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,
chills, headache, nausea or vomiting.
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.
Usually scars do not form unless genetically prone. Deep partial thickness burns destroy the epidermis and dermis. Seven to ten days after injury skin buds and hair follicles appear. The healing process includes excision of the wound and a skin graft from another area of unburned skin and can take up to several weeks to months to heal
Third degree burns (full thickness injury) destroys the epidermis, dermis and subcutaneous tissue. Muscle and bone may also be damaged. The skin has a dry leather appearance. Edema forms and the wound requires to be cut to relieve the pressure. All of the nerve endings are destroyed so the individual does not feel any pain.
Major burns vary depending on body size. A major burn for an adult is 20% of total body surface area (TBSA) and 10% of TBSA in children and elderly. The TBSA of a burn is
2

measured by the “rule of nines” or the Lund and Bowder Chart. Major burns also include injury to face, genitals, and airway regardless of the percentage of injury. Major burns cause large tissue destruction and activation of the inflammatory response. Major burns activate the sympathetic nervous system and release glucagon, insulin, catecholamines and cortisol. There are 2 phases to burn injuries: Burn shock phase and hypermetabolic phase.
During burn shock circulating mediators (tumor necrosis factor and interleukins) are released to start the systemic inflammatory response which causes an increase in capillary permeability. Edema starts to occur and leads to tissue ischemia. After the first few hours of injury there is a shift of fluid and electrolytes from the intra vascular to the interstitial spaces to help with tissue perfusion from the burn. Due to this rapid shift in fluid it is important that the intravascular volume is replaced to avoid burn shock. If burn shock occurs, the plasma volume is inadequate and unable to maintain preload, cardiac output and tissue hypoperfusion.
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
patient.