21.2 Burn Assessment, Inhalation Injury & Resuscitation

Pathophysiology of Thermal Injury & Burn Depth Classification

Severe thermal burns induce both localized tissue coagulation and a massive systemic inflammatory response. In burns exceeding $20%$ Total Body Surface Area (TBSA), widespread release of vasoactive mediators (histamine, bradykinin, prostaglandins, thromboxane $A_2$, tumor necrosis factor-alpha) triggers extensive capillary endothelial hyperpermeability, profound plasma extravasation into the interstitial third-space, and systemic hypovolemic/distributive burn shock.

Jackson's Burn Wound Model

Locally, thermal injury organizes into three distinct concentric histological zones:

1. Zone of Coagulation: The central area of maximal thermal contact. Complete cellular necrosis and microvascular thrombosis occur instantaneously. This tissue is nonviable and forms the avascular eschar requiring surgical debridement.
2. Zone of Stasis: The intermediate zone surrounding the central coagulation zone. Characterized by compromised microvascular perfusion, cellular ischemia, and endothelial swelling. This zone is potentially salvageable with aggressive, timely fluid resuscitation and avoidance of hypothermia. Inadequate resuscitation converts the zone of stasis into nonviable coagulation necrosis ("burn wound conversion").
3. Zone of Hyperemia: The outermost peripheral zone. Exhibits prominent vasodilation and increased blood flow secondary to local inflammatory mediator release. This tissue uniformly recovers viability within 7 to 10 days unless complicated by invasive secondary infection.

                         JACKSON'S CONCENTRIC ZONES OF BURN INJURY

                ┌────────────────────────────────────────────────────────┐
                │ ZONE OF HYPEREMIA (Outermost)                          │
                │ • Marked vasodilation & inflammatory hyperemia         │
                │ • Fully viable tissue; heals spontaneously             │
                │   ┌────────────────────────────────────────────────┐   │
                │   │ ZONE OF STASIS (Intermediate)                  │   │
                │   │ • Ischemia, sluggish microvascular perfusion   │   │
                │   │ • SALVAGEABLE with timely fluid resuscitation  │   │
                │   │ • Converts to necrosis if hypoperfusion occurs │   │
                │   │   ┌────────────────────────────────────────┐   │   │
                │   │   │ ZONE OF COAGULATION (Central)          │   │   │
                │   │   │ • Irreversible tissue necrosis         │   │   │
                │   │   │ • Thrombosed microvessels; eschar      │   │   │
                │   │   │ • Requires excision and skin grafting  │   │   │
                │   │   └────────────────────────────────────────┘   │   │
                │   └────────────────────────────────────────────────┘   │
                └────────────────────────────────────────────────────────┘

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Clinical Classification of Burn Depth

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Total Body Surface Area (%TBSA) Calculation

Accurate calculation of the burned Total Body Surface Area (%TBSA) is essential to determine fluid resuscitation volumes and assess burn center transfer criteria. Overestimating %TBSA leads to fluid overload, while underestimating causes acute tubular necrosis and burn shock.

The Adult Rule of Nines

The adult body is divided into anatomical regions representing multiples of $9%$:

• Head and Neck: $9%$ (entire anterior face/neck $4.5%$, entire posterior head/neck $4.5%$)
• Anterior Torso (Chest and Abdomen): $18%$
• Posterior Torso (Upper and Lower Back): $18%$
• Each Upper Extremity: $9%$ (entire right arm $9%$, entire left arm $9%$; anterior $4.5%$, posterior $4.5%$ each)
• Each Lower Extremity: $18%$ (entire right leg $18%$, entire left leg $18%$; anterior $9%$, posterior $9%$ each)
• Perineum and External Genitalia: $1%$

The Palmar Method

For scattered, patchy, or irregular burns, the patient's palmar surface (including the palm and all five extended fingers) equals approximately $1%$ of their Total Body Surface Area. Clinicians assess how many "patient palms" are required to cover the burned patches.

[!IMPORTANT] THE GOLDEN RULE OF TBSA CALCULATION: First-degree burns (superficial erythema without blisters, such as sunburn) are STRICTLY EXCLUDED from %TBSA calculations. Only partial-thickness (second-degree) and full-thickness (third-degree) burns are included in fluid calculations. Counting superficial erythema results in severe fluid over-resuscitation ("fluid creep"), causing abdominal compartment syndrome and acute pulmonary edema.

Pediatric Differences: The Lund-Browder Chart

Children have a dramatically larger head-to-body surface area ratio and smaller lower extremities than adults. Using the adult Rule of Nines in infants causes gross estimation errors. Under the Lund-Browder Chart:

• In an infant, the head accounts for $18%$ of TBSA, while each leg accounts for only $14%$.
• For every year of age past 1 year, the head decreases by $1%$ while each lower extremity increases by $0.5%$, until adult proportions are attained at approximately 10 years of age.

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Fluid Resuscitation: The Parkland (Baxter) Formula

Formal intravenous fluid resuscitation is indicated for all adult patients with partial- and full-thickness burns involving $\ge 20%$ TBSA (or $\ge 10%$ TBSA in pediatric patients).

The 24-Hour Formula

$\text{Total 24-Hour Crystalloid Volume} = 4\text{ mL} \times \text{Body Weight (kg)} \times \%\text{TBSA (2nd and 3rd degree burns only)}$

• Fluid of Choice: Lactated Ringer's (LR) solution. Balanced crystalloid solutions match physiological electrolyte osmolarity and provide sodium lactate buffers. Normal saline ($0.9%\text{ NaCl}$) is avoided in massive resuscitation because its high chloride concentration ($154\text{ mEq/L}$) induces severe hyperchloremic non-anion gap metabolic acidosis and impairs renal perfusion.
• The Two-Interval Administration Schedule:
  1. First 8 Hours: Administer $50%$ of the total calculated volume within the first 8 hours FROM THE EXACT TIME OF THE BURN INJURY (NOT from the time of hospital arrival!). Any intravenous fluid already administered by EMS or referring clinics is subtracted from this 8-hour total.
  2. Next 16 Hours: Administer the remaining $50%$ of the calculated volume evenly over the subsequent 16 hours.

Clinical Example of Resuscitation Timing

• Scenario: A 75-kg male sustains $30%$ TBSA partial- and full-thickness burns at 12:00 PM. He arrives in the emergency department at 2:00 PM (2 hours post-injury) having received $500\text{ mL}$ LR en route.
• Calculation:
  • Total 24-hour volume $= 4\text{ mL} \times 75\text{ kg} \times 30 = 9,000\text{ mL}$ LR.
  • First 8-hour requirement $= 50% \text{ of } 9,000\text{ mL} = 4,500\text{ mL}$.
  • This $4,500\text{ mL}$ must be completed by 8:00 PM (8 hours post-injury).
  • Since 2 hours have already elapsed and $500\text{ mL}$ was infused, the patient requires $4,500 - 500 = 4,000\text{ mL}$ over the remaining 6 hours.
  • Initial infusion rate $= 4,000\text{ mL} / 6\text{ hours} = 667\text{ mL/hour}$.
  • The remaining $4,500\text{ mL}$ is infused over the subsequent 16 hours ($281\text{ mL/hour}$).

Clinical Monitoring & Dynamic Titration

The Parkland formula is merely a starting guide. Fluid infusion rates must be titrated up or down hourly by $10%\text{ to }20%$ based on objective physiological endpoints:

• Adult Target Urine Output: $0.5\text{ to }1.0\text{ mL/kg/hour}$ (approximately $30\text{ to }50\text{ mL/hour}$ in an average adult).
• Pediatric Target Urine Output: $1.0\text{ to }2.0\text{ mL/kg/hour}$ (in children weighing $<30\text{ kg}$).
• High-Voltage Electrical Burns & Crush Injuries: Extensive deep muscle necrosis releases massive amounts of myoglobin and potassium into the circulation. To prevent myoglobin cast precipitation and acute tubular necrosis, target an adult urine output of $1.5\text{ to }2.0\text{ mL/kg/hour}$ ($75\text{ to }100\text{ mL/hour}$) until urine is visibly clear of pigment, and administer IV sodium bicarbonate to alkalinize the urine (target urine $pH > 6.5$).
• Danger of "Fluid Creep": Excessive over-resuscitation beyond target urine outputs drives fluid into non-burned tissues, precipitating life-threatening abdominal compartment syndrome (intra-abdominal pressure $>20\text{ mmHg}$), severe extremity compartment syndrome, ocular compartment syndrome, and acute respiratory failure.

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Upper Airway Inhalation Injury & Airway Protection

Inhalation injury is the single most important predictor of burn mortality, increasing the expected mortality of any given burn by $>20%$. Injury occurs along two distinct anatomical segments:

1. Supraglottic Upper Airway Thermal Injury: Direct heat transfer to the nasopharynx, epiglottis, and vocal cords. True thermal burns rarely penetrate below the vocal cords because the upper airway acts as an efficient heat exchanger, rapidly cooling superheated air.
2. Subglottic Lower Airway Chemical Tracheobronchitis: Inhalation of toxic smoke particulates, aldehydes, sulfur dioxide, and acid fumes causes chemical injury to bronchiolar epithelium, ciliary paralysis, mucosal sloughing, airway casting, and severe bronchospasm.

Clinical Signs Demanding Immediate Proactive Intubation

Progressive glottic, pharyngeal, and aryepiglottic edema develops rapidly over the first 12 to 24 hours post-injury as fluid resuscitation expands third-spaced interstitial tissues. Clinicians must maintain a low threshold for early preemptive endotracheal intubation when signs of upper airway burn are present:

• History of fire trapped within a closed, enclosed space;
• Deep facial, perioral, or neck burns;
• Singed nasal vibrissae (hairs) and singed eyebrows;
• Soot deposits in the oral cavity, palate, posterior pharynx, or tongue;
• Carbonaceous (soot-laden) sputum;
• Development of hoarseness, brassy cough, or deep phonation changes;
• Inspiratory stridor, tachypnea, or intercostal retractions (indicates $>85%$ airway lumen occlusion).

[!WARNING] THE INHALATION AIRWAY TRAP: In an acute burn patient with perioral soot and mild hoarseness, oxygen saturation may remain completely normal ($98%\text{ to }100%$) during the first few hours. Do not be falsely reassured by a normal pulse oximetry reading or clear lung auscultation. Attempting endotracheal intubation 8 to 12 hours later, when massive supraglottic edema has converted the vocal cords into an unrecognizable mass of swollen gelatinous tissue, frequently results in a catastrophic "cannot intubate, cannot ventilate" scenario requiring emergency surgical cricothyroidotomy.

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Toxic Inhalation Syndromes: Carbon Monoxide & Cyanide

Patients rescued from enclosed structural fires frequently suffer from toxic asphyxiant inhalations that prevent cellular ATP generation:

                         TOXIC INHALATION RESUSCITATION PATHWAY

                   Victim Rescued from Enclosed Space Fire
                                     │
                       100% Normobaric Oxygen via NRB
                                     │
             ┌───────────────────────┴───────────────────────┐
             ▼                                               ▼
   CARBON MONOXIDE (CO)                            HYDROGEN CYANIDE (HCN)
   • Affinity 200x > Oxygen                        • Inhibits Cytochrome c Oxidase
   • SpO2 falsely reads 100%                       • Profound Cellular Dysoxia
   • Send Blood Co-Oximetry (COHb)                 • Severe Lactic Acidosis (>8-10 mmol/L)
             │                                               │
     ┌───────┴───────┐                                       ▼
     ▼               ▼                             INTRAVENOUS HYDROXOCOBALAMIN
   COHb <25%       COHb >25%                       (5g IV Cyanokit over 15 min)
   (No signs)     (or >15% Pregnant,               • Binds CN -> Cyanocobalamin
     │             Coma, Ischemia)                 • Excreted harmlessly in urine
     ▼               │
  Continue           ▼
  100% O2       HYPERBARIC OXYGEN
  (until         THERAPY (HBO)
  COHb <5%)     (Reduces half-life
                 to ~20-30 min)

1. Carbon Monoxide (CO) Poisoning

• Mechanism: Carbon monoxide binds hemoglobin with an affinity 200 to 250 times greater than oxygen, forming carboxyhemoglobin (COHb). This directly displaces oxygen from binding sites and shifts the oxyhemoglobin dissociation curve sharply to the left (Haldane effect), preventing oxygen release to peripheral tissues. CO also binds intracellular myoglobin and mitochondrial cytochrome oxidase, halting ATP production.
• The Pulse Oximetry Fallacy: Standard two-wavelength pulse oximeters measure light absorbance at 660 nm and 940 nm, cannot distinguish carboxyhemoglobin from oxyhemoglobin, and falsely report normal or near-normal values ($99%\text{ to }100%$). Clinicians must obtain an arterial or venous blood gas with co-oximetry to measure the carboxyhemoglobin level.
• Treatment Protocol:
  • Administer $100%$ high-flow normobaric oxygen via a tight-fitting non-rebreather mask (or endotracheal tube). This accelerates CO dissociation from hemoglobin, reducing the half-life of COHb from 300 minutes on room air down to 60 to 90 minutes on $100%\text{ }O_2$.
  • Indications for Hyperbaric Oxygen (HBO) Therapy:
    1. Carboxyhemoglobin level $> 25%$ in non-pregnant patients;
    2. Carboxyhemoglobin level $> 15%$ in pregnant women (fetal hemoglobin binds CO with higher affinity, and fetal tissue is uniquely vulnerable to hypoxic death);
    3. Any documented history of loss of consciousness, syncope, or seizure;
    4. Unresolved neurological deficits, confusion, or severe delirium;
    5. Evidence of acute myocardial ischemia (angina, ischemic ECG changes, or elevated troponin);
    6. Severe refractory metabolic acidosis ($pH < 7.25$).
  • HBO delivers $100%\text{ }O_2$ at 2.5 to 3 atmospheres absolute, reducing COHb half-life to 20 to 30 minutes and preventing delayed neuropsychiatric sequelae.

2. Hydrogen Cyanide (HCN) Poisoning

• Mechanism: Generated during the incomplete combustion of nitrogen-containing synthetic materials, polyurethane foam, plastics, insulation, and synthetic carpets. Inhaled cyanide binds with high affinity to ferric iron ($Fe^{3+}$) within mitochondrial cytochrome c oxidase (Complex IV) of the electron transport chain. This completely halts oxidative phosphorylation, uncouples cellular respiration, and prevents cells from utilizing oxygen (histotoxic hypoxia), forcing anaerobic glycolysis.
• Diagnostic Hallmarks:
  • The combination of soot in the pharynx and severe, refractory metabolic lactic acidosis (serum lactate $> 8\text{ to }10\text{ mmol/L}$) in an enclosed-space fire victim is virtually diagnostic of cyanide poisoning.
  • Central venous oxygen saturation ($ScvO_2$) or mixed venous oxygen saturation is paradoxically elevated ($>80%\text{ to }85%$), reflecting inability of peripheral tissues to extract circulating oxygen.
• Definitive Antidote: Hydroxocobalamin (Cyanokit):
  • Administer $5\text{ g}$ IV infused over 15 minutes (pediatric dose $70\text{ mg/kg}$). A second $5\text{ g}$ dose can be repeated if hemodynamic instability or lactic acidosis persists.
  • Mechanism: Hydroxocobalamin contains cobalt that binds cyanide with higher affinity than cytochrome oxidase, forming non-toxic cyanocobalamin (vitamin $B_{12}$), which is excreted safely in the urine.
  • Clinical Note: Causes transient reddish discoloration of the skin and dark red "burgundy" urine, and temporarily interferes with colorimetric laboratory assays (bilirubin, creatinine, co-oximetry).
  • Historical Warning: The traditional cyanide antidote kit containing sodium nitrite is avoided in burn patients because nitrites induce methemoglobinemia, which severely worsens oxygen-carrying capacity in patients with concurrent carbon monoxide poisoning.

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Circumferential Burns & Emergency Escharotomy

Full-thickness third-degree burns produce rigid, inelastic, leathery eschar. During vigorous fluid resuscitation, progressive interstitial edema expands beneath the unyielding eschar, creating dangerous tourniquet and compartment syndromes:

Indications for Surgical Escharotomy

1. Circumferential Torso / Chest Burns:
   • Edema expanding against the rigid chest eschar severely restricts diaphragmatic descent and chest wall compliance.
   • Produces progressive hypoventilation, rapidly escalating peak airway pressures ($>40\text{ cm }H_2O$) on the mechanical ventilator, refractory hypercapnia, and hypoxemia.
2. Circumferential Extremity Burns:
   • Intracompartmental tissue pressure escalates, exceeding capillary perfusion pressure ($>30\text{ mmHg}$). This compresses venous return, followed by arterial inflow, producing limb-threatening ischemic compartment syndrome.
   • Signs: Severe pain out of proportion (in partial-thickness borders), deep distal paresthesias, tense woody firmness, progressive pallor, delayed capillary refill ($>3\text{ seconds}$), and loss of distal arterial Doppler flow signals.

Procedural Technique of Bedside Escharotomy

• Escharotomy is performed at the bedside under sterile conditions using an electrocautery unit or scalpel. Local anesthesia is generally unnecessary through third-degree full-thickness eschar (which is anesthetic).
• Chest Incisions: Longitudinal bilateral incisions along the anterior axillary lines, joined across the lower rib margin by a transverse subcostal incision, creating a "U-shaped" release that frees the anterior thoracic plate.
• Extremity Incisions: Longitudinal mid-lateral or mid-medial incisions along the anatomical neutral axes of the limb, extending across burned joints from non-burned tissue to non-burned tissue.
• Depth of Incision: Incise only through the full thickness of the leathery eschar and superficial dermis until the subcutaneous fat pops open and herniates slightly outward. Do NOT incise the deep investing muscle fascia (fasciotomy is reserved for underlying high-voltage electrical injury or refractory compartment syndrome). Avoid major superficial nerves (ulnar nerve at the medial epicondyle; common peroneal nerve at the fibular head).

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American Burn Association (ABA) Burn Center Transfer Criteria

Patients meeting any of the following criteria should be transferred to an accredited American Burn Association burn center following initial stabilization:

1. Partial-thickness (second-degree) burns involving $>10%$ TBSA;
2. Burns involving sensitive cosmetic or functional anatomical zones: the face, hands, feet, genitalia, perineum, or overlying major synovial joints;
3. Third-degree (full-thickness) burns of any size in any age group;
4. Electrical burns, including high-voltage, low-voltage, and lightning strike injuries;
5. Chemical burns from industrial acids, alkalis, or corrosive organics;
6. Inhalation injury of any severity;
7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality (e.g., severe heart failure, renal failure, cirrhosis);
8. Burn injury accompanied by concomitant traumatic mechanical injury (e.g., fractures) where the burn injury poses the greatest immediate risk of morbidity or mortality;
9. Burned children in hospitals without specialized pediatric personnel or equipment;
10. Burn injury requiring specialized social, emotional, or long-term rehabilitative intervention.