It is important to understand what happens to the skin and the body after a burn in order to treat the injury properly. When you provide the right emergency care quickly and effectively, the patient’s wound has a better chance of healing.

Burn injuries are complex wounds that most commonly affect the upper extremities (the arms, head and neck) and the trunk. There are two ways to look at the pathophysiology of these burns:

Local response to burn injury

The direct effect of heat on the tissue causes cellular proteins to coagulate. The body reacts to the burn, and this reaction influences the circulation in the wound and surrounding area.

The Jackson Model of Burns describes three zones of tissue injury:

Zone of Coagulation

The zone of coagulation is the area of maximum damage. In this zone, the direct effect of the heat has resulted in irreversible tissue necrosis. Blood vessels are destroyed, which causes ischemia in the area. Because of this, proteins become denatured and cells die. The extent of this zone mostly depends on the temperature of the heat source and the duration of exposure.

Zone of Stasis

The zone of stasis is the area surrounding the central zone of necrosis. In this zone, there is reduced blood flow that may lead to ischemia. The circulation of the skin and subcutaneous tissue is compromised. This zone may progress to full necrosis unless the ischemia is reversed. If resuscitation is inadequate, the ischemia will worsen and therefore the burn depth will increase.

Zone of Hyperemia

The zone of hyperemia is the area surrounding the Zone of Stasis. Inflammatory mediators such as histamine, serotonin, prostaglandins and bradykinin are produced in this zone. These mediators affect vascular integrity and thereby make the blood vessels more permeable, leading to edema. The tissues of this area eventually return to normal. The zone of hyperemia may involve the whole body in major burns (i.e. adults with a Total Body Surface Area (TBSA) burned >20% and children with a TBSA burned >15%).

Systemic response to burn injury

The skin is the largest organ of the body. It isolates the interior from the outside environment chemically, thermally, biologically and mechanically. A burn injury affects these functions, which causes inflammatory mediators to be released and neurons to be stimulated.

In large burns (>15% TBSA burned) the following general effects occur, which are often clinically significant:

The circulation is affected due to loss of water, electrolytes and proteins (mainly albumin), causing increased vascular permeability. This results in hypovolemia and the formation of edema. Correction of hypovolemia during the shock phase may be life-saving in the first few hours after the burn.

A hypermetabolic response is characterized by tachycardia, hypertension, peripheral insulin resistance and increased protein and lipid catabolism. This leads to an increased resting energy expenditure, hyperthermia, total body protein wasting, muscle wasting and stimulated synthesis of acute-phase proteins (e.g. cortisol, catecholamines and glucagon).

Immunosuppression increases the risk of infection due to depression of the immune mechanism.

Impairment of barrier function of the gut leads to translocation of bacteria. Early enteral feeding can prevent this.

Systemic inflammatory response affects the lungs, resulting in Acute Respiratory Distress Syndrome (ARDS), even when no inhalation injury has occurred.

Long-term growth changes in children due to an increased central deposition of fat, decreased muscle growth, decreased bone mineralization, and decreased longitudinal growth of the body.