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This returns cold blood from the extremities to central
circulation and can result in systemic hypothermia.
*
Initial Frostbite Treatment
Rapid rewarming of affected area in 104 °F-108 °F water
bath, not radiant heat
Ibuprofen 400-600 mg PO QID
Antibiotic prophylaxis to cover Staph, Strep, Pseudomonas
Pentoxifylline 400 mg PO TID
Elevation of limb with splinting to decrease movement
No smoking, caffeine, or chocolate
Tetanus prophylaxis
Three-phase bone scan may identify “at-risk” tissue
Acute Interventions
For stable patients with severe frostbite, rapid extrication to
a center with interventional radiology capabilities within 12
hours is indicated.
Arterial catheterization can identify and treat
vasospasm and microvascular thrombosis with tPA or
heparin.
Reversal of local microvascular thrombosis may
restore perfusion before irreversible necrosis and
ischemia occur.
Several studies have shown significant decrease in
amputation and tissue loss with this aggressive
protocol.
Early regional sympathectomy of an affected extremity is
controversial.
PROGNOSIS
Tissue necrosis may be superficial with underlying viable tissue.
Complete demarcation usually takes several weeks. Therefore,
amputation should not be considered until complete tissue loss
is established.
Cold intolerance and an increased susceptibility to cold injury
are likely in the affected part or extremity.
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STEVENS-JOHNSON SYNDROME
AND TOXIC EPIDERMAL
NECROLYSIS
ETIOLOGY
Both Stevens-Johnson syndrome (SJS) and toxic epidermal
necrolysis (TEN) have widespread necrosis of the superficial
portion of the epidermis.
*SJS/TEN is commonly associated with sulfonamides,
trimethoprim-sulfamethoxazole, oxicam NSAIDs,
chlormezanone, and carbamazepine. However, a single
offending drug is identified in <50% of cases.
Antibiotic-associated SJS/TEN presents ∼7 days after drug
is first taken.
Anticonvulsant-associated SJS/TES can present up to 2
months after drug is first taken.
TEN can also be caused by staphylococcal infections in
immunocompromised patients.
CLASSIFICATION
SJS: total involvement <10% TBSA. Widespread erythematous
or purpuric macules or flat atypical targets are present.
Overlap SJS-TEN: total cutaneous involvement of 10%-30%
TBSA. Widespread purpuric macules or flat atypical targets are
present.
TEN with spots: total cutaneous involvement of >30% TBSA.
Widespread purpuric macules or flat atypical targets are
present.
TEN without spots: total cutaneous involvement >10% TBSA.
Large epidermal sheets present. No purpuric macules or
targets.
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PRESENTATION
Initial symptoms can be a 2- to 3-day prodrome of nonspecific
findings like fevers, headaches, and chills.
Symptoms of mucosal irritation like conjunctivitis, dysuria,
and/or dysphagia may be present. These symptoms are
followed by mucosal and cutaneous lesions.
Mucosal irritation, typically at two or more sites. Involved sites
may include vaginal, urinary, respiratory, gastrointestinal, oral,
and/or conjunctival.
Skin lesions are diffusely present
Lesions are typically erythematous macules with purple,
possibly necrotic centers.
Nikolsky sign is typically positive (rubbing the skin causes
exfoliation of outermost layers and/or a new blister to form).
Differential diagnosis of acute, diffuse blistering includes
staphylococcal scalded skin syndrome, pemphigus vulgaris,
pemphigus foliaceus, paraneoplastic pemphigus, bullous
pemphigoid, acute graft vs host disease, and linear IgA
dermatosis.
Diagnosis of SJS/TEN is largely clinical and can be confirmed
by skin biopsy and histology.
TREATMENT
Discontinue all potentially offending drugs.
Transfer to a burn ICU for fluid/electrolyte monitoring, dressing
changes, and temperature regulation is recommended.
Débride flaccid bullae. Initial wound care with dressing changes
until extent of skin loss is known.
Empiric systemic antibiotics have been associated with
increased mortality and are not indicated.
Consider hemodialysis to remove potentially offending drugs
with long half-lives.
Early ophthalmology consultation. Over 50% of SJS/TEN
patients can develop symblepharon or entropion.
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Can involve other consultant services (pulmonary, urology,
OB/GYN, gastroenterology) as needed.
Administration of steroids and IVIG is controversial. TEN is
known to overexpress FAS, which promotes apoptosis of
keratinocytes by binding to the FAS/CD95 receptor. IVIG blocks
the CD95 receptor and has been efficacious in small series of
TEN patients.
OUTCOMES
SJS has a mortality of between 1% and 5%. TENS has a mortality of
up to 44%.
PEARLS
1. The Parkland formula is only a guide to approximate fluid
replacement. Real-time monitoring of urine output (0.5 cc/kg/h
adults, 1 cc/kg/h in children) is the most important indicator of
adequate resuscitation.
2. Be wary of inhalation injury and have a low threshold for early
endotracheal intubation.
3. Wounds that are not closed by 3 weeks (through healing on
their own or skin grafting) are at high risk for hypertrophic scar
formation.
4. Electrical injury can cause harm via multiple mechanisms,
including cutaneous burns from arc or clothing fire, deep tissue
burns from current flow along bones, concomitant traumatic
injury, and cardiac arrhythmia.
5. Compartment syndrome is treated with decompressive
fasciotomy.
6. The most important immediate frostbite intervention is rapid
rewarming in a 104 °F-108 °F water bath.
QUESTIONS YOU WILL BE ASKED
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1. How does a skin graft survive?
a. *Initially the graft survives by imbibition or diffusion of
nutrients from the surrounding serum (first 48 hours).
b. Inosculation (days 2-3) connections forming between vessels
in the skin graft and from the recipient site.
c. Revascularization, with new blood vessel ingrowth into the
graft (days 5-7).
2. How should we deal with exposed ear cartilage?
a. Sulfamylon is the preferred topical wound dressing because
it has good cartilage penetration.
b. Small amounts of exposed cartilage can be resected with
primary closure.
c. Large amounts may require temporal-parietal flap closure
with skin grafting.
3. What factors cause a skin graft to fail?
a. Shear forces
b. Infection or inadequate débridement
c. Fluid collection beneath the graft (hematoma most common,
seroma)
d. Poor nutrition
4. How is compartment syndrome diagnosed and treated?
a. Compartment syndrome is a clinical diagnosis, typically
made using the 6 “P’s” (see above). Measurement of
intracompartmental pressures is a useful adjunct when
clinical diagnosis is unclear or the patient is unresponsive.
Compartment syndrome requires compartment release of
the affected areas, typically the forearm and/or hand.
b. *Diagnosis: absolute pressure ≥30 mm Hg or pressure within
20 mm Hg of the diastolic blood pressure is also diagnostic
of compartment syndrome.
5. Which is worse: acid burns or alkali burns?
Alkali. Alkali burns will continue to extend deeper into tissues
until the source is removed or diluted. Acid injury is typically
limited to the exposed area.
6. Who is at risk for frostbite?
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1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Any patient with cutaneous dilation, decreased awareness of
their surroundings, or loss of instinct to seek shelter.
THINGS TO DRAW
1. Draw basic schematic of percent burn percentage per body part
(Fig. 10-1).
2. Draw incision lines for escharotomy (Fig. 10-3).
Recommended Readings
Arnoldo B, Klein M, Gibran NS. Practice guidelines for the management of
electrical injuries. J Burn Care Res. 2006;27(4):439‐447.
Bruen KJ, Ballard JR, Morris SE, Cochran A, Edelman LS, Saffle JR.
Reduction of the incidence of amputation in frostbite injury with thrombolytic
therapy. Arch Surg. 2007;142(6):546‐551. discussion 551–553
Friedstat JS, Klein MB. Acute management of facial burns. Clin Plast Surg.
2009;36(4):653‐660.
Gerull R, Nelle M, Schaible T. Toxic epidermal necrolysis and Stevens-Johnson
syndrome: a review. Crit Care Med. 2011;39(6):1521‐1532.
Hazin R, Ibrahimi OA, Hazin MI, Kimyai-Asadi A. Stevens- Johnson syndrome:
pathogenesis, diagnosis, and management. Ann Med. 2008;40(2):129‐138.
Klein MB, Moore ML, Costa B, Engrav LH. Primer on the management of face
burns at the University of Washington. J Burn Care Rehabil. 2005;26(1):2‐6.
Mohr WJ, Jenabzadeh K, Ahrenholz DH. Cold injury. Hand Clin.
2009;25(4):481‐496.
Palao R, Monge I, Ruiz M, Barret JP. Chemical burns: pathophysiology and
treatment. Burns. 2010;36(3):295‐304.
Schulz JT, Sheridan RL, Ryan CM, MacKool B, Tompkins RG. A 10-year
experience with toxic epidermal necrolysis. J Burn Care Rehabil.
2000;21(3):199‐204.
Sterling J, Gibran NS, Klein MB. Acute management of hand burns. Hand Clin.
2009;25(4):453‐459.
*
Denotes common in-service examination topics.
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11
Burn Reconstruction
Megan Lane and Ayana K. Cole-Price
OVERVIEW
TECHNIQUES IN ACUTE BURN CARE
THAT CAN DECREASE LONG-TERM
RECONSTRUCTIVE NEEDS
Please see Chapter 10: Burns for appropriate resuscitation of
thermal injuries.
Fasciotomies, entrapment release, and repair of any ocular
injuries are critical in the acute burn period.
Use sheet grafts when possible and full-thickness grafts for the
hands and face with attention to the aesthetic units of the face.
Initiate early motion and pressure garments as soon as
possible.
Apply splints with hands in intrinsic plus and joints in extension
to prevent flexion contracture.
For patients with eyelid burns, tarsorrhaphy in the first weeks
following burn can be helpful in preventing exposure
keratopathy.
Exposed cartilage and severe microstomia require urgent
reconstruction in the subacute period.
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MAJOR RECONSTRUCTIVE
CHALLENGES FOLLOWING BURN
INJURIES
Burn Contractures
Tight, shortened scars from tissue deficit.
Can form across joint creating limitation of movement.
Can involve more than skin: causes shortening and fibrosis
of underlying muscle, fascia, and joints.
More common on flexor surface because flexors are
stronger and flexed position is position of comfort.
Assessment of contracture should include description of
functional limitation, presence of joint involvement, quality
of scarred skin, condition, and a vailability of surrounding
tissue.
Nonoperative treatments include occupational therapy and
pressure garments.
Pressure garments thought to reduce hypertrophic scarring
and contractures by reorienting collagen fibers and reduce
fiber thickness.
Scar Deformity
Risk factors: wound closure, infection, Fitzpatrick scale
Characteristics of problematic scars: poor pliability,
hypertrophic scarring, tissue loss, uneven surface, pigment
change, fragility, chronic open wounds
Have high suspicion for malignancy Marjolin’s ulcer in
chronic wounds, which have been persistent for years
Pigment and Hair Loss
Pigment
Hyperpigmentation and hypopigmentation can develop
at the burn site or the donor site.
Topical treatment options: hydroquinones and retinoids
can be used for hyperpigmentation.
Lasers additionally useful. Pulsed dye can be utilized
for red scars and fractionated CO2 laser can soften
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thick scars.
Hair Loss
Can occur in grafted region or in region of deep burn
without grafting.
Small areas addressed with excision and tissue
rearrangement, large areas with tissue expansion.
Micrografts can be used for eyebrows and moustache
region.
Excess hair from thick grafting can be treated with
laser (Alexandrite or Nd:YAG) or electrolysis.
Timing for Reconstructive Surgery
Urgent Reconstructive Surgeries
Severe microstomia
Exposed cartilage
Release of vital structures (eg, eyelid, exposed cornea)
Semi-elective Procedures (Should Be Done Within First
Few Months to 1 Year)
Release of joint limited by range of motion
Progressive deformities
Elective Procedures (Should Be Done After 1 Year to Allow
Scars to Mature)
Aesthetics
Hypertrophic scars
SURGICAL TECHNIQUES
CONTRACTURE RELEASE
Linear incision through scar overlying point of maximum
tightness, oriented perpendicular to line of contracture.
Incise skin and then keep area on tension and carefully push
with scalpel.
If contracture persists, may need to release underlying fascia,
muscle, tendon, or joint.
Commonly paired with local tissue rearrangement.
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LOCAL TISSUE REARRANGEMENTS
(SEE CHAPTER 4)
For example, the standard Z-plasty (Fig. 11-1).
Figure 11-1 Z-plasty.
Like contracture release, the central limb of Z-plasty is
perpendicular to the area of scar being released.
Prior to inset, assess the transposition of the Z. If the Z does not
transpose, deepen the Z-plasty.
Jumping man and series of Z-plasties are commonly used within
burn reconstruction, particularly in web spaces or in joint
contractures.
GRAFTS
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