Burns Assessment and Resuscitation — TBSA Accuracy, Fluid-Creep Volumes, Inhalation Grades and Excision Timing

The burn is the injury you both overestimate and undertreat. In burn medicine, the percentage of the burned body surface area (TBSA-B) to the total body surface area (TBSA) is a crucial parameter to ensure adequate treatment and therapy — and inaccurate estimations of the burn extent can lead to wrong medical decisions resulting in considerable consequences for patients, including over-resuscitation, complications due to fluid aggregation from burn edema, or non-optimal distribution of patients.^[1] Burn depth and burn size are the two crucial determinants for assessing patients suffering from burns, and getting them right is what adapts the appropriate treatment in modern burn care.^[3]

The numbers behind that warning are stark. The poll of experts confirmed deviations of burn depth/size estimates of up to 62% in relation to the mean value of all participants — and in comparison to the computer-based method, overestimation of up to 161% was found.^[3] Inaccurate estimation of burn size impacts initial management directly, including unnecessary transfer to burn centres and fluid overload during resuscitation.^[2] Three traps decide the viva: the eye that overestimates size, the urine output that reassures falsely while lactate stays high, and the inhalation injury diagnosed from history instead of bronchoscopy.

A 34-year-old man arrives after a garage fire with mixed-depth burns of trunk and arm, soot around the mouth, and a hoarse voice. His mate estimates "about 15%", the triage nurse writes "25%", and his urine output sits at 35 mL/h on 500 mL/h of crystalloid. The examiner wants your TBSA method with its error numbers, what the resuscitation volumes actually run at with which endpoints, how you grade the inhalation injury and what it does to mortality, whether he meets referral criteria, what his Baux-based prognosis is, when you excise, and how you feed him. This page answers each with the number from the paper beside it.^[1][9][11]

Overview & Definition — size and depth decide everything

Burn assessment is the measurement of two things: how much skin is burned (TBSA-B as a proportion of TBSA) and how deep the injury goes — because in burn medicine the TBSA-B proportion is the crucial parameter that ensures adequate treatment and therapy.^[1] The three traditional bedside methods still of great practical relevance were developed from the middle of the 20th century: the Lund Browder Chart, the Rule of Nines, and the Rule of Palms — and they share one assumption, specific fixed values for different body parts' surface as a proportion of the TBSA.^[1]

That shared assumption is the flaw. Due to the missing consideration of differences regarding sex, age, weight, height, and body shape, these methods have practical limitations — a child is not a scaled adult, and neither is the morbidly obese patient.^[1] Modern three-dimensional computer-based systems consider patients' body characteristics and allow a very realistic burn size assessment, and electronic documentation systems such as BurnCase 3D allow accurate burn size assessment with complete medical documentation.^[1]

Classification — size bands and depth judgments

Classify first by size, because size drives resuscitation and referral. The resuscitation cohorts in this topic enter at ≥15% TBSA (sepsis and creep cohorts) and ≥20% TBSA (ABRUPT resuscitation cohort) — those are the bands where hourly resuscitation documentation, burn-centre care, and mortality modelling begin.^[10][4] The validation manikins behind the accuracy numbers span small burns under 20%, medium burns 20–49%, and large burns over 49% across infant, child and adult body shapes.^[2]

Classify second by depth, because depth drives excision and mortality. Burn depth and burn size together are the crucial determinants — yet the same poll that found 62% deviations confirms depth is judged as variably as size, which is why the examiner tests whether you re-assess depth rather than trusting the first estimate.^[3] In the elderly this matters most: the over-65s arrive with less TBSA but a far higher proportion of deep burn — 41% deep share against 23.3% in the young — and that deep proportion helps explain their excess mortality.^[32]

Epidemiology & Risk — the misestimation burden and the referral gap

The epidemiology of burns assessment is an epidemiology of error. Deviations of burn depth/size estimates reach up to 62% around the expert mean, with overestimation up to 161% against computer measurement — so the system over-transfers and over-fills.^[3] The consequence chain is explicit: inaccurate estimation drives unnecessary transfer to burn centres and fluid overload during resuscitation.^[2]

The referral gap proves it. Across 2036 adult admissions, 1416 (70%) met ABA referral criteria — yet of the 952 burns treated entirely at nonburn centres, 48% met referral criteria but were not transferred.^[17] The burns kept back cluster exactly where the exam expects: the most common burns treated at nonburn centres included injuries to the hand, wrist, face, neck, and lower extremity.^[17] The price of that gap is absolute: all deaths occurring at nonburn centres met referral criteria.^[17]

Chemical burns are uncommon but testable: 99 patients admitted for chemical burns formed 3.3% of total admissions in the Hong Kong series.^[27] The burns most often kept back at nonburn centres — hand, wrist, face, neck, lower extremity — are exactly the functional and cosmetic areas where the examiner expects a low referral threshold.^[17]

Pathophysiology — leak, hypermetabolism, and the two prices of error

Burn shock is a capillary-leak shock. The early events include an exaggerated inflammatory state, injury to the endothelium, and increased capillary permeability, which all culminate in shock — and that is why initial resuscitation is based on crystalloids: because of the increased capillary permeability occurring during the first 24 h.^[6] Understanding these processes is critical to effective management, and modern resuscitation answers with individualized fluid titration and monitoring along with colloid-based adjuncts — yet despite these developments, complications from over-resuscitation still occur.^[6]

The second phase is hypermetabolic. Severe burn causes a persistent and prolonged hypermetabolic state with increased catabolism, muscle wasting and cachexia — metabolic rates can surpass twice normal, and failure to meet them causes impaired wound healing, organ dysfunction, and susceptibility to infection.^[33] Protein handling is perverse: protein supplementation appears preferentially distributed to the burn wound rather than the skeletal muscle pool, so the muscle wastes while the wound drinks.^[35]

Insufficient resuscitation and over-resuscitation both kill, and the topic prices both. Under-resuscitation leaves lactate and base deficit abnormally high even while urine output and MAP look maintained — the Jeng cohort held UO above 30 mL/h and MAP above 70 mm Hg yet serum lactate and base deficit remained abnormally high on average through 48 hours.^[10] Over-resuscitation buys respiratory failure and compartment syndromes, with intra-abdominal hypertension as the named mechanism — the explicit reason the least-fluid doctrine exists.^[8] Fluid creep is the term applied to a resuscitation requiring more fluid than predicted by standard formulas; it is common today and is linked to several serious edema-related complications.^[8]

Presentation & the First Look — what the examiner watches you do first

Present the assessment in the order the resuscitationist needs it: size, depth, airway, perfusion, referral trigger. State your TBSA method and its error aloud — the EasyTBSA application had the greatest accuracy at -0.01% (SD 3.59%), followed by the Rule of Palms (3.92%, SD 10.71%), the Lund-Browder Chart (4.42%, SD 5.52%) and the Rule of Nines (5.05%, SD 6.87%) — so name the method and accept the overestimation bias.^[2] Re-estimate depth on the second look, because the 62% deviation means your first depth call is a draft, not a diagnosis.^[3]

Read the airway before the fluids. Smoke inhalation injury is an independent risk factor for mortality and its management is inherently complex — so hoarseness, soot, facial burns and confinement history trigger bronchoscopy, never reassurance.^[12] Inhalation injury diagnosed through history does not predict mortality from burns — bronchoscopy grades and ventilation need do.^[13]

Read perfusion with five numbers, not one. Mean arterial pressure, heart rate, urine output and lactate are the most established markers — but the evidence says lactate is the superior metabolic endpoint marker, and no single universal resuscitation endpoint has yet emerged, so integrate MAP, HR, UO, lactate and base deficit together.^[9]

Scoring & Classification — quote volumes with their variability shadow

Classify resuscitation by what was actually given, never by formula memory. In ABRUPT — 379 adults with ≥20% TBSA and hourly documentation for 48 hours across 21 burn centres — two-thirds (253) were resuscitated with albumin and one-third (126) with crystalloid alone.^[4] Albumin patients received more total fluid than crystalloid patients (5.2 ± 2.3 vs 3.7 ± 1.7 mL/kg/% TBSA burn/24 hours) — but they were older, had larger and deeper burns, higher SOFA scores and more inhalation injury, and albumin was started when initial crystalloid rates ran above expected targets, improving the in-to-out ratio.^[4] The headline for the viva: the fluid received in the first 24 hours was at or above the Parkland Formula estimate.^[4]

Quote the review behind it. Across 48 publications and 3196 patients from 1980–2015, mean 24-hour fluid infused for all studies was 5.2±1.1mL/kg per %TBSA — with great ranges of the means and high standard deviations compared with the original Baxter publication.^[5] The mean 24-hour urinary output reported in 30 studies was 1.2±0.5mL/kg per hr — far above the yardsticks below, which is the point.^[5] Burns with inhalation injuries received significantly more fluid than non-inhalation burns (5.0±1.3 versus 3.9±0.9mL/kg per %TBSA).^[5] The review verdict stands: burn units currently administer volumes larger than Parkland formula with great patient variability.^[5]

Quote the single-centre creep audit exactly. Among 196 consecutive resuscitations of ≥15% TBSA burns, total crystalloids in the first 24 hours were 6.3 +/- 2.9 mL/kg/%TBSA, with 76% of all resuscitations receiving more than 4.3 mL/kg/%burn — the upper limit predicted by Baxter.^[7] Hourly urine output in the first 24 hours was 1.2 +/- 0.7 ml/kg/h — and despite awareness of fluid creep, the centre had not substantially reversed it, primarily through failure to titrate down infusion rates and by accepting higher than recommended urine output.^[7] Nearly 40% of the 24-hour Parkland volume had already been given before burn-centre arrival (1.5 +/- 1.0 mL/kg/%burn) — excessive pre-burn-centre fluid continues to contribute.^[7]

Secondary Assessment & Hospital Reception — the door re-measures everything

Treat the burn-centre door as a second assessment, because the field size is wrong and the field fluid is already 40% of the day's volume. Re-measure TBSA with the method whose error you can quote — EasyTBSA -0.01% against Nines +5.05% — and re-triage transfer need against the ABA pattern: hand, wrist, face, neck and lower-extremity burns are the ones most often wrongly kept back.^[2][17] Re-titrate fluids downward from the pre-arrival rate rather than inheriting it, because failure to titrate down is the documented reason creep never reversed.^[7]

Resuscitation — crystalloids first, least fluid always, five endpoints together

Since 1968, when Baxter and Shires developed the Parkland formula, little progress has been made in fluid therapy for burn resuscitation — despite haemodynamic monitoring, goal-directed therapy, and new colloid and crystalloid solutions.^[6] Burn patients receive a larger amount of fluids in the first hours than any other trauma patients.^[6] The fluid rule for the first day is explicit: initial resuscitation is based on crystalloids because of the increased capillary permeability occurring during the first 24 h — with colloids accepted only after that window, and not all colloids.^[6] One named exclusion carries its regulator: since the Pharmacovigilance Risk Assessment Committee alert from the European Medicines Agency concerning hydroxyethyl starches, solutions containing this component are not recommended for burns.^[6]

Run the resuscitation on five endpoints together. Mean arterial pressure, heart rate, urine output and lactate are the most established markers — lactate is the superior metabolic endpoint marker — yet no single universal resuscitation endpoint has yet emerged, so integrate MAP, HR, UO, lactate and base deficit and let no single number decide.^[9] The traditional yardsticks remain urinary output of 30 to 50 mL/h and mean arterial pressure above 70 mm Hg — but the prospective comparison found partial correlations between those traditional variables and lactate/base deficit were low, and on average serum lactate and base deficit remained abnormally high while UO and MAP were maintained.^[10] That is why the modern doctrine reads: resuscitate with the least amount of fluid to provide adequate organ perfusion, recognising urine output as a poor resuscitation target, with transpulmonary thermodilution-type monitoring where available.^[8]

Inhalation Injury — history never rules it out, bronchoscopy grades decide

Scope every at-risk airway within 24 hours. The RAND/UCLA panel — 15 anaesthetists, intensivists and plastic surgeons rating 140 statements by DELPHI — judged appropriate: initial intubation with ≥ 8.0 mm endotracheal tubes, lung-protective ventilatory strategies, initial bronchoscopic lavage, serial lavage for severe injury, nebulised heparin and salbutamol for moderate-severe injury, and N-acetylcysteine for moderate injury.^[11] The same panel judged inappropriate: non-protective ventilation, high-frequency oscillatory or percussive ventilation, and prophylactic systemic antibiotics and corticosteroids.^[11] The evidence review agrees: bronchoscopy, permissive hypercapnia, nebulized heparin and hydroxocobalamin have support; high-frequency oscillation and surfactant are unproven but not shown harmful; prophylactic antibiotics and corticosteroids are not recommended — with most inhalation evidence at Level 3 or below for lack of large human studies.^[12]

Quote the grades with their outcomes. Carboxyhemoglobin rises significantly with higher abbreviated-injury-score grade, and ARDS incidence climbs by grade — 0, 22, 57 and 80% at 24 hours — with severe grades (2 and 3) predicting ARDS at 24 and 72 hours and ventilator days beyond 21 after adjustment for age, TBSA and full-thickness extent.^[15] The three-level Australian split makes it viva-ready: mortality 2.3% (3/128) for none/mild, 7.4% (6/81) for moderate, and 30.7% (4/13) for severe — with median ventilation 26, 84 and 94 hours respectively — and only severe injury independently predicting death (odds ratio 20.4, 95% CI 1.74 to 239.4) while moderate injury independently prolongs ventilation (OR 2.25).^[16] The Korean refinement adds the two independent mortality predictors together: mechanical ventilation (adjusted OR 9.787) and severe inhalation injury on bronchoscopy (adjusted OR 45.357) — while inhalation injury diagnosed through history alone does not predict mortality.^[13]

Quote the additive mortality for disposition. Among 1058 patients, 373 (35%) had inhalation injury by bronchoscopy and/or ventilation-perfusion scan — and inhalation injury alone increased mortality by a maximum of 20%, pneumonia by a maximum of 40%, with approximately 60% when both were present, maximal in the midrange of baseline risk.^[14]

Excision Timing — hold both papers, counsel the tension honestly

Two high-quality answers disagree, and the examiner wants both. The systematic review across low- and high-income countries (16 trials) found length of stay shorter with early excision in both settings, mortality lower with late excision in both settings (confirmed in elderly high-income subgroup), and sepsis reduced with early excision in both — with heterogeneous age, timing, TBSA, inhalation and resource definitions limiting firm conclusions for low-middle-income practice.^[21] The TriNetX cohort of 6158 excisions within 14 days (72.5% under 20% TBSA, 60.1% excised at 0–3 days) found the opposite mortality direction after propensity matching: mortality 3.84% for 0–3-day excision against 6.09% for 8–14-day excision, wound infection 37.84% for 0–3 days against 42.48% for 4–7 days, and hypertrophic scarring 22% for 0–3 days against 28% for 4–7 days — with no difference in myocardial dysfunction, transfusion or sepsis.^[22]

Counsel it straight: early excision has substantially decreased invasive burn-wound infection and secondary sepsis — yet most deaths in severely burned patients are still due to burn-wound sepsis or inhalation complications, so excision timing is argued on infection and stay, never as a substitute for resuscitation and airway control.^[23]

Sepsis — the ABA trigger with its measured limits

Sepsis is the primary cause of death in burn patients — defined as severe organ dysfunction attributed to the host's disordered response to infection — against a background of hypovolaemia, immune, inflammatory and metabolic derangement.^[24] Diagnosis is uniquely hard because the hypermetabolic systemic inflammation masks typical signs, which is why burns were historically excluded from high-impact sepsis studies.^[24]

Use the 2007 ABA criteria as a trigger, never as a rule-out. The six items are: temperature above 39°C or below 36°C; progressive tachycardia above 110 beats per minute; progressive tachypnea above 25 breaths per minute (or minute ventilation above 12 L/minute ventilated); thrombocytopenia below 100,000/μl (not before day 3); hyperglycemia (untreated glucose above 200 mg/dl, insulin drip above 7 units/hour, or >25% increased insulin need over 24 hours); and feed intolerance beyond 24 hours (distension, residuals twice the feed rate, or diarrhoea above 2500 mL/day) — with more than three criteria triggering concern for infection.^[25] Quote its limits alongside it: the trigger's receiver-operating area for bacteraemia is 0.638 (95% CI 0.573-0.704), with only heart rate and temperature correlating on multivariate analysis — so the trigger prompts cultures and source control, never certainty.^[25]

Special Burns — electrical and chemical

High-tension electrical injury is a deep-tissue injury wearing a small skin wound. Electrical burns divide into flash (thermal) and high-tension injury — the latter usually from greater than 1000 volts, producing the characteristic entry and exit wound — and its optimal management has evolved into urgent exploration and debridement, aggressive redebridement, and early wound closure.^[26]

Chemical burns keep injuring until decontaminated. In the 99-patient series, immediate surgical debridement failed to achieve faster recovery than irrigation or wet packs — continuous water irrigation beat wet packs for earlier recovery and remains the most preferred decontamination method in acute chemical-burn management.^[27]

Complications, Thresholds & Referral — the door, the creep, and the transfer

The creep complications are named together: respiratory failure and compartment syndromes including intra-abdominal hypertension — the price of late-20th-century urine-output-based strategies that the least-fluid doctrine exists to prevent.^[8] The two bedside traps are quantified: 40% of the day's Parkland volume already given before burn-centre arrival, and urine outputs of 1.2 ml/kg/h accepted as adequate while lactate and base deficit stay abnormal.^[7][10]

The referral threshold is pattern-based. The ABA criteria capture 70% of admissions — and the misses cluster in hand, wrist, face, neck and lower-extremity burns kept at nonburn centres, where every death had met criteria.^[17] Counsel the transfer the same way: misestimated size drives unnecessary transfer outward and untransferred need drives preventable death inward — so re-measure, then decide.^[2][17]

Prognosis — rBaux with lactate and comorbidity

The revised Baux score is a reliable mortality predictor with a known boundary. Across 21 studies the AUC ranges 0.682 to 0.99 with a summary AUC of 0.93 (CI 0.91–0.95) — but with diminished prediction at both extremes of age.^[18] Lactate sharpens it: in 222 severe burns (median age 55, TBSA 24.5%, mortality 17%), age plus TBSA alone reaches AUC 0.906, and adding admission lactate lifts it to 0.938 — with further ICU scores adding only marginally.^[19] Comorbidity counts independently: among 90 ventilated patients with ≥15% TBSA (median age 45.7, TBSA 36.5%), only the revised Baux score and the updated Charlson index independently predict inpatient mortality and time to death, with a combined ROC of 0.920.^[20]

Special Populations — children need surface-area maths, the elderly need depth respect

Children are underestimated by adult maths. In 110 children with ≥15% TBSA resuscitated by weight-based Parkland, the BSA-based Galveston formula underpredicted fluid given over the first 24 hours while Parkland and Cincinnati predictions did not differ from fluids given.^[28] The mechanism is explicit: the Parkland formula works well for normal-weight adults but underestimates when applied indiscriminately to paediatric patients — and in children under 23 kg the height-free Galveston-3/4 power model correlates with the Du Bois Galveston at R2 0.997, most critically under 10 kg.^[29]

The elderly are overkilled by small burns. Mortality rises with TBSA and age, falling 2.9% per five years (11.6% over twenty years, steepest in the oldest) — with fire the commonest and deadliest cause and no gender effect.^[30] Their physiology diverges: the lethal-dose-50 burn size has not moved in three decades, with longer stays, more premorbidity, no excess infection or sepsis but significantly more multi-organ failure — alongside delayed hypermetabolism, hyperglycaemic/hyperlipidaemic excess, inverted inflammation, immune compromise and delayed wound healing from progenitor-cell change.^[31] Their anatomy explains part of it: over-65s arrive with smaller TBSA (13% vs 22.5%) but identical deep area, hence a deep share of 41% vs 23.3% — with mortality 48% vs 24% (OR 2.9) rising to twelvefold (OR 12.02) after TBSA and deep-share adjustment.^[32]

Feed everyone early, dose protein by weight, cap glucose and fat. Most clinicians advocate early enteral nutrition with high-carbohydrate formulas, individualized and adjusted through recovery — with no consensus on optimal timing, route, amount or composition beyond that direction.^[33] The ESPEN-endorsed specifics are: early enteral feeding; protein 1.5–2 g/kg in adults and 3 g/kg in children; glucose capped at 55% of energy and 5 mg/kg/h with blood glucose ≤8 mmol/l by continuous infusion; early trace-element and vitamin substitution; fat ≤30% of energy; energy by Toronto equation (Schoffield in children) without calorimetry accepting overfeeding risk; and non-nutritional hypermetabolism control by propranolol, oxandrolone, early surgery and thermo-neutral rooms.^[34] The physiology caveat stays beside it: protein favours wound over muscle, calorimetry should set calories with trophic feeding initially to prevent overfeeding, and protein targets remain controversial within a multidisciplinary muscle-loading and pharmacological programme.^[35]

Evidence, Guidelines & Regional Differences — who proved what

No single fluid owns this topic — since Baxter and Shires (1968) little has advanced in burn fluid therapy itself, while monitoring, goal-directed concepts and new solutions circled without settling the crystalloid-colloid choice.^[6] ABRUPT owns the modern practice description (albumin for the sicker, larger, deeper, more dysfunctional; I/O ratio improved; volumes at/above Parkland) and the Shah review owns the historical verdict (volumes above Parkland with great variability; inhalation costs extra).^[4][5] The RAND/UCLA panel and the Deutsch review own the inhalation consensus boundary together (lavage/heparin/NAC/permissive hypercapnia supported; prophylactic antibiotics and steroids inappropriate; evidence Level ≤3).^[11][12] ESPEN owns the nutrition specifics (early enteral, protein, glucose/fat caps, adjuncts) with calorimetry as the acknowledged gold standard it modifies.^[34][35] The rBaux literature owns prognosis (summary AUC 0.93) with its age-extreme and comorbidity caveats carried by the same papers.^[18][20]

Exam Pearls — the one-liners that score

• TBSA-B proportion is the crucial treatment parameter; the three classic methods assume fixed body-part shares and ignore sex, age, weight, height and shape.^[1]
• EasyTBSA -0.01% beats Palms +3.92, Lund-Browder +4.42 and Nines +5.05; misestimation buys transfer and overload.^[2]
• Expert deviations reach 62% with 161% overestimation vs computer — re-measure at the door.^[3]
• ABRUPT: 253 albumin vs 126 crystalloid; 5.2 ± 2.3 vs 3.7 ± 1.7; first-24h at/above Parkland.^[4]
• Review: 5.2±1.1 mean with wide variability; UO 1.2±0.5; inhalation 5.0±1.3 vs 3.9±0.9.^[5]
• Parkland 1968 Baxter/Shires; crystalloids first 24 h for leak; HES not recommended post-EMA.^[6]
• Creep audit: 6.3 +/- 2.9 with 76% above 4.3; UO 1.2 +/- 0.7; never reversed for untitrated rates and high UO tolerance.^[7]
• UO a poor target; least fluid for perfusion; creep buys respiratory failure and compartment syndromes.^[8]
• MAP/HR/UO/LA established with LA superior; no single endpoint; integrate all five.^[9]
• Yardsticks 30 to 50 ml/hr and MAP >70 fail while lactate/BD stay high in 53 patients ≥15%.^[10]
• RAND/UCLA: ≥ 8.0 mm tubes, lung-protective, lavage, heparin/salbutamol/NAC yes; HFOV/HFPV, prophylactic abx/steroids no.^[11]
• Inhalation independent mortality risk; bronchoscopy/hypercapnia/heparin/hydroxocobalamin supported; evidence ≤Level 3.^[12]
• Severe bronchoscopy OR 45.357 with ventilation OR 9.787; history alone non-predictive.^[13]
• Inhalation 35% of 1058; mortality +20 alone, +40 pneumonia, +60 both.^[14]
• COHb rises with AIS; ARDS 0/22/57/80% at 24 h; grades 2–3 predict ARDS and >21 vent days.^[15]
• Three-level: deaths 2.3/7.4/30.7%, vent 26/84/94 h, severe OR 20.4.^[16]
• Referral: 2036 admissions, 70% qualify, 48% of 952 kept back, hand/face/neck/leg cluster, all nonburn deaths qualified.^[17]
• rBaux AUC 0.682 to 0.99, summary 0.93, weak at age extremes.^[18]
• Age+TBSA 0.906 rises to 0.938 with lactate in 222 severe burns.^[19]
• rBaux plus Charlson independent in 90 ventilated ≥15%; ROC 0.920.^[20]
• Excision SR: stay shorter early, mortality lower late, sepsis lower early — heterogeneous, no LMIC conclusion.^[21]
• Excision 0–3 days: deaths 3.84 vs 6.09%, infection 37.84 vs 42.48%, hypertrophic 22 vs 28%.^[22]
• Early excision cut invasive infection; deaths still sepsis/inhalation; burns immunosuppress.^[23]
• Sepsis defined as organ dysfunction from disordered host response; the primary death cause.^[24]
• ABA six-item trigger at >3 with AUC 0.638; only HR/temp correlate — trigger cultures, never certainty.^[25]
• Electrical >1,000 V entry/exit; urgent exploration, aggressive redebridement, early closure.^[26]
• Chemical 99 cases (3.3%); debridement no faster; continuous irrigation beats wet packs and stays preferred.^[27]
• Paediatric 110 ≥15%: Galveston underpredicted, Parkland/Cincinnati matched.^[28]
• Parkland underestimates under 23 kg; Galveston-3/4PM matches Du Bois at R2 0.997, worst under 10 kg.^[29]
• Elderly fire commonest/deadliest; mortality −2.9%/5y and −11.6%/20y.^[30]
• Elderly LD50 frozen decades; MOF rises without infection excess; hypermetabolic/wound delay.^[31]
• Elderly TBSA 13 vs 22.5% but deep 41 vs 23.3%; deaths 48 vs 24% (OR 2.9, adjusted 12.02).^[32]
• Hypermetabolism to 2× normal; early enteral high-carb, individualized.^[33]
• ESPEN: early enteral, protein 1.5–2/3, glucose ≤55%/5 with ≤8 mmol/l, fat ≤30%, Toronto/Schoffield, adjuncts.^[34]
• Protein favours wound over muscle; calorimetry with trophic start; targets controversial.^[35]