Burns & Thermal Injury

Meet the patient

A 40-year-old man is brought to the emergency department 40 minutes after a kitchen flash-fire. He has flame burns across his chest, abdomen and both arms, an estimated 25 percent of his body surface. There is soot around his mouth and nose, his nasal hairs are singed, and his voice is hoarse.[2][11]

This single patient carries every decision that defines burn care, and the order is not negotiable. The airway comes first — hoarseness and soot mean the upper airway is already injured and will swell shut, so he is intubated now, before it is lost. Only then do you assess depth and surface area, start the Parkland clock from the time of the burn, cool the wound, and arrange transfer to a burns unit. Get that order wrong and the patient dies of asphyxiation in a body that was otherwise survivable.[1][2]

What a burn is — the wound itself is the disease

A burn is coagulative destruction of the skin and, in deeper injuries, of subcutaneous fat, fascia, muscle and bone — produced when thermal, chemical, electrical or radiant energy arrives faster than the tissue can dissipate it. The plastics and dermatology perspective that separates modern burn care from generic resuscitation is this: the wound itself is the disease, and every decision about depth, surface area, dressing, the timing of excision and grafting, and rehabilitation is taken to preserve function in the hands, face and over joints and to limit the late scarring that dominates a survivor's life.[2][9]

Burns are among the most devastating yet most preventable of traumas. The World Health Organization attributes more than 180,000 burn deaths a year to burns, the overwhelming majority in low- and middle-income countries, where open-flame cooking, kerosene heaters, unsafe wiring and absent smoke alarms converge. The skill of burn assessment rests on three pillars: accurate depth and surface area, airway protection (inhalation injury kills by oedema and obstruction — intubate early), and fluid resuscitation titrated to urine output (under-resuscitation causes burn shock, over-resuscitation causes oedema, compartment syndrome and abdominal compartment syndrome). Circumferential full-thickness burns demand escharotomy; electrical burns hide deep injury behind a small entry wound and need cardiac monitoring and a search for myoglobinuria; chemical burns demand copious irrigation, with calcium gluconate gel for hydrofluoric acid.[1][2]

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Classification — two axes, depth and surface area

Every burn is described on two independent axes: depth and TBSA. Depth governs healing potential and the need for surgery; TBSA governs the systemic fluid response. First-degree (epidermal) burns are excluded from the TBSA calculation because they do not produce the capillary leak that drives burn shock.[1]

Depth — the five grades

Depth is the single most important wound-level decision, because it predicts whether the wound heals spontaneously from epithelial appendages within two to three weeks (no scar), heals slowly with scarring (may need a graft), or will not re-epithelialise and must be excised and grafted. The discriminators are blanching, capillary refill, pinprick sensation, moisture and the appearance of the surface.[2][6]

Depth is not fixed at the moment of injury — it can deepen over the first 48 to 72 hours. A burn that looks superficial dermal on day one can become deep dermal or full-thickness if the zone of stasis is lost to under-resuscitation, infection or desiccation. This is why serial re-assessment at 24 and 48 hours, with moist occlusive dressings or biological membranes to keep the wound environment optimal, is standard practice.[2][9]

Surface area — Rule of Nines, Lund-Browder, palm

Count only partial-thickness (2nd degree) and deeper burns in the TBSA. Superficial epidermal (1st degree) erythema is excluded. A common and dangerous error is to fold sunburn-like erythema into the Parkland calculation.[5][6]

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The Lund-Browder chart corrects the Rule of Nines for children, whose head is proportionally much larger — up to 19 percent in an infant — and whose legs are smaller. Applying the adult Rule of Nines to a young child underestimates the head and overestimates the legs, under-resuscitating the most dangerous region. This is a classic and lethal error; always use Lund-Browder in children.[4]

Epidemiology — a disease of poverty and the domestic kitchen

Burns are overwhelmingly a disease of poverty and domesticity. Smolle and colleagues' systematic review found the highest incidence and mortality in the WHO South-East Asian and African regions: flame burns dominate in adults and scalds in children under five. Risk clusters in the home kitchen, around open fires, kerosene stoves and hot bathwater; occupational electrical and chemical burns cluster in construction, electrical and chemical industries.[1]

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In a child, always weigh non-accidental injury. Suspect it when the history is inconsistent with the injury, presentation is delayed, the burn has a stocking-glove or doughnut (central sparing) distribution suggestive of forced immersion, or there are associated signs of neglect. Assessing a burned child is also safeguarding that child.[4]

Pathophysiology — Jackson's zones, capillary leak, and the hypermetabolic state

The Jackson model — three concentric zones

The local response to a burn is the Jackson zones — three concentric zones within and around the wound at the moment of injury. This model is what separates burn surgery from simple wound care, because the central zone is dead but the middle zone is salvageable, and good resuscitation, dressings and infection control are precisely the measures that rescue it.[2]

The zone of stasis is the tissue the resuscitation is fought for. Under-resuscitation, desiccation, infection or a continued inflammatory cascade converts it into the zone of coagulation — the burn deepens, more tissue is lost, and the eventual scar and graft burden worsen. Every action in the first 48 hours is, in part, an attempt to save the zone of stasis.[1]

Systemic — capillary leak, burn shock, hypermetabolism

A burn exceeding roughly 20 percent TBSA in adults (10 percent in children) produces a generalised increase in capillary permeability throughout the body — not only at the burn site. Inflammatory mediators (histamine, bradykinin, serotonin, prostaglandins, leukotrienes, thromboxane, IL-1, IL-6, TNF-alpha) circulate and drive a massive transcapillary leak of fluid, electrolytes and protein into the interstitium. The result is the oedema of burn shock and a steep fall in intravascular volume, cardiac output and urine output over the first 8 to 12 hours.[2][3]

This is the rationale for the Parkland formula: crystalloid in a calculated volume over the first 24 hours to replace the leak. After 24 hours the leak partly resolves and colloid (protein) is introduced. Under-resuscitation gives hypovolaemic (burn) shock with multi-organ dysfunction; over-resuscitation tracks fluid into the soft tissues and may precipitate compartment syndrome of a limb or abdominal compartment syndrome — the syndrome called fluid creep.[3][5]

A profound hypermetabolic response then sets in: resting energy expenditure can reach 1.5 to 2 times baseline in burns over 40 percent TBSA, driven by catecholamines, cortisol and glucagon, with fever, tachycardia, muscle catabolism, immune suppression and impaired wound healing. This is why early enteral nutrition (within 24 to 48 hours) is a treatment, not a comfort measure — it blunts the catabolic drive, protects the gut mucosa and lowers bacterial translocation and Curling's ulcer risk.[2]

Clinical presentation — how deep, how much, where

The bedside questions are three: how deep, how much, and where.[1]

Depth signs. A superficial dermal burn is red, moist, blistering and exquisitely painful, with brisk blanching and refill — the capillaries are alive. A deep dermal burn is drier, paler or mottled, with sluggish capillary refill and reduced pinprick sensation. A full-thickness burn is dry, leathery and insensate (the nerves are destroyed), often white, grey or charred, with no blanching. A painless burn is a deep burn — one of the most important rules in the specialty.[6][9]

Surface area is the Rule of Nines, Lund-Browder or palm method — always excluding first-degree erythema.[1]

Special sites each carry a specific threat and lower the threshold for burns-unit referral: the face (inhalation injury, eye injury, cosmetic), the hands (function — the position of safety), the feet (mobility), the perineum and genitals (infection risk, micturition), and skin over major joints (contracture).[1]

Inhalation injury presents with soot in the mouth or sputum, singed nasal and facial hairs, hoarseness, stridor, a history of exposure in an enclosed space, and altered consciousness from carbon monoxide poisoning. Hoarseness or stridor is a pre-emergency warning — the airway will close as oedema worsens, so the patient is intubated early, before the airway is lost.[11]

Differential diagnosis — not every blister is a burn

Not every blistering or desquamating eruption is a burn, and several mimics are life-threatening in their own right.[1]

The key bedside discriminator is the history. A thermal burn has a clear heat-source history; TEN or SJS has a drug exposure, SSSS an infectious prodrome in a child, phytophotodermatitis plant-plus-sun. The distribution differs too — thermal burns follow a splash, scald or flame pattern, while TEN is symmetrical and mucosal.[2]

The bedside round — ABCDE before the burn

The ABCDE primary survey is performed before any burn assessment, because an obstructed airway or a tension pneumothorax from associated trauma will kill the patient before the burn does.[1]

The focused burn assessment

1. History — mechanism (flame, scald, electrical, chemical), time of burn (for the Parkland clock), enclosed space (inhalation), first aid already given, tetanus status, comorbidities, drugs, and — for a child — whether the history fits the injury.
2. Airway and breathing — signs of inhalation injury; assess oxygenation.
3. Depth assessment — blanching (press with a glass slide or finger), capillary refill, pinprick sensation, moisture, appearance; document on a body chart.
4. TBSA — Rule of Nines or Lund-Browder; confirm small or patchy burns with the palm method.
5. Special sites — face and eyes (fluorescein staining for corneal burns), ears (cartilage — mafenide acetate), hands (neurovascular, position of safety), perineum, joints.
6. Circumferential burns — document any circumferential full-thickness burn of a limb or chest; check distal perfusion and chest expansion.
7. Neurovascular distal to the burn — pulses, capillary refill, sensation — to detect early compartment syndrome.[6][9]

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Investigations — clinical diagnosis, tests serve the resuscitation

Burns are a clinical diagnosis. Investigations serve the resuscitation, the hunt for complications, and the assessment of inhalation and electrical injury — not the diagnosis itself.[1]

Inhalation injury is diagnosed clinically and confirmed bronchoscopically — carbonaceous material, oedema, erythema or mucosal necrosis in the airway is diagnostic.[11] Carbon monoxide poisoning is detected by an elevated carboxyhaemoglobin and treated with 100 percent oxygen (hyperbaric oxygen is considered in selected severe cases, though the evidence is debated).

Management — resuscitation, in the right order

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First aid and pre-hospital care

Cooling with running water for 20 minutes, ideally begun within three hours of the burn, reduces pain, limits depth progression and improves outcome. Ice must not be used — it causes vasoconstriction that worsens the zone of stasis, can produce frostbite on top of the thermal injury, and risks systemic hypothermia, especially in children.[2]

Airway and breathing

In any suspected inhalation injury, secure the airway early by endotracheal intubation before oedema makes it impossible. Indications include hoarseness, stridor, significant facial burns with soot or singed hairs, and altered consciousness. Give 100 percent oxygen via a non-rebreather mask pending intubation — this treats carbon monoxide poisoning (the CO half-life falls from around 320 minutes on room air to around 80 minutes on 100 percent oxygen). Arrange bronchoscopy to grade the inhalation injury.[11]

Fluid resuscitation — the Parkland (Baxter) formula

For major burns (over 10 percent TBSA in adults, over 5 percent in children), calculate the first 24 hours of fluid with the Parkland formula.[3][5]

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Children need maintenance fluid (with glucose) on top of the calculated resuscitation volume, because their glycogen stores are limited. From 24 hours onwards, capillary leak has largely resolved and colloid (albumin) is introduced at a reduced rate, with oral or enteral intake encouraged as tolerated.[3][4]

Analgesia, tetanus and the escharotomy

Analgesia: burns are extremely painful. Give intravenous morphine 0.1 mg/kg (titrated, repeated as needed) or fentanyl, with paracetamol as baseline. Never give intramuscular analgesia in a major burn — absorption is unreliable in shock. Cover the wound to reduce air-current pain.[1]

Tetanus prophylaxis: all burns are tetanus-prone wounds. Check immunisation status and give tetanus toxoid (and immunoglobulin if the wound is contaminated and the patient is not immune) per local protocol.[1]

Escharotomy: a circumferential full-thickness burn of a limb or the chest forms an inelastic eschar. As oedema accumulates beneath it, distal perfusion is compromised (limb) or chest expansion is restricted (thorax). A surgical escharotomy — incisions through the eschar to subcutaneous fat along the lateral and medial aspects of the limb or the anterior chest — relieves the pressure. It is a bedside procedure under sedation, and the incision should be bloodless (a full-thickness burn is insensate). Indications include a cool, pulseless or painful distal limb, falling pulse-oximetry, paraesthesia, and reduced chest expansion. A fasciotomy (deeper, through fascia) is needed for electrical burns and deep thermal injury with muscle involvement.[1]

Management — definitive and stepwise

Minor (outpatient) burns

Minor burns — small partial-thickness burns under 10 percent TBSA in adults (under 5 percent in children), not involving special sites, not circumferential — are managed as outpatients.[6]

Dressing choice follows depth and exudate. Hydrocolloids (occlusive, autolytic) suit clean superficial partial-thickness burns. Silver sulfadiazine 1 percent remains the topical antimicrobial standard — broad-spectrum (gram-positive including some MRSA, gram-negative including Pseudomonas, and some fungal), painless on application, but sulfa-based (contraindicated in sulfa allergy and pregnancy near term) and causes a transient leucopenia in roughly 5 to 15 percent of patients. Mafenide acetate 10 percent penetrates cartilage and eschar and is preferred for ear burns (to prevent suppurative chondritis) but is painful on application and can cause a metabolic acidosis (carbonic anhydrase inhibition). Biological and biosynthetic membranes (Biobrane, Suprathel) suit clean superficial partial-thickness burns and reduce pain and dressing changes.[12]

Major burns — definitive surgical management

Definitive management of a major burn is surgical and undertaken in a burns unit. The principle of modern burn surgery is early tangential excision and split-thickness skin grafting (STSG) of deep dermal and full-thickness burns, ideally within the first 3 to 5 days — removing the necrotic eschar (a culture medium for infection), reducing the inflammatory and hypermetabolic burden, shortening stay and improving survival. Early excision is what changed burn mortality in the late 20th century, and it is now standard.[2][9]

Antibiotics are NOT given prophylactically in burns — they do not prevent wound infection, they select resistant organisms, and they are reserved for documented infection (cellulitis, bacteraemia, sepsis) guided by culture. The single most important infection-prevention measure is early excision and closure of the wound.[2]

The position of safety for the burned hand

The hand is the single most important functional unit in burn rehabilitation, and a burned hand held in the wrong position for two weeks will contract into a useless claw. The position of safety (anti-deformity position) splints the hand in: wrist extended 20 to 30 degrees, metacarpophalangeal joints flexed 70 to 90 degrees, interphalangeal joints fully extended, thumb abducted and opposed. This lengthens the collateral ligaments and the palmar skin so that, when oedema and scarring contract, they do not pull the hand into the classic contracture (wrist flexed, MCPs extended, IPs flexed, thumb adducted).[9]

Specific subtypes — electrical and chemical burns

Electrical burns

Electrical injury is deceptively dangerous because the skin wound is small but the deep tissue injury is large — current follows the path of least resistance through nerves, blood vessels and muscle, sparing the high-resistance skin. The entry wound may be a tiny charred puncture, the exit wound similarly small, and in between muscle, nerve and vessel may be destroyed. Vigilance for deep injury is everything.[2]

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Chemical burns

Chemical burns differ from thermal burns because the injuring agent keeps damaging tissue until it is removed or neutralised. The first principle is copious, prolonged irrigation with water (most agents) for at least 20 minutes — and longer for alkalis.[8]

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Hydrofluoric acid is the most feared chemical burn because the fluoride ion chelates calcium and magnesium, producing deep, excruciating pain disproportionate to the visible injury, progressive tissue necrosis, life-threatening hypocalcaemia and hypomagnesaemia, and fatal ventricular arrhythmia. The specific antidote is calcium gluconate.[8]

Special sites

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Complications — local, systemic, late

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Curling's ulcer deserves its own line: an acute stress ulceration of the duodenum (and sometimes stomach) in severe burns (and, by analogous pathophysiology, head injury — Cushing's ulcer). Modern prophylaxis — early enteral feeding and acid suppression in major burns — has made it uncommon, but bleeding or perforation in a major burn is still Curling's until proven otherwise.[7]

Prognosis and disposition

Prognosis is governed by age, TBSA, inhalation injury and comorbidity. The classic Baux score (age plus percent TBSA) gives a rough mortality estimate — a score over 100 historically implied near-certain death, though modern care has substantially improved survival beyond it. The revised Baux score adds inhalation injury (age plus percent TBSA plus 17 if inhalation injury present) and predicts in-hospital mortality more accurately.[10]

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Disposition. Minor burns (small partial-thickness, not special sites, not circumferential) are managed as outpatients. Major burns and all special-site, electrical, chemical, inhalation and circumferential burns are referred to a burns unit.[6]

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Special populations

Children. The TBSA threshold for a major burn is lower (over 5 percent). Children have a larger surface-area-to-mass ratio, so fluid needs per kg are higher and they desiccate and become hypothermic faster. The Lund-Browder chart must be used (the adult Rule of Nines underestimates the head and overestimates the legs). Maintenance fluid with glucose is added to the Parkland resuscitation. Non-accidental injury must be considered whenever the history is inconsistent, presentation is delayed, or the pattern is stocking-glove, doughnut (central sparing from forced immersion) or a contact pattern suggesting a heated object.[4]

The elderly. Skin is thinner, so the same insult produces a deeper burn. Comorbidities (cardiac, respiratory, diabetes) limit reserve, and mortality at any given TBSA is higher. Polypharmacy (beta-blockers, anticoagulants) complicates resuscitation and surgery.[1]

Electrical injury. Cardiac monitoring, rhabdomyolysis and deep-tissue surveillance as above.[1]

Pregnancy. The fetus is vulnerable to maternal hypovolaemia and hypoxia; resuscitation must be aggressive, the patient positioned to avoid aortocaval compression, and fetal monitoring instituted for viable pregnancies.[1]

Evidence, guidelines and regional differences

The Parkland (Baxter) formula (Baxter, 1968) — 4 mL per kg per percent TBSA of crystalloid, half in the first 8 hours — remains the most widely taught resuscitation formula. Its simplicity is its strength, but it has been criticised for the fluid creep syndrome (over-resuscitation leading to oedema, compartment syndrome and abdominal compartment syndrome) seen since the 2000s. The Modified Brooke formula (2 mL per kg per percent TBSA) was developed in response, and many modern units use a goal-directed (urine-output-titrated) approach regardless of the starting formula.[3][5]

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Prevention

Burns are largely preventable, and prevention is the most cost-effective intervention at a population level. WHO and national programmes target smoke alarms and home fire-escape plans; lowering hot-water thermostat settings (to under 50 degrees Celsius) to prevent scalds; child-resistant cigarette lighters; safe cooking stoves; fireworks regulation; electrical and chemical safety with training and PPE; and first-aid education ("cool with running water for 20 minutes"). The dermatology and plastics team contributes through school and community education and tertiary prevention — early excision, grafting, pressure garments and rehabilitation.[1]

The mantra

The mantra: airway first, cool for 20, Parkland to urine, escharotomy for the circumferential burn — and never let the airway swell shut while you measure the area.[1]

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Ward-round test — three stems, thirty seconds each

Stem 1 — the flash-fire patient with soot around the mouth (answer)

A 40-year-old man has 25 percent TBSA flame burns to the chest, abdomen and arms. There is soot around his mouth, his nasal hairs are singed, and his voice is hoarse. What is the first intervention, and why? Model: Intubate now. Hoarseness and soot are signs of inhalation injury, and the upper-airway oedema that follows will close the airway within hours. The lethal, recurring error is delaying intubation in the hope that the patient "looks fine." Secure the airway before it is lost, give 100 percent oxygen for carbon monoxide poisoning, arrange bronchoscopy, and only then assess depth and TBSA and start the Parkland clock from the time of the burn.[11]

Stem 2 — the 25 percent TBSA burn and the Parkland calculation (answer)

A 70 kg adult has a 25 percent TBSA partial-thickness burn, sustained 2 hours ago. What is the Parkland volume for the first 24 hours, and how much is given in the first 8 hours? Model: Parkland = 4 mL x 70 kg x 25 = 7,000 mL of Ringer lactate over the first 24 hours. Half — 3,500 mL — goes in the first 8 hours from the time of the burn (so the clock started 2 hours ago; 6 hours remain for that first half), and the remaining 3,500 mL over the next 16 hours. Titrate to urine output 0.5 mL/kg/h. Remember to count only partial-thickness and deeper burns, never first-degree erythema, and to watch for fluid creep.[3]

Stem 3 — the hydrofluoric acid burn on the finger (answer)

A laboratory worker spills hydrofluoric acid on his finger; he has severe deep pain out of proportion to a small area of erythema. What is the sequence of management, and what is the antidote? Model: First, copious irrigation with water. Then apply calcium gluconate gel 10 percent (mixed with a lubricant) and massage in repeatedly until the pain resolves. For deep, extensive or digital involvement, give intradermal or intra-arterial calcium gluconate 10 percent. Monitor the ECG and serum calcium and magnesium — fluoride chelates calcium and magnesium, and fatal hypocalcaemic arrhythmia can follow even small burns. The fluoride ion keeps damaging tissue until it is neutralised, which is why HF is more feared than other acid burns.[8]

References

1. [1]Smolle C, Cambiaso-Daniel J, Forbes AA, et al. Recent trends in burn epidemiology worldwide: A systematic review Burns, 2017.PMID 27600982
2. [2]Jeschke MG, van Baar ME, Choudhry MM, et al. Burn injury Nat Rev Dis Primers, 2020.PMID 32054846
3. [3]Guilabert P, Usúa G, Martín N, et al. Fluid resuscitation management in patients with burns: update Br J Anaesth, 2016.PMID 27543523
4. [4]Jeschke MG, Herndon DN. Burns in children: standard and new treatments Lancet, 2014.PMID 24034453
5. [5]Alvarado R, Chung KK, Cancio LC, Wolf SE. Burn resuscitation Burns, 2009.PMID 18539396
6. [6]Kiwan O, Hassanin S, Ekwobi C, et al. What You Need to Know About: Assessment of Burns and Initial Management Br J Hosp Med (Lond), 2025.PMID 41134176
7. [7]Kanchan T, Geriani D, Savithry KS Curling's ulcer - have these stress ulcers gone extinct? Burns, 2015.PMID 25440842
8. [8]Pan CS, Lee CC, Yu JH, et al. Assessing the efficacy and safety of calcium gluconate soaking as a treatment modality for hydrofluoric acid burns Burns, 2025.PMID 40088690
9. [9]Tredget EE. Management of the acutely burned upper extremity Hand Clin, 2000.PMID 10791166
10. [10]Belayneh ES, Abebe MW, Fikremariam M, et al. Accuracy of the revised Baux score for predicting in-hospital mortality of patients with burns: A retrospective cohort study from Ethiopia J Plast Reconstr Aesthet Surg, 2026.PMID 42399141
11. [11]Dries DJ, Endorf FW Inhalation injury: epidemiology, pathology, treatment strategies Scand J Trauma Resusc Emerg Med, 2013.PMID 23597126
12. [12]Tan H, Wasiak J, Paul E, et al. Effective use of Biobrane as a temporary wound dressing prior to definitive split-skin graft in the treatment of severe burn: A retrospective analysis Burns, 2015.PMID 25767062