Pathophysiology and types of burnsBMJ 2004; 328 doi: https://doi.org/10.1136/bmj.328.7453.1427 (Published 10 June 2004) Cite this as: BMJ 2004;328:1427
- Shehan Hettiaratchy, specialist registrar in plastic and reconstructive surgery,
- Peter Dziewulski, consultant burns and plastic surgeon
- Pan-Thames Training Scheme, London
- St Andrews Centre for Plastic Surgery and Burns, Broomfield Hospital, Chelmsford
Understanding the pathophysiology of a burn injury is important for effective management. In addition, different causes lead to different injury patterns, which require different management. It is therefore important to understand how a burn was caused and what kind of physiological response it will induce.
The body's response to a burn
Burn injuries result in both local and systemic responses.
The three zones of a burn were described by Jackson in 1947.
Zone of coagulation—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.
Zone of stasis—The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults—such as prolonged hypotension, infection, or oedema—can convert this zone into an area of complete tissue loss.
Zone of hyperaemia—In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion.
These three zones of a burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.
The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area.
Cardiovascular changes—Capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of tumour necrosis factor α. These changes, coupled with fluid …