Jackson’s Burn Wound Model provides a model for understanding the pathophysiology of a burn wound. Primary injury is the zone of coagulation nearest to the heat source . This zone has irreversible tissue necrosis at the centre of the burn due to exposure to heat, chemicals or electricity. The extent of the injury is dependent on the duration and the temperature of exposure .
Zone of Ischaemia is the zone surrounding the central zone of necrosis in which there is a reduction in the dermal circulation. This is a damaged but potientially viable tissue. This ischemic zone may progress to full necrosis unless the ischemia is reversed. If the ischemia is not relieved, for example when resuscitation and wound care are suboptimal, then persisting ischaemia will worsen, and the burn depth will increase.
The third zone of hyperaemia is at the periphery of the burn characterised by a reversible increase in blood flow and inflammation. Fig.5. JACKSONS ZONESOF TISSUE INJURY.
BURN CENTER REFERRAL CRITERIA [7]
A burn center may treat adults, children, or both.
Burn injuries that should be referred to a burn center include:
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. Third degree burns in any age group. 4. Electrical burns, including lightning injury.
5. Chemical burns.
6. Inhalation injury.
7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality. 8. Any patient with burns and concomitant trauma (such as fractures) 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 will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols. 9. Burned children in hospitals without qualified personnel or equipment for the care of children. 10. Burn injury in patients who will require special social, emotional, or rehabilitative intervention. BURN SHOCK RESUCITATION The history of burn resuscitation began over a century ago. However complete appreciation of fluid loss severity in burns was not apparent until the enlightening studies of Frank P Underhill[8], who studied the victims of Rialto Theatre fire in 1921. His concept that burn shock was due to intravascular fluid loss was further elucidated by Cope and Moore,[9] who conducted studies on patients from the Coconut Grove disaster in 1942. They developed the concept of burn edema and introduced the body-weight formula for fluid resuscitation of burn patients. In 1952, Evans[10] developed a burn surface area-weight formula for computing fluid replacement in burns which became the first simplified formula for fluid resuscitation for burn patients. Surgeons at the Brooke Army Medical Centre modified the original Evans formula and this became the standard for the next 15 years. A number of methods for accomplishing adequate volume replacement therapy have been advocated in the more than 40 years since the introduction of the Evans’ formula in 1952. The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid oedema formation, due to vasodilation, increased microvascular permeability, and increased extravascular osmotic activity. These reactions are due to chemical mediators of inflammationand to the direct heat effect on the microvasculature. Histamine release is the cause of earliest stage of vasodilatation and increased venous permeability . Oxygen-free radicals which are released from polymorphonuclear leucocytes cause damage to the cell membranes and would activate the enzymes catalyzing the hydrolysis of prostaglandin precursor. This results in rapid formation of prostaglandin . Norepinephrine release is inhibited by prostaglandins and may thus be of importance in controlling the adrenergic nervous system which gets activated in response to thermal injury. Increase in vacuoles number and open endothelial intercellular junctions are the morphological interpretations of the changes in the functional ultrastructure of the blood lymph barrier following …show more content…
Consequently, the volume predicted by a resuscitation formula must be altered according to the individuals response to therapy. In optimizing fluid resuscitation in severely burned patients, the amount of fluid should be just enough to maintain vital organ function without causing iatrogenic pathological