Management of patients with burn injury

Dr Aidah Abu Elsoud Alkaissi

An-Najah National University

Faculty of Nursing

Incidence of burn• In USA 2 milion people require medical

attention for burn injury, 51,000 require acute hospital admission, 4500 people die from burn and related inhalation injuries

• Young children and elderly people are at particularly high risk for burn injury

• The skin is thin and fragile

• Alimited eriod of contact with haet can create a fukk thicknes burn

Incidence of burn

• Most burn injuries occur in the home, in the kitchen, in the bath room – scald or impropr use of electrical appliances around water sources

• Narses can play an active role in preventing fires and burns by teaching prevention concept and promoting legislation related to fire safety

• Promoting the use of smoke alarms has had the greatest impacton decreasing fire deaths

Gerontologic consideration• Reduced mobility• Changes in vision• decreased sensation in the feet and hands place elderly

people at high risk for burn injury• Scalds and flames are the leading causes• They have difficulty in extinguishing the fire and

removing themselves from the burn source• Thinning and loss of elasticity of the skin in the elderly

predispose them to a deep injury from a thermal insult that might cause a less severe burn in a younger person

• Chronic illness decreases the older person´s ability to withstand the multisystem stresses imposed by burn injury

Pathophysiology of burns• Burn are caused by a transfere of energy from a heat source to

the body• Heat may transferred through conduction or electromagnetic

radiation• Burns are categorized as thermal ( include electric burns) ,

radiation, chemical• Tissue destruction results from coagulation, protein

denaturation, or ionization of cellular contente• The skin and the mucous of the upper airways are the sites of

tissue destruction• Deep tissues including the viscera, can be damaged by

electrical burns or through prolonged contact with a heat source

Pathophysiology of burns• Disruption of the skin can lead to increased fluid loss,

infection, hypothermia, scarring, compromised immunity, and changes in function, appearance and body image

• The depth of the injury depends on the temp of the burning agent and the duration of contact with the agent

• For example in the case of scald burns in adults, one second of contact with hot tap water at 68.9 c may result in a burn that destroys both the epidermis and the dermis, causing a full thickness (third degree) injury

• Fifteen seconds of exposure to hot water at 56.1 c results in a similar full-thickness injury

Classification of Burns

• Burn depth. Are classified according o the depth of the tissue destruction as superficial partial thickness injuries, deep partial thickness injuries or full thickness injuries

• Burn depth determines whether epithelialization will occur

• Determining burn depth can be difficult even for the experienced burn care provider

• The categories of superficial partial thickness, deep partial thicjkness and full thickness burns are similar to , but not the same as first, second and third degree

Classification of Burns• The wound is painful, a superficial partial thickness

burn, the epidermis is destroyed or injured and a portion of the dermis may be injured

• The damaged skin may be painful and appear red and dry as in sunburn or it may be blister

• A deep partial thickness burn involves destruction of the epidermis and upper layers of the dermis and injury to deeper portion of the dermis

• Capillary refill follows tissue blanching• Hair follicle remain intact• Deep partial thickness burns take longer to heal and are

more likely to result in hypertrophic scars

Classification of Burns• A full thickness burn involves total destruction

of epdermis and dermis and in some cases underlying tissue as well

• Wound color ranges widely from white to red, brown, or black.

• The burn area is painless because never fibers are destroyed

• The wound appears leathery, hair follicles and sweat glands are destroyed

Classification of Burns

• The following factors are considered in determining the depth of the burn:

• How the injury occur

• Causative agent, such as flame or scalding liquid

• Temperature of the burning agent

• Duration of contact with the agent

• Thickness of the skin

Extent of body surface area injured

• Various methods are used to estimate the TBSA affected by burns among them are the rule of nines, the Lund and Browder method and the palm method

Rule of nine

• An estimation of TBSA involved in a burn is simplified by using rule of nine

• It is a quick way to calculate the extent of burn

• The sytem assigns percentages in multiples of nine to major body surfaces

Lund and browder method

• Recognizes the percantages of TBSA of various anatomic parts especially the head and legs and changes with growth

• By dividing the body into very small areas and providing and estimate of the proportion of TBSA accounted for by such parts , one can obtain a reliable estimate of the TBSA burned

Palm method

• In patient with scattered burns, a method to estimate the percantage of burn is the palm method

• The size of the patient´s palm is approximately 1% of TBSA

Local and systemic resposes to burns

• Burns that do not exceed 25% TBSA produce a primarily local response

• More than 25% produce both a local and a systemic response and considered major burn injury

• System response is due to the release of cytokines and other mediators into the systemic circulation

• The release of local mediators and chanes in blood flow , tissue edema and infection can cause progression of the burn injury

Local and systemic resposes to burns

• Pathologic changes resulting from major burns during the initial burn-shoch period include tissue hypoperfusion and organ hypofunction secondary to decreased cardiac output followed by a hyperdynamic and hypermetabolic phase

• The intial systemic event after a major burn injury is hemodynamic instability, resulting from loss of capillary integrity and a subsequent shift of fluid, sodium and protein from the intravascular space into the interstitial spaces

• Hemodynamic instabiliy involves cardiovascular, fluid and electrolyte, blood volume. Pulmonary and other mechanism

Cardiovascular response• Hypovolemia is the immediate consequences

of fluid loss resulting in decreased perfusion and oxygen delivery

• Cardiac output decreases before any significant changes in blood volume is evident

• As fluid loss continues and vascular volum decreases, cardiac output continues to fall and blood pressure drops

• This is the consent of burn shock

Cardiovascular response• In response the sympathetic nervous system releases

catecholamines, resulting in an increase in peripheral resistance (vasoconstriction) and an increase in pulse rate

• Peripheral vasoconstriction further decreases cardiac output

• Myocardial contractility may be suppressed by the release of inflammatory cytokine necrosis factor

• Prompt fluid resuscitation maintain the blood pressure in the low normal range and improves cardiac output

• Despite adequate fluid resuscitation cardiac filling pressures (central venous pressure, pulmonary artery pressure and pulmonary artery wedge pressure ) remain low during the burn-shock period)

Cardiovascular response• If inadequate fluid resuscitation occurs, distributive

shock will occur• Generally the greatest volume of fluid leak occurs in

the first 24-36 hours after the burn, peaking by 6-8 h• As the capillaries begin to regain their integrity, burn

shock resolves and fluid returns to the vascular compartment

• As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases

• If renal and cardiac function is adequate , urinary output increases

• Diuresis continue for several days

Burn edema• Local swelling due to thermal injury is often extensive• Edema is defined as the presence of excessive fluid in

the tissue spaces• In burns involving less than 25% TBSA, the loss of

capillary integrity ans shift of fluid are localized to the burn itself, resulting in blister formation and edema only in the area of injury

• Pat with more severe burns develop massive systemic edema

• Edema is usually maximal after 24 h• It begins to resolve 1-2 days post-burn and usually is

completed in 7-10 days postinjury

Burn edema• Edema in burn wounds can be reduced by avoiding excessive

fluid during the early post-burn period• Unnecessary over resuscitation will increase edema formation

in both burn tissue and non-burn tissue• As edema increases in circumferential (encompassing) burns,

pressure on small blood vessels and nerves in the distal extrimities causes an obstruction of blood flow and consequent ischemia

• This complication is known as compartment syndrome• The physician may need to perform an escharotomy, a surgical

incision into the eschar (a slough or dry scab that forms, for example, on an area of skin that has been burnt or exposed to corrosive agents)

(devitalized tissue resulting from a burn), to relieve the constricting effect of the burned tissue

Effects on fluids, electrolytes and blood volume

• Circulating blood volume decreases dramatically during burn shock

• In addition, evaporative fluid loss through the burn wound may reach 3-5 l or more over a 24 hour period until the burn surfaces are covered

• During burn shock, serum sodium levels vary in response to fluid resuscitation

• Hyponatremia (sodim depletion) is present• Hyponatremia is common during the first week of the acute

phase as water shifts from the interstitial to the vascular space

Effects on fluids, electrolytes and blood volume

• Immediately after burn injury, hyperkalemia (excessive potasium) results from massive cell destruction

• Hypokalemia (potasium depletion) may occur later with fluid shifts and inadequate potassium replacement

• At the time of burn injury, some red blood cells may be destroyed and other damaged, resulting in anemia

• Despite this the hematocrit may be elevated due to plasma loss

• Blood loss during surgical procedures, wound care, diagnostic studies and ongoing hemolysis further contribute to anemia

• Blood transfusions are required periodically to maintain adequate hemoglobin levels for oxygen delivery

Effects on fluids, electrolytes and blood volume

• Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin times occur with burn injury

Pulmonary response

• Inhalation injury is the leading cause of death in fire victims

• Half of these deaths could have been prevented with use of a smoke detector

• Burn victims mke it out of a burning home safely• Once they are outside they mat be realize that loved ones ,

pets or valuable items are still inside the burning home• They then reenter the burning home and are overcome

with toxic smoke and fumes and become disoriented or unconcious

Pulmonary response• Inhalation injury has asignificant impact on survivability of

a bburn pat• Deterioration in severely burned patients can occur without

evidence of a smoke inhalation injury• Bronchoconstriction caused by release of histamine,

serotonin and thromboxane, a powerful vasoconstrictor as well as chest constriction secondary to circumferential full thickness chest burns causes this deterioration

• One third of all burn patients have pulmonary problem related to the burn injury

• Even without pulmonary injury, hypoxia (oxygen starvation) may be present

Pulmonary response• Early in the postburn period, catecholamine

release in response to the stress of the burn injury alters peripheral blood flow, therby reducing oxygen delivery to the periphery

• Later hypermetabolism and continued catecholamine release lead to increased tissue oxygen consumption which can lead to hypoxia

• To ensure that adequate oxygen is available to the tissue, supplemental oxygen may be needed

Pulmonary response• Pulmonary ijuries fall into several categories, upper

airway injury, inhalational injury bellow the glottis , including carbon monoxide poisining and restrictive defects

• Upper air way injury results from direct heat or edema• It is manifested by machanical obstruction of the upper

airway, including the pharynx and larynx• Because of the cooling effect of rapid vaporization in

the pulmonary tract, direct heat injury does not normally occur bellow the level of bronchus

• Upper airway injury is treated by early nasotracheal or endotracheal intubation

Pulmonary response• Inhalation injury below the glottis results from inhaling th

products incomplete combustion (Burning) or noxious gases• These products include carbon monoxide, sulfer oxide,

nitrogen oxide, aldehydes, cyanide, ammonia, chloride, phosgene, benzene and halogen (One of the chemical elements chlorine, bromine, or iodine)

• The injury results directly from chemical irritation of the pulmonary tisues are the alveolar level

• Inhalation injuries below glottis cause loss of ciliary action, hypersecretion, severe mucosal edema and bronchospasm

• The pulmonary surgactant is reduced, resulting in atelectasis (collapse of alveoli)

Pulmonary response• Expectoration of carbon particles in the sputum is the cardinal

sighn of this injury• Carbon monoxide is probably the most common cause of

inhalation injury because it is a byproduct of the combustion of organic material and is therefore present in smoke

• The pathophysiology effects are due to tissue hypoxia a result of carbon monoxide combining with hemoglobin to form carboxyhemoglobin which competes with oxygen for available hemoglobin sites

• The effinity of hemoglobin for carbon monoxide is 200 times greater than that for oxygen

• Treatment usually consists of ealy intubation and mechnical ventilation with 100% oxygen

Pulmonary response• Some ptients require only oxygen therapy, depending on the extent of

pulmonary injury and edema• Administering 100% O2 is essential to accelerate the removal of

carbon monoxide from the hemoglobin molecule restrictive defects arise when edema develops under full-thickness burns encircling the neck and thorax

• Chest excursion may be greatly restricted resulting in decreased tidal volume

• In such situation escharotomy is necessary• Pulmonary abnormalities are not always immediately apparent• Motre than half of all burn victims with pulmonary involvement do

not intially demonstrate pulmonary signs and symptoms• Any pat with possible inhalation injury must be observed for the least

24 h for respiratory complications

Pulmonary response

• Airway obstruction may occur very rapidly in hours

• Decreased lung compliance, decreased arterial oxygen levels and respiratory acidosis may occur gradually over the first 5 days after a burn

Indication of possible pulmonary damages include

• History indicating that the urn occured in an enclosed area• Burns of the face and neck• Signed nasal hair• Hoarseness , voice change, dry cough, stridor, sooty sputum• Bloody sputum• Labored breathing or tachypnes (rapid breathing) and other

signs of reduced oxygen levels• Erythema and blistering of the oral or pharyngeal mucosa

Pulmonary response• Serum carboxyhemoglobin levels and arterial blood gas

levels are frequently used to assess for inhalation injuries• Bronchoscopy and xenon 133 ventilation –perfusion scans

can be used to aid diagnosis in the early postburn period• Pulmonary function studies may be useful in diagnosing

decreased lung compliance or obstructed airflow• Pulmonary complications secondary to inhalation injuries

include acute respiratory failure and acute respiratory distress syndrome (ARDS)

• Respiratory failure occurs when inmairment of ventilation and gas exchange is life threatening

Pulmonary response• The immediate intervention is intubation and

mechanical ventilation

• If ventilation is impaired by restricted chest excursion, immediate chest escharotomy is needed

• ARDS may develop in the first few days after the burn injury secondary to systemic and pulmonary responses to the burn and inhalation injury

Other systemic responses• Renal function may be altered as a result of decreased blood

volume• Destruction of red blood cells at the injury site in free

hemoglobin in the utine• If muscle damage occurs (from electric burns e..) myoglobin

is released from the muecle cells and excreted by the kidney• Adequate fluid volume replacement restores renal blood

flow, increasing the glomerular filtration rate and urine volume

• If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resultinh in acute tubular necrosis and renal failure

Other systemic responses• The immunologic defences of the body are greatly

altered by burn injury• Serious burn injury diminishes resistance to the infection• As a result sepsis remains the leading cause of death in

thermally injured patients• The loss of skin integrity is compounded by the release

of abnormal inflammatory factors, altered levels of immunglobulins and serum complement, impared neutrophil function and a reduction in lymphocytes (lymphocytopeni)

• Research suggest that burn injury results in loss of T-helper.cell lymphocytes

Other systemic responses• There is a significant impairement of the production and

release of granulocytes and macrophages from bone marrow after burn injury

• The resulting immunosuppression places the burn patient at high risk for sepsis

• Loss of skin results in an inability to regulate body temperature

• Burn patients may therefore exhibit low body temperature in the early hours after injury

• As hypermetabolism resets (Something set again) core temperature, burn patients become hyperthermic for much of the postburn period, even in the abscence of infection

Other systemic responses• Two potential gastrointestinal complications may occur,

paralytic ileus (absence of intestinal peristalsis) and Curling´s ulcer, decreased peristalsis and bowel soynds are manifestations of paralytic ileus resulting from burn trauma

• Gastric distention and nausea may lead to vomiting unless gastric decompression is intiated

• Gastric bleeding secondary to massive physiologic stress may be signaled by occult blood in the stool, regurgitation of coffee ground material from the stomachor bloody vomitus

• There are suggest gastric or deuodenal erosion (Curling´s ulcer).

Medical care• Laboratory:

• CBC show eleveted hematocrit due to hemoconcentration and later decreased hematocrit may mean vascular damage to endothelium, white blood cell count may increase due to inflammatory response to the trauma and wound infection

• WBC count may increase due to inflammatory response to the trauma and wound infec tion

Medical care• WBC can be as high as 30,000 mm3 initially, biut

resolves within 2 days• Leukopnia may occur as a side efect from silver

sulfadiazine or SIRS• Thrombocytopenia may result within the first 72 hours

because of hemodilution and potential microthrombi, protein and albumin are decreased

• Because of protein loss from increased vascular permeability, coagulation studies usually will show increased prothrombin and partial thromboplastin time during the first 72 hours after injury as a result of leakage of clotting factors from the intravascular space

Medical care• Electrolytes may show initially hyperkalemia resulting

from injury, later changing to hypokalemia when duiretic phase begins, sodium initially decreased with fluid loss and later changes to hypernatremia when renal system attempt to conserve water, alkaline phosphatase elevated, glucose elevated from stress reaction, albumin decreased, BUN and creatinine elevated because of renal dysfunction

• Carboxyhemoglobin may be done to identify carbon monoxide poisining with inhalation injury

Medical care• Radiography: chest x-ray used to identify

complications that may occur as a result of inhalation injury or with fluid shifting from rapid replacement

• Arterial blood gases: used to identify hypoxia or acid base imbalances, acidosis may be noted because of decreased renal perfusion, hypercapnia and hypoxia may occur with carbon monoxide poisining

Medical care• Lung scan:to identifymagnitude of lung damage from

inhalation injury• Electrocdiogram: used to identify myocardial

ischemia or dysrhythmias that may occur with burns or electrolyte imbalances

• Analgesics: required to reduce pain associated with tissue damage and nerve injury

• Tetanus toxiod: required to provide immunity against infective organisms

• Antimicrobials:required to treat infection

Medical Care• surgery: required for skin grafting, fasciotomy,

debridement, or repair of other injuries

• IV fluid: massive amount of IV fluids may be required for fluid resuscitation immediately post burn and will be required for maintenance of fluid balance as shifting occurs