FACTORS DETERMINING SEVERITY OF BURNS
- Size of burn Body part involved
- Depth of burn
- Mechanism of injury
- Age of patient
- History of cardiac, pulmonary, renal, or hepatic disease
- Injuries sustained at time of burn.
TISSUE RESPONSE TO BURN INJURY
- Localized responses - burn injury cause immediate tissue changes known as zones of injury.
- The zone of coagulation is the innermost zone in which protein has been coagulated and the damage is irreversible.
- Zone of stasis - most cells in this area are viable even though blood vessels have been damaged and perfusion is decreased. Highly sensitive and risk for necrosis because of inflammatory response & resultant edema, ischemia, cellular dehydration and infection
- Zone of hyperemia - blood flow is increased from vasodilation and circulating vasoactive mediators. It brings leukocytes and nutrients to the area to promote wound healing within zone of stasis.
- The depth of a burn depends on the temperature of the burning agent and the length of time it is contact with the skin.
Early tissue damage may occur at temperatures of 104° C and irreversible damage to the dermis occurs at temperatures of 158° C.
Direct injury to the skin
Heat from an external source is conducted to the skin
It denatures the cells
Various cellular enzyme system and cellular system fail
Sodium potassium pump fails
Cell necrosis as temperature rises
Free radicals are produced
- 1.zone of coagulation→damaged skin coagulates →tissue destroyed
- 2.Zone of stasis→ surrounding inflammation→tissue edematous and impaired blood flow→ skin is initially viable → eventually die from ischemia
- 3.zone of hyperemia →vasodialation→red appearance
SYSTEMIC RESPONSE –
- More than 25% of TBSA is considered as major burn.
- Major burn effects every organ system.
- They are associated with-
- Massive fluid shifts from the intravascular to the interstitial space
- Edema of uninjured tissues
- Hemodynamics instability
- Hypoperfusion of tissues and organs
SYSTEMIC EFFECTS OF MAJOR BURNS
- l. Hyper metabolism
- 2.Myocardial depression
- 4.Inflammatory release of vasoactive mediators
- 5.Renal tubular damage
- 6.Decreased G I blood flow
- 7.Suppressed cellular immunity
- 8.Catabolism of fat and muscle
- 9.Clotting abnormalities
- 10.Early destruction of RBC's
- Cardiac output : CO is decreased
Because of the release of catecholamines, eg: (epinephrine and norepinephrine), vasopressin (antidiurectic hormone) and angiotensin II.
- These produce a intense vasoconstriction, which increases systemic vascular resistance and cardiac workload.
- Tachycardia and blood pressure may transiently elevated. Which increases the capillary force and promotes burn edema.
- With adequate fluid resuscitation, cardiac function continues to be depressed due to myocardial depressant factor and other vasoactive- mediators released by injured cells and the inflammatoy response.
- Fluid loss can be as much as 20 times greater than the normal and continue until the wound is healed.
- Such loss coupled with protein loss
- Patient is at risk for electrolyte imbalances such as hyperkalemia, hyponatermia, or hypernatermia.
- Edema - forms rapidly after burns.
- Reaches maximum within 12 to 24 hours and subsides within 72hours.
- Cause- inflammatory response and vasoactive mediators that produce vasodilation and increased capillary permeability.
- When the capillary permeability is reestablished, protein, because of its large size is unable to move back into the intravascular space, thus significant hypoproteinemia takes place.
- Even though lymphatic resorption remains intact, the system becomes overloaded and significant localized and systemic edema occurs.
Pulmonary responses -
- Smoke, chemical irritants, oropharyngeal swelling from fluid resuscitation and hypo proteinemia are factors believed to contribute to the development of pulmonary edema.
- Pulmonary edema, increased pulmonary vascular resistance and increased systemic vascular resistance caused by mediators such as serotonin increase the workload of lungs making bçeathing difficulty.
Renal and GI responses -
- Blood flow to kidney, liver and GI is reduced by hypovolemia, peripheral vasoconstriction and a significant release of antidiurectic hormone placing the patient at risk of kidney failure, hepatic failure and paralytic ileus. Breakdown of small intestine may occur
Gastric and duodenal ulcer with bleeding can occur related to stress. Cholecystitis and pancreatitis may also be seen.
Hypermetabolism and impaired nutrition follow burn shock.
- A negative nitrogen balance begins at the onset of the burn from tissue destruction, protein loss and the stress response.
- It continues through out the acute phase.
- The patient is vulnerable to significant weight loss due to fluid loss and loss of solid body mass secondary to increased metabolism
Immune response -
- The break in the skin integrity destroys the body's first line of defense and complex immune changes result in bone marrow depression, decreased immunoglobin production, suppression of complement and shorter life span of red blood cells.
- Damaged tissues trigger the release of the inflammatory cytokine cascade, which impairs the function of lymphocytes, macrophages and neutrophils, increasing the risk for infection.
- Nutritional deficits further compromise the patients ability to fight infection. Infection leads to sepsis and multisystem organ dysfunction.
Psychological responses -
- During the emergent phase patient may be in a state of disbelief and shock, which may be followed by anger, Irritability or frustration.
- In -70% of burn Injury, after 48 hours, the period of delirium with manifestation such as fluctuating of alertness; nightmares, insomnia, severe anxiety, withdrawl behavior ,resistance to treatment or hostility.
- These reactions are thought to be related to stress induced metabolic disturbances.
- Patients may have tendency for suicide.Depressed patient must be looked carefully.
- For those patients who remain dependent, psychological problems are likely to continue throughout rehabilitation and discharge.
- Infection - endogenous or exogenous
- Renal compromise
- Fluid volume deficit
- Gastrointestinal disorders
- Electrolyte imbalances
- Hepatic injury
- Respiratory insufficiency or ARDS
- Psychological disturbances.
- Physical examination
- Laboratory profile
- As with all trauma victims, a primary and secondary trauma survey, including assessment of A,B,C as well as vital signs, is done.
- Other assessment parameters specific to the burn injury focus on the extent and severity of burn injury and inhalation injury