Emergency and Disaster

Nursing Course

BURNS
Prepared by: Basel AbdulQader
RN,BSN
Supervised by : Manar Nabulsi
RN,Ph.D
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
 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 .
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,
Introduction

raising the issue of collaborative holistic

approaches and continuing education to
preserve knowledge and skills specially related
to resuscitate burn victims.
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 1970’s through
1.5 millions in 1990’s .
Epidemiology
And a decrease in number of deaths is
significantly noticed, as in 1970’s , the
number of deaths related to burns was
estimated to be 12000 deaths per annum,
compared to 4000 deaths in 1990’s .
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 (1970’s 30%
TBSA, 1990’s 80% TBSA).
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.
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.
The Skin Overview
Mechanism of injury & Biomechanics

The energy agents that can cause burns are:

Energy

Thermal Chemical Electrical

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
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
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.
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.
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 102°F to 103°F
(38.8°C–39.4°C) are common as "fever
spikes."
 Healing a large surface area requires much
energy; glucose is the primary metabolic fuel.
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.
.
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.
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 .
 )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.
 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
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.
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.
Extend of burn
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.)
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.
 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 elastic—may or

 may not be sensitive to touch; sensitive to

cold air.
 Hair does not pull out easily
Third degree
 Destruction of epithelial cells—epidermis 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.
Rule of nine
Thermal injuries
 The most common
Type of injuries

 Varies according to severity

 The prognosis is better.
Electrical injuries
 The type of current
 Duration of contact to electrical source
 Location of electrical source
 Causes necrosis in skin , tetany, cardiac
dysrhythmias
Chemical burns
 Chemical agents either alkaline or acidic, or
petroleum based products. (alkaline
penetrate more than acidic)
 painful
 Identify neutralizing agent
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
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.
Nursing process
 Nursing assessment
 Severity of Burns
 Severity of burns is determined by:
 Depth—first, second, third degree
 Extent—percentage of TBSA
 Area of the body burned—face, hands,
feet, perineum, and circumferential
burns require special care.
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
Nursing interventions

 Stop the burning process if possible

 Remove all clothing and jewelry
 Ensure patent airway
 Prepare for incubation
 Cannulate two veins
Fluid resuscitation formulas
 First 24 hours—4 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
 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
Treatment
 Hydration therapy
 Escharotomy
 Grafts
 Flabs
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.
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.