Physical Exam

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, lifethreatening 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), 465485. 