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)
Causes of SUPERFICIAL PARTIAL-THICKNESS
(similar to first degree)
Low intensity flash
Superficial partial-thickness: Skin involvement
Possibly a portion of the dermis
Superficial partial-thickness: Symptoms
Pain that is soothed by cooling
Superficial partial-thickness: Wound appearance
Reddned; blanches with pressure
Minimal or no edema
Superficial partial-thickness: Recuperative course
Complete recovery within a week
Causes of DEEP PARTIAL -THICKNESS
(similar to Second Degree)
Deep Partial-thickness: Skin involvement
Portion of deeper dermis
Deep Partial-thickness: Symptoms
Sensitive to cold air
Deep Partial-thickness: Wound appearance
Mottled red base
Deep Partial-thickness: Recuperative course
Recovery within 2-4 wks
Some scarring and depigmentation
Infection may convert it to full thickness
Causes of FULL-THICKNESS
(Similar to Third Degree)
Prolonged exposure to hot liquids
Full-thickness: Skin involvement
sometimes subcutaneous tissue
Hematuria (blood in the urine)
hemolysis (Blood cell destruction)
Possible entrance and exit wounds (electrical burn)
Full-thickness: Wound appearance
Broken skin with fat exposed
Full-thickness: Recuperative course
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
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.
(For patients with SCATTERED burns)
Size of the patients palm excluding the digits is approx. 1% of the TBSA.
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)
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)
If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resulting in tubular necrosis and renal failure.
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)
low body temps in early hrs. due to skin loss
hypothermic during postburn period
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
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
central venous pressure, or pulmonary artery pressure if indicated.
signs of hypovolemia or fluid overload
Monitor urine output at least hourly
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.
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.
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.
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.
Should be used together w/antimicrobial therapy.
Seperate dressings used for silver and antimicrobial agent.
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
skin from living / recently deceased humans.
revascularization occurs within 48 hrs.
may be left in place for several wks.
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
split thickness autografts
can be expanded and cover 1.5-9 times more than a given donor site area.
Skin mesher used
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.
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