ICU · Resuscitation
Severe burns management
Also known as Burn resuscitation · Parkland formula · Inhalation injury · Total body surface area (TBSA) · Lund and Browder chart · Burn depth classification · Superficial dermal burn · Deep dermal burn · Full thickness burn · Escharotomy · Burn centre transfer criteria · Revised Baux score · Fluid creep · Carbon monoxide poisoning in burns · Cyanide toxicity in burns
Severe burns (20% TBSA in adults, 10% in children/elderly) require ICU admission for fluid resuscitation, airway management, and wound care. Burn depth is classified by tissue layer: superficial epidermal (erythema, not counted in TBSA), superficial dermal (painful, blistering, blanching), deep dermal (pale, sluggish capillary refill, may need grafting), and full thickness (dry, leathery, painless, requires excision and grafting). TBSA is estimated by the Rule of Nines (adult: head 9, arm 9, leg 18, trunk 18 front and 18 back) or, preferably in children, the Lund-Browder chart which corrects for the proportionally larger head. Fluid resuscitation uses the Parkland formula (4 mL x kg x %TBSA in first 24h, half in first 8h from time of burn) using crystalloid (Hartmann's preferred — less hyperchloraemia than saline), titrated to urine output (0.5 mL/kg/h adult, 1 mL/kg/h child). Inhalation injury: suspect in enclosed space fires, facial burns, stridor, carbonaceous sputum — early intubation. Monitor for carbon monoxide and cyanide toxicity (house fires). Escharotomy for circumferential burns compromising circulation/ventilation. Infection is the leading cause of late mortality. Nutrition: early enteral feeding (within 6h) reduces bacterial translocation.
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Target exams
Red flags
Burn assessment
Total Body Surface Area (TBSA)
[1]The Rule of Nines and Lund-Browder chart agree in the adult but diverge sharply below school age. Re-assess TBSA at 24h — overestimation in the field is common (mean overestimate ~5-10%), and the initial number drives the entire first-day fluid prescription. Modern smartphone-assisted and computer-vision tools (BurnCase 3D) reduce inter-observer variability but the Lund-Browder chart remains the bedside standard.[10][11]
Burn depth
Superficial (1st degree)
Epidermis only
- Erythema, pain, no blisters (like sunburn)
- NOT counted in TBSA calculation
- Heals in 3-5 days without scarring
- Treatment: simple analgesia, moisturiser
Partial-thickness (2nd degree)
Into dermis
- Superficial partial: blisters, very painful, moist, blanching. Hair intact.
- Deep partial: less painful (nerve damage), pale, may not blanch. Hair lost.
- Counted in TBSA
- Heals in 2-3 weeks (superficial) or may need grafting (deep)
Full-thickness (3rd degree)
Through entire dermis
- Dry, leathery, white/black, painless (nerves destroyed), no blanching
- Counted in TBSA
- Will NOT heal without skin grafting
- Eschar forms — may need escharotomy if circumferential
Four-tier depth classification (examiner-preferred)
Examiners increasingly expect the modern four-tier scheme, because the boundary between a deep-dermal and a full-thickness burn determines whether a wound will heal spontaneously (within 3 weeks) or needs excision and grafting. Bedside assessment is wrong in ~30% of intermediate-depth burns; laser Doppler imaging (LDI) at 48-72h improves accuracy where available.[7][9]
Superficial epidermal
1st degree — epidermis
- Sunburn pattern: erythema, no blisters, blanches briskly, very painful
- Skin appendages intact; heals in 3-6 days by desquamation, no scar
- EXCLUDED from TBSA — do NOT add to Parkland formula
- Treatment: cool running water 20 min, simple analgesia, moisturiser, aloe
Superficial dermal
2nd degree — superficial papillary dermis
- Blisters, moist and glistening pink, blanches rapidly, exquisitely painful (intact nociceptors)
- Hair follicles and sweat glands intact — re-epithelialise from these in 10-14 days
- Counted in TBSA
- Treatment: de-roof blisters, non-adherent dressing, antimicrobial silver dressing; expect healing without scar
Deep dermal
2nd degree — deep reticular dermis
- Pale/mottled pink, sluggish or absent capillary refill, decreased sensation (nerve damage); hair may be lost
- Few surviving appendages → re-epithelialisation slow (>3 weeks) or stalls; high risk of hypertrophic scar
- Counted in TBSA
- Likely needs surgical excision and split-thickness skin grafting (STSG). LDI at 48-72h clarifies depth.
Full thickness
3rd degree — entire dermis ± subcutis
- Dry, leathery, waxy white / cherry-red / black; painless (nerves destroyed); no blanching
- No epithelial regrowth possible — WILL NOT heal without grafting (or contract from edges)
- Counted in TBSA; the rigid eschar may require escharotomy if circumferential
- Treatment: early tangential excision (within 72h-1 week) and STSG; 4th degree extends to muscle/bone
Fluid resuscitation — Parkland formula
Burn fluid resuscitation protocol
Calculate fluid requirement (Parkland formula)
Volume (first 24h) = 4 mL x weight (kg) x %TBSA. Example: 70 kg adult with 40% TBSA burn = 4 x 70 x 40 = 11,200 mL in first 24h. Use Hartmann solution (Ringer lactate) — preferred over normal saline (less hyperchloraemic acidosis).<Cite id="9" />
Give half in first 8 hours (from time of BURN, not admission)
Critical: the 8-hour clock starts from the TIME OF BURN, not from hospital arrival. If patient presents 3h after burn, give the first half in the remaining 5h. Rate = (half total volume) / (8 - hours since burn). The other half is given over the next 16h.
Titrate to urine output — the formula is a STARTING POINT
Target urine output: 0.5 mL/kg/h (adults), 1 mL/kg/h (children <30 kg). Adjust fluid rate every hour based on urine output. If urine output too low: increase fluid rate by 20-30%. If too high: decrease rate. The Parkland formula overestimates in some patients — titration is essential.
Second 24h: add colloid + maintenance
After 24h, capillary leak resolves. Add colloid (albumin 5%) for ongoing losses. Start maintenance fluids (glucose-containing for children). Reduce crystalloid. Begin enteral nutrition.
Parkland worked example and pitfalls
Worked example — 70 kg adult, 40% TBSA flame burn at 10:00
Step 1 — total 24h volume
4 mL x 70 kg x 40% = 11,200 mL Hartmann in 24h (from 10:00 to 10:00 next day).
Step 2 — first-half rate (10:00-18:00)
Half = 5,600 mL over the first 8h = 700 mL/h. If the patient arrives at 13:00 (3h post-burn), the remaining 5,600 mL must go in the 5 hours to 18:00 = 1,120 mL/h. Recalculate on every delayed presentation.
Step 3 — second-half rate (18:00-10:00)
Remaining 5,600 mL over the next 16h = 350 mL/h.
Step 4 — hourly titration
Hour 1 urine output 20 mL (target 35 mL/h for a 70 kg adult at 0.5 mL/kg/h): increase rate by 25%. Hour 2 output 60 mL: hold rate. Sustained UO >1 mL/kg/h without diuretics = cut rate by 20-30% to avoid fluid creep and abdominal compartment syndrome.
Modified Brooke (2 mL/kg/%TBSA)
Resuscitation formula
- Originated from observations that resuscitation volumes were climbing; advocates a LOWER starting point (2 mL/kg/%TBSA in first 24h).
- Goal: limit fluid creep and its complications (oedema, compartment syndrome, ARDS).
- Titrate to the SAME urine-output target as Parkland; if UO falls you add fluid rather than starting high.
- Preferred by many burn centres for the patient WITHOUT inhalation injury; the two formulas converge if you titrate properly.
Parkland (4 mL/kg/%TBSA)
Resuscitation formula
- The classic starting point (Baxter, 1968); still the most widely taught.
- Tends to OVER-resuscitate when followed uncritically (modern series give 5-6 mL/kg/%TBSA in practice, the origin of fluid creep).
- Add 1-2 mL/kg/%TBSA extra for inhalation injury and delay >2h post-burn.
- Use crystalloid ONLY for the first 24h (colloid leaks through the open capillaries in the first day).
Children <30 kg
Maintenance + resuscitation
- Children need a glucose-containing MAINTENANCE fluid in addition to resuscitation (limited glycogen, risk of hypoglycaemia).
- Parkland resuscitation volume + 4-2-1 maintenance (or D5-0.45%NaCl at Holliday-Segar rate).
- Higher urine-output target: 1 mL/kg/h.
- Use weight-based everything; a 10 kg child with 30% TBSA burn is a major burn and a burn-centre transfer.
Inhalation injury
Supraglottic vs infraglottic injury
The anatomical division of inhalation injury predicts the clinical course. The larynx is an efficient heat exchanger: it almost always absorbs enough thermal energy to protect the subglottis from direct thermal damage, so true lower-airway thermal injury is rare except with steam (water vapour carries ~4000x the heat capacity of dry air). The infraglottic lesion is therefore chemical, not thermal.[3][12]
Supraglottic (thermal)
Above the vocal cords
- Direct thermal injury to mouth, oropharynx, supraglottic larynx → mucosal oedema that peaks at 24-48h.
- Signs: singed nasal/vibrissae hairs, soot in mouth, swollen uvula, hoarse voice, stridor (late, ominous).
- Airway obstruction is the threat — progressive over hours; intubate BEFORE oedema closes the glottis.
- Steam injuries are the exception that CAN reach the lower airway (high heat capacity of water vapour).
Infraglottic (chemical)
Below the vocal cords
- Chemical injury from smoke toxins (acrolein, hydrogen chloride, ammonia, nitrogen oxides) dissolving in the airway lining fluid.
- Bronchospasm, mucosal sloughing, loss of ciliary clearance, mucous plugging, atelectasis, then chemical pneumonitis → ARDS over 24-72h.
- Signs: cough, wheeze, carbonaceous sputum, hypoxaemia, falling compliance; CXR initially normal.
- Surfactant disruption and bronchial blood flow loss drive the pneumonia/ARDS phase; nebulised heparin/NAC reduce airway casts.
Systemic toxins (CO + cyanide)
Combustion products absorbed
- Carbon monoxide: binds Hb 240x tighter than O2; pulse oximetry falsely reads ~SpO2 99%. Check COHb; treat with 100% O2 (halves COHb half-life from 320 to 80 min); hyperbaric O2 for COHb >25%, neuro signs, or pregnancy.
- Cyanide: from burning plastics/wool; blocks cytochrome c oxidase → anion-gap metabolic (lactic) acidosis with NORMAL saturation and NORMAL COHb. Antidote: hydroxocobalamin 5 g IV (preferred — does not impair tissue oxygen-carrying capacity).
- House fire + coma + severe metabolic acidosis = cyanide until proven otherwise; give hydroxocobalamin empirically.
- Sodium thiosulfate and the older cyanide antidote kit (amyl/sodium nitrite) are alternatives but risk methaemoglobinaemia and hypotension.
Management bundle — the first 24 hours
The first hour is airway, then fluid. Everything else (wound care, analgesia, tetanus, NG tube, catheter, transfer decision) is layered onto a stable ABC platform. The order matters: securing the airway before oedema closes it is the single most time-critical intervention in burns.[1][9]
First-24h burns management bundle
A — Stop the burning process and secure the airway
Remove clothing (preserve heat and chemicals), cool with running water 20 min (within 3h of burn — comfort, not the delayed 20-min myth). Assess airway: enclosed fire, facial burn, stridor, carbonaceous sputum → EARLY intubation (oedema peaks 24-48h; delayed = cricoid pressure on a distorted, oedematous airway and a surgical airway). C-spine precautions in any fall/jump to escape.
B — 100% oxygen and breathing
100% O2 by high-flow mask for ALL major burns (drives CO off haemoglobin; COHb half-life ~320 min on air, ~80 min on 100% O2). Check COHb and lactate. Intubate and ventilate lung-protectively if GCS <8, inhalation injury with respiratory failure, or deep burns >60% TBSA. Rehearse RSI — the burnt airway swells fast; smaller tube (6.0-7.0) if facial oedema.
C — Circulation: Parkland fluid + access + monitoring
Two large-bore IV cannulae through UNBURNED skin where possible. Calculate Parkland: 4 mL x kg x %TBSA Hartmann, half in first 8h from time of burn. Titrate hourly to UO 0.5 mL/kg/h (adult), 1 mL/kg/h (child). Insert urinary catheter (mandatory for >20% TBSA to titrate). Monitor HR, BP, capillary refill, lactate. Arterial line if >30% or vasoactive drugs.
D — Disability: analgesia and GCS
Burns hurt — titrated IV opioid (morphine 0.1 mg/kg or fentanyl 1-2 mcg/kg) in small repeat boluses; avoid IM (absorption unreliable in shock). Do NOT under-treat pain. Check GCS — depressed GCS in a burn patient is CO/cyanide, head injury, or hypoxia until proven otherwise. Pupils before opioid.
E — Exposure, estimate TBSA and depth, temperature control
Log-roll to assess back. Estimate TBSA with Lund-Browder (child) or Rule of Nines + palm method. Cover wounds with cling film / sterile saline-soaked dressings — NOT creams at this stage (impairs later assessment). Keep patient WARM: burns cause massive heat loss; hypothermia worsens coagulopathy and shock.
F — NG tube (>20% TBSA), tetanus, bloods
Insert NG tube for >20% TBSA (gastric stasis and Curling ulcer prophylaxis; PPI). Tetanus status — give tetanus toxoid +/- immunoglobulin. Bloods: FBC, U&E, CK (electrical), coagulation, group and save, COHb, lactate, beta-hCG (women of childbearing age). CXR, ECG (electrical/chemical/lightning).
G — Escharotomy for circumferential full-thickness burns
Bedside escharotomy if circumferential full-thickness burn of the chest (restricting ventilation), a limb (compromising perfusion — check pulses, capillary refill, pulse oximetry distally), or abdomen (raised intra-abdominal pressure). No anaesthesia needed — full-thickness burns are painless.
H — Burn centre referral / transfer
Apply the ABA transfer criteria (below) early — the decision and the call to the burns unit should be made in the first hour, not after 24h of failed resuscitation. Keep the patient warm, the lines secured, and the documentation (TBSA, time of burn, mechanism, photographs) complete for the receiving centre.
Escharotomy
[1]Bedside escharotomy technique
Indicators that the eschar needs releasing
Chest: rising peak airway pressures, falling tidal volume, accessory-muscle use, inability to ventilate despite high pressures. Limb: cool/pale distal limb, absent pulses (late sign — by the time pulses go, perfusion is dire), prolonged capillary refill, falling distal SpO2, tight/hard limb. Abdomen: intra-abdominal pressure >25 mmHg via bladder, oliguria, falling cardiac output, raised peak pressures.
Chest escharotomy
Two longitudinal incisions along the anterior axillary lines from clavicle to costal margin, joined transversely across the upper abdomen (subcostal) and below the clavicles. This releases the constricting eschar and restores chest-wall excursion. Diathermy for haemostasis; pack the wounds.
Limb escharotomy
Medial and lateral longitudinal incisions the full length of the burn, along the safe (inter-muscular septa) lines — medial and lateral mid-axial of the arm, medial and lateral of the forearm, medial and lateral of the leg (avoid the peroneal nerve at the fibular head and the ulnar nerve at the elbow). Incise skin and eschar down to fat; the underlying muscle is NOT released unless there is a true compartment syndrome (then a formal fasciotomy).
After the release
Re-check distal pulses, capillary refill, SpO2 and airway pressures — improvement is immediate. Dress with non-adherent gauze. The escharotomy wounds themselves may need skin grafting later. If no improvement, suspect a deeper compartment syndrome and proceed to fasciotomy.
Burn centre transfer criteria
[1] [1]Burns by mechanism
The mechanism predicts the hidden injury. The surface TBSA is only the visible part; deep muscle, conduction injury, and chemical penetration can dwarf the cutaneous estimate and demand extra fluid, fasciotomy, or specific antidotes.[1][9]
Flame / flash
Dry heat, high intensity
- Most common major-burn mechanism; deep partial to full thickness; high inhalation-injury risk in enclosed fires.
- Standard Parkland resuscitation; check CO/cyanide; high proportion of full-thickness wounds needing grafting.
- Circumferential injury common (clothing ignition) → escharotomy vigilance.
Scald (liquid/steam)
Moist heat
- Commonest in children and elderly; usually superficial-to-deep dermal; depth related to temperature and contact time.
- Stocking/glove or sharply demarcated "dunk" distribution in a child raises non-accidental injury — safeguarding referral.
- Lower inhalation risk than flame; TBSA estimation often the main challenge.
Electrical
Low & high voltage
- Surface TBSA MASSIVELY underestimates injury — current follows the path of least resistance through deep tissues (muscle, nerve, vessel).
- Look for entry and exit wounds; check CK and urine for myoglobin (dark urine, positive blood on dipstick but few RBC); alkalinise urine (bicarbonate) and force diuresis; fasciotomy for compartment syndrome in unburned limbs.
- Cardiac: arrhythmia (including VF) at presentation — ECG and cardiac monitoring for at least 24h. Lightning can cause immediate asystole/VF.
- Long-term: cataracts, peripheral neuropathy, delayed AV-node disease.
Chemical
Acid / alkali / hydrofluoric
- ALKALI injuries are WORSE than acid — saponification of fat + liquefaction necrosis continues until neutralised; copious water irrigation for 1-2h+.
- Acid causes coagulative necrosis (a self-limiting eschar); still irrigate copiously, remove all clothing (caregiver contamination).
- Hydrofluoric acid: systemic hypocalcaemia and hypomagnesaemia (fluoride binds Ca/Mg) → fatal arrhythmia. Antidote: topical/intra-arterial calcium gluconate; monitor ECG and ionised calcium.
- Never try to chemically neutralise (the reaction generates heat) — irrigation with WATER is the universal first step.
Contact / radiation
Prolonged contact, tar, sun
- Contact burns (exhaust pipe, iron) are small but deep; check depth carefully.
- Hot tar: cool with water, then dissolve with a lipid solvent (medieval oil / sunflower oil) — do NOT peel.
- Radiation burns (local) vs acute radiation syndrome (whole body): the latter adds immunosuppression, marrow failure, GI syndrome.
Prognosis — Baux and Revised Baux
The Revised Baux does not capture comorbidity, mechanism (electrical and chemical add independent mortality), or the quality of the receiving burn centre's care, but it remains the most widely quoted bedside burn mortality number. Examiners expect you to know the inhalation term and that an RB >110 is roughly a coin-toss survival.[1][5]
Complications and ongoing management
Early (0-48h)
Resuscitation phase
- Airway obstruction from inhalation injury
- Hypovolaemic shock (massive fluid shifts)
- Carbon monoxide + cyanide toxicity
- Compartment syndrome (circumferential burns)
- Hypothermia (loss of skin thermoregulation)
Late (>48h)
Infection/metabolic phase
- INFECTION (#1 cause of late mortality) — wound sepsis, pneumonia, line infection
- Hypermetabolic state (2x normal metabolic rate) — nutrition critical
- Acute kidney injury (myoglobin from electrical burns, ATN from hypoperfusion)
- Stress ulcer (Curling ulcer) — PPI prophylaxis
- DVT (immobility) — prophylaxis
- Scar formation, contractures
Infection in burns — the leading cause of late death
Infection (wound sepsis, ventilator-associated pneumonia, catheter-related bloodstream infection) is the dominant cause of late burn mortality. The burn wound is a vast, protein-rich, avascular necrotic surface that is rapidly colonised by skin flora, then Gram-negatives (Pseudomonas, Klebsiella, Acinetobacter), then MRSA and Candida. The Surviving Sepsis After Burn Campaign (2023) adapts the general SSC framework for the burn patient, in whom the systemic inflammatory response is universally present and therefore useless as a sepsis trigger.[4]
Burn wound infection
Local
- Early colonisation (skin flora) → invasive wound infection by day 3-5 (Gram-negatives, then MRSA/fungal).
- Signs of invasive infection: conversion of partial to full-thickness, rapid eschar separation, haemorrhagic discoloration, ecthyma gangrenosum (Pseudomonas).
- Prevention: early excision and grafting, topical antimicrobials (silver sulfadiazine, mafenide, nanocrystalline silver dressings).
- Prophylactic systemic antibiotics are NOT recommended (selects resistance); treat proven infection on cultures.
Burn pneumonia
Lower respiratory
- Driven by inhalation injury, intubation, and aspiration; the dominant late respiratory threat.
- Surveillance cultures, lung-protective ventilation, oral chlorhexidine, semi-recumbent positioning, daily sedation holds.
- Empiric therapy for late-onset VAP covers Pseudomonas/Acinetobacter/MRSA; narrow on culture.
Catheter-related bloodstream infection
Iatrogenic
- Burns patients need many lines and for a long time — high CRBSI burden.
- Subclavian preferred (lowest infection, per 3SITES) when feasible; femoral avoided; daily review with prompt removal.
- Central-line bundle (maximal sterile barrier, chlorhexidine prep, ultrasound guidance) is non-negotiable.
Nutrition and the hypermetabolic state
The burn hypermetabolic state is the largest sustained metabolic stress in medicine: resting energy expenditure rises to 1.5-2x normal in burns >40% TBSA, driven by inflammatory mediators (catecholamines, IL-1, IL-6, TNF, cortisol) and sustained for months. Without aggressive nutrition the patient catabolises wound-healing protein, loses graft take, and dies of infection.[1]
Nutrition strategy in major burns
Start EARLY enteral feeding (within 6h)
Early enteral nutrition (within 6h of burn) maintains gut mucosal integrity, reduces bacterial translocation, blunts the hypermetabolic response, and lowers infection. NG or post-pyloric tube; delay beyond 48h worsens outcomes. TPN is reserved only for the small minority who cannot tolerate enteral feeds.
Calorie target
Use a validated formula (e.g. Toronto/Schofield, or the Harris-Benedict x 1.5-2 in major burns). TheCurreri formula (25 x kg + 40 x %TBSA) overestimates; modern indirect calorimetry is the gold standard. Aim for 30-35 kcal/kg/day in adults, more in children.
Protein target
1.5-2.0 g/kg/day protein (nitrogen loss is massive and sustained). Track pre-albumin and CRP weekly. Adequate protein is the single most important determinant of graft take and wound healing.
Pharmacologic modulation (selected centres)
Beta-blockade (propranolol) blunts the catecholamine-driven hypermetabolism and reduces tachycardia, fatty infiltration of the liver, and insulin resistance. Oxandrolone (anabolic steroid) and recombinant human growth hormone are used in specialist centres; insulin/glucose control targets 6-10 mmol/L.
Glucose control
Burn-induced insulin resistance is universal; hyperglycaemia impairs wound healing and immunity. Target glucose 6-10 mmol/L with an insulin infusion; avoid hypoglycaemia. Glutamine supplementation (enteral) reduces infection in some trials.
Landmark trials and references
Jeschke MG, van Baar ME — Burn injury (Nature Reviews Disease Primers 2020)
Type
Authoritative Primer — the definitive modern synthesis of burn pathophysiology and management
Scope
Pathophysiology of the burn wound (local + systemic), the hypermetabolic response, fluid resuscitation (Parkland vs modified Brooke), inhalation injury, infection, nutrition, and surgical management
Key teaching
Severe burns trigger a sustained systemic inflammatory and hypermetabolic state (~2x resting energy expenditure for months) that drives the late complications (infection, catabolism, scarring); outcomes hinge on early resuscitation, early excision/grafting, and early nutrition
Clinical bottom line
The single best one-stop reference for the CICM/FFICM burns question; quote it for the physiology, the resuscitation principles, and the rationale for early enteral feeding
Enkhbaatar P, Pruitt BA Jr — Smoke inhalation injury (Lancet 2016)
Type
Authoritative Lancet review of the pathophysiology and clinical management of smoke inhalation injury
Key concepts
The supraglottic (thermal) vs infraglottic (chemical) distinction; airway oedema peaks at 24-48h (early intubation); systemic toxins (CO binds Hb 240x; cyanide blocks cytochrome c oxidase); nebulised heparin + N-acetylcysteine reduce airway casts
Clinical bottom line
The reference for the inhalation-injury question: intubate early, give 100% O2, check COHb AND lactate (cyanide clue), and use lung-protective ventilation plus airway-cast clearance (heparin/NAC) for the infraglottic injury
Dries DJ, Endorf FW — Inhalation injury: epidemiology, pathology, treatment strategies (Scand J Trauma 2013)
Type
Comprehensive narrative review
Epidemiology
Inhalation injury complicates ~10-20% of major burns and DOUBLES mortality at any given TBSA; it adds 1-2 mL/kg/%TBSA to fluid requirements
Key teaching
Severity grading (bronchoscopic — mild/moderate/severe by soot, oedema, mucosal sloughing); the role of high-frequency percussive ventilation, bronchoscopy, and nebulised heparin/NAC; antibiotics only for proven infection
Clinical bottom line
The reference that quantifies the mortality impact of inhalation injury and justifies the additional fluid and the aggressive airway-cast clearance strategy
Osler T, Glance LG, Hosmer DW — Revised Baux score (J Trauma 2010)
Type
Retrospective analysis of the US National Burn Repository (>39,000 burn patients) deriving and validating a mortality model
Innovation
Added an inhalation-injury term (+17 points) to the original Baux (Age + %TBSA), fitted by logistic regression
Result
Revised Baux predicted mortality more accurately than the original; RB ~60 ≈ 10% mortality, ~90 ≈ 30%, ~110 ≈ 50%, >140 ≈ >90%
Clinical bottom line
The most widely used bedside burn-mortality score — a single number to set expectations and guide goals-of-care discussions; not a futility tool (individual outcomes, especially in children, vary widely)
Greenhalgh DG, Hill DM — Surviving Sepsis After Burn Campaign (Burns 2023)
Type
International consensus recommendations for the diagnosis and management of sepsis and infection in burn-injured patients
Problem addressed
The standard SSC framework (SIRS criteria) is useless in burns — every major burn patient is persistently tachycardic, tachypnoeic, and leukocytotic; a burn-specific definition of sepsis and infection was needed
Key recommendations
Burn sepsis = infection PLUS organ dysfunction (not SIRS); surveillance cultures; early source control (excision of infected eschar); NO prophylactic systemic antibiotics; bundle the line, lung, and wound-prevention strategies; procalcitonin and trends in the clinical picture over single values
Clinical bottom line
The burn-specific sepsis guideline — replaces blanket SIRS-based triggers with burn-adapted infection definitions and prevention bundles; the reference when asked how sepsis is diagnosed in a burn patient
ISBI Practice Guidelines for Burn Care, Part 2 (Burns 2018)
Type
International Society for Burn Injuries practice guidelines — global consensus
Scope
Initial assessment, fluid resuscitation (Parkland and modified Brooke with titration to urine output), inhalation injury, wound care, infection control, and surgical management
Key teaching
Reaffirms crystalloid-only for the first 24h (colloid leaks in the open-capillary phase); Lund-Browder for TBSA; early excision and grafting; pain management; and the principle that the formula is a STARTING POINT titrated to urine output
Clinical bottom line
The international standard-of-care reference; cite for the resuscitation formula, the depth/TBSA assessment, and the early-excision principle
Rowan MP, Cancio LC — Burn wound healing and treatment: review and advancements (Crit Care 2015)
Type
Comprehensive critical-care-focused review of burn wound biology and treatment
Key concepts
Depth classification and the dynamic conversion of partial to full-thickness; the role of early tangential excision and split-thickness skin grafting; topical antimicrobials (silver sulfadiazine, mafenide, nanocrystalline silver); biological and skin-substitute dressings; negative-pressure wound therapy
Clinical bottom line
The reference for wound care in the ICU: why depth matters (heals vs graft), what the topical agents do, and the rationale for early excision; cite for the management of the burn wound itself
Choi J, Patil A — Computer-vision reappraisal of TBSA (JAMA Surgery 2022)
Type
Cross-sectional reappraisal applying a computer-vision TBSA tool to compare Rule of Nines vs Lund-Browder vs palm-method estimations
Key finding
Inter-observer TBSA estimation is highly variable; the Rule of Nines is least accurate in children and in patchy burns; the palm method (patient's palm + digits ≈ 1% TBSA) is reliable for small/partial burns; computer-assisted 3D mapping (BurnCase 3D) reduces variability most
Clinical bottom line
TBSA estimation is the single biggest source of resuscitation error; use Lund-Browder (especially in children), correct the palm method to the patient's OWN palm-plus-digits, and re-assess at 24h — the initial field estimate is often 5-10% too high
Sherren PB, Hussey J — Lethal triad in severe burns (Burns 2014)
Type
ANZ-focused intensive-care review of the lethal triad (hypothermia, acidosis, coagulopathy) and the resuscitation of severe burns
Key teaching
Severe burns re-create the trauma lethal triad — heat loss through the lost skin, lactic acidosis from under-perfusion, and coagulopathy from consumption and hypothermia; aggressive warming, adequate (titrated) fluid, and correction of coagulopathy are as important as the Parkland number
Clinical bottom line
Reframes burn resuscitation as a trauma-style damage-control problem; directly relevant to CICM/FFICM practice and the rationale for keeping the burn patient warm and coagulation-normal
Erickson MJ, Enkhbaatar P, Lee JO — Inhalation Injury (Semin Plast Surg 2024)
Type
Contemporary review updating the diagnosis and management of inhalation injury
Key updates
Bronchoscopic grading, the additive effect of inhalation injury on mortality and fluid requirement, lung-protective ventilation, nebulised heparin/NAC, the role of high-flow nasal cannula and ECMO in refractory hypoxaemia, and the management of CO and cyanide toxicity
Clinical bottom line
The up-to-date reference for inhalation injury — pair with the 2016 Lancet Enkhbaatar review for the exam answer; emphasises early intubation and 100% O2 with empiric hydroxocobalamin for the house-fire patient
SAQ — Burn fluid resuscitation and the Parkland formula
10 minutes · 10 marks
A 60 kg woman has sustained 40% TBSA partial- and full-thickness flame burns in a house fire 1 hour ago. She is conscious, BP 100/60, HR 120, with soot in the oropharynx and a hoarse voice. The registrar asks for the fluid prescription for the next 24 hours.
SAQ — Escharotomy and abdominal compartment syndrome in burns
10 minutes · 10 marks
A 45-year-old man with a 55% TBSA full-thickness flame burn, including circumferential burns to the chest and lower legs, has received 6 L of Hartmann`s over the first 8 hours. His ventilator peak pressures are rising, his urine output has fallen to 10 mL/h, and his bladder pressure reads 28 mmHg.
Clinical pearls
Red flags
Common exam pitfalls
References
- [1]Jeschke MG, van Baar ME, Choudhry MA, Chung KK, et al. Burn injury Nat Rev Dis Primers, 2020.PMID 32054846
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