pathophysiology of burns
Major thermal injuries are accompanied by marked pathophysiological and immunological changes. These have been extensively detailed by Arturson (1985 pp.129-146) and Britto et al (1999 pp.103-112).
The burn wound syndrome (Adapted from Arturson 1985)
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the burn wound
- oedema with fluid/ electrolyte losses
- leads to hypovolaemic shock if fluid resuscitation not carried out
- wound infection
- hypermetabolic state (catabolic)
- pronounced weight loss
- multiple organ dysfunction/ failure
- pulmonary insufficiency (airway damage/ hypoxia/ respiratory failure)
- renal insufficiency (dehydration/ direct effects of myoglobin and haemoglobin metabolism)
- gastro-intestinal tract (dilatation/ ileus/ ulceration during recovery)
The effects of heat
As temperature rises, proteins are at risk of being denatured. Over 40°C cells begin to malfunction, and over 45°C cellular repair mechanisms fail and cells die. When temperatures reach 60°C vessels thrombose and tissue becomes necrotic. An object heated to 70°C will cause burning within 1 second (Cooper 2003 p.184).
Surviving tissues are then confronted with the acute inflammatory response, which results in the increase in capillary permeability that gives rise to the massive loss of fluid and electrolytes from the burn injury surface.
The thickness of skin affects susceptibility to burning – the skin on the palms of the hands and that on the soles of the feet, for example is thick and more resistant to burning than that of the forearms etc.
Where the area of burn wound exceeds 20% total body surface, there is a risk that the protective inflammatory response becomes counter productive, with pro-inflammatory mediators ‘flooding the system’ and overwhelming the body. The systemic inflammatory response syndrome (SIRS) is the common end-point of a number of bodily insults, including trauma, sepsis and burns, and a major source of mortality in critical care medicine (Greaves et al 2001 p.205).
Rigorous fluid resuscitation and infection prevention and treatment is required, with organ system support as required. This management starts at the triage stage, through an assessment of suitability for burn centre transfer, to the Advanced Trauma Life Support system of acute medical management (ABCDE etc) (Britto et al 1999 pp.101-104).
Mortality prediction
Several tools have been developed with which to attempt to estimate the probability of death from burn injuries. These tools assist in the audit of care.
Ryan et al (1998 pp.362-366) describe one such method of assessing risk of mortality and hospital length of stay for burn patients attending Massachusetts General Hospital and the Shriners Burns Institute in Boston, USA. The prediction tool relies on the presence or absence of 3 risk factors;
- burn size >40% body surface area
- >60 years of age
- presence of inhalation injury
Patient mortality is then calculated as 0.3% with no risk factors; 3% with 1; 33% with 2 and 90% with all three factors.
references
- Arturson M.G. (1985), ‘The Pathophysiology of severe thermal injury’, Journal of burn care and rehabilitation 6:129-146
- Britto J.A., Moganasundram S., Phipps A.R. (1999), ‘Thermal, chemical and explosive injuries’, Chapter 10 in ‘Trauma : A Scientific Basis for Care’, Alpar E.K., Gosling P. (Ed) Arnold Publishing
- Cooper P.N. (2003), ‘Injuries and death caused by heat and electricity’, Chapter 14 in ‘Forensic Medicine: Clinical and Pathological Aspects’, Payne-James J.J., Busuttil A., Smock W. (Ed) 2003 Greenwich Medical Media
- Greaves I., Porter K.M., Ryan J.M. (2001), ‘Trauma Care Manual’, Arnold Publishing
- Ryan C.M., Schoenfeld D.A., Thorpe W.P., Sheridan R.L., Cassen E.H., Tompkins R.G. (1998), ‘Objective estimates of probability of death from burn injuries’, NEJM 338: 362-366