Effects
of burn injury
• local;
• regional;
• systemic.
Local effects
Tissue
damage
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.
Inflammation
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.
Infection
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
Circulation
Limb circulation may be compromised. Direct damage to a main limb vessel
is unlikely, although it may occur from high-
Systemic
effects from burning
Fluid
loss
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.
Inhalation
injury
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.
Systemic
complications
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.