Emergency and Disaster Nursing Course

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Emergency and Disaster Nursing Course

• BURNS

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Contents

• Objectives
• Introduction
• Mechanism of injury and Biomechanics of burns
• Types of burn injuries
• Signs and symptoms based on the pathophysiology
• Nursing process application
• Research utilization
• References

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Objectives

• At the end of this scientific presentation , each
  one of the students shall be able to -
• Identify burn traumas, types and degrees.
• Discuss the common mechanisms of injury
  associated with burn traumas.
• Discuss the pathophysiologic changes according to
  burn effects and manifestations.
• Apply the nursing process in dealing with burn
  clients including assessment, diagnosis,
  planning ,implementation and evaluation .

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Introduction

• Burn patients experience lots of disastrous
  problems , embarking from the initial events of
  the injury , and through periods of
  hospitalizations and rehabilitation .
• Caring of burn victims in any emergency
  department is very stressful and challenging for
  the health team members including nurses ,
  physicians , occupational therapist and even
  psychiatrists and dietitians,

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Introduction

• raising the issue of collaborative holistic
  approaches and continuing education to preserve
  knowledge and skills specially related to
  resuscitate burn victims.

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Epidemiology

• During the past two decades ,trends of burn
  incidence, hospitalization , and deaths shown all
  a decrease caused by the emphasis on preventive
  education and implementing of safety measures .
• The American experience with burn injuries
  revealed a dramatic decrease in burn cases
  estimated from 2.5 millions in 1970s through 1.5
  millions in 1990s .

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Epidemiology

• And a decrease in number of deaths is
  significantly noticed, as in 1970s , the number
  of deaths related to burns was estimated to be
  12000 deaths per annum, compared to 4000 deaths
  in 1990s .
• Also the great advances in treating burn shocks,
  which had been considered the leading cause of
  death for many years, were shown improving
  mortality rates (1970s 30 TBSA, 1990s 80
  TBSA).

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Epidemiology

• About the Jordanian experience with burn
  patients, the latest figures and numbers from the
  burn unit at JUH reveal that in 2005 , the number
  of admissions was 86 patients , 3 of them were
  died only.
• Another study made by Haddadin K. Amayreh W. for
  non-aacidental pediatric burn patients in Burn
  Unit, Farah Royal Jordanian Rehabilitation
  Centre/King Hussein Medical Centre.

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Epidemiology

• revealed after 7 years of this retrospective
  study that more than 70 of burn victims were
  below the year of 6 yrs and in absence of their
  parents.
• Also found that the major method of burn was
  scald burns associated to boiling water effect.
• And child abuse was one of the most
  indicators of burn accidents.

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The Skin Overview
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Mechanism of injury Biomechanics

• The energy agents that can cause burns are

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Pathophysiologic Changes

• Skin and soft tissue injury
• Zone Of Coagulation
• Area of coagulation affected
• Zone Of Stasis
• Capillary occlusion, decreased perfusion Edema
  formation 24-48 hrs
• Zone Of Hyperemia
• Increased blood flow results from inflammatory
  processes

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Pathophysiology

• Plasma loss and vascular responses
• Intravascular volume loss
• Diminished tissue perfusion
• Release of vasoactive agents
• Capillary semipermiability Lost
• Moving of fluids and substances like proteins
  from the intravascular to interstitial space
• Hyperemia
• hypovolemia

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Hemodynamic changes

• Lessened circulating blood volume results in
  decreased cardiac output initially and increased
  pulse rate.
• There is a decreased stroke volume as well as a
  marked rise in peripheral resistance (due to
  constriction of arterioles and increased
  hemoviscosity).
• This results in inadequate tissue perfusion,
  which may in turn cause acidosis, renal failure,
  and irreversible burn shock.

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Hemodynamic

• Electrolyte imbalance may also occur.
• Hyponatremia usually occurs during the 3rd to
  10th day due to fluid shift.
• The burn injury also causes hyperkalemia
  initially due to cell destruction, followed by
  hypokalemia as fluid shifts occur and potassium
  is not replaced.

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Metabolic Demands

• Catecholamine release appears to be the major
  mediator of the hypermetabolic response to burn
  injury.
• "Burn fever" is common and is dependent on depth
  of burn and percentage of TBSA involved.
  Temperatures of 102F to 103F (38.8C39.4C)
  are common as "fever spikes."
• Healing a large surface area requires much
  energy glucose is the primary metabolic fuel.

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Metabolic change

• Because total body glucose stores are limited and
  stored liver and muscle glycogen is exhausted
  within the first few days postburn, hepatic
  glucose synthesis (gluconeogenesis)
• Despite all nutritional support, it is almost
  impossible to counteract a negative nitrogen
  balance the sooner a burn wound is closed, the
  more rapidly a positive nitrogen balance is
  reached.
• .

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Renal changes

• Glomerular filtration may be decreased in
  extensive injury.
• Without resuscitation or with delay, decreased
  renal blood flow may lead to high oliguric renal
  failure and decreased creatinine clearance.
• Hemoglobin and myoglobin, present in the urine of
  patients with deep muscle damage often associated
  with electrical injury, may cause acute tubular
  necrosis and call for a greater amount of initial
  fluid therapy and osmotic diuresis.

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Pulmonary Changes

• hyperventilation and increased oxygen consumption
  are associated with major burns.
• The majority of deaths from fire are due to smoke
  inhalation.
• fluid resuscitation and the effects of burn shock
  on cell membrane potential may cause pulmonary
  edema, contributing to decreased alveolar
  exchange.
• Initial respiratory alkalosis resulting from
  hyperventilation may change to respiratory
  acidosis .

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Pulmonary (CO poisoning)

• Carbon monoxide (CO) is a colorless, odorless,
  tasteless, nonirritating gas produced from
  incomplete combustion of carbon-containing
  materials.
• Affinity of hemoglobin for CO is 200 times
  greater than for oxygen.

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Hematologic Changes

• Release of thromboxane A2 leads to
  Thrombocytopenia, abnormal platelet function,
  depressed fibrinogen levels, inhibition of
  fibrinolysis, and a deficit in several plasma
  clotting factors occur postburn.
• Anemia results from the direct effect of
  destruction of red blood cells due to burn
  injury, reduced life span of surviving red blood
  cells, and blood loss during diagnostic and
  therapeutic procedures

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Immunologic change

• The loss of the skin barrier and presence of
  eschar favor bacterial growth.
• Hypoxia, acidosis, and thrombosis of vessels in
  the wound area impair host resistance to
  pathogenic bacteria.
• Burn wound sepsis
• The wound will be fully colonized in 3 to 5 days.
  
• Seeding of bacteria from the wound may give rise
  to systemic septicemia.

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Gastrointestinal changes

• As a result of sympathetic nervous system
  response to burn trauma, peristalsis decreases,
  and gastric distention, nausea, vomiting.
• Ischemia of the gastric mucosa and other
  etiologic factors put the burn patient at risk
  for duodenal and gastric ulcer, manifested by
  occult bleeding and, in some cases,
  life-threatening hemorrhage.

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Extend of burn
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Extend of burn

• First degree
• Pink to red slight edema, which subsides
  quickly. In about 5 days, epidermis peels, heals
• Pain may last up to 48 hours relieved by
  cooling. spontaneously.
• (Sunburn is a typical example.)

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Extend

• Second degree
• Superficial
• Pink or red blisters form (vesicles)
  weeping, Takes several weeks to heal.
• edematous, elastic. Scarring may occur.
• Superficial layers of skin are destroyed wound
  moist and painful.

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• Second degree
• Deep dermal
• white and red edematous reddened Takes several
  weeks to heal.
• areas blanch on pressure. Scarring may occur.
• May be yellowish but soft and elasticmay or
• may not be sensitive to touch sensitive to cold
  air.
• Hair does not pull out easily

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Third degree

• Destruction of epithelial cellsepidermis and
  Eschar must be removed. Granulation tissue dermis
  destroyed.forms to nearest epithelium from wound
• Reddened areas do not blanch with
  pressure.margins or support graft.
• Not painful inelastic coloration varies
  from For areas larger than 3-5 cm.
• tissue is called eschar.Expect scarring and loss
  of skin function.
• Destruction of epithelium, fat, muscles, and Area
  requires debridement, formation of bone.

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Rule of nine
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Thermal injuries

• The most common
• Type of injuries
• Varies according to severity
• The prognosis is better.

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Electrical injuries

• The type of current
• Duration of contact to electrical source
• Location of electrical source
• Causes necrosis in skin , tetany, cardiac
  dysrhythmias

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Chemical burns

• Chemical agents either alkaline or acidic, or
  petroleum based products. (alkaline penetrate
  more than acidic)
• painful
• Identify neutralizing agent

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Inhalation burns

• May be upper airway (supraglottic) and incur
  injury in minutes to hours or may involve lower
  airway and cause adult respiratory distress
  syndrome (ARDS). This can occur in as little as 4
  hours of burn

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Nursing care for burn patients

• Assessment
• with all trauma victims, a primary and
  secondary trauma survey, including assessment of
  airway, breathing, and circulation as well as
  vital signs, is done. Other assessment parameters
  specific to the burn injury focus on extent and
  severity of burn injury and inhalation injury.

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Nursing process

• Nursing assessment
• Severity of Burns
• Severity of burns is determined by
• Depthfirst, second, third degree
• Extentpercentage of TBSA
• Area of the body burnedface, hands, feet,
  perineum, and circumferential burns require
  special care.

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Nursing diagnosis

• Impaired Gas Exchange related to inhalation
  injury
• Ineffective Breathing Pattern related to
  circumferential chest burn, upper airway
  obstruction, or ARDS
• Risk for Infection related to loss of skin
  barrier and altered immune response
• Body Image Disturbance related to cosmetic and
  functional sequelae of burn wound

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Nursing interventions

• Stop the burning process if possible
• Remove all clothing and jewelry
• Ensure patent airway
• Prepare for incubation
• Cannulate two veins

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Fluid resuscitation formulas

• First 24 hours4 mL of Ringer's lactate weight
  in kg TBSA burned.
• One-half amount of fluid is given in the first 8
  hours, calculated from the time of injury. If the
  starting of fluids is delayed, then the same
  amount of fluid is given over the remaining time.
  Remember to deduct any fluids given in the
  prehospital setting

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• Patient's weight 70 kg TBSA burn 80
• 4 mL 70 kg 80 TBSA 22,400 mL of Ringer's
  lactate
• 1st 8 hours 11,200 mL or 1,400 mL/hour
• 2nd 16 hours 11,200 mL or 700 mL/hour

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Treatment

• Hydration therapy
• Escharotomy
• Grafts
• Flabs

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summary

• Burn is not traumatic not only for the patient,
  but also for the family , so the care giver must
• ensure the the holistic care approach dealing
  with the victim.

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Refrences

• mo, L., Kravitz, M. (1993). The management of
  acute burn and burn shock resuscitation. AACN
  Clinical Issues in Critical Care Nursing, 4(2),
  351-366.
• nster, A. M., Smith-Meek, M., Sharkey, P.
  (1994). The effect of early surgical intervention
  on mortality and cost effectiveness in burn care.
  Burns, 20(1), 61-64.
• Smith, D. J., Thompson, P. D., Gardner, W. L.,
  Rodrigues, S. L. 1994. Burn wounds Infection and
  healing. American Journal of Surgery, 167(1A),
  465-485.