Effects of burn injury
The effects of the burn upon the patient can be considered as:
Heating of tissue results in direct cell rupture or cell necrosis. At the periphery the cells may be viable, but injured. In addition, collagen is denatured and damage to the peripheral microcirculation occurs. The capillaries are either thrombosed where the damage is severe or in less damaged areas there is increased capillary permeability such that the tissues become oedematous and 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 the former may progress to the latter.
There is a marked and immediate inflammatory response. In the areas least damaged by burning, this is manifest simply as erythema. The precise cause of this immediate vasodilation may represent a neurovascular response similar to Lewis’s triple response. Mild areas of erythema resolve within a few hours. More severely damaged tissue may develop a more prolonged inflammatory response. Macrophages produce inflammatory mediators or cytokines (e.g. transforming growth factor-p) and phagocytose necrotic cells. Neutrophils and later lymphocytes provide protection against infection.
Damaged tissue separates by an active cellular process described as desloughing, generally complete by 3 weeks.
The damaged tissue represents a nidus for infection. Burn wounds will almost inevitably be colonised by microorganisms within 24—48 hours and this may remain as a local wound or regional infection. There may in addition be a bacteraemia or septicaemia and metastatic infections may develop at other sites. Bacteraemia is a common cause of fatality in a severe burn and may occur at any time from the first day until the point when all the wounds have entirely healed. Beta-haemolytic streptococci and pseudomonas produce protease enzymes that prevent skin graft adhesion.
Regional problems in burns
Limb circulation may be compromised. Direct damage to a main limb vessel is unlikely, although it may occur from high- tension electrical burns. If there is gross oedema in a limb following burning, the swelling and tissue tension may lead to venous obstruction. This is particularly likely where there is circumferential burn tissue (eschar) which is incapable of distending. There is also the possibility of a muscle compartment syndrome affecting the flexors and/or extensor compartments of the upper limb or any compartment of the lower limb. The circulation of the intrinsic muscles of the hand may be compromised by oedema alone and this may lead on to ischaemic fibrosis and contractures. The accumulation of large quantities of interstitial fluid in the hand will inflate the elastic tissues of the hand, tending to drive it into a claw posture (metacarpal—phalangeal joint extension, proximal interphalangeal joint flexion).
Systemic effects from burning
Fluid may be lost from damaged capillaries either by visible external loss or internally into the tissues from oedema in the region of the burn. In addition, there may be more extensive oedema of the region or even of the entire body. It is likely that this is mediated by cytokines acting on the microcirculation. Prevention of hypovolaemia is the most important function in early burn resuscitation. Effective fluid replacement will minimise the risk of other systemic complications.
Multiple organ failure
There may be progressive failure of renal or hepatic function or heart failure. The precise cause of these complications is uncertain and has often been attributed to fluid loss, ‘toxaemia’ from infection, or uncontrolled overreaction of the inflammatory response to sepsis. Multiple organ failure may, however, occur without obvious systemic infection.
These occur in those trapped in enclosed spaces. They are particularly common in association with burns of the head and neck. Various parts of the respiratory tract may be injured. The inhalation of hot gases causes a thermal burn to the upper airway. This is manifest early on by stridor, hoarseness, cough and respiratory obstruction. Inhalation of the products of combustion causes a chemical burn to the bronchial tree and lungs. This is manifest by hypoxia, acute respiratory distress syndrome and respiratory failure; it may be of delayed onset. Systemic absorption of, in particular, carbon monoxide (but also hydrogen cyanide from burning plastics) causes poisoning. Carbon monoxide displaces oxygen from haemoglobin to form carboxyhaemoglobin, reducing the oxygen-carrying capacity of the blood. It also has intracellular effects. Patients who survive the original incident may arrive confused or unconscious. Inhalation injury has an additive effect on mortality in all burns.
There are well-documented systemic complications in association with burns such as Curling’s (gastric or duodenal) ulcer that may result in acute haematemesis. Immunosuppression increases the risk of septic complications. Later, there is a catabolic response to trauma with severe weight loss. Nonspecific complications include urinary tract infection from catheterization, deep vein thrombosis and pulmonary embolism.
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