Residency · Residency · Critical Care

Burns and Inhalation Injury

Burn Assessment and Classification

Burn Depth Classification

Burn Depth

Accurate assessment of burn depth determines the need for surgical intervention, the expected healing time, and the overall prognosis. Superficial or first-degree burns involve only the epidermis and present as painful, erythematous skin without blistering, healing completely within 5 to 7 days. The common sunburn is the prototypical example. Superficial partial-thickness or superficial second-degree burns extend through the epidermis into the superficial dermis, producing painful, blistering wounds that blanch with pressure and typically heal within 10 to 21 days with minimal scarring, as the deeper dermal appendages remain intact to provide a source of epithelial regeneration.

Deep partial-thickness or deep second-degree burns extend into the deeper dermis, destroying most of the dermal appendages. These wounds are less painful due to nerve damage, appear mottled pink or white, and do not blanch with pressure. Healing takes 21 to 35 days and results in significant scarring; many deep partial-thickness burns ultimately require skin grafting. Full-thickness or third-degree burns destroy the entire epidermis and dermis, presenting as painless, leathery or waxy wounds with no blanching. These wounds cannot regenerate from dermal remnants and require excision and grafting. Fourth-degree burns extend beyond the dermis into fascia, muscle, or bone and represent the most devastating injury.

Total Body Surface Area (TBSA)

Accurate estimation of burn size is essential because it directly determines fluid resuscitation requirements and triage decisions. The Rule of Nines divides the adult body surface into regions, each representing approximately 9 percent: the head (9 percent), each upper extremity (9 percent), the anterior trunk (18 percent), the posterior trunk (18 percent), each lower extremity (18 percent), and the perineum (1 percent). The Lund-Browder chart provides greater accuracy by adjusting body surface proportions for age, which is particularly important in children where the head represents a proportionally larger area. The palm method, in which the patient's palm with fingers represents approximately 1 percent TBSA, is useful for estimating scattered or irregular burn patterns. Only partial-thickness and full-thickness burns are included in the TBSA calculation for fluid resuscitation purposes.

Burn Center Referral Criteria (ABA)

The American Burn Association has established specific criteria for referral to a burn center, reflecting the specialized resources required for optimal management. These include partial-thickness burns exceeding 10 percent TBSA, full-thickness burns of any size, burns involving the face, hands, feet, genitalia, perineum, or major joints, chemical or electrical burns, inhalation injury, patients with pre-existing medical conditions that may complicate burn management, and children in hospitals lacking pediatric burn expertise.

Initial Resuscitation

Airway Assessment

Airway management in the burn patient demands a high index of suspicion and early intervention. Clinical indicators suggestive of inhalation injury include a history of burns sustained in an enclosed space, facial burns, singed nasal hairs or eyebrows, carbonaceous sputum, hoarse voice, and stridor. The critical principle is that early intubation is mandatory when inhalation injury is suspected because upper airway edema progresses rapidly over 12 to 24 hours, and once significant edema develops, intubation may become technically impossible, necessitating a surgical airway.

Direct visualization on laryngoscopy may reveal oropharyngeal erythema, soot deposits, and mucosal edema, confirming the need for definitive airway management. The largest endotracheal tube that can be safely placed should be used, anticipating significant airway edema that will progressively narrow the airway around the tube. Nasal intubation should be avoided in patients with facial burns.

Fluid Resuscitation — Parkland Formula

The Parkland formula provides the initial framework for fluid resuscitation in major burns: 4 mL multiplied by body weight in kilograms multiplied by the percentage of TBSA burned, using Lactated Ringer's solution. Half of the calculated volume is administered in the first 8 hours from the time of the burn (not from the time of hospital arrival), with the remaining half infused over the subsequent 16 hours. The target endpoint for resuscitation is a urine output of 0.5 to 1 mL/kg/hr in adults and 1 to 2 mL/kg/hr in children.

It is essential to understand that the Parkland formula is a starting point, not a rigid prescription. Actual fluid requirements frequently exceed the calculated prediction, particularly in the setting of concomitant inhalation injury, delayed resuscitation, or electrical burns. Conversely, excessive resuscitation beyond the Parkland prediction, termed "fluid creep," is a recognized iatrogenic complication that can produce devastating consequences including abdominal compartment syndrome, extremity compartment syndrome, and pulmonary edema. Intra-abdominal pressure should be monitored via bladder pressure measurement, with pressures exceeding 20 mmHg prompting concern for abdominal compartment syndrome. Albumin 5 percent may be introduced after 12 to 24 hours to reduce ongoing crystalloid requirements. Resuscitation endpoints include urine output, lactate clearance, and base deficit correction; CVP-guided resuscitation should be avoided.

Colloid Strategy

The addition of albumin 5 percent colloid after the first 12 to 24 hours, once capillary leak begins to subside and the administered colloid will remain intravascular, may reduce total fluid volume requirements by 30 to 50 percent compared to crystalloid alone. There is no consensus on the optimal timing of colloid introduction, and practice varies among burn centers. Hydroxyethyl starch must be avoided due to its association with increased acute kidney injury.

<image>Burn resuscitation protocol flowchart. Entry: "Burn patient arrival — assess burn depth and TBSA." Left panel: Rule of Nines body diagram with labeled percentages for each body region (adult). Center: Parkland formula calculation example for 80 kg patient with 40% TBSA burn showing hourly infusion rates for first 8 hours and subsequent 16 hours. Right panel: monitoring checklist with targets: urine output 0.5-1 mL/kg/hr (dial gauge graphic), MAP >65 mmHg, lactate trending down, base deficit improving. Below: troubleshooting algorithm — if urine output inadequate: bolus 250 mL LR, increase rate by 10-20%; if excessive fluid requirements (>6 mL/kg/%TBSA): consider colloid (albumin 5%), check for missed injuries, assess for compartment syndrome (abdominal and extremity compartment pressure measurements), consider vasopressin. Warning box: signs of fluid creep — IAP >20, extremity compartment pressures rising, inability to ventilate (peak pressures increasing).</image>

Inhalation Injury

Types

Inhalation injury encompasses three distinct pathological processes that may occur alone or in combination. Upper airway thermal injury results from direct heat damage to supraglottic structures, producing edema and potential obstruction. This injury rarely extends below the vocal cords because the upper airway efficiently dissipates heat, protecting the lower airways from thermal damage. Peak edema occurs at 12 to 24 hours.

Lower airway and tracheobronchial injury is a chemical rather than thermal injury, caused by combustion byproducts including acrolein, hydrochloric acid, and phosgene. These chemicals cause direct mucosal injury leading to epithelial sloughing, cast formation that obstructs small and medium airways, and atelectasis. The associated inflammatory response increases capillary permeability, producing pulmonary edema.

Systemic toxicity from carbon monoxide and hydrogen cyanide poisoning represents the third component, which may be rapidly fatal and requires specific recognition and treatment.

Diagnosis

Bronchoscopy is the gold standard for diagnosing and grading lower airway inhalation injury. The grading system progresses from Grade 0 (no injury) through Grade 1 (mild edema and soot deposition), Grade 2 (moderate edema with bronchorrhea), and Grade 3 (severe edema with mucosal sloughing and partial obstruction) to Grade 4 (complete obstruction with necrosis). Chest radiography is often normal in the initial hours and may not demonstrate changes until 24 to 72 hours after injury. Technetium-99m DTPA scanning can detect increased pulmonary epithelial permeability but is rarely used in the acute setting.

Management

Ventilatory support follows lung-protective principles with tidal volumes of 6 to 8 mL/kg of ideal body weight, though higher levels of PEEP may be required to maintain alveolar recruitment in the setting of airway edema and cast formation. Therapeutic bronchoscopy plays an important role in removing carbonaceous debris, mucus plugs, and fibrin casts that can cause progressive airway obstruction and atelectasis.

A nebulized treatment protocol has shown benefit in observational studies. Nebulized heparin at 5,000 to 10,000 units every 4 hours prevents fibrin cast formation within the airways. N-acetylcysteine 20 percent at 3 mL nebulized every 4 hours serves as a mucolytic agent. Albuterol at 2.5 to 5 mg nebulized every 4 hours provides bronchodilation. This combination protocol has been associated with reduced reintubation rates and atelectasis in observational studies. Prophylactic systemic antibiotics should be avoided as they increase antimicrobial resistance without demonstrating benefit. Tracheostomy should be considered when prolonged mechanical ventilation is anticipated, and contrary to earlier concerns, does not carry increased infection risk in burn patients.

Carbon Monoxide Poisoning

Carbon monoxide binds to hemoglobin with 200 to 250 times the affinity of oxygen, forming carboxyhemoglobin (COHb) and producing tissue hypoxia through both impaired oxygen carrying capacity and a leftward shift of the oxyhemoglobin dissociation curve. Symptoms correlate roughly with COHb levels: headache at 10 to 20 percent, confusion and nausea at 20 to 40 percent, coma and seizures at 40 to 60 percent, and death above 60 percent.

A critical clinical principle is that pulse oximetry is unreliable in CO poisoning because conventional pulse oximeters cannot distinguish carboxyhemoglobin from oxyhemoglobin, producing falsely normal SpO2 readings. Diagnosis requires COHb measurement via co-oximetry, obtained from an arterial blood gas with co-oximetry analysis.

Treatment with 100 percent oxygen via non-rebreather mask or mechanical ventilation reduces the CO half-life from 4 to 5 hours on room air to 60 to 90 minutes. Hyperbaric oxygen (HBO) further reduces the half-life to 20 to 30 minutes and may reduce the incidence of delayed neurological sequelae. Indications for HBO include COHb above 25 percent, loss of consciousness, neurological symptoms, cardiac ischemia, and pregnancy (fetal hemoglobin has higher CO affinity, making the fetus particularly vulnerable). Treatment with 100 percent oxygen should continue until COHb falls below 5 percent and symptoms have resolved.

Hydrogen Cyanide Poisoning

Hydrogen cyanide is generated from the combustion of synthetic materials including plastics, nylon, and polyurethane, making it a common co-toxicant in structural fires. The mechanism involves inhibition of cytochrome c oxidase in the mitochondrial electron transport chain, blocking aerobic metabolism and forcing cells to rely on anaerobic glycolysis. The hallmark finding is persistent lactic acidosis despite adequate carbon monoxide treatment and fluid resuscitation.

Hydroxocobalamin (Cyanokit) at 5 g IV over 15 minutes is the preferred antidote, binding cyanide to form cyanocobalamin (vitamin B12) which is renally excreted. It is safe and effective with minimal side effects, the most notable being transient red discoloration of skin and urine and interference with colorimetric laboratory assays. Sodium thiosulfate at 12.5 g IV provides an alternative with slower onset, acting as a sulfur donor for the rhodanese enzyme that converts cyanide to thiocyanate. The older antidotes amyl nitrite and sodium nitrite, which form methemoglobin to bind cyanide, are dangerous in CO co-poisoning because they further reduce oxygen-carrying capacity.

Burn Wound Management

Escharotomy

Full-thickness circumferential burns produce a rigid, inelastic eschar that can act as a constricting band around extremities or the chest. On extremities, this constriction produces vascular compromise manifesting as absent pulses, cyanosis, and paresthesias. On the chest, eschar restricts chest wall expansion, causing rising peak airway pressures and inadequate tidal volumes.

Escharotomy involves longitudinal incisions through the eschar along the lateral and medial aspects of the affected extremity or the anterior axillary lines on the chest. Because full-thickness burns destroy cutaneous nerve fibers, the procedure is painless and does not require anesthesia. Timing is critical: escharotomy should be performed within 6 hours of the development of signs of compromise.

Topical Antimicrobial Comparison

Topical Antimicrobials

Several topical antimicrobial agents are used for burn wound care, each with distinct advantages and limitations. Silver sulfadiazine 1 percent provides broad-spectrum coverage and painless application but carries a risk of leukopenia and impairs wound healing assessment by creating a white pseudo-eschar. Mafenide acetate (Sulfamylon) penetrates eschar well, making it particularly useful for deep burns, but application is painful and it inhibits carbonic anhydrase, potentially producing metabolic acidosis. Silver-containing dressings such as Acticoat and Mepilex Ag provide sustained silver release with less frequent dressing changes. Bacitracin and polymyxin are appropriate for superficial burns and facial burns.

Surgical Management

Early excision and grafting within 72 hours for deep partial-thickness and full-thickness burns has been shown to reduce infection risk, length of hospital stay, and mortality compared to the older approach of serial debridement. Split-thickness skin autograft from unburned donor sites remains the gold standard for definitive wound coverage. When donor sites are limited, temporary coverage options include allograft (cadaveric skin), xenograft (porcine skin), Integra (a dermal regeneration template), and Biobrane. For massive burns exceeding 80 percent TBSA with severely limited donor sites, cultured epithelial autograft (CEA) provides a means of expanding available autologous tissue.

Systemic Complications

Hypermetabolic Response

The hypermetabolic response to major burns is the most extreme of any critical illness, with metabolic rate increasing by 100 to 200 percent above baseline. This response persists for 12 to 24 months post-burn, far exceeding the acute hospital phase. It is mediated by a massive catecholamine surge, elevated cortisol and glucagon, and inflammatory cytokines, producing muscle wasting, insulin resistance, hepatic steatosis, and immune suppression.

Pharmacological modulation of the hypermetabolic response has become an important component of burn care. Propranolol reduces metabolic rate by 15 to 20 percent and preserves lean body mass, as demonstrated by Herndon et al. Oxandrolone, an anabolic steroid at 10 mg orally twice daily, improves nitrogen balance and wound healing. Insulin infusion targeting glucose below 180 mg/dL provides both glycemic control and an anabolic effect.

Nutritional support demands aggressive enteral feeding initiated within 4 to 6 hours of the burn, earlier than for other ICU populations, as this has been shown to attenuate the hypermetabolic response. Caloric targets should be determined by the Toronto formula or indirect calorimetry, as predictive equations are particularly inaccurate in burn patients. Protein requirements are 1.5 to 2.0 g/kg/day to offset massive protein losses through wound exudate. Gastric feeding is preferred, with post-pyloric access utilized if gastroparesis develops.

Infection

Infection is the leading cause of death after the first 72 hours in patients with major burns. Burn wound infection is defined by quantitative culture showing greater than 10^5 organisms per gram of tissue, while invasive wound infection occurs when bacteria penetrate into viable tissue and cause systemic sepsis. Recognizing sepsis in burn patients is challenging because the baseline hypermetabolic state produces tachycardia and elevated metabolic rate that mimic standard SIRS criteria. The American Burn Association has therefore developed burn-specific sepsis criteria, which include temperature above 39 or below 36.5 degrees Celsius, progressive tachycardia, progressive tachypnea, thrombocytopenia, new hyperglycemia in a previously tolerant patient, and inability to continue enteral feeding. Prophylactic systemic antibiotics are not recommended as they increase antimicrobial resistance without reducing infection rates.

Venous Thromboembolism

Burn patients are at high risk for VTE due to the hypercoagulable state induced by the burn injury, prolonged immobilization, and frequent central venous catheter placement. Pharmacological prophylaxis with enoxaparin 40 mg subcutaneously daily should be initiated once any coagulopathy has resolved and there is no active bleeding. Mechanical prophylaxis with intermittent pneumatic compression should be applied from admission.

<image>Inhalation injury management algorithm. Entry point: "Suspected inhalation injury (enclosed space fire, facial burns, stridor, carbonaceous sputum)." First branch: Airway assessment — if stridor, voice changes, or significant pharyngeal edema → immediate endotracheal intubation (largest tube possible). If stable airway → close monitoring q1h for 24 hours with low threshold for intubation. Second tier: Obtain COHb level (co-oximetry) and assess for cyanide poisoning (lactate >10 mmol/L with adequate resuscitation). CO treatment: 100% O2 → assess for HBO criteria (COHb >25%, LOC, pregnancy, cardiac ischemia). Cyanide treatment: hydroxocobalamin 5g IV. Third tier: Bronchoscopy within 24 hours for grading and therapeutic lavage. Fourth tier: Ventilator management (lung-protective) + nebulized heparin/NAC/albuterol protocol. Monitoring panel: serial COHb, lactate, bronchoscopy, chest imaging evolution over 72 hours.</image>

Key Clinical Pearls

• Intubate early in suspected inhalation injury — upper airway edema peaks at 12-24 hours and can make intubation impossible; use the largest ETT possible
• Pulse oximetry is unreliable in carbon monoxide poisoning — always obtain co-oximetry ABG; treat with 100% O2 until COHb <5%
• The Parkland formula (4 mL/kg/%TBSA) is a starting guide only — titrate to urine output 0.5-1 mL/kg/hr; excessive resuscitation ("fluid creep") causes abdominal and extremity compartment syndrome
• Suspect cyanide poisoning when lactic acidosis persists despite adequate CO treatment — hydroxocobalamin 5 g IV is the preferred antidote
• Circumferential full-thickness burns require escharotomy within 6 hours if signs of vascular or ventilatory compromise develop
• The hypermetabolic response in major burns is the most extreme of any critical illness (100-200% increase in REE) — propranolol reduces metabolic rate and preserves lean body mass
• Do NOT use prophylactic systemic antibiotics in burn patients — they increase antimicrobial resistance without reducing infection rates
• Early enteral nutrition (within 4-6 hours) attenuates the hypermetabolic response and improves outcomes in major burns

References

1. Jeschke MG, van Baar ME, Choudhry MA, et al. Burn injury. Nat Rev Dis Primers. 2020;6(1):11.
2. ISBI Practice Guidelines Committee. ISBI practice guidelines for burn care. Burns. 2016;42(5):953-1021.
3. Herndon DN, Tompkins RG. Support of the metabolic response to burn injury. Lancet. 2004;363(9424):1895-1902.
4. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347(14):1057-1067.
5. Mosier MJ, Gibran NS. Surgical excision of the burn wound. Clin Plast Surg. 2009;36(4):617-625.

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