# Burns and Inhalation Injury: Anesthetic Management

## Introduction

Burn injuries present unique physiologic and pharmacologic challenges to the anesthesiologist. Management encompasses the acute resuscitation phase, repeated operative debridement and grafting procedures, and long-term reconstructive surgery. Inhalation injury compounds the complexity by adding airway compromise and pulmonary dysfunction to an already hypermetabolic, catabolic state.

## Classification of Burn Injuries

### Burn Depth

Superficial (first-degree) burns affect the epidermis only, producing erythema and pain, and heal without scarring (such as sunburn). Superficial partial-thickness (second-degree) burns extend through the epidermis and into the superficial dermis, producing blisters that are moist and painful, and heal in 10 to 14 days. Deep partial-thickness burns extend into the deep dermis, produce less pain due to nerve destruction, and may require grafting. Full-thickness (third-degree) burns destroy the entire dermis, are painless with a leathery and waxy appearance, and require excision and grafting. Fourth-degree burns extend to fascia, muscle, or bone.

### Estimating Burn Size

The Rule of Nines for adults assigns 9% to the head, 9% to each upper extremity, 18% to the anterior trunk, 18% to the posterior trunk, 18% to each lower extremity, and 1% to the perineum. The Lund-Browder chart is more accurate, especially in children, as it adjusts for age-related body surface area proportions. The palm method, in which the patient's palm including fingers represents approximately 1% TBSA, is useful for small or patchy burns.

| Burn Depth | Old Term | Layers Involved | Appearance | Sensation | Healing |
|---|---|---|---|---|---|
| Superficial | 1st degree | Epidermis only | Erythema, dry | Painful | Heals without scarring (3–7 days) |
| Superficial partial-thickness | 2nd degree (superficial) | Epidermis + superficial dermis | Blisters, moist, pink | Very painful | Heals in 10–14 days |
| Deep partial-thickness | 2nd degree (deep) | Epidermis + deep dermis | White/red, less moist | Decreased (nerve destruction) | May require grafting |
| Full-thickness | 3rd degree | Entire dermis destroyed | Leathery, waxy, white/brown | Painless | Requires excision and grafting |
| 4th degree | 4th degree | Fascia, muscle, bone | Charred, exposed structures | Painless | Requires excision; may need amputation |

| Rule of Nines (Adult) | Body Region | %TBSA |
|---|---|---|
| Head and neck | | 9% |
| Each upper extremity | | 9% each |
| Anterior trunk | | 18% |
| Posterior trunk | | 18% |
| Each lower extremity | | 18% each |
| Perineum | | 1% |

## Pathophysiology of Major Burns

### Acute Phase (0-72 hours)

The acute phase is characterized by massive capillary leak and third-spacing of fluid driven by the release of inflammatory mediators. Hypovolemic shock results from intravascular volume depletion. Myocardial depression occurs with decreased cardiac output. A systemic inflammatory response produces generalized edema, including airway edema in burns exceeding 20 to 30% TBSA.

### Hypermetabolic Phase (>72 hours)

The metabolic rate may increase by 150 to 200% in large burns. A hyperdynamic cardiovascular state develops with increased cardiac output and decreased SVR. Oxygen consumption, CO2 production, and glucose utilization all increase. Protein catabolism with muscle wasting and negative nitrogen balance ensues. Drug metabolism is altered by increased hepatic blood flow and enzyme induction. Immunosuppression increases susceptibility to sepsis.

![Parkland formula calculation and fluid resuscitation timeline for major burns](burn-fluid-resuscitation.png)

## Inhalation Injury

### Types

Supraglottic thermal injury occurs when hot gases and steam cause edema and obstruction of the upper airway (oropharynx, larynx), which may progress rapidly. Infraglottic chemical injury results from toxic products of combustion (acrolein, hydrogen chloride, phosgene) that cause tracheobronchial inflammation, mucosal sloughing, bronchospasm, and ARDS. Systemic toxicity involves carbon monoxide and cyanide poisoning.

### Clinical Indicators of Inhalation Injury

Clinical indicators include an enclosed-space fire, facial burns, singed nasal hairs, and eyebrow or eyelash burns. Soot in the oropharynx or sputum, hoarseness, and stridor are important findings. Carbonaceous sputum, wheezing, and dyspnea suggest lower airway involvement. Altered mental status raises concern for carbon monoxide or cyanide poisoning.

### Carbon Monoxide Poisoning

Carbon monoxide binds hemoglobin with 240 times the affinity of oxygen, forming carboxyhemoglobin. It shifts the oxyhemoglobin dissociation curve to the left, impairing oxygen unloading to tissues. Pulse oximetry is unreliable because SpO2 reads falsely normal, as the device cannot distinguish carboxyhemoglobin from oxyhemoglobin. Diagnosis requires co-oximetry on an arterial blood gas to measure the carboxyhemoglobin level. Treatment consists of 100% FiO2, which reduces the carboxyhemoglobin half-life from 4 to 6 hours to 60 to 90 minutes. Hyperbaric oxygen is indicated for carboxyhemoglobin levels above 25%, neurologic symptoms, or pregnancy.

### Cyanide Poisoning

Cyanide is generated from the combustion of synthetic materials such as polyurethane, nylon, and wool. It inhibits cytochrome oxidase (complex IV) in the mitochondrial electron transport chain. The presentation includes unexplained lactic acidosis and cardiovascular collapse despite adequate oxygenation. The preferred treatment is hydroxocobalamin (Cyanokit) at 5 g IV over 15 minutes, with sodium thiosulfate as an alternative.

## Airway Management

Early intubation is mandatory when inhalation injury is suspected because airway edema can progress rapidly over 12 to 24 hours, making delayed intubation extremely dangerous. Direct or video laryngoscopy is used, and smaller ETT sizes should be available due to edema. Once intubated, an uncut endotracheal tube should be secured with umbilical tape rather than adhesive tape, which will not adhere to burned skin. Nasal intubation should be avoided in facial burns. Flexible bronchoscopy is used for diagnosis, with findings including erythema, edema, soot, and mucosal ulceration below the cords. Early tracheostomy should be considered for patients requiring prolonged ventilation with extensive facial and neck burns.

## Fluid Resuscitation

### Parkland Formula (Modified Baxter)

The Parkland formula calculates the first 24 hours of fluid resuscitation as 4 mL/kg multiplied by the percentage of TBSA burned, using lactated Ringer's solution. Fifty percent is administered in the first 8 hours (calculated from the time of injury, not hospital arrival), and the remaining 50% over the next 16 hours. Fluid is titrated to a urine output of 0.5 to 1 mL/kg/hr in adults and 1 to 2 mL/kg/hr in children. "Fluid creep" (excessive resuscitation) must be avoided because it leads to abdominal compartment syndrome, pulmonary edema, and extremity compartment syndrome.

### Colloid Use

Albumin 5% may be introduced after 8 to 24 hours when capillary integrity begins to restore. It reduces total fluid volume requirements in some protocols.

## Anesthetic Considerations for Burn Surgery

### Pharmacologic Changes

**Succinylcholine is contraindicated** from 24 hours post-burn until at least 1 to 2 years after complete healing due to upregulation of extrajunctional acetylcholine receptors, which causes life-threatening hyperkalemia. Nondepolarizing agents such as rocuronium and cisatracurium should be used instead, and doses may need to be increased because of receptor upregulation and increased volume of distribution. Opioid requirements increase due to tolerance, the hypermetabolic state, and altered pharmacokinetics. Volatile agents are well tolerated with no specific contraindication. Propofol clearance may be increased, requiring higher infusion rates.

### Blood Loss and Transfusion

Burn excision and grafting are among the most hemorrhagic surgical procedures. Blood loss is estimated at 50 to 75 mL per 1% TBSA excised for full-thickness burns. Preparation for massive transfusion is essential, and topical hemostatic agents and surgical technique (tangential excision versus fascial excision) help manage bleeding. Hemoglobin should be maintained above 7 to 8 g/dL, with a higher threshold of above 10 g/dL potentially appropriate in the acute resuscitation phase.

### Temperature Management

Burn patients are at extreme risk of hypothermia due to loss of the skin barrier and the hypermetabolic state. The operating room temperature should be maintained at 28 to 33 degrees Celsius. All IV fluids and blood products should be warmed, and forced-air warming should be used on unburned areas. Hypothermia worsens coagulopathy, increases metabolic demands, and delays wound healing.

### Vascular Access

Peripheral IV access may be difficult due to burns, and lines may be placed through burned skin if necessary. Central venous access, intraosseous access, or venous cutdown may be required. An arterial line is needed for beat-to-beat monitoring and frequent blood sampling.

![Anesthetic considerations timeline for burn patients from acute phase through reconstruction](burn-anesthetic-timeline.png)

## Pain Management

Burn pain is among the most severe forms of pain and has both background (continuous) and procedural (dressing changes, debridement) components. A multimodal approach includes opioids (morphine, hydromorphone, methadone for background pain), ketamine (0.1 to 0.3 mg/kg/hr), acetaminophen, and gabapentin or pregabalin.

**Ketamine** is particularly valuable in burn patients because it provides analgesia, sedation for dressing changes, and opioid-sparing effects. Regional anesthesia should be used when feasible, including peripheral nerve blocks and neuraxial techniques for lower extremity burns. Anxiety and PTSD should be addressed with benzodiazepines, dexmedetomidine, and psychiatric support.

## Clinical Pearls

Succinylcholine must be avoided from 24 hours after a burn until at least 1 to 2 years post-healing because the hyperkalemic response can be fatal. Pulse oximetry is unreliable in carbon monoxide poisoning, and co-oximetry for carboxyhemoglobin levels should always be obtained. Early intubation saves lives in inhalation injury because airway edema can convert a manageable airway to an impossible one within hours. Burn resuscitation with the Parkland formula is a starting point, not a fixed prescription; fluids should be titrated to urine output and clinical response, with vigilance for fluid creep. Operating room temperature is a critical variable, and hypothermia in burn patients is dangerous and should be aggressively prevented.

![Mechanisms of inhalation injury: thermal, chemical, and systemic toxic effects](inhalation-injury-mechanisms.png)

## References

1. Bittner EA, Shank E, Woodson L, Martyn JA. Acute and perioperative care of the burn-injured patient. *Anesthesiology*. 2015;122(2):448-464.
2. Palmieri TL. Inhalation injury: research progress and needs. *J Burn Care Res*. 2007;28(4):549-554.
3. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. *Anesthesiology*. 2006;104(1):158-169.
4. ISBI Practice Guidelines Committee. ISBI Practice Guidelines for Burn Care. *Burns*. 2016;42(5):953-1021.
