Burns Classification and Management

Zone of Coagulation (Central Zone)

• Represents irreversibly damaged tissue at the injury epicenter with temperatures exceeding the denaturation threshold of cellular proteins (typically >65°C)
• Coagulation necrosis occurs through denaturation of structural and enzymatic proteins, cellular membrane disruption, and cell death via necrosis (not apoptosis, due to severity of injury)
• Characterized histologically by complete loss of cellular architecture with no viable cells
• This zone determines the actual burn depth and is essentially irreversible; all tissue in this zone will be lost regardless of intervention

Zone of Stasis (Intermediate Zone)

• Surrounds the coagulation zone with intermediate heat exposure and incomplete protein denaturation
• Tissue viability in this zone depends critically on perfusion; viable cells with compromised but intact membranes coexist with inflammatory mediators
• Progressive tissue ischemia develops over 24-48 hours due to microvascular thrombosis (caused by endothelial damage, activation of tissue factor, and platelet aggregation), increased tissue edema, and progressive hypoxia
• This zone is potentially salvageable through aggressive fluid resuscitation and reducing edema; inadequate resuscitation causes expansion of this zone into irreversible necrosis
• Contains inflammatory cells and cytokines including TNF-α, IL-1, IL-6, IL-8, and bradykinin that drive both local and systemic inflammation

Zone of Hyperemia (Peripheral Zone)

• Outermost zone with minimal temperature elevation showing inflammatory response without cell death
• Characterized by vasodilation mediated by histamine and prostaglandins, increased capillary permeability, and hyperemia that appears as erythema
• Generally resolves completely with restoration of normal perfusion within 7-10 days without scarring
• Contains activated mast cells, macrophages, and endothelial cells actively secreting inflammatory mediators

Systemic Inflammatory Response and Fluid Shifts

• Large burns (>20% TBSA in adults, >10% in children/elderly) trigger a systemic inflammatory response syndrome (SIRS) even without sepsis, driven by bacterial translocation, damaged epithelial barriers, and massive cytokine release
• Increased capillary permeability occurs in burned and unburned tissue through the release of vasoactive mediators (histamine, prostaglandins, leukotrienes, platelet-activating factor, bradykinin), leukocyte sequestration, and complement activation
• This causes massive third-spacing with fluid shifting from intravascular to interstitial and intracellular compartments; edema develops not only in burned areas but throughout the body in severe burns
• Peak edema formation occurs 24-48 hours post-injury; fluid losses can be 3-4 times the volume of visible burn
• The inflammatory response contributes to multi-organ dysfunction: acute kidney injury (from hypovolemia and myoglobinuria if muscle is involved), acute respiratory distress syndrome (ARDS), hepatic dysfunction, and immunosuppression with increased infection risk

Metabolic and Hemodynamic Consequences

• Massive hypermetabolic state develops with metabolic rate increasing to 1.5-2 times normal, mediated by catecholamines, cortisol, and thyroid hormones
• Persistent tachycardia and elevated cardiac output (hyperkinetic circulation) develop as the body attempts to maintain oxygen delivery despite ongoing losses
• Progressive cooling of core temperature occurs (burn shock), and hypothermia is common in the first 24-48 hours despite appearing as a "hot" injury
• Myocardial depression develops in severe burns through circulating depressant factors, reduced preload from fluid losses, and increased afterload
• Blood viscosity increases from hemoconcentration (due to fluid losses exceeding protein losses initially), worsening microcirculatory flow

Inhalation Injury Pathophysiology

• Thermal injury to airways causes direct coagulation necrosis of respiratory epithelium with massive edema; steam inhalation is particularly damaging due to higher heat capacity than dry air
• Chemical injury from combustion products (carbon monoxide, hydrogen cyanide, hydrogen sulfide, chlorine, phosgene) causes:
• Carbon monoxide (CO): binds hemoglobin with affinity 200-250× that of oxygen, forming carboxyhemoglobin and impairing oxygen delivery despite normal PaO2; also impairs cytochrome oxidase activity
• Hydrogen cyanide: binds cytochrome c oxidase, blocking aerobic metabolism even when oxygen is available
• Acrolein and other aldehydes: directly damage respiratory epithelium and cause pulmonary edema
• Massive airway edema develops within minutes to hours, potentially causing complete obstruction
• Circumferential burns of the thorax cause escharotomy-requiring restriction of chest wall expansion, impairing ventilation
• Smoke inhalation increases risk of mortality 3-4 fold compared to burns without inhalation injury

Electrical Burns Unique Pathophysiology

• Current flows along path of least resistance (typically heart, CNS, muscle); enters at contact point and exits at grounding point
• Tetanic muscle contraction from sustained stimulation of motor nerves can cause tetanus-like rigidity, crush injuries from violent contraction, and compartment syndrome
• Deep muscle injury (rhabdomyolysis) occurs disproportionate to surface injury as current heats deep tissues
• Myoglobin release from muscle necrosis (myoglobinuria) causes acute kidney injury through:
• Precipitation of myoglobin in renal tubules (Tamm-Horsfall protein interaction)
• Direct tubular toxicity
• Vasoconstriction of renal vessels
• Aciduria exacerbates precipitation
• Cardiac dysrhythmias occur from direct current effect on myocardium; asystole or ventricular fibrillation can be immediate or delayed
• Neurological injury can include spinal cord damage from violent contraction or direct heating, causing paresis or paralysis

Thermal Burns (85% of all burns)

• Flame/contact burns: most common cause of hospitalized burns; associated with clothing ignition, house fires, vehicle fires, campfire exposure
• Scalding injuries: second most common cause overall; predominantly affects children <5 years in home settings with hot water, hot liquids (coffee, soup, tea), and steam; also affects elderly from impaired mobility and sensation
• Hot surfaces: contact with stoves, heaters, machinery; risk increases with alcohol intoxication and impaired consciousness
• Outdoor exposures: sun exposure (rarely causes full-thickness burns but significant cumulative damage), campfires, grills

Electrical Burns (5% of all burns)

• Household current (110-240V): causes mostly superficial injuries but can cause cardiac dysrhythmias
• High-voltage contact (>1000V): particularly dangerous with deep tissue injury, high mortality rate; occupational in utility workers, electricians; also occurs from contact with power lines
• Lightning strikes: rare but extremely high mortality; causes unique pattern of injury with entry/exit wounds and potential for cardiac arrest and neurological injury

Chemical Burns (10% of all burns)

• Alkali (calcium oxide, sodium hydroxide, potassium hydroxide): cause liquefactive necrosis with saponification of fats and deep penetration; typically more severe than acid burns of equivalent concentration
• Acids (hydrofluoric acid, sulfuric acid, phosphoric acid): cause coagulative necrosis with protein denaturation; form eschar limiting further penetration; hydrofluoric acid is particularly dangerous due to fluoride ion toxicity causing hypocalcemia and hyperkalemia
• Hydrocarbons and organic compounds: tar, asphalt, white phosphorus
• Occupational exposure: construction workers, industrial workers, laboratory personnel

Radiation Burns

• Ultraviolet radiation: cumulative exposure over lifetime, primarily causes superficial burns and increased melanoma risk
• Ionizing radiation: rare outside occupational/industrial accidents or nuclear incidents; can cause deep tissue injury

Risk Factors for Burn Injury

• Age extremes: children <5 years (curiosity, poor coordination, inability to escape) and elderly >65 years (impaired mobility, sensation, reaction time, thin skin); account for disproportionate mortality
• Substance use: alcohol and drug intoxication impair judgment, reaction time, and ability to escape; found in 30-40% of adult burn admissions
• Male gender: 2-3× higher incidence, likely related to occupational exposure and risk-taking behavior
• Low socioeconomic status: associated with inadequate heating systems, overcrowding, reduced fire safety measures
• Psychiatric illness: suicide attempts account for 5-10% of adult burns; untreated mental illness associated with higher burn risk
• Impaired sensation/mobility: neuropathy, spinal cord injury, arthritis, dementia predispose to prolonged contact with heat source
• Seizure disorder: convulsions near heat sources increase risk
• Occupational exposure: military personnel, firefighters, industrial workers in high-temperature environments
• Environmental/structural factors: lack of smoke detectors, unattended cooking, faulty heating systems, overcrowded housing, blocked exits

Burn Depth Classification (Determines Healing Potential and Scarring)

Superficial (First-Degree) Burns

• Clinical appearance: bright red, dry, intact skin with no blistering; painful to touch
• Physiological basis: injury limited to epidermis; melanocytes are damaged but dermal structures preserved
• Sensation: extremely painful due to intact sensory nerve endings and inflammatory response
• Blanching: erythema blanches completely with pressure
• Healing: complete healing within 3-7 days without scarring; epidermis regenerates from basal layer
• Examples: typical sunburn, minor scald exposure
• NOT typically included in TBSA calculations in standard practice (though this varies by institution)

Partial-Thickness (Second-Degree) Burns: Superficial Dermal

• Clinical appearance: bright red or mottled appearance with clear fluid-filled blisters (fragile bullae) present; extremely painful
• Physiological basis: injury extends through epidermis into papillary dermis but preserves deeper dermal structures and adnexal structures (hair follicles, sweat glands)
• Sensation: very painful due to exposed sensory nerve endings; patients withdraw from touching
• Blanching: erythema blanches with pressure
• Hair pull test: hair pulls out easily (distinguishes from deeper burns where hair is firmly attached to remaining dermis)
• Healing: spontaneous healing within 1-2 weeks through re-epithelialization from preserved dermal structures; minimal scarring if infection is prevented
• Examples: scalding from hot water, brief flame contact, minor contact burns

Partial-Thickness (Second-Degree) Burns: Deep Dermal

• Clinical appearance: mottled appearance with white/tan areas mixed with red; blisters may be present but are less prominent; may appear leathery
• Physiological basis: injury extends through most of the dermis but preserves deeper structures and some skin appendages; border between viable and non-viable tissue is indistinct
• Sensation: markedly diminished pain sensation compared to superficial second-degree; touch sensation may be absent but deep pressure sensation preserved
• Blanching: slow or incomplete blanching; capillary refill may be prolonged (>2 seconds)
• Hair pull test: hair strongly attached; does not pull out easily
• Healing: slower healing over 2-3 weeks with significant risk of hypertrophic scarring and contractures; often requires skin grafting; depth of injury may worsen over first 24-48 hours due to expanding zone of stasis
• Examples: prolonged scald exposure, contact with hot objects, flame burns with brief to moderate contact

Full-Thickness (Third-Degree) Burns

• Clinical appearance: waxy, leathery, translucent or opaque eschar; may appear charred (black) or white depending on temperature and tissue composition
• Physiological basis: complete destruction of epidermis and dermis with extension into subcutaneous tissue; all skin appendages destroyed and non-viable
• Sensation: painless because nerve endings are destroyed; patient may feel pain around the edges of the burn (zone of stasis) but not in the burn itself
• Blanching: no blanching; eschar does not turn white with pressure
• Hair pull test: hair is firmly attached to remaining dermis or moves as a unit; no individual hair movement
• Healing: cannot heal by re-epithelialization alone due to complete loss of skin appendages; requires surgical excision and grafting; any healing without grafting occurs through slow contraction from wound margins and scarring
• Examples: prolonged flame exposure, contact with hot objects >65°C for extended time, electrical burns, chemical burns with deep penetration
• Hyperextension: may appear painless, which can be misinterpreted as minor injury by patients (classic trap); loss of sensation does not mean loss of severity

Fourth-Degree Burns

• Clinical appearance: charred black eschar with visible muscle, bone, or organ tissue beneath
• Physiological basis: destruction extends through all skin layers into subcutaneous fat, muscle, and potentially bone
• Associated findings: may show visible muscle charring, bone exposure, or organ tissue
• Healing: always requires surgical excision; amputation often necessary if limbs involved; extremely high mortality
• Examples: prolonged flame exposure, electrical burns with severe current flow through extremities, contact with extremely high temperatures

Total Body Surface Area (TBSA) Estimation

Rule of Nines (for adults)

• Head and neck: 9%
• Each upper extremity: 9%
• Anterior trunk: 18%
• Posterior trunk: 18%
• Each lower extremity: 18%
• Genitalia: 1%

Lund-Browder Chart (more accurate for small burns and children)

• More precise percentages based on body region and age
• Necessary for children because head and extremities represent different proportions than adults (children have larger heads)
• Preferred for accurate TBSA calculation in clinical practice

Systemic Manifestations of Burn Injury

Burn Shock (Hypovolemic Shock with Inflammatory Components)

• Pathophysiology: combination of massive fluid losses into third space (interstitial edema from increased capillary permeability) and circulating depressant factors
• Clinical presentation:
• Tachycardia (compensatory increase in heart rate; heart rate often increases 1 beat per minute for each 1% TBSA burned acutely)
• Hypotension (late sign indicating severe shock; develops after 6-24 hours if resuscitation inadequate)
• Decreased urine output (oliguria or anuria)
• Altered mental status (agitation initially, then lethargy as shock worsens)
• Cool, clammy skin with poor perfusion peripherally despite core being warm
• Lactic acidosis from tissue hypoperfusion
• Timing: begins immediately at time of injury; peak occurs at 6-24 hours post-injury; may last 48-72 hours in severe burns

Inhalation Injury Presentation

• Acute presentation:
• Singed nasal hairs, carbonaceous sputum, or soot in mouth/oropharynx indicating airway involvement
• Stridor (indicates laryngeal edema)
• Hoarseness from vocal cord damage
• Difficulty swallowing
• Wheezing or crackles on auscultation
• Hypoxemia with normal-to-low carboxyhemoglobin (in contrast to classic teaching, carboxyhemoglobin is often not markedly elevated in non-fatal inhalation)
• Progressive respiratory distress within minutes to hours
• Severe inhalation injury can cause complete

Bedside assessment (the initial "test")

• Depth: judged by color, blistering, blanching, sensation, and the hair pull test — pain and brisk blanching mean viable dermis; a painless, non-blanching, leathery eschar means full thickness. Depth is dynamic and may declare itself only at 48–72 hours as the zone of stasis converts.
• TBSA: Rule of Nines for rapid adult field estimation; Lund–Browder chart is the reference standard, particularly in children, whose head is proportionally larger. For patchy or small burns use the palmar method — the patient's palm plus fingers approximates 1% TBSA. Superficial (first-degree) burns are excluded from TBSA.

Laboratory and imaging workup in major burns

• ABG with co-oximetry: the confirmatory test for carbon monoxide poisoning. Pulse oximetry is falsely normal because carboxyhemoglobin absorbs light like oxyhemoglobin, and PaO2 is normal because dissolved oxygen is unaffected — only direct carboxyhemoglobin measurement makes the diagnosis.
• Lactate: a markedly elevated lactate with a narrow arteriovenous oxygen difference in an enclosed-space fire suggests cyanide toxicity; treat empirically, since cyanide levels return too late to be useful.
• Fiberoptic bronchoscopy: gold standard for inhalation injury, showing soot, mucosal edema, erythema, and ulceration. Chest radiograph is typically normal initially and does not exclude injury.
• CK, urine myoglobin, ECG, potassium: mandatory after electrical injury to detect rhabdomyolysis and dysrhythmia.
• Baseline CBC, chemistry, type and screen, and pregnancy testing.

Immediate stabilization (ATLS/ABLS sequence)

• Stop the burning process: remove clothing, jewelry, and chemical residue; irrigate chemical burns copiously with water. Do not attempt chemical neutralization (exothermic) and do not apply ice — vasoconstriction extends the zone of stasis.
• Airway: early intubation for stridor, hoarseness, deep facial burns, or progressive edema. Airway swelling is time-dependent and worsens with resuscitation; waiting for failure makes the airway unobtainable.
• 100% oxygen by non-rebreather for suspected CO poisoning — it shortens carboxyhemoglobin half-life several-fold; hyperbaric oxygen is considered for severe poisoning, neurologic findings, or pregnancy.
• Hydroxocobalamin is the antidote of choice for suspected cyanide toxicity in smoke inhalation; avoid nitrite-based kits, which induce methemoglobinemia and further impair oxygen carriage.

Wound and supportive care

• Analgesia: IV opioids (e.g., fentanyl or morphine); avoid IM/SC routes given unreliable absorption in shock.
• Tetanus immunization per CDC/ACIP.
• Topical antimicrobials: silver sulfadiazine (avoid on the face, in sulfa allergy, and near term/in neonates), mafenide acetate for eschar and cartilage penetration, or silver-impregnated dressings. Systemic prophylactic antibiotics are not recommended.
• Early enteral nutrition, high-protein, to blunt the hypermetabolic response.

Airway and pulmonary

• Upper airway obstruction (emergency): progressive laryngeal edema, worsened by resuscitation fluid; heralded by stridor and hoarseness. Intubate early.
• Carbon monoxide and cyanide toxicity (emergency): headache, confusion, or coma with a normal pulse oximetry reading and normal PaO2; unexplained severe lactic acidosis suggests cyanide.
• ARDS and pneumonia: mucosal sloughing, cast formation, and impaired ciliary clearance; new infiltrates with rising oxygen requirement.

Circulatory and renal

• Burn shock/AKI: third-spacing and hypoperfusion; oliguria despite resuscitation. In electrical burns, rhabdomyolysis produces tea-colored urine, urine dipstick positive for blood with no red cells, and markedly elevated CK.
• Compartment syndrome and constrictive eschar (emergency): circumferential extremity burns cause loss of pulses and pain on passive stretch; circumferential torso burns cause rising airway pressures. Treat with escharotomy.
• Abdominal compartment syndrome (emergency): a complication of over-resuscitation; oliguria with elevated bladder pressure, distended abdomen, and difficult ventilation.

Infectious

• Burn wound sepsis (emergency): loss of the epithelial barrier plus burn-induced immunosuppression; Pseudomonas aeruginosa (green discoloration, sweet odor), Staphylococcus aureus, and later Candida. Signs are wound conversion to deeper injury, graft loss, hypothermia, thrombocytopenia, and glucose intolerance rather than classic fever alone.
• Toxic shock syndrome: classically in small burns in children — fever, rash, and shock out of proportion to wound size.

Gastrointestinal, metabolic, and treatment-related

• Curling ulcer: stress-related gastroduodenal ulceration from splanchnic hypoperfusion; presents as GI bleeding.
• Hypermetabolism with muscle catabolism, hyperglycemia, and hypothermia from lost skin barrier.
• Mafenide acetate: carbonic anhydrase inhibition → non-anion-gap metabolic acidosis. Silver sulfadiazine: leukopenia and kernicterus risk in neonates.
• Succinylcholine after roughly the first 24–48 hours: extrajunctional acetylcholine receptor upregulation causes life-threatening hyperkalemia (emergency) — use a non-depolarizing agent.

• Airway before fluids: the single best next step in a patient from an enclosed-space fire with singed nasal hairs, carbonaceous sputum, hoarseness, or stridor is early intubation — not calculating the Parkland formula. Edema is progressive and worsened by resuscitation.
• Normal pulse oximetry does not exclude carbon monoxide poisoning. Order ABG with co-oximetry for carboxyhemoglobin and start 100% oxygen. The common distractor is reassurance based on a 99% SpO2 or a normal PaO2.
• Parkland timing is from the moment of injury, not from ED arrival — a patient arriving 3 hours post-burn must receive the first half over the remaining 5 hours. Fluid is lactated Ringer's, titrated to urine output, per ABA/ABLS; colloid and prophylactic systemic antibiotics are the classic wrong answers.
• First-degree burns are excluded from TBSA. Sunburn does not count. Use Rule of Nines for adults and the Lund–Browder chart for children, whose heads occupy a larger proportion of surface area.
• Painless, leathery, non-blanching burn = full thickness, and it is more severe, not less. Pain preservation argues for a salvageable partial-thickness wound.
• Circumferential full-thickness burn with a cold, pulseless limb or rising ventilator pressures → escharotomy at the bedside; fasciotomy is reserved for true compartment syndrome, typically after electrical injury.
• Electrical injury association tested most: surface wounds underestimate deep muscle necrosis. Expect rhabdomyolysis, hyperkalemia, and dysrhythmia — check CK, urine myoglobin, and an ECG, and target a higher urine output.
• Alkali burns penetrate deeper than acids (liquefactive vs coagulative necrosis); irrigate copiously and never neutralize. Hydrofluoric acid is the exception requiring calcium gluconate for hypocalcemia.
• Avoid succinylcholine beyond the first day post-burn because of receptor upregulation and hyperkalemic arrest.