Management of patients with burn injury

1
Management of patients with burn injury

• Dr Aidah Abu Elsoud Alkaissi
• An-Najah National University
• Faculty of Nursing

2
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

3
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

4
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

5
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

6
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

7
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

8
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

9
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

10
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

11
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

12
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

13
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

14
Palm method

• In patient with scattered burns, a method to
  estimate the percantage of burn is the palm
  method
• The size of the patients palm is approximately
  1 of TBSA

15
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

16
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

17
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

18
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)

19
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

20
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

21
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

22
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

23
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

24
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

25
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

26
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

27
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

28
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

29
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)

30
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

31
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

32
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

33
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

34
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

35
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

36
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

37
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

38
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

39
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).

40
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

41
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

42
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

43
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

44
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

45
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