23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies

Burn Injury Classification and Surface Area Estimation

Care of the severely burned patient in the intensive care unit requires precise quantification of burn depth and Total Body Surface Area (%TBSA) to guide fluid resuscitation, wound care, and systemic organ support.

Classification of Burn Depth

Burn wounds are classified pathologically by the depth of cutaneous injury:

• Superficial (First-Degree): Involves the epidermis only. Manifests as painful erythema and dry skin without blistering (e.g., classic mild sunburn). Capillary refill is rapid. Heals within 3 to 6 days without scarring. Superficial burns are strictly EXCLUDED from %TBSA calculations for fluid resuscitation.
• Superficial Partial-Thickness (Superficial Second-Degree): Involves the epidermis and the papillary dermis. Characterized by thin-walled, fluid-filled blisters, weeping erythematous bases, brisk capillary refill, and severe pain to air exposure. Typically heals in 1 to 3 weeks without grafting.
• Deep Partial-Thickness (Deep Second-Degree): Extends into the deeper reticular dermis. Appears mottled pink to waxy white, dry, with diminished or sluggish capillary refill. Sensation to light pinprick is diminished due to dermal nerve ending destruction, though pressure sensation remains intact. Often requires surgical excision and autografting to prevent hypertrophic scarring.
• Full-Thickness (Third-Degree): Destroys the entire epidermis and dermis into subcutaneous fat. The wound appears hard, leathery, charred, or porcelain white (eschar) with visible thrombosed thrombophlebitic subcutaneous vessels. It is completely insensate, dry, and lacks capillary blanching. Mandates early surgical tangential excision and skin grafting.
• Fourth-Degree: Extends beyond subcutaneous tissue into underlying fascia, muscle, tendon, or bone. Commonly seen in high-voltage electrical injuries and prolonged entrapment.

Wallace Rule of Nines

In adult patients, %TBSA of partial- and full-thickness burns is estimated using the Wallace Rule of Nines:

• Head and Neck: $9\%$ (anterior $4.5\%$, posterior $4.5\%$)
• Anterior Torso: $18\%$ (chest $9\%$, abdomen $9\%$)
• Posterior Torso: $18\%$ (upper back $9\%$, lower back/buttocks $9\%$)
• Each Upper Extremity: $9\%$ (anterior $4.5\%$, posterior $4.5\%$)
• Each Lower Extremity: $18\%$ (anterior $9\%$, posterior $9\%$)
• Perineum and Genitalia: $1\%$

For scattered, non-contiguous, or patchy burns, the Palmar Surface Method is utilized: the patient's entire hand (palm plus all five fingers held together) represents approximately $1\%$ of their total body surface area.

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Burn Shock, Resuscitation Formulas, and Fluid Creep

Pathophysiology of Burn Shock

Extensive burns ($> 20\%\text{ TBSA}$) produce a biphasic hemodynamic response. The initial phase (burn shock) spans the first 24 to 48 hours and is a complex combination of hypovolemic, distributive, and cardiogenic shock. Thermal injury stimulates an overwhelming release of inflammatory mediators (histamine, prostaglandins, leukotrienes, thromboxane $A_2$, bradykinin, and reactive oxygen species), causing widespread disruption of microvascular endothelial tight junctions. Protein-rich plasma extravasates rapidly into the interstitial space—not only in burned tissue, but throughout the entire body—culminating in marked hypovolemia, hemoconcentration, and cellular ischemia.

Resuscitation Formulas: Parkland vs. Modern ABA Consensus

1. The Classic Parkland Formula: $\text{Total 24-Hour Volume (mL)} = 4\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA}$
   • Administered using a balanced crystalloid (Lactated Ringer's).
   • Timing: $50\%$ of the calculated volume is infused over the first 8 hours from the exact time of injury (NOT from hospital arrival). The remaining $50\%$ is infused over the subsequent 16 hours.
2. The Modern American Burn Association (ABA) Consensus Update: Extensive clinical evidence demonstrated that rigid adherence to the $4\text{ mL/kg/\%TBSA}$ Parkland formula systematically over-resuscitates burn patients. Current ABA guidelines recommend a lower starting fluid rate:
   • Thermal and Chemical Burns in Adults: $2\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA}$
   • High-Voltage Electrical Burns: $3\text{ to }4\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA}$
   • Balanced crystalloid (Lactated Ringer's or Plasma-Lyte) is preferred; 0.9% normal saline should be avoided due to the development of severe hyperchloremic metabolic acidosis.

Physiological Titration: Urine Output Targets

Resuscitation formulas provide only an initial estimate of fluid requirements. Once initiated, the crystalloid rate must be adjusted upward or downward by $10\%\text{ to }20\%$ hourly based strictly on physiological endpoints:

• Standard Adult Target: $0.5\text{ mL/kg/h}$ ($30\text{ to }50\text{ mL/h}$).
• High-Voltage Electrical Injury / Pigmenturia: High-voltage currents traverse deep muscular tissue, generating intense internal heat that induces extensive rhabdomyolysis and myoglobinuria. To prevent myoglobin precipitation in renal tubules and acute tubular necrosis, target a higher urine output of $1.0\text{ to }1.5\text{ mL/kg/h}$ ($75\text{ to }100\text{ mL/h}$) until the urine clears gross pigment.

The Hazard of "Fluid Creep"

Fluid creep refers to the insidious administration of crystalloids far exceeding calculated physiological requirements, commonly driven by automated infusion protocols, reliance on CVP rather than urine output, or treating transient oliguria with excessive fluid boluses. Fluid creep precipitates disastrous complications:

• Abdominal Compartment Syndrome (ACS): Retroperitoneal and visceral edema markedly increases intra-abdominal pressure ($> 20\text{ mmHg}$), compromising renal perfusion and elevating diaphragms to impair lung compliance.
• Extremity Compartment Syndrome: Severe interstitial swelling within unburned limbs enclosed by rigid muscular fascia.
• Acute Respiratory Failure: Alveolar-capillary barrier disruption causing non-cardiogenic pulmonary edema.
• Wound Conversion: Elevated interstitial pressures compress dermal capillary venules, converting viable partial-thickness burns into ischemic full-thickness wounds.

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Inhalation Injury and Airway Management

Inhalation injury independently doubles the mortality of thermal burns and increases the risk of ARDS and pneumonia by up to 20-fold. It encompasses three distinct clinical pathophysiological entities:

1. Supraglottic Thermal Injury

The upper airway possesses tremendous heat-exchange capacity; therefore, true thermal heat injury is almost exclusively confined to structures above the vocal cords (pharynx, larynx, epiglottis). Superheated gases cause acute thermal injury that triggers progressive laryngeal edema. Airway edema develops rapidly over 12 to 24 hours, even if the patient appears comfortable on initial presentation.

2. Subglottic Chemical Injury

Combustion of synthetic materials produces toxic aldehydes, sulfur dioxide, acrolein, and hydrogen chloride. These water-soluble chemicals react with respiratory mucosal moisture to form strong acids and bases below the vocal cords. The result is extensive tracheobronchial mucosal sloughing, ciliary paralysis, impaired mucous clearance, and the formation of obstructive fibrin-cellular airway casts. This precipitates severe atelectasis, distal air trapping, and profound ventilation-perfusion ($V_A/Q$) mismatch.

• Management: Lung-protective ventilation, aggressive pulmonary hygiene, therapeutic bronchoscopy for airway cast removal, and aerosolized nebulized heparin (5,000–10,000 units) combined with N-acetylcysteine (NAC 20%) every 4 hours to dissolve casts.

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Carbon Monoxide vs. Cyanide Toxicity

Patients trapped in structural fires are frequently exposed to two deadly systemic asphyxiants: Carbon Monoxide (CO) and Hydrogen Cyanide (HCN).

Carbon Monoxide Toxicity

• Mechanism: Carbon monoxide binds to hemoglobin with an affinity approximately 200 to 250 times greater than oxygen, producing Carboxyhemoglobin (COHb). COHb shifts the oxyhemoglobin dissociation curve sharply to the left, impairing oxygen unloading to tissues. Additionally, CO binds directly to intracellular myoglobin and mitochondrial cytochrome c oxidase, inducing cellular hypoxia and free-radical generation.
• Diagnostic Trap: Standard dual-wavelength pulse oximetry ($\text{SpO}_2$) measures light absorption at 660 nm and 940 nm; it cannot distinguish between oxyhemoglobin and carboxyhemoglobin. A patient with a lethal COHb level of 50% will display a falsely reassuring $\text{SpO}_2$ of $99\%\text{ to }100\%$. Arterial blood gas with co-oximetry is mandatory to directly measure COHb.
• Treatment: Immediate high-flow $100\%\text{ O}_2$ via non-rebreather mask or endotracheal tube. Oxygen competes with CO for hemoglobin binding sites, reducing the elimination half-life of CO from 320 minutes on room air down to 60 to 90 minutes on $100\%\text{ O}_2$.
• Hyperbaric Oxygen (HBO at 2.5–3.0 ATA) further reduces the half-life to 20 to 30 minutes and reduces delayed neurological sequelae. Indications for HBO include:
  • $\text{COHb} > 25\%$ (or $> 15\%\text{ to }20\%$ in pregnant patients due to fetal hemoglobin affinity)
  • Loss of consciousness or transient syncope
  • Persistent neurological deficits or altered mental status
  • Acute myocardial ischemia or ischemic ECG changes
  • Severe, unexplained metabolic acidosis

Cyanide Poisoning

• Mechanism: Cyanide is produced during the combustion of nitrogen-containing synthetic polymers (plastics, polyurethane foam, nylon, wool). Inhaled cyanide gas binds with extreme affinity to the ferric (${\text{Fe}}^{3+}$) iron of cytochrome $a_3$ within cytochrome c oxidase (Complex IV) of the mitochondrial electron transport chain. This halts aerobic oxidative phosphorylation, completely arresting cellular ATP production. Cells convert immediately to anaerobic metabolism despite normal or high arterial oxygen tension.
• Clinical Presentation: Suspect cyanide toxicity in any closed-space smoke inhalation victim who presents with:
  1. Severe Lactic Acidosis: Serum lactate $\ge 8\text{ to }10\text{ mmol/L}$ (a lactate $\ge 10\text{ mmol/L}$ in closed-space smoke exposure has $> 85\%$ sensitivity for toxic cyanide levels).
  2. Refractory Hypotension and Shock: Bradycardia, cardiovascular collapse, and seizures.
  3. Arterialization of Venous Blood: Because tissues are unable to extract oxygen from hemoglobin, central venous and mixed venous oxygen saturation are markedly elevated ($\text{ScvO}_2 > 85\%\text{ to }90\%$), narrowing the arteriovenous oxygen content difference.
• Definitive Antidote: Hydroxocobalamin (Cyanokit):
  • Administer $5\text{ g}$ IV infusion over 15 minutes (may repeat once to a total of $10\text{ g}$). Hydroxocobalamin contains a cobalt center that binds cyanide with higher affinity than cytochrome $a_3$, forming non-toxic cyanocobalamin (Vitamin $\text{B}_{12}$), which is excreted harmlessly in the urine.

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Environmental Emergencies: Accidental Hypothermia and Heat Stroke

Accidental Hypothermia

Defined as an involuntary drop in core body temperature $< 35^\circ\text{C}$ ($< 95^\circ\text{F}$). Core temperature must be measured using a low-reading esophageal, bladder, or rectal probe (esophageal is most accurate in intubated patients):

• Mild ($32^\circ\text{C}\text{ to }35^\circ\text{C}$): Vigorous shivering, tachycardia, tachypnea, ataxia, cold diuresis.
• Moderate ($28^\circ\text{C}\text{ to }32^\circ\text{C}$): Shivering ceases, altered mental status, hyporeflexia, bradycardia, hypotension.
• Severe ($< 28^\circ\text{C}$): Coma, severe bradycardia, pulmonary edema, ventricular fibrillation, asystole.

Electrocardiographic Hallmarks

• Osborne (J) Waves: A distinctive, positive deflection at the junction of the QRS complex and the ST segment, most prominent in the precordial leads. The height of the J-wave is proportional to the degree of hypothermia.
• Prolongation of all ECG conduction intervals (PR, QRS, and QTc intervals).
• Bradyarrhythmias, junctional rhythms, "slow" atrial fibrillation, and ventricular fibrillation (VF).

Rewarming Strategies and Arrest Protocols

• Mild-to-Moderate: Passive external rewarming (warm blankets, ambient room temperature) and active external rewarming (forced warm air blankets).
• Severe / Hemodynamically Unstable: Active internal/core rewarming: warmed IV fluids ($40^\circ\text{C}\text{ to }42^\circ\text{C}$), warm humidified ventilator circuit ($42^\circ\text{C}$), and warm bladder, pleural, or peritoneal irrigation.
• Hypothermic Cardiac Arrest: The cold myocardium is refractory to defibrillation and pharmacological cardioversion. Deliver up to 3 initial defibrillation shocks and withhold repeated epinephrine until core temperature reaches $> 30^\circ\text{C}$, as medications accumulate and cause lethal rebound toxicity when the patient rewarms. Continue chest compressions continuously.
• Extracorporeal Life Support (ECLS / VA-ECMO): The gold standard for hypothermic arrest or refractory shock with core temperature $< 28^\circ\text{C}$. ECMO provides complete circulatory support and rapid rewarming ($1^\circ\text{C}\text{ to }2^\circ\text{C}$ per hour).

Heat Stroke

Heat stroke is a medical emergency defined by a core body temperature $> 40^\circ\text{C}$ ($> 104^\circ\text{F}$) accompanied by central nervous system dysfunction (delirium, ataxia, seizures, or coma).

• Classic (Non-Exertional) Heat Stroke: Occurs during environmental heat waves in elderly, unhoused, or chronically ill individuals with impaired thermoregulation; anhidrosis (dry skin) is common.
• Exertional Heat Stroke: Occurs in young athletes or military recruits performing strenuous exertion in hot, humid weather; diaphoresis is frequently preserved.

Complications and Emergency Management

Heat stroke causes widespread systemic inflammatory response, endothelial injury, rhabdomyolysis, acute kidney injury, disseminated intravascular coagulation (DIC), and acute liver failure.

• Immediate Rapid Cooling: The cornerstone of therapy; mortality is directly correlated with the duration of hyperthermia. Cool immediately to a target core temperature of $< 38.5^\circ\text{C}\text{ to }39^\circ\text{C}$ within 30 minutes.
  • Exertional: Cold-water immersion is the most effective modality, achieving cooling rates $> 0.2^\circ\text{C/min}$.
  • Classic / Frail: Evaporative and convective cooling (spraying lukewarm water over the exposed body while high-velocity industrial fans blow continuously).
• Pharmacological Contraindications: Antipyretics (acetaminophen, NSAIDs) are completely ineffective and strictly contraindicated. The hypothalamic thermoregulatory set-point in heat stroke is normal (unlike fever); antipyretics do not reduce temperature and worsen hepatic necrosis and coagulopathy. Shivering should be treated with low-dose intravenous benzodiazepines to prevent endogenous heat production.