2 Albert Einstein Medical Center, Philadelphia, PA, USA
Background
Definition of disease
Burns are a heterogeneous disease characterized by tissue injury due to cellular damage from a transfer of energy with local and systemic consequences.
Incidence/prevalence
The incidence of burn injuries has declined over the past several decades but remains a leading cause of accidental death in the USA and worldwide.
About 1 million burn injuries occur annually in the USA and about 50 000 require hospitalization.
Burn‐related mortality is estimated to occur approximately every 3 hours in the USA and there are about 250 000 burn‐related deaths per year worldwide.
Etiology
The most common etiologies of burn are scald and flame injuries.
The next most common in decreasing order of frequency are contact, electrical, and chemical burns.
About 65% occur at home, 17% at work, 5% during recreation, 5% are self‐inflicted, and the rest undisclosed.
Pathology/pathogenesis
Typically, the severity of injury is determined by four factors: temperature of an object, amount of time in contact, location of injury, and specific heat of the object (or its ability to transfer energy). These factors contribute to burn depth and size, which are the ultimate determinants of severity of injury.
Reversible protein degradation occurs above 40°C with permanent denaturation and coagulative necrosis starting at 45°C.
The area of injury can be divided into three zones:
Coagulation (non‐viable).
Stasis (salvageable).
Hyperemia (inflamed but viable).
The early goal is to prevent progression of the zone of stasis and death of this tissue.
Systemic inflammatory response syndrome
When a burn injures 20–30% of the total body surface area (TBSA), systemic manifestations occur. Release of inflammatory mediators results in macro‐ and microcirculatory dysfunction and multiorgan damage. Large fluid shifts occur from ‘third spacing’ of intravascular fluid and protein from capillary leakage and increased insensible fluid loss from open wounds and enhanced metabolic activity.
In severe cases, burn shock occurs, which shares components of depressed myocardial function in combination with decreased intravascular volume.
Fluid resuscitation is a necessity but over‐resuscitation can exacerbate formation of edema and cardiogenic dysfunction.
Within 48 hours, production and release of catecholamines, glucocorticoids, glucagon, and dopamine results in a hypermetabolic/catabolic state. Glycogenolysis and insulin resistance cause hyperglycemia, and increased lipolysis and proteinolysis provide further substrate for gluconeogenesis.
In severe burns, protein loss can occur at a rate of up to 25 g/m2 of burned tissue per day and is associated with impaired wound healing and immunity.
Initial resting energy expenditure at time of admission is 140% of normal and can remain elevated at 110% 2–3 years later.
Oliguria and kidney injury may develop without adequate resuscitation.
Hepatic dysfunction occurs, and mucosal atrophy occurs in the gut.
Depression of the reticuloendothelial system leads to decreased quantity and impaired functioning of immunologic cells.
Most of these pathophysiologic mechanisms have been shown to correlate with severity of injury, and can improve with wound excision and closure.
Evolution of injury
Without early and aggressive care by experienced providers, multiorgan failure and death can rapidly develop.
Whereas partial thickness burns heal spontaneously from epidermal remnants and rarely scar, full thickness burns heal slowly from the wound edges.
This slow process in combination with impaired immunity, weakened nutrition, and necrotic tissue substrate provide a viable environment for infection to develop, which is the leading cause of death in burns.
As wounds heal, they contract and form hypertrophic scars, leaving functional and aesthetic deformities.
Predictive/risk factors for fire death
Risk factor
Relative risk
Age >85 years
4.6
Age <5 years
1.4
African‐American
6.9
American‐Indian
5.3
Other notable risk factors include mental or physical illness, use of sedative or illicit drugs, and military personnel.
Prevention
Primary prevention
Multiple public health measures have contributed to a reduced incidence of burn injuries in the past two decades.
The advent of and improvement in fire alarms have led to improved fire detection and the use of fire friendly materials, and sprinkler systems limit spread of fire after it develops.
Safety mechanisms on electric devices, cooking appliances, and mechanical objects in addition to emergency exit routes at home and workplaces reduce the frequency and severity of injuries.
Increased public awareness with educational programs in conjunction with improved fire professional proficiency have led to reduced incidence and more rapid triage and management of burn traumas.
Diagnosis
Differential diagnosis
Differential diagnosis
Features
Frostbite
Tissue injury more likely to be symmetric and in sensitive areas including digits, nose, and ears
Appears as second degree burns and are often diffuse, affecting mucous membranes as well and accompany history of medication use or recent infection
Typical presentation
Burns can occur in people of all ages and oftentimes patients or their families are a reliable source for mechanism of injury. In unaccompanied young children or in those with cognitive impairments, one should search for other clues.
In fire and smoke‐related incidents patients may present covered in soot with associated clothing damage.
More common scald, flame, and contact injuries will present with erythema, blistering, severe pain and tenderness, or anesthesia at the site of injury depending on the severity.
Electrical or chemical burns are more likely to be associated with specific recreational or occupational histories and but may otherwise have a similar physical presentation.
Clinical diagnosis
History
Several important features of a history are useful in triaging a burn patient. The AMPLE (allergies, medications, past medical history, last meal, events) history is applicable to all trauma patients.
The source of the burn (e.g. scald, electrical, chemical) is important for assessment and management of the injury.
One should ascertain whether the patient was entrapped in a closed space, how much time has passed since the injury occurred, and whether there was loss of consciousness.
Tetanus status should be ascertained.
Physical examination
Evaluation of airway, breathing, and circulation, disability, and exposure are paramount in primary examination.
Dyspnea or stridor, coughing up sputum, and singed hairs should raise suspicion for airway injury.
Circumferential chest or extremity burns can impair breathing or circulation, respectively.
One should maintain a relatively low threshold for intubation as rapid progression of airway edema can progress to a surgical emergency.
Disability or altered consciousness may suggest other underlying conditions such as carbon monoxide or cyanide poisoning, hypoxia, or other conditions.
Exposing the patient both removes a source of potential continued injury and permits assessment of extent of injury.
In conjunction with a complete secondary examination, thorough assessment of burn size and depth is important to both guide initial management and to establish a baseline, as burns are dynamic and can convert to larger wounds over time depending on the recovery of the zone of stasis.
Burn size can be estimated using the rule of nines or a Lund and Browder chart, and is critical for determining resuscitation, prognosis, disposition, nutritional support, and the need for potential surgical interventions.
After estimating the amount of burnt TBSA, the Parkland formula can be used to guide fluid resuscitation:
%TBSA × weight (kg) × 4 mL = total first 24 hour fluid requirement. Half should be given within the first 8 hours and the additional half over the subsequent 16 hours.
While the Parkland formula is a useful tool, fluid resuscitation should ultimately be determined by clinical and laboratory findings. Generally, burns of <15% TBSA do not require resuscitation.
In adults, the most important endpoint of resuscitation is urine output with a goal of 30 mL/h in adults or 0.5–1 mL/kg/h.
Since significant capillary leakage occurs early following injury, resuscitation with crystalloids, not colloids, is the mainstay of resuscitation during the first 12–24 hours (primarily lactated Ringers’ solution).
Consideration should be given to colloids if fluid requirements far exceed those suggested by the Parkland formula.
Nutrition requirement calculations are available at: http://www.surgicalcriticalcare.net/Resources/burn_nutrition.php.
Disease severity classification
As shown in Table 38.1, burn degree can be determined by identifying various clinical findings. Historically, burns were described by several anatomic levels or ‘degrees’ (Figure 38.2). Today they are more commonly described by partial or full thickness, which focuses more on treatment distinction.
Laboratory diagnosis
List of diagnostic tests
CBC, BMP, serum lactate, and ECG for all patients with burns >10% TBSA.
ABG or VBG and carboxyhemoglobin level for enclosed space injury.
Capnography and peak expiratory flow rates are useful adjuncts if available.
Wound biopsy is the gold standard for diagnosing infection if suspected.
List of imaging techniques
CSR when there is concern for inhalation injury.
Laser Doppler imaging when clinical assessment is inadequate to assess burn extent.
Bronchoscopy or laryngoscopy should be used for airway injury.
Potential pitfalls/common errors made regarding diagnosis of disease
Tendency to focus on burn injury instead of triaging for all immediately life‐threatening injuries via ABCs.
Inadequate history.
Failure to recognize airway injuries or potential for expansion of injury as edema increases following resuscitation.
Treatment
Treatment rationale
In general, superficial burns can be managed conservatively.
Second degree or greater burns will require medical attention.
During triage, two large bore IVs should be placed for early resuscitation in case it becomes apparent resuscitation will be necessary, and amount can be determined using the Parkland formula.
2–4 days/sloughed epidermis replaced by regenerating keratinocytes
Second degree superficial (partial)
Superficial (papillary) dermis
Blanching erythema, moist with blistering, extremely tender
1–2 weeks/epidermis regenerates from dermal appendages
Second degree deep (full)
Deep (reticular) dermis
White intermixed with erythema, less blanching, drier with potential blood blisters, less and variably painful
3–4 weeks/regeneration from wound edges as appendages are lost, scarring is typical, often managed surgically
Third degree (full)
Subcutaneous
White or charred with eschar, dry and leathery, non‐blanching, insensate
Variable, managed surgically
Fourth degree (full)
Muscle or bone
Charred with eschar, insensate
Variable, managed surgically
Patients with concerning airways or with significant injuries meeting transfer criteria should be intubated or transferred to a burn center, respectively.
Succinylcholine should not be used to intubate a burn patient if intubating after 72 hours because of the risk of severe hyperkalemia.
Prophylactic systemic antibiotics should be avoided as they have not been shown to lower risk of invasive wound infections.
Efforts should be made to initiate early enteral feeding as management of nutrition is critical to healing. TPN should be avoided as it has been shown to increase mortality in burn patients.
Circumferential deep burns should undergo urgent escharotomy.
Blisters >2 cm should be gently debrided and inspected.
Wound treatment is geared towards limiting loss of additional tissue, preventing bacterial invasion, and decreasing evaporative losses.
Superficial partial wounds should be treated with topical antimicrobials with attempts to minimize painful dressing changes.
Deep partial thickness wounds can be treated similarly if small.
In larger wounds and in full thickness burns, the wound should be excised and covered with autologous, meshed, split thickness skin graft or non‐meshed material if in a cosmetically sensitive area.
If wounds are too extensive for autologous grafting, skin substitutes may be used.
Optimal timing of burn wound excision is within 48 hours to minimize risk for infection and expedite hospital stay and can be accomplished in a single or staged manner if the burn area is large or donor site scarce.
When to hospitalize
Partial thickness burns greater than 10–20% TBSA, with a lower threshold for transfer in patients younger than 10 or older than 50 years.
Burns that involve the face, hands, feet, genitalia, perineum, or major joints.
Third degree burns in any age group.
Electrical burns, including lightning injury.
Chemical burns.
Inhalation injury.
Burn injury in patients with pre‐existing medical disorders that could complicate management, prolong recovery, or affect mortality.
Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burns unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols.
Burned children in hospitals without qualified personnel or equipment for the care of children should be moved to hospitals with specialist facilities.
Burn injury in patients who will require special social, emotional, or rehabilitative intervention.
Criteria for non‐burn center hospital admission
Partial thickness burn of 5–10% TBSA in patients aged <10 or >50 years.
Mild to moderate voltage injury.
Suspected but not definitive inhalation injury.
Circumferential injury not meeting burn center referral criteria.
Managing the hospitalized patient
ABCs guide initial urgent management (e.g. intubation for airway concern, hyperbaric or high flow oxygen for carbon monoxide poisoning, urgent escharotomy for circumferential burns).
Immediate assessment of burn depth and severity with gentle debridement if necessary and pain control.
Determination of fluid requirements using the Parkland formula and initiation of resuscitation with a goal urine output of 0.5–1 mL/kg.
Transfer to burn center if indicated.
Placement of nasogastric tube for prevention of gastric ileus in large wounds.
Application of topical antimicrobials.
Application of an appropriate dressing for superficial and partial thickness injuries with biologic or non‐biologic antimicrobial dressings.
Early excision and grafting more extensive burns with autograft, allograft, or dermal substitute.
Determination of nutrition requirements and early post gastric or parenteral nutrition initiation.
Medical management to blunt catecholamine surge and catabolic response (commonly propranolol).
Reassessment of wounds to assess for larger wound conversion and graft take.
Superficial, PT, or grafts, Gram+ cocci Superficial, PT, or grafts, active against MRSA PT, broad coverage Superficial grafts, fungal coverage only DD or FT, intermediate eschar penetration, broad spectrum DD or FT, excellent eschar penetration, broad spectrum especially against Pseudomonas, poor against Staphylococcus Broad spectrum, can be left in place for up to 1 week PT, can be left in place until healing is complete, requires clean wound for adherence PT, can be left in place until healing is complete, reduces evaporative losses
For PT wounds, to conserve dermal appendages if spared by injury For DD or FT For significant partial thickness or deeper injuries. Split thickness typically employed acutely, whereas full thickness is usually reserved for post‐burn reconstruction if at all. Autografting is ideal. Dermal substitutes can be used to replenish the normal properties of skin following full thickness excision. Allograft, dermal/epidermal substitutes, and cultured skin substitutes used for extensive and/or irregular wounds For circumferential burns of chest, extremity, or over joints For compartment release if injury has impaired perfusion to a compartment for 4–6 hours To release tension and prevent release contracture over a mobile area
DD, deep dermal; FT, full thickness; PT, partial thickness.
Prevention/management of complications
Over‐resuscitation or ‘fluid creep’ should be monitored because it can rapidly cause pulmonary edema, arrhythmias, compartment syndromes, and conversion of superficial to more extensive wounds.
Extensive blood loss with tangential excisions is common and can be minimized by operating within 24 hours of injury or applying a tourniquet or local vasoconstrictive agents during the operation.
Mafenide can cause metabolic acidosis due to carbonic anhydrase inhibition.
Silver nitrate can cause hyponatremia and methemoglobinemia; the latter can be treated with methylene blue.
Silver sulfadiazine can cause neutropenia.
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