Burn Injury Research Paper

Burn injuries cause several physiological changes within in the body. A burn can come from thermal, chemical or electrical environments. The location and severity of the burn will determine the morbidity and mortality outcome. The risk of death increases with age, inhalation injury and burn area. Burns can cause tissue damage, electrolyte imbalance and organ system failure. There are several different depths of burns: First degree, Second degree, and Third degree. First degree burns (partial thickness injury) include the epidermis only. The affected skin is able to maintain water vapor and protect against bacteria. Local pain and erythema are present.
Blisters appear after 24 hours of injury. The person may experience localized edema,
In most cases no treatment is needed unless there is a need for rehydration. Second degree burns are classified as superficial partial thickness injury or deep partial thickness. Superficial partial thickness burns appear with fluid filled blisters a few minutes after injury. Pain is present and gets worse due to the nerves being exposed to air as the blisters break.
This type of wound heals in 3 to 4 weeks if the individual has normal nutritional intake.
Clinical manifestations include hypovolemia, acidosis, organ injury and multiorgan dysfunction.
Intravenous fluid replacement such as Lactated Ringers are necessary to restore the circulating blood volume.
Hypermetabolic phase occurs when fluid resuscitation (into the vascular system) is effective. This response causes a massive shift in catecholamines and corticosteroids causing increased cardiac oxygen consumption and cardiac work. Proteins and amino acids are mobilized to meet the metabolic and energy demands. Lean body mass is lost and alters the immune function and would healing. Hypermetabolism can lead to physiological exhaustion and death, if left untreated. Techniques used to amend the hypermetabolic response include early surgical intervention, warm environment (28-33 C), catabolic nutritional support and pharmacological agents such as insulin and ß- antagonists. The clinical manifestations are systemic hypertension, increased muscle protein degradation, persistent tachycardia (up to 2 years post burn), insulin resistance, elevated core temperature, liver dysfunction and hyperventilation. Urine output is an accurate sign of successful fluid replacement in a burn