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Burns are classified according to tissue depth destruction

superficial partial-thickness (similar to 1st degree)
deep partial-thickness (similar to 2nd degree)
full-thickness (similar to 3rd degree)

(similar to first degree)

Low intensity flash

Superficial partial-thickness: Skin involvement

Possibly a portion of the dermis

Superficial partial-thickness: Symptoms

Hyperesthesia (supersensitivity)
Pain that is soothed by cooling

Superficial partial-thickness: Wound appearance

Reddned; blanches with pressure
Minimal or no edema
Possible blisters

Superficial partial-thickness: Recuperative course

Complete recovery within a week
no scarring

(similar to Second Degree)

Flash flame

Deep Partial-thickness: Skin involvement

Upper dermis
Portion of deeper dermis

Deep Partial-thickness: Symptoms

Sensitive to cold air

Deep Partial-thickness: Wound appearance

Mottled red base
Broken epidermis
weeping surface

Deep Partial-thickness: Recuperative course

Recovery within 2-4 wks
Some scarring and depigmentation
Infection may convert it to full thickness

(Similar to Third Degree)

Prolonged exposure to hot liquids
Electric current

Full-thickness: Skin involvement

Entire dermis
sometimes subcutaneous tissue
Connective tissue

Full-thickness: Symptoms

Pain free
Hematuria (blood in the urine)
hemolysis (Blood cell destruction)
Possible entrance and exit wounds (electrical burn)

Full-thickness: Wound appearance

pale white
Broken skin with fat exposed

Full-thickness: Recuperative course

Eschar sloughs
Grafting necessary
Scarring and loss of contour and function
Loss of digits or extremity possible

Estimating the TBSA
Rule of nines method

Head - 9% (includes anterior & posterior)
Each arm - 9%
Anterior trunk - 18%
Posterior trunk - 18%
Private's - 1%
Each leg - 18%

Lund and Browder Method
(More precise)

a method for estimating the extent of burns that allows for the varying proportion of body surface, especially head & legs, in persons of different ages. It is used instead of the rule of nines for children, in whom the head occupies a larger area and the lower limbs a smaller area than in adults.

Palmer Method
(For patients with SCATTERED burns)

Size of the patients palm excluding the digits is approx. 1% of the TBSA.

Cardiovascular changes

Fluid loss (> from 24-36hrs after burn)
vascular volume decreases
CO decreases and BP drops
this is onset of burn shock.
increase in peripheral resistance (vasoconstriction)
increase pulse rate

Fluid and Electrolyte alterations (emergent phase)

Edema forms within 4 hours.
Generlized dehydration (plasma leaks through damaged capillaries)
Reduction in blood volume (Secondary to plasma loss, fall of BP, and CO)
Decreased urinary output (Secondary to fluid loss, decreased renal flow, Na and H2O retention caused by increased adrenocortical activity, Hemolysis of RBC's)
Potassium (K+) excess
Sodium (Na+) deficit
Metabolic acidosis (loss of bi-carb ions accompanies Na loss)
Hemoconcentration (elevated hematocrit)

Fluid and Electrolyte alterations in the Acute phase
begins 48-72 hours after the burn injury

Hemodilution (decreased hematocrit)
Increased urinary output
Sodium (Na+) deficit
Potassium (K+) deficit (occurs occasionally in this phase)
Metabolic acidosis

Pulmonary Alterations

Upper airway injury from inhalation of direct heat(>302 F,150C)
Bronchoconstriction (caused by release of histamine, serotonin, and thromboxane - vasoconstrictors)
Lower airway (below glottis)
Tissue hypoxia due to carboxyhemoglobin)
Loss of ciliary action
severe mucosal edema
Pulmonary surfactant reduced = actelectasis (expectoration of carbon particles in sputum is the cardinal sign of this injury)

Renal alterations

If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resulting in tubular necrosis and renal failure.

Immunologic alterations

High risk for infection and sepsis
Loss of skin integrity is compounded by the release of abnormal inflammatory factors,
altered levels of immunoglobulins and serum complement
impaired neutrophil function
reduction in lymphocytes (lymphoctyopenia)

Thermoregulatory alterations

low body temps in early hrs. due to skin loss
hypothermic during postburn period

Gastrointestinal alterations

GI distention and nausea
Mucosal barrier becomes permeable (allows for overgrowth of GI bacteria)
Risk for abdominal compartment syndrome (ACS) - increased abdominal distention from fluid shift into abdominal cavity.
decreased urine output
respiratory insufficiency.
bladder pressure >25 mmHg may indicate increasing abdominal pressure.

Two main GI complications:

Paralytic ileus (absence of intestinal peristalsis)
-Maintain NG tube on low intermittent suction until bowel sounds resume. (this measure relieves gastric and abdominal distention, prevents vomiting)
Auscultate for bowel sounds, abdominal distention.

Curling's Ulcer - (gastric or duodenal erosion)
- assess gastric aspirate for pH and blood. (Acidic pH indicates need for antacids or histamine blockers. Blood indicates poss. gastric bleeding)
- Occult blood in stool may indidcate gastric or duodenal ulcer
- Administer histamine blockers and antacids as prescribed (these meds reduce gastric acidity and risk of ulceration)

Order of importance for burn patient.

A patent airway is ensured
Adequate peripheral circulation is established in any burned extremity.
A secure IV catheter is inserted w/LR solution infusing at a rate to maintain 30 mL/h
An indwelling urinary cath. is inserted
Adequate pain relief is attained
Wounds are covered with a clean, dry sheet, and the pt. is kept comfortably warm.

Emergency procedures at the burn scene.
Extinguish the flames

stop drop and roll
anything available to smother the flames

Cool the burn

Cover wound with some type of cloth dipped in cool water to help halt burning process.
NEVER apply ice directly to burn.
NEVER wrap person in ice
NEVER use cold soaks or dressings for longer than several minutes.
May lead to tissue damage or hypothermia

Remove restrictive objects

Helps allow for assessment and to prevent constriction secondary to rapidly developing edema.

Cover the Wound

Cover ASAP (minimize bacterial contamination)
Maintains body Temp.
Decreases pain by preventing air contact.
DO NOT use ointments and salves or apply any medications

Irrigate of chemical burns

brush off the chemical agent
remove clothes immed.
rinse all contact body areas
flush eyes if necessary

Management of Fluid using Parkland Formula

The Parkland Formula is as follows.
2 to 4mL Patient's weight in kg %BSA = Fluid for first 24 hrs (ml)
Afterwards, the first half of this amount is delivered in the first 8 hours, and the remaining half is delivered in the remaining 16 hours.

IV solution to use

Isotonic electrolyte solutions - most common

Nursing interventions during fluid resuscitation

Observe V/S
central venous pressure, or pulmonary artery pressure if indicated.
urine output
signs of hypovolemia or fluid overload
Monitor urine output at least hourly
Weight daily.

Evaluation of the effectiveness of fluid resuscitation:

Hypovolemia is a major risk factor immediately after the burn injury. Overresuscitation might cause fluid overload.
Output and weight provide information about renal perfusion, adequacy of fluid replacement, and fluid requirement and fluid status.
Serum electrolytes with normal limits
Urine ouput between 0.5 and 1.0 mL/kg/h
Blood pressure higher than 90/60 mmHg
HR < 120 beats/min
Exhibits clear sensorium
Voids clear yellow urine with specific gravity within normal limits.

Plan of care during the Emergent / Resuscitative phase.

First aid
Prevention of shock
Prevention of respiratory distress
Detection and treatment of additional injuries.
Wound assessment and initial care.

( Increasing PaCO2 and decreasing PaO2 sat. may indicate need for mechanical ventilation)

Goals during the Emergent / Resuscitative phase

Maintenance of adequate tissue oxygenation
Mainitain patent airway and adequate airway clearance.
Restoration of optimal fluid and electrolyte balance and perfusion of vital organs.
Maintenance of adequate body temperature
Control of pain
Minimization of pt's and family's anxiety

Infection prevention following a burn injury

Primary source of bacterial infection is the pt's intestinal tract.
- Early interal feeding is one strategy to help avoid increased intestinal permeability and prevent early endotoxin translocation.
Major secondary source is the environment.
- private rooms
- increased airflow within pt rooms to create positive airflow
- low humidification to prevent bacterial growth
- limited use of cloth (curtains, window treatments etc..)
- cap, gown, mask and gloves (all caregivers/visitors)
- hand hygiene
- antidust and dirt collection areas
- Aseptic technique when caring directly with wounds

topical antibacterial therapy drugs
Silver sulfadiazine (SILVADENE) Indication:

Most bactericidal agent
Minimal penetration of eschar

Silvadene nursing implications

Watch for leukopenia 2-3 days after initiation of therapy
Anticipate formation of pseudoeschar (proteinaceous get) which is removed easily after 72 hrs.

Silver Nitrate indications:

Bacteriostatic and fungicidial
Does not penetrate eschar

Silver Nitrate implications:

Monitor serum Na+ and K+ levesl
Silver nitrate solution is hypotonic and acts as wick for Na+ and K+.
Protect bed linen and clothing from contact with silver nitrate, which STAINS everything it touches BLACK.

Mafenide acetate (Sulfamylon) indications:

Effective against gram (+/-) organisms.
Diffuses rapidly through eschar
in 10% strength, it is the agent of choice for electrical burns because of it's ability to penetrate thick eschar.

Mafenide acetate (Sulfamylon) implications:

Monitor ABG's and discontiue if prescribed, if acidosis occurs
A strong carbonic anhydrase inhibitor that my reduce renal buffering
May cause metabolic acidosis
Premedicate pt. with an analgesic before applying
Agent causes severe burning pain up to 20 min. after appl.

Acticoat implications:

effective against gram (+/-) organisms and some yeasts and molds.
Delivers a uniform, antimicrobial concentration of silver to the burn wound.

Acticoat nursing implications:

Do not use oil-based products or topical antimicrobials with Acticoat burn dressing.
Keep Acticoat moist, not saturated.
May produce a "pseudo eschar" from silver application
Can be left in place for 3-5 days.

Wound dressing

Don not wrap to tightly
peripheral pulses must be ck'd freq.
burned extremities elevated on two pillows
Extremities are wrapped DISTAL TO PROXIMAL to the heart.
if pulse's are deminished = crucial sign that needs addressed

Natural wound debridement

Dead tissue naturally seperates from the body. Tissue underneath gradually liquefy the fibrils of collagen.
Antibacterial topical agents slow this natural process / healing

Mechanical wound debridement

use of surgical scissors, scalpels, forceps etc...
Usually done with daily dressing changes.
Wet to dry dressings are not advocated because of the chance of removing viable cells along w/necrotic tissue.

Chemical debridement

Should be used together w/antimicrobial therapy.
Seperate dressings used for silver and antimicrobial agent.

Surgical debridement

Initiated early in wound management before natural seperation of eschar is allowed to occur.
Rduced the incidence of sepsis
High risk of extensive blood loss

Homografts (allografts)

skin from living / recently deceased humans.
best protection
revascularization occurs within 48 hrs.
may be left in place for several wks.

Heterografts (xenografts)

Usually taken from pigs.
temporary covering (superficial paritia - thickness)
offers excellent pain control while wound epithelializes.

(CEA) cultured epithelial autograft:

Permanent coverage of large wounds when harvesting of skin or autografting is not an option.
grafts are thin and fragil, can shear easily
longer hospital stays, costs
more reconstructive procedures.


Patient's own skin
Not rejected

split thickness autografts

can be expanded and cover 1.5-9 times more than a given donor site area.
Skin mesher used
Scar formation
Allows the remaining donor site to retain sweat glands and hair follicles and minimizes donor site healing time.

Full thickness and pedicle flaps autografts

Commonly used for reconstructive surgery, which may take place months or years after the initial injury.

Burn patho

heat transfer from 1 site to another→coagulation, protein denaturation, or ionization of cellular contents→tissue destruction→↑ fluid loss, infection, hypothermia, scarring, compromised immunity, & changes in function, appearance, & body image

The depth of burn injury depends on

temp of burning agent
duration of contact w/burn agent

Burns that do not exceed 20% TBSA produce a

primarily local response

Burns that exceed 20% TBSA may produce

both a local & systemic response & are considered major burn injuries

Systemic response from burns is caused by

release of cytokines & other mediators into the systemic circulation; release of local mediators & changes in blood flow, tissue edema, & infection can cause burn injury progression

Pathophysiologic changes resulting from major burns during the initial burn-shock period include

-tissue hypoperfusion & organ hypofunction secondary to ↓ CO, followed by hyperdynamic & hypermetabolic phases; maximal response seen in burns >60% TBSA

Initial systemic event after a major burn injury is

hemodynamic instability resulting from loss of capillary integrity & shift of fluid, Na+, & protein from intravascular space into interstitial spaces which leads to hypovolemia

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