Luka Bakar

01Pathophysiology

Burn injury triggers a cascade of local and systemic events that the exam tests repeatedly. Understanding these mechanisms is what separates correct answers from plausible distractors.

At the local level, the burn wound is best understood through Jackson's three-zone model. The innermost zone of coagulation is the area of direct thermal contact where proteins undergo irreversible denaturation and tissue necrosis occurs immediately. Surrounding this is the zone of stasis, where perfusion is compromised but cells remain viable for 24 to 48 hours. This is the zone you are trying to salvage with adequate resuscitation, because inadequate fluid delivery or secondary insults (infection, hypotension, edema) will convert this zone into further necrosis. The outermost zone of hyperemia has increased blood flow due to local inflammatory mediators and will recover spontaneously. Exam vignettes that describe "burn wound deepening" over the first 48 hours are testing your knowledge that the zone of stasis converted due to under-resuscitation or infection.

Systemically, burns greater than 20% TBSA produce a systemic inflammatory response. Damaged endothelium releases inflammatory cytokines (TNF-alpha, IL-1, IL-6), causing a dramatic increase in capillary permeability. Protein-rich fluid shifts from the intravascular space into the interstitium (third-spacing), producing profound hypovolemic shock that is not hemorrhagic in nature. This is why the Parkland formula uses crystalloid and why the first 8 hours demand the greatest fluid volume: the capillary leak is maximal during this early window. The exam will test this timing repeatedly.

Burn-induced hypermetabolism is one of the most extreme catabolic states in medicine, with metabolic rates rising to 150 to 200% of baseline. Catecholamine surge drives tachycardia, hyperglycemia, and muscle protein breakdown. This is the rationale behind early enteral feeding and the use of agents like oxandrolone or propranolol in selected patients to blunt the hypermetabolic response.

Immunosuppression follows large burns because of both a shift from Th1 to Th2 immune response and a reduction in neutrophil and macrophage function. This makes burn patients highly susceptible to infection, particularly from Pseudomonas aeruginosa and Staphylococcus aureus. Burn wound sepsis remains the leading cause of death in patients who survive the initial resuscitation period.

Two classic complications arise directly from the stress physiology of burns. Curling ulcer is a stress ulcer of the duodenum caused by mucosal ischemia secondary to systemic hypoperfusion and is prevented with proton pump inhibitors or H2 blockers. Marjolin ulcer is a squamous cell carcinoma arising in a chronic burn scar, typically appearing years to decades after the injury. Both are named complications that appear as isolated questions on exams.

02Classification and Clinical Manifestation

Burn Depth Classification

TBSA Estimation: Rule of Nines (Adults)

Key modifier for children: In pediatric patients, the head represents a proportionally larger TBSA and the legs a smaller one. A child's head is approximately 18% at birth and decreases with age, while the legs increase proportionally. The Lund-Browder chart is the most accurate tool for pediatric TBSA estimation and is preferred over the Rule of Nines in children.

Palm method: The patient's own palm (including fingers) approximates 1% TBSA and is useful for estimating small or scattered burns.

Important: Only partial-thickness and full-thickness burns are included in TBSA calculations for fluid resuscitation. Superficial (first-degree) burns are excluded.

Classification by Burn Etiology

03Diagnostic Workup

The diagnosis of a burn is clinical. There is no single laboratory test that confirms "burn injury." The workup is instead focused on three goals: (1) accurate classification of depth and extent to guide resuscitation, (2) identification of associated injuries (inhalation, CO/cyanide, electrical), and (3) monitoring for complications.

TBSA and depth assessment are performed at the bedside. This is the "best initial test" for determining management. The Rule of Nines is rapid and practical for adults, but the Lund-Browder chart is the most accurate method, particularly in children where body proportions differ from adults.

For patients with suspected inhalation injury, the best initial step is securing the airway. The gold standard for diagnosing inhalation injury is fiberoptic bronchoscopy, which reveals erythema, edema, carbonaceous deposits, and mucosal sloughing in the tracheobronchial tree. However, do not delay intubation to obtain a bronchoscopy: if clinical signs of upper airway compromise are present (stridor, hoarseness, progressive edema), intubate first. A chest X-ray is often normal in the first 24 to 72 hours of inhalation injury, so a normal film does not rule it out.

For carbon monoxide poisoning, pulse oximetry is unreliable because conventional pulse oximeters cannot distinguish oxyhemoglobin from carboxyhemoglobin, producing falsely normal SpO2 readings. The correct test is a COHb level on co-oximetry from an arterial blood gas. Normal COHb is less than 3% in nonsmokers. Symptoms correlate roughly with levels: headache at 10 to 20%, confusion at 20 to 40%, coma and death above 40 to 60%.

For cyanide toxicity (common in enclosed-space fires involving burning plastics, wool, or silk), a direct cyanide level can be measured but results are often delayed. A practical surrogate is a persistently elevated serum lactate (>10 mmol/L) that does not improve with supplemental oxygen, which strongly suggests concurrent cyanide poisoning.

In electrical burns, the internal injury is almost always worse than what the skin surface suggests. Order a CK, urine myoglobin, and BMP to evaluate for rhabdomyolysis and hyperkalemia. Continuous cardiac monitoring and a 12-lead ECG are mandatory, as arrhythmias (ventricular fibrillation with AC current, asystole with DC/lightning) can be immediate or delayed.

Burn wound infection is diagnosed clinically by changes in wound appearance (focal discoloration, green exudate from Pseudomonas, rapid eschar separation) and confirmed with quantitative wound biopsy. The threshold of $>{10}^5>10^5$ colony-forming units per gram of tissue differentiates infection from colonization.

04Management & Treatment

Step 1: Scene Safety and Stopping the Burn. The very first action is to remove the patient from the source and stop ongoing injury. For chemical burns, copious water irrigation is the treatment, not neutralization (exothermic neutralization reactions cause additional thermal injury). Alkali burns require prolonged irrigation (30 minutes or more) because alkali penetrates deeply via liquefactive necrosis.

Step 2: Airway. This is the most critical early decision. Upper airway edema from thermal or inhalation injury can progress rapidly over the first 12 to 24 hours. If you see facial burns, singed eyebrows/nasal hairs, carbonaceous sputum, hoarseness, or stridor, the "next best step" is early endotracheal intubation. Do not wait for worsening obstruction. This is a "do not delay" answer on exams.

Step 3: Breathing and CO/Cyanide. Administer 100% oxygen via non-rebreather mask immediately. This is simultaneously diagnostic and therapeutic: it is the treatment for CO poisoning, reducing the half-life of COHb from approximately 5 hours (room air) to 60 to 90 minutes. Hyperbaric oxygen is indicated for COHb levels above 25%, neurological symptoms, pregnancy, or cardiac ischemia, where it reduces the half-life to approximately 20 to 30 minutes. For concurrent cyanide poisoning, hydroxocobalamin is the preferred antidote because it does not further compromise oxygen-carrying capacity (unlike the nitrite component of the older cyanide antidote kit, which induces methemoglobinemia).

Step 4: Fluid Resuscitation. Any burn over 20% TBSA in adults (or over 10% in children) requires IV fluid resuscitation. The Parkland formula is the most tested formula:

$$V=4\text{ mL}\times \text{body weight (kg)}\times \mathrm{\%}\text{TBSA burned}V\; =\; 4\backslash \; \backslash text\{mL\}\; \backslash times\; \backslash text\{body\; weight\; (kg)\}\; \backslash times\; \backslash \%\backslash text\{TBSA\; burned\}$$

Half of this calculated volume is given in the first 8 hours from the time of the burn injury, and the remaining half is infused over the subsequent 16 hours. The fluid of choice is Lactated Ringer's solution (isotonic crystalloid without dextrose for adults). The critical pitfall tested on exams is: the 8-hour clock starts from the time of injury, not time of arrival to the hospital. If a patient was burned 2 hours ago, you have only 6 hours remaining to deliver the first half.

The formula is a starting point, not a fixed prescription. Titrate fluids to urine output: 0.5 mL/kg/hr in adults, 1 mL/kg/hr in children. Over-resuscitation causes abdominal compartment syndrome and pulmonary edema ("fluid creep"), while under-resuscitation causes burn wound conversion and renal failure.

Step 5: Wound Care and Topical Agents. After resuscitation is initiated, wounds are debrided and covered with topical antimicrobials. The drug pharmacology here is a favorite exam topic:

Step 6: Escharotomy. If a circumferential full-thickness burn is present on an extremity or the chest, the inelastic eschar acts like a tourniquet as underlying edema develops. This causes compartment syndrome in extremities (loss of distal pulses, pain, paresthesias) or respiratory failure from restricted chest wall expansion. The treatment is escharotomy: a bedside longitudinal incision through the eschar along the mid-lateral or mid-medial lines. Because the burn is full-thickness, no anesthesia is needed for the incision through the eschar itself.

Step 7: Nutrition and Stress Ulcer Prophylaxis. Burns produce the most intense hypermetabolic state of any injury. Begin enteral feeding within 6 to 12 hours using a high-calorie, high-protein formula. Caloric needs can be estimated with the Curreri formula: $25\text{ kcal/kg/day}+40\text{ kcal}\times \mathrm{\%}\text{TBSA burned}25\backslash \; \backslash text\{kcal/kg/day\}\; +\; 40\backslash \; \backslash text\{kcal\}\; \backslash times\; \backslash \%\backslash text\{TBSA\; burned\}$. Administer a PPI or H2 blocker to prevent Curling ulcer.

Step 8: Surgical Management. Full-thickness burns and deep partial-thickness burns that will not epithelialize within 3 weeks require excision and grafting. The standard is tangential excision of necrotic tissue followed by split-thickness skin autograft (STSG). Early excision (within the first 72 hours) improves survival by reducing the inflammatory burden and infection risk. For patients with limited donor sites (very large TBSA burns), temporary coverage with cadaveric allograft, xenograft (porcine), or synthetic skin substitutes is used as a bridge.

Burn Center Referral Criteria

Any of the following warrants transfer:

• Partial-thickness burns >10% TBSA

• Burns involving the face, hands, feet, genitalia, perineum, or major joints

• Full-thickness burns of any size

• Electrical burns (including lightning)

• Chemical burns

• Inhalation injury

• Burns with pre-existing medical conditions that may complicate management

• Burns with concomitant trauma (if burn is the greater risk)

• Pediatric burns at hospitals without pediatric capabilities

• Burns requiring specialized social, emotional, or rehabilitative support (e.g., suspected abuse)

05Differential Diagnosis & Distractors

06Traps & High-Yield Pearls

The most common trap on burn questions involves the Parkland formula timing. Students frequently calculate the correct total volume but then deliver the first half based on the time of hospital arrival rather than the time of injury. The 8-hour clock begins at the moment of the burn. If a patient arrives 3 hours after injury, you must deliver the remaining first-half volume in 5 hours, not 8. This is tested in virtually every burn question that involves a calculation.

A second classic mistake is relying on pulse oximetry in carbon monoxide poisoning. The vignette will describe a house fire victim with normal SpO2 but altered mental status, and the student who trusts the oximeter reading will miss the diagnosis. The correct answer is always a COHb level on co-oximetry. Pulse oximetry reads carboxyhemoglobin as oxyhemoglobin, producing the falsely reassuring number.

Students also confuse the topical antimicrobials. Mafenide acetate is the only agent that penetrates eschar and cartilage, making it uniquely suited for ear burns (preventing suppurative chondritis), but its side effect is metabolic acidosis via carbonic anhydrase inhibition. Silver sulfadiazine is the default agent but does not penetrate eschar and causes a benign, self-limited leukopenia that does not require stopping the drug.

Another high-yield pitfall involves electrical burns. The surface injury misleads because the true damage is internal, following the path of least resistance through nerves and vessels. The exam will present a patient with small entrance and exit wounds who then develops rhabdomyolysis, hyperkalemia, cardiac arrhythmias, or compartment syndrome. The "next best step" in any electrical burn with dark urine is aggressive IV fluid resuscitation targeting urine output of 1 to 2 mL/kg/hr along with urine alkalinization to prevent myoglobin-induced acute tubular necrosis.

Finally, be vigilant for the child abuse vignette. An immersion scald burn in a toddler with uniform depth, sharp lines of demarcation, no splash marks, and a stocking-glove or buttock distribution should immediately raise suspicion. The correct next step is not just treating the burn; it includes reporting to child protective services and obtaining a skeletal survey to evaluate for occult fractures.

The core competency being tested across burn questions is the ability to integrate clinical assessment (depth, TBSA, mechanism, and associated injuries) into a logical management sequence: secure the airway before calculating fluids, calculate fluids from the correct time zero, choose the right topical agent for the right anatomic location, recognize when escharotomy is needed, and identify the complications that each burn mechanism uniquely produces.