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Treatment of Acute Burns

January 19, 2023 - read ≈ 28 min



Eric Emberton, MD


Dennis P. Orgill, MD, PhD


Mechanism of action of thermal burns 

Skin is a complex organ that protects humans from bacterial infection and minimizes fluid loss.  It is composed of two structural layers:  the epidermis which forms a barrier for fluid loss and the underlying dermis which is a thick collagenous structure that provides structural integrity to the skin.

Burns cause cell death most commonly from heat but also can occur from chemicals, electricity, or radiation.  Thermal burns occur by heat transfer into the skin and there is a relationship between the temperature applied at the surface of the skin and the duration of injury.  Because of the low thermal conductivity of skin, most injuries occur within 1 mm of the skin surface.  Subsequent vascular and immunological changes can cause burns to deepen over time which can be minimized by proper initial treatments.

Burns have been traditionally classified into 1st, 2nd and 3rd degree burns with 1st degree burns being superficial and involve just the epidermis.  These burns generally heal within a few days without scarring.  In contrast 2nd degree burns involve a portion of the dermis and their healing is related to the depth of injury.  3rd degree burns involve the entire dermis and do not contain any regenerative elements.  As such, these burns heal either by migration of cells from the edges or through reconstructive surgery such as skin grafts or flaps that bring in new cells to the injured area.  An uncommon type of burn is a 4th degree burn which involves tissues deep to the s1kin such as muscle and bone.  These burns require long contact periods of a heat source.

Optimal management of deep 2nd degree to 4th degree burns typically involves debridement and replacement with skin grafts or a dermal substitute, as the regenerative elements have been destroyed and will result in little to no wound healing.  Burn injuries may contain a mixture of different depths, and in areas of thicker skin, may take several days to fully declare.

Thermal burns result in a prolonged contact to a heat source, and length and temperature usually are directly correlated to the degree of burn (see figure).  This is true not only for heat, but also for cold as frostbite represents a unique type of soft tissue injury pattern from cold exposure with injury patterns similar to those for heat (see table).

The area closest to the heat source is the zone of coagulation, which is the area that is almost entirely necrotic or has sustained irreversible injury.  Below this is a zone of stasis and edema, an area of reduced blood flow and moderate injury to cellular structure.  This area is of particular importance as this is the area resuscitation efforts are attempting to salvage by preventing infection and hypoperfusion.  Superficial burns may be converted to deeper burns if improper management is undergone.  The next layer is the zone of hyperemia, which is an area of increased blood flow around 7 days after injury as a result of inflammatory cytokines from the injury.


This represents a type of thermal injury with exposure to the extreme cold versus extreme heat.  Risk factors for developing frostbite can be found in the table below.

Risk Factors for Developing Frostbite

• Homelessness
• Winter season
• Alcohol/tobacco use Inadequate shelter
• Moisture
• Malnutrition
• Immobilization
• Extremes of age
• Vasculopathy
• Diabetes
• Prolonged cold exposure

Most often, the “end organs” are damaged (distal extremities, digits, nose, ears) as they are the most vulnerable.  Normal skin perfusion is about 250mL per min but drops to virtually zero in temperatures below 0 degrees Centigrade due to vasoconstriction.  The venous system can then freeze, resulting in venous congestion then ultimately reduced perfusion.

Like injury from heat, cold injures tissues by direct contact, dehydration due to swelling, ice crystal formation leading to alteration in cell physiology, stasis, and eventually reperfusion injury.  Extracellular ice crystals first form, with continued exposure resulting in intracellular crystals and cellular damage.  This can result in increased osmotic gradient, membrane rupture and cell death.  This can result in a cytokine mediated inflammatory response and reperfusion injury. Again, like heat, frost bite injuries have a zone of coagulation, zone of stasis, and a zone of hyperemia. Also, frostbite is classification is like that of burns.

Classification of FrostbiteFindings
First DegreeCentral pallor with surrounding erythema and/or edema, desquamation, dysethesia, numbness
Second DegreeSkin blistering with milky fluid, erythema/edema
Third DegreeFull thickness skin loss, hemorrhagic blisters
Fourth DegreeFull thickness tissue loss including muscle, bone, tendon, etc, usually resulting in loss of the entire part.

When presented with a frostbitten patient, one should follow the ATLS algorithm.  Temperature exposed and duration should be ascertained.  Initial exam of the patient doesn’t accurately define extent of injury, as rewarming will result in edema, typically 3-5 hours later and last close 7 days.  Blisters may start to appear over the next 24 hours.  Eschar formation takes longer, usually 10-15 days.  If the entire digit/limb is lost, it may take weeks for the line of demarcation to form with mummification of the extremity.

Initial treatment should include covering the injuries, removing the patient from the elements, removing wet clothing.  Do not vigorously rub as this can cause further damage. It is also important to not rewarm the patient until it is certain that further exposure to freezing won’t occur, as this thawing/re-freezing can worsen the overall injury.  Underlying comorbidities should be addressed.  Core body temperature should be corrected prior to pronouncing dead if patient arrives in cardiac arrest.  Mild hypothermia should be treated with warm room and warm blankets or Bair hugger.  Moderate hypothermia should be treated with warmed intravenous fluids.

Warm water baths at 40-42 degrees Celsius can be used to warm affected extremities.  Severe hypothermia may need to be treated with cardiopulmonary bypass.  Anti-inflammatories can be used for pain control.  Continued clinical exams should follow re-warming. 

For second degree frostbite, drainage of the milky white blisters is controversial in the literature.  Hemorrhagic blisters should be left alone.  Early surgical debridement is not indicated, as some tissue can be reclaimed.  One should await full demarcation prior to attempts at debridement.  Amputation should be delayed up to six weeks, unless the area autoamputates.  As with the burn patient, hypotension should be avoided, and aggressive wound care to prevent infection should be priorities.

Patients should avoid cold exposure to affected area for a year.  They should be advised to wear proper clothing when exposed to the cold.  They should be counselled to avoid alcohol and tobacco.  Patients should be approached by multiple teams to best manage them, and there should be a low threshold to transfer the patient to a comprehensive healthcare center.

Chemical Burns

There are a variety of chemical burns that can result in injury.  It is important to identify the specific chemicals involved and to read the Material Safety Data Sheets (MSDSs). These are easily found on the internet.  Some have specific management.  We will cover a few common ones that may be encountered here.

Most common encountered chemical burns include acids, alkalis and irritants.  Most commonly, these are the result of spill or ingestion, either accidental or with ill intent.  Some of the commonly encountered ones are listed below:

ClassSpecific Compound
AcidSulfuric, nitric, hydrofluoric*, hydrochloric, acetic acid, formic, phosphoric, phenols, chloroacetic acid
BaseHydroxides (sodium, potassium, calcium), Hypochlorites (sodium, calcium), ammonia, phosphates, silicate, sodium carbonate, lithium hydride.
OxidantHome bleaches, peroxides, chromates, magnates
MiscWhite phosphorus, metals, hair coloring agents, airbag injury
VesicantsMustard gas

Initial exposure prompts copious irrigation to affected areas.  Any contaminated garments should be immediately removed from the patient, but PPE should be donned by the healthcare providers to protect themselves from exposure.  For ingestions, endoscopic examination is warranted.  One should not give emetic agents or neutralizing agents after ingestion.  For example, combining a base to an acid or vice versa to neutralize creates an exothermic reaction and can exacerbate the injury.  It may also increase the risk of aspiration.  Steroids, antibiotics or prophylactic renal/hepatic therapies are currently not recommended.  For phenol burns, polyethylene glycol is a better irrigate than water.

Disc batteries are a particular problem in children.  This can result in esophageal burns as well as burns along the GI tract that may result in perforation.  Endoscopic retrieval and radiographic tracking of these materials is warranted.

Supportive care is warranted.  For skin lesions, these are treated with local wound care and may require grafting if severe enough.  Esophageal burns should be monitored for stricture.  Eye burns should be closely followed and may result in corneal scarring/blindness.  Tarsorrhaphy may be required to protect the cornea from further ulceration.

Hydrofluoric Acid burns

This represents a unique chemical burn.  Hydrofluoric acid (HF) is used in cleaning agents, rust removals, semiconductor, fertilizer, and plastic manufacturing.  At low concentrations (<20%), its relatively safe but becomes more dangerous >20% concentrations.  However, if misdiagnosed and ignored for over 24 hours, then could progress along the pathway of higher concentration burns.  At >50% concentrations, the acidity increases significantly, and it behaves like a strong acid with immediate corrosive damage immediately seen.  Most HF burns are at lower concentrations, so this is rare.  The challenge with HF is that it has high tissue penetration due to his lipophilic nature, and releases hydrogen and fluoride ions in the presence of calcium and magnesium.  This results in local hyperkalemia, neuronal depolarization, and intense pain at the site of injury, and this ‘pain out of proportion’ is a hallmark of this type of chemical burn.  Systemically, patient should manifest nausea, vomiting, abdominal pain, convulsions, hypotension, and cardiovascular collapse.  Renal impairment, acidosis, electrolyte disturbances can also be seen.

Treatment is multimodal, and may require a mixture of topical, infiltrative, intra-arterial agents as well as surgery.  The idea is the deactivation of the fluoride ion, which is the main causative agent of these burns.  Calcium gluconate gel is standard of care in the United States, with older magnesium or ammonium-based compounds used to precipitate an insoluble fluoride salt.  These were less effective or had some systemic toxicity when compared to the former.  Calcium gluconate gel can also be made at bedside using a water-soluble lubricant (see Table).

LubricantCalcium Additive
75mL25mL of 10% calcium gluconate
100mL2.5g of calcium gluconate
Apply above every 30 minutes initially and massage in until some pain relief, then apply every 4 hours.  Monitor for pain relief.  May require large quantities due to surface area and degree of penetration that may require next steps if no pain relief.

For injectable calcium gluconate, should use smallest needle possible (27gauge or smaller) to inject 5-10% calcium gluconate subcutaneously.  This usually isn’t required for those that had concentrations <20%.  If on exam there is presence of a central hard gray area with surrounding erythema or continued pain after use of the gel, then this is indicated.  To avoid elevated compartment pressures, a limit of 0.5mL per phalanx should be adhered to.  Calcium chloride is avoided as the calcium salts are produced in high concentrations can be toxic to tissues.  The risk of infection and hypercalcemia should also be considered.

Intra-arterial calcium infusion is rarely used, and is reserved for severe burns with unrelenting pain despite calcium gel therapy.  This was originally used for high concentration HF burns where infiltration didn’t have a sufficient safety profile.  This requires intensive monitoring as its usually reserved for the extremities, particularly the hand, and cannulation of the brachial artery, which is typically done, has a high morbidity.  Complications (nerve palsies, carpal tunnel syndrome, hypercalcemia, arterial spasm) are higher with this method and it’s not readily used except in severe burns.  50mL of 4% calcium gluconate is given over 4-hour period and repeated every 12 hours until free from pain.

Surgical debridement is typically reserved for blisters and eschars to allow better penetration of calcium, but isn’t usually the mainstay of treatment.  The exception is the patient with > 5% total body surface area with >50% concentration with complications (i.e., arrythmia).  As with most chemical burns, staged debridements are often necessary to make sure all necrotic tissue is removed.

Electrical Burns

Electrical injury can be classified as low voltage or high voltage injuries.  Low-voltage current is considered is usually in the range of 110-120V and usually results in tetany whereas high voltage injury is often greater than 500V and results in deep burns.  However, electrical field strength (area of contact and the voltage encountered) also plays a role in the degree of injury.  Type of current also plays a role, with AC (alternating current) typically causing more damage than DC (direct current).

Electrical injuries are concerning in the sense that external manifestations don’t always adequately or accurately represent the internal damage.  Often times, it’s difficult to find the exit and entry point and this may represent the only external manifestation of electrical injury.  Because skin is a good insulator, electricity will travel the path of least resistance, which is usually through the muscle.  As a result, muscle injury and myonecrosis is common, resulting in significant edema and leading to compartment syndrome and rhabdomyolysis.

In general, muscle closest to bone is the most susceptible, as bone represents an area of increased resistance thus greater heat generation, worsening the muscle injury.  This also explains why areas across joints tend to suffer most damage, as a high volume of the cross-sectional area is made up of high resistant tissues thus more current travels through a smaller area of low resistance.

Low field strength will be accompanied by a sensation of shock and typically don’t result in significant injury.  However, high field strength injuries can lead to significant thermal damage that may result in protein coagulation, necrosis, hemolysis, thrombosis.  This leads to massive tissue edema, swelling and may lead to intravascular depletion and compartment syndrome.  Concerns for compartment syndrome should be treated promptly (see figure/table).  Compartment pressures can be measured in suspected cases but should not delay treatment if diagnosis is suspected.  Rhabdomyolysis, myoglobinuria and electrolyte disturbances can ensue resulting cardiopulmonary collapse and renal failure.

The SIX “p’s” of compartment syndrome

ParesthesiasUsually 1st sign, loss of 2-point discrimination or vibratory sensation.
PainPain out of proportion to exam findings.  Most sensitive is pain on passive stretch.
pulse deficitCan present early due to venous outflow obstruction resulting in increased perfusion pressure
PallorOccurs later, usually poor prognostic indicator.
PoikliothermiaCold limb, usually a late finding
paralysisUsually due to ischemic neuritis, late finding >6 hours after onset.  Usually is permanent once develops.
Compartment PressuresTreatment
0-10mmHg (Normal)None needed
11-20mmHg (Mild Elevation)Serial exams, elevation
21-30mmHg (Moderate Elevation)Frequent exams, elevation, low threshold for fasciotomy
>30mmHgFasciotomy indicated
↑ The delta pressure (Diastolic pressure – Compartment pressure) can also be used, a ∆Pof <30mmHg is indication for immediate fasciotomy.
*While these are important numbers, compartment syndrome is a clinical diagnosis and fasciotomy should be performed if suspected, especially in the comatose patient.

Cardiac manifestations are also common.  Patients with electrical injury should undergo strict cardiac monitoring for arrythmias for no less than 24 hours.  Initial EKG should be obtained.  Associated electrolyte abnormalities should be corrected in a judicious manner.  External wounds should be treated similar to thermal burns, but it’s usually the internal injury that is the more major player.

Patient presenting with suspected electrical burns should be managed along the ATLS algorithm.  Life threatening and limb threatening injuries should be first addressed.  Labs and EKG should be obtained, and depending on severity of assessment, patient should be monitored in the hospital for at least 24 hours vs the ICU.  Patients should be transferred to a burn center with a multidisciplinary team suited to address all potential problems and complications.


While the focus of this article is primarily on thermal injury, we will briefly cover radiation exposure.  Ionizing radiation damages cells both directly and indirectly by creation of oxidative species.  Metabolically active cells (lining of GI tract, skin, stem cells) are among the most radiosensitive, thus among the most prone to injury.  Patients with connective tissue disorders seem to be more prone to injury.  Those on certain medications also seem to be more radiosensitive (actinomycin D, doxorubicin, bleomycin, 5-fluorouricil, methotrexate).  Areas of thinner skin and the extremities are more sensitive.  Hair follicles are also sensitive, with hair on the scalp being the most but the skin being more resistant compared to skin elsewhere.

Contaminated particles can cause both external and internal damage.  Inhaled dust, especially in children, can be particularly dangerous for long term sequelae.  Open wounds can be a source of internal contamination and should be addressed.  When patients present suspected of radiation exposure, you should first don personal protective equipment and address the patient’s acute, life-threatening injuries first.  Once stabilized, the patient’s contaminated clothing should be removed, and patient cleansed of debris/particulate.  Care should be taken to not to shake the material to shower the room with radioactive material.  Roll the clothes into a sheet and dispose of in a proper labeled container.

Removal of clothing typically remove 90% of materials.   The rest of the body should be surveyed, and priority given to open wounds as this can lead to significant radiation exposure.  All visible debris and metallic pieces should be removed.  If using a radiation detector, a piece of lead can be placed between the detector and wound to see if counter decreases.  Once addressed, the wound should be cleansed and covered with waterproof drapes.  Irrigate gently with warmed water or saline, ensuring to capture irrigate in radioactive labeled container.  Blot dry with gauze and dispose of in radioactive container.  Repeat these steps as many times as necessary.  Burns should be treated like any other thermal or chemical burn with the consideration that the eschar is radioactive. 

Next, attention should be turned to the face and orifices.  Using a cotton-tipped applicator, survey for radioactive material in the mouth, ears, and nose.  For oral contamination, frequent mouth rinsing and tooth brushing is recommended, with 3% hydrogen peroxide rinses being useful.  Eyes should be evaluated for foreign bodies and damage to the globe.  The eyes are then irrigated copiously with fluid collected in appropriate disposal container.  Care should be taken to avoid flushing irrigation into the nasolacrimal duct; thus, irrigation should be carried out in a medial to lateral direction.  If the external auditory canal is contaminated, irrigation with a bulb syringe should be performed if the tympanic membrane is intact.  Nasal decontamination should follow similar route.  Patient should blow their nose followed by irrigation with lukewarm water or saline with the patient leaning forward to avoid swallowing contaminated fluid.

Skin and hair should then be decontaminated.   Lukewarm water should be used (cold water can close pores and trap material).  The area can be gently sponged with a mild soap.  Following all decontamination, one should resurvey the areas with a radiation detector to make sure adequate decontamination has been processes. 

Radiation exposure symptoms depends on dose of radiation.  GI manifestations can be prognostic.  Early and severe nausea, vomiting, diarrhea and GI upset may signify significant radiation injury and is associated with high mortality.  The LD50 (median radiation dose with 30 day mortality of 50%) is approximately 4.5Gy.

Manifestations of acute skin injury from radiation occurs <30 days from exposure.  Depending on the duration and amount of exposure, injury consists of erythema that goes away in a few days to desquamation and ischemic dermal necrosis.  High enough doses may result in a second hyperemic phase that occurs 1-2 weeks later.  This is an erythematous reaction that peaks by 2 weeks, usually after 6 Gy of exposure.  Area is warm, burning, itching, and tender as a result of the damaged cells in the basal layer of the epidermis, and may fade away with doses <6 Gy.  Hair loss may be seen at 3 weeks, and may be temporary or permanent if dose is >7 Gy.   If doses of 14 Gy is reached, dry desquamation occurs.  This consists of dry, scaly skin due to sebaceous gland loss.  Doses of >18 Gy result in moist desquamation, which resembles a deep partial thickness burn with epidermolysis and blistering.  At these doses, ischemic dermal necrosis may be seen at 1-2 months.  These wounds may heal with wound care but may persist for years.  These are the wounds that require flap reconstruction.  Late sequelae of radiation exposure occurs many years later and will not be discussed here.

Skin manifestations are just the tip of the iceberg in terms of damage.  Underlying organs are can also be damaged with symptoms related to the organ damaged.  Myelosuppression can occur due to bone marrow damage, requiring supportive care with colony stimulating factors and blood transfusions for support.

Radiation associated with nuclear blasts create a multitude of issues.  Within a certain radius will be significant blunt trauma from the blast shockwave.  Outside of this, heat will result in significant thermal burns.  Radiation is also a major issue as fall out can be carried many miles away by the elements. A nuclear blast is about 50% blast, 35% thermal energy, 4% initial ionizing radiation (within first minute of blast) then 10% fallout, and about 1% EMP.  By this breakdown, one can see the extent of aftermath expected to be encountered following nuclear detonation.

Initial Assessment and Treatment

When assessing the burn patient, priorities to primary survey in trauma care can’t be overly emphasized.  The airway, breathing and circulation should first be managed.  The patient should then be assessed for any neuro-deficit, assigned a GCS and treated accordingly.  The patient should then be exposed from head to toe to fully assess extent of injury.  The TBSA (or total body surface area) involved in the burn can be estimated using the figure below (Rule of 9’s in adults and the Lund-Browder chart for age-based estimation).  Another general rule is that the palm of the patient represents 1%, so a general estimate can be obtained by using that as a guide, or the practitioner’s own hand, for estimating TBSA. 

However, during this time, the patient should be kept as warm as possible as hypothermia can lead to worse outcomes, particularly infectious.  Upon initial assessment, it is important to note criteria that would prompt urgent transfer to a burn center after the patient has been stabilized for transport.

Criteria for Transfer to a Burn Center in the US

• >10% TBSA partial-thickness burns
• Third-degree burns
• Burns involving face, hands, feet, genitalia/perineum, major joints
• Electrical or chemical burns
• Inhalation Injury
• Burns with trauma that increases risk of death or complications
• Burns with pre-existing medical condition that increases risk of death or complications
• Burns in children
• Burns in patients who require specialized social, emotional or rehabilitative help

For this reason, a good history involving mechanism, timing and prior health conditions are of utmost importance.  Patients with suspected inhalation injury or involved in house fires (one where upholstery or other industry made products are contained) or high suspicion of carbon monoxide poisoning should be intubated immediately for airway protection.  Concerning physical exam findings include poor mentation, soot in nares/throat, singed nose hairs.  Once resuscitation efforts ensure, airway edema will result and rapid deterioration with difficult airway could follow.

There are multiple formula’s used to assess for fluid management, the one that is most widely accepted now is: 2ml x body weight (in kg)x %TBSA where the % TBSA is >20%, and this estimates the amount of fluid a patient should receive in 24 hours

Those with <20% can take in PO with IV supplement titrated to meet their fluid goals.  For resuscitation, we prefer an isotonic fluid such as Lactated Ringer’s with an osmolarity similar to that of plasma (290 osm).  We would recommend avoiding fluids that would make the patient more acidotic as these patients are already acidotic and adding to this would result in worsening the acidosis.  Traditionally, the Parkland formula was used but this usually led to over resuscitation.  A foley catheter should be placed as urine output is the primary endpoint of resuscitative efforts.  The goal urinary output varies by age group (see table).  There had been some shift to personalized endpoints for patients, but in the setting on acute management, this is a sufficient generalized protocol to follow.

AgeGoal urinary output
>1230-50cc per hour

Avoidance of over-resuscitation is critical.  This can lead to prolonged intubation, edema, and eventual abdominal compartment syndrome (see figure for signs, symptoms and management). 

Circumferential burns can lead to compartment syndrome in the extremities and inability to ventilate in the chest/back.  These patients are most often those involved in thermal injury in which the heat source is open flame.  These patients almost always have full thickness burns characterized by leathery skin.  Any signs of compartment syndrome should prompt emergent escharotomy.  These are full thickness skin incisions down to the fascia.  In the case of electrical burns, compartment syndrome often arises due to the internal injury without significant evidence of external burns.  Patients suspected of compartment syndrome in this instance should undergo emergent fasciotomies to preserve life and limb. Release of myoglobin from dying muscle can result in renal failure and release of potassium can result in life threatening cardiac arrythmias. For this reason, patient should be undergoing strict cardiac monitoring and correction of electrolyte derangements. They should also receive IV resuscitation to prevent renal failure. Giving the patient bicarbonate to alkalinize the urine is theorized to be helpful but should be carefully monitored to prevent systematic alkalosis and hypernatremia.  Loop diuretics and osmotic diuretics (such as mannitol) can be used for diuresis, but care must be taken to avoid hypoperfusion.

Burn wounds are initially dressed with nonstick gauze over the wound bed covered with dry gauze.  Petroleum based gauze dressings are a popular choice for dressing the wounds.  Topical antimicrobials such as silver sulfadiazine (Silvadene), silver nitrate, bacitracin, and mafenide acetate are commonly used in the United States.  Twice daily dressing changes are sometimes needed due the amount of effluent from the wounds.  Wound care should be aggressive as this is the key to infection prevention, along with correction of the deadly triad.  Prophylactic systemic antibiotics are no longer indicated, and should be given only if active infection is suspected.  Those with Staphyloccocus aureus, Pseudomonas aeruginosa, and Acinetobacter are particularly concerning due to increased antibiotic resistance in these organisms.  In patients with suspected infection, broad spectrum antibiotics should be given and tailored to cultures.

After the patient is stabilized, one can start preparing the wound bed for grafting.  This should be done after correction of the deadly triad (hypothermia, coagulopathy, acidemia).  This should not be done in the field, but rather in a controlled setting as it is not part of the resuscitative efforts.  Wound grafting results in normalization of fluid and heat losses for the patient.  Excision of all devitalized tissue should be carried out tangentially utilizing a guarded blade down to a layer of capillary bleeding.  This can result in significant blood loss (as high as 100-200ml per 1% TBSA excised), and so we recommend gauze soaked in dilute epinephrine to assist in hemostasis.

Large burns may need to be carried out in a staged approach for this reason.  Blood products should be available, with attention not just paid to packed red blood cells, but plasma and platelets as well.  One institution advocates for FFP to be given at a rate of 0.5ml per kg body weight per % TBSA involved once TBSA exceeds 30% for the first 24 hours then colloid at the same rate following this.  Another option for excision, more so for deep burns involving entire dermis, would be excision down to fascia utilizing cautery which would result in better hemostasis and early grafting, but would result in sensory loss and significant cosmetic deformity.  In case of bone/cartilage involvement, this should also be debrided and may require coverage with local or distant flap.  Timing for excision of devitalized tissue is within a week of injury.

Split thickness skin graft harvested from the patient provides the ideal coverage option.  This is harvested typically with an air-powered dermatome (Stryker dermatome), but can also be harvested using a Watson knife or similar.  The thickness typically ranges from 2-5mm, or 0.08-0.2 inches.  Some providers injection local anesthetic and/or dilute epinephrine under the harvest site to not only provide a platform for even harvest, but also provide pain relief and hemostasis.  These can be meshed at a 2:1 or 3:1 ratio to increase the surface area covered, especially in the patient that has little native skin to harvest.

The donor site can be covered with silver foam or petroleum gauze and allowed to re-epithelialize over the ensuing weeks, then re-harvested.  New skin grafts should be placed in a clean, healthy wound bed with overlying petroleum-based gauze and dressings applied.  The grafts should be sewn to the native tissue with dissolvable suture, going from ‘ship to shore’ (from graft to native edge), with care taken to make sure there is no tenting in the skin graft thus to prevent loss of graft.  For the same reason, fluid collections under the graft should be evacuated.  Graft that does not take should be debrided.  In a pinch, dermal substitutes or allograft (cadaver skin) can be used to cover the wounds, but it must be noted the increased infection risk.  Over joints, either full thickness grafts or local flaps should be used for coverage.  This helps prevent significant contracture and functional loss.  Long term management of burn scars/contractures is a complex topic and beyond the scope of this text.


The burn patient represents a complex problem as often a burn patient doesn’t present with isolated burn injury, but rather as a complex trauma patient.  It is important to emphasize that the trauma algorithm should be followed and the primary survey shouldn’t be ignored.  In the acute phase, treating life threatening injuries should be addressed first then attention turned to addressing the acute burns then burn reconstruction.


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    Image (eschar) adapted from: Escharotomy – Procedure Instructions An unlikely … | GrepMed
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