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Management of patients with burn injury


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 ... – PowerPoint PPT presentation

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Title: Management of patients with burn injury

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 persons
    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
  • 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
  • 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
  • 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

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

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
  • The size of the patients 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
  • 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

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

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
  • Hypokalemia (potasium depletion) may occur later
    with fluid shifts and inadequate potassium
  • At the time of burn injury, some red blood cells
    may be destroyed and other damaged, resulting in
  • 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

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
  • 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
  • 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
  • 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
  • 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

Pulmonary response
  • Airway obstruction may occur very rapidly in
  • 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

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
  • 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 Curlings 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
    (Curlings 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

Medical care
  • Lung scanto 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
  • Antimicrobialsrequired 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
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