. Effective fluid replacement will minimise the risk of other systemic complications .
(2) Multiple organ failure - There may be progressive failure of renal or hepatic function or heart failure. The precise cause of these complication is uncertain and has often been attributed to fluid loss, toxaemia from infection.
(3) Inhalation Injury - These occur in those trapped in enclosed space. They are particularly common in association with burns of the head and neck. The inhalation of hot gases cause thermal burn to the upper airway. This is manifested early by stridor, hoarseness, cough and respiratory obstruction . Inhalation of product of combustion causes a chemical burn to the bronchial tree and lungs. This is manifested by hypoxia , Acute Respiratory Distress Syndrome (ARDS) and respiratory failure. Carbon monoxide displaces oxygen from haemoglobin to form carboxyhaemoglobin thus reducing oxygen carring capacity of blood.
Systemic Complication in association with burn such as Curling's ulcer that may results in haematemesis. Immunosupression increases the risk of septic complication.
Nonspecific Complications - Includes urinatory tract infection due to catheterisation, deep vein thrombosis and pulmonary embolism.

Management Of Burn Patient

First Aid -
(1) Stop the burning process, flames from burning clothing or from burning inflammable substances on the skin surface shouls be extingwished by wrapping the patient in a fire blanket. In electrical burn any live current is to be switched off.
(2) Cooling the burn surface - Immediate cooling of the part should continue for 20 minutes. Irrigation with cold water is useful in chemical burn. Hypothermia should be avoided , do not use ice or ice water. Ideal temperature of cooling water is 15 o C. The burn is wrapped in a clean linen and transported to hospital.

Emergency Treatment - The management of major burn injury is -

1. A - Airway.
2. B - Breathing and ventilation.
3. C - Circulation.
4. D - Disability - neurological status.
5. E - Environmental control - keep warm.
6. F - Fluid resuscitation.
In severe fascial and neck burn early endotracheal intubation or tracheostomy should be considered. Early escharotomy is needed in circumferential chest and limb burns where respiratory or circulatory disturbance is observed. Altered consciousness may due to
carbon monoxide poising.

It is important to take a detail history of patient with burn injury. A detail physical examination and examination of burned area is carried out. Good notes and drawing of burn areas are needed. Small burns may be managed on an out patient basis with arrangement for further dressing either at a hospital followup clinic or by a general practioner.Patients with major burns should be treated in a burn unit. Indications for referral to burn units are -
1. Burn requiring fluid resuscitation.
2. Burn of face, hand, feet, perenium and genitalia.
3. Full thickness burn > 5% of total body surface area.
4. Circumferential limb or chest burn.
5. Electric burn.
6. Chemical burn.
7. Burn in children and elderly.
8. Associated medical condition or pregnancy.
9. Associated other trauma.

Fluid resuscitation - It is important to secure a large bore intravenous line. Blood samples are taken for Haemoglobin,urea , electrolyte and grouping cross matching. Blood gas and blood analysis for carbon monoxide are required in unconscious patients. There are many guids to fluid resuscitation, the most widely used in UK is the-
Parkland Formula - (Fig. - 8) Resuscitation fluid volume for the first 24 hours -
3 to 4 × total body surface area (%) × body weight. Half of this fluid is given in first 8 hours and other half is given over remaining 16 hours. Hartmann solution is used , but other isotinic fluid may be used. The above formulae are only guide and the adequacy of fluid resuscitation is best monitered by clinical assessment. Urinary output is the best guide to adequate tissue perfusion, in an adult one should aim at 30 to 50 ml of urine output / Hr.



Fig. 8.



Fig. 9.

The skin is the largest organ in the body representing about 16% of the adult body weight . Damage from burn result in fluid loss by (a) Evaporation (b) By exudative fluid. These losses are approximately in proportion to the size of burn injury as assessed by total body surface area (TBSA). The fluid shift results in systemic oedema in burn involving > 25% of TBSA. A large capillary leak of intravascular fliud occurs over first 36 hours after injury. This leak is also sufficient to allow the passage of smaller macromolecules notable albumin into the extravascular space. When colloid solution are used in the resuscitation of patient with major burn, the colloid leaks into the extravascular space and thus alters the intra and extra vascular osmotic pressure and prolongs edema, which impairs tissue function and healing. Hence crystalloid solution is favoured over colloid solution for the early management of burn.
As a rule intravenous fluid is required by children aged < 12 years and with > 10% TBSA injury. In individuals aged > 12 Years and with > 15% TBSA injury .
Hartmann's solution is given for burn resuscitation. The correct balance should be maintained between too much and too little fluid In most instances urinary output is used as primary guide.

Temperature - Major burns interfere with the thermoregulatory function of the skin. Burn causes local hyperaemia, raising the temperature of the skin surface. Heat is lost by radiation and convection . Breach in integrity result in heat lost through the latient heat of evaporation . All these heat loss result in fall in core body temperature. But due to hyperaemia the patient feels hot and seeks cooling despite fall in core body temperature. This process must be arrested early in burn management before the adverse effect of hypothermia impairs coagulation, cardiovascular and CNS. Patient with major burns must be kept in warm and humid environment.
Nutrition - Patients with major burn should have a wide bore nasogastric tube passed early in their resuscitation,this decompress the stomach and enables a high calorie diet to be given. Nutrition requirement after burn exceeds those for any other type of trauma, delay or failure to meet this requirement impairs healing, increase catabolic response to injury and increase the risk to infection. Ryles tube feeding should be started as early as possible with the help of a dietitian.
Dressing - dermal burns with erythema and no blister do not require dressing. Burns of the face are generally treated by open dressing because of difficulty of dressing. Where there is much crust it is necessary to apply an ointment. Burns of the trunk and limbs are usually dressed. Burn should be inspected by a doctor to check the area and depth before application of dressing. Superficial dermal burns with blisters are usually dressed to absorb exudate, prevent desiccation, provide pain releaf, encourage epithelisation and prevent infection. Most major burns are treated with daily silver sulphadiazine ointment dressing.
Infection - There is a controversy about the use of routine antibiotic administration. A burn surface will become colonized by micro organisms within 24 tp 48 hours.There may in additionbe a bacteraemia and septicaemia and metastatic infection may develop at other sites.Bacteraemia is a common cause of death in severe burn. The administration of a broad spectrum antibiotics on a routine basis is likely to produce resistant organism. Children suffering from burn wound are often given routine antibiotics to prevent the possibility of metastatic infection.Almost any organism may colonise a wound. Betahaemolytic streptococci are likely to delay healing and should be treated. Staphylococcus aurens is a frequent pathogen. Pseudomonas grow on raw surface. These organisms are best treated by local antiseptic preparations , although if there is evidence of cellulitis, antibiotics should be administered . Frequent swab cultures is to be taken and if there is fever blood culture should be taken. Monitoring the onset or progress of infection should consists of -
1. Daily temperature measurement.
2. Frequent wound swab culture.
3. Wound inspection by a doctor at the time of dressing.
4. Blood culture.

Surgical Treatment - Partial thickness burns should heal without surgical intervention, but full thickness burns require surgical management. There are two alternative treatment for deep burns.
(1) One can wait for spontaneous desloughing and apply split thickness skin graft at 3 weeks. This policy has the advantage that early operation can be avoided, but has the disadvantage of slow healing and greater scarring.
(2) Alternatively early excision of the burn is carried out with the application of skin cover by a skin graft or a flap. This has the advantage of obtaining rapid healing and early restoration of function and at the same time minimises the risk of adverse scarring. Where facilities allow the policy of early operation for deep burns is preferred. Early excision and skin grafting is the technique used for deep dermal burns, usually preferred within 48 hours.This technique requires considerable experience in the interpretation of the wound bed.The layers of the burned tissue are shaved with a split skin grafting knife until a healthy bleeding bed is reached,upon which the partial thickness skin grtft is applied. The healing process of deep dermal burn can be expedited by this method with no scarring. Surgery of this is associated with considerable blood loss, limbs should be operated with the assistance of a tourniquet. On the trumk it may be necessary to use a diluted infusion of adrenaline subcutaneously. After excision of the burnt tissue,skin cover is given by split thickness skin autograft cover. This is removed from a donor site on an unburned area of skin. Care should be taken to produce the least possible cosmetic deficit. With extensive burn, the thighs are the first choise and other sites on the limbs and trunk may be used as donor sites. The skin graft can be meshed to expand its area.The skin can then be stretched and the cut ends opened out into small diamond shaped wounds. Meshed skin also has the advantage that it allows free drainage of fluid from beneath the graft area.

Surgical reconstruction of burn injury - The major complication of burn injury is scarring. Hypertrophic scar or Keloid scar can be prevented by the application of pressure, and patients are routinely given Lycra pressure garments to wear continuously for 14 months. Where burn scar crosses a joint, contractures may occur. Later surgical reconstruction may be needed to release these contracture.


Mobilisation and Rehabilitation - early excision and skin cover and early mobilisation of the patient reduces the incidence of complication such as infection and deep vein thrombosis. Now a days most burn units have an intensive program of physiotherapy and mobilisation without which the limb would progress to joint contracture.