Pathophysiology of Burn
Following systemic changes takes place in the human body following a burn injury:
- Inflammation and edema
- Altered hemodynamics
- Immunosuppression
- Hypermetabolism
- Decreased renal flow
- Increased gut mucosal permeability
- Infection & septicemia.
Fig. 1: Degree of Burn
1. Inflammation and Edema:-
- Burn injury causes a massive release of inflammatory mediators which produce the first vasoconstriction of the skin capillaries followed by rebound vasodilatation, increased capillary permeability, and edema, locally and in distant organs.
- The generalized edema occurs in response to changes in both burned and unburned skin as plasma osmotic pressure decreases and interstitial osmotic pressure increases as a result of the protein loss induced by increased capillary permeability, edema forms in the burned and unburned tissues.
- The edema is greater in the burned tissues because of lower interstitial pressure.
- The swelling in the tissue further compresses the blood vessels cutting off blood flow in the tissues.
2. Altered Hemodynamics:
- Massive loss of fluid from the blood results in reduced blood volume, putting excessive strain on the heart.
- This reflects adversely on the normal metabolic functioning of other vital organs such as lungs, kidneys, and liver, which are dependent on critical blood pressure to work properly.
- In this situation, the patient goes into a hypovolemic shock.
3. Hypermetabolism:
- Burn injury sets off massive inflammatory reactions due to which the metabolic rate shoots up as the body tries to fight the effects of pain, inflammation, and tissue destruction.
- This increases the demand for oxygen and blood flow to the tissues, with associated increases in respiration and heart rate.
- The energy reserve of the body is depleted at a very rapid rate to keep up with this suddenly increased metabolic rate.
4. Renal System
- Renal system dysfunction is caused by diminished blood volume and cardiac output, resulting in decreased renal blood flow and glomerular filtration rate.
- Other stress-induced hormones and mediators such as angiotensin, aldosterone, and vasopressin further reduce renal blood flow immediately after the injury.
- This results in oliguria, which if left untreated will cause acute tubular necrosis and renal failure. Early fluid replenishment therapy decreases the chances of renal failure and improves the associated mortality rate.
5. Gastrointestinal System
- Gastrointestinal system dysfunction is highlighted by mucosal atrophy, changes in digestive absorption, and increased intestinal permeability.
6. Immunosuppression
- There is a global depression of immune function in a burn patient, which is the reason allograft skin survives on burn wounds for a long time.
- Burned patients are thus at great risk for a number of infectious complications, including bacterial wound infection, pneumonia, and fungal and viral infections.
7. Infection and Septicemia
- Loss of skin cover, even if partial, can lead to infections because of damage to the skin's protective barrier.
- Ideally small, shallow burns may need only to be kept clean and to have an antibiotic cream applied for it to heal. However, the onset of secondary infection, even in a superficial shallow burn may lead to the down gradation of the wound. Infected burn wounds end up with deep and extensive skin loss which may aggravate.
- In addition, damaged skin and other body tissues serve as excellent culture media for infective organisms. The wound is easily infected because the skin can no longer act as a barrier against invading micro-organisms. This massive invasion of pathogens into the body overwhelms the immune system and the patient may develop septicemia.
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