Burn resuscitation and shock management

Overview

Burn resuscitation is the management of plasma-volume loss after thermal injury during the period when the microvascular barrier is failing and the patient's effective circulating volume is collapsing into the wound and into uninjured tissue. The clinical decision space is bounded by two failure modes: under-resuscitation and over-resuscitation. Over-resuscitation produces fluid creep, abdominal compartment syndrome, and orbital compartment syndrome ^[22,28,31]. Fluid resuscitation is the mainstay of preventing burn shock and the foundation for initial stabilization ^[25].

The 2024 American Burn Association (ABA) Clinical Practice Guideline on Burn Shock Resuscitation is the current field standard for adults with burns of 20% TBSA or greater and addresses the first 48 hours after injury ^[1]. The 2008 ABA practice guideline, which it largely supersedes, established formal resuscitation for adults and children with burns greater than 20% TBSA using crystalloid in the 2–4 mL/kg/%TBSA range over the first 24 hours titrated to urine output ^[2]. Modern practice is heterogeneous: the ABRUPT multicenter prospective trial reported that in 2023 most North American patients received first-24-hour volumes at or above Parkland-formula prediction ^[26].

This page treats the umbrella scope. The detailed protocol for crystalloid resuscitation lives at [[fluid-resuscitation-in-burns]]; single-agent colloid pages live at [[albumin-resuscitation-in-burns]] and [[ffp-resuscitation-in-burns]].

Pathophysiology

After severe thermal injury, both local and systemic vascular permeability increase, intravascular fluid extravasates, and effective circulating volume falls progressively, producing a distributive shock with a large interstitial component ^[5]. Baxter and Shires first documented in 1968 that restoration of the functional extracellular fluid in severe burns required greater volumes delivered at a faster rate than had previously been anticipated, and that circulatory hemodynamics in the first 24 to 30 hours post-burn were closely correlated with maintenance of that volume; after that window, changes in circulatory status appeared unrelated to ongoing fluid administration ^[3].

Three mechanisms drive the volume loss. Local burn-tissue and generalized non-burn-tissue edema occur initially through histamine release that increases microvascular permeability ^[4]. Burn-tissue edema is also driven by direct thermal injury to endothelial cells and by increased burn-tissue osmolarity; non-burn-tissue edema is attributed to severe hypoproteinemia caused by protein flux into the injured tissue ^[4]. Cell damage occurs with ischemia from decreased perfusion, and additional damage occurs with reperfusion through formation of oxygen radicals ^[4].

Endothelial glycocalyx shedding is an early process in severe burn injury and increases with patient age and injury severity, with direct consequences on vascular function, permeability, and probably coagulation ^[6]. Generalized edema increases with burn-wound size in parallel with elevated interleukin-2 and endothelin-1 levels, reduced C1 esterase inhibitor levels, and leukocytosis in the first week after injury, consistent with dynamic interactions among endothelium, cytokine stimulation, leukocytosis, complement, and platelet activation that promote microvascular permeability ^[7].

Cardiac dysfunction is part of burn shock and is not solely a downstream consequence of preload reduction. Myocardial damage and cardiac dysfunction occur immediately following severe burn, even before a significant fall in blood volume from increased capillary permeability ^[8]. Young and elderly subjects show greater diminution of burn-induced cardiac contractile function than adult subjects, related to differences in intracellular calcium availability ^[60].

Assessment

Hourly urine output is the most widely used resuscitation endpoint. The 2008 ABA practice guideline targets approximately 0.5–1.0 mL/kg/h in adults and 1.0–1.5 mL/kg/h in children ^[2]. Yowler and Fratianne stated the goal more compactly: the ideal burn resuscitation formula does not exist, but urine output 0.5–1 mL/kg/h in adults and 1–1.5 mL/kg/h in children is the target whichever formula is used ^[21]. Urinary output of 30–50 mL/h and a mean arterial pressure greater than 70 mm Hg continue to be the yardsticks by which burn patients are resuscitated in many centers ^[13].

Biochemical markers add a layer urine output cannot resolve. Kamolz et al. reported that the initial Day-0 lactate level separates survivors from non-survivors, with a 68% survival rate when lactate clears to normal within 24 hours versus 32% when it remains supranormal; measuring lactate and lactate clearance helps detect critically injured patients and informs whether to escalate or modify therapy ^[9]. Mean base deficit less than -6 mmol/L is associated with more florid systemic inflammatory response, more prevalent acute respiratory distress syndrome, and more severe multiple organ failure ^[10].

A 2014 systematic review compared urine output against alternative endpoints. Hemodynamic monitoring as a resuscitation endpoint was associated with an increased survival signal (RR 0.58; 95% CI 0.42–0.85; P < 0.004) versus hourly urine output, but when analysis was restricted to randomized controlled trials there was no survival advantage of hemodynamic monitoring over urine output ^[11]. Intrathoracic blood volume (ITBV) from transpulmonary thermodilution may be a reliable preload indicator in life-threatening burns, but Holm et al. observed that ITBV-guided resuscitation administered significantly larger crystalloid volumes than Parkland prediction ^[12]. Bak et al. simultaneously recorded preload variables, global systolic function, and oxygen transport by three separate methods and found no need to increase total fluid volume within 36 hours of a major burn, although early signs of central circulatory hypovolemia at 12 hours supported more rapid initial infusion ^[61]. Inoue et al. observed that hourly urine output remains an effective and practical guide for managing burn patients within permissive hypovolemia ^[14].

The 2024 ABA guideline does not recommend transpulmonary thermodilution–derived variables to guide burn shock resuscitation ^[1]. The same guideline does recommend selective monitoring of intra-abdominal and intraocular pressure ^[1]. The [[fluid-resuscitation-in-burns]] page treats endpoint titration in protocol detail.

Management

Vascular access

Vascular access in burn shock prioritizes flow. Peripheral large-bore intravenous lines, often through burned skin, are the dominant first route at the cut-off TBSA for formal resuscitation; Greenhalgh's ISBI/ABA survey of practice reported that 15% TBSA was the typical cut-off for initiating resuscitation, and that most respondents preferred peripheral IVs (70%) with central lines used by 47.5% of centers ^[62]. Wolf et al. found that time to intravenous access was an independent predictor of mortality in children with massive burns, underlining the load-bearing nature of early access ^[20].

Central venous access is needed when peripheral access fails, when monitoring requires it, or when prolonged infusion of vasoactive or hyperosmolar agents is anticipated. Femoral-vein central access can be safely employed in burn patients ^[18]. A Chinese national expert consensus identifies deep vein catheterization as an important method to prevent and treat burn shock in severe burn patients, monitor hemodynamic changes, and provide venous nutritional support ^[19].

Peripherally inserted central catheters (PICCs) are an alternative for ongoing care. A survey of 44 US burn centers found that 37% of burn units use PICC lines as part of their treatment protocol ^[16]. Fearonce et al. reported that the catheter-related bloodstream infection rate was 0 per 1000 line days for PICCs compared with 6.6 per 1000 line days for conventional central venous catheters in burn patients, although PICCs are not adequate for the fluid volumes typically required during burn shock resuscitation and serve better for ongoing care ^[15]. Li et al. documented an overall upper-extremity venous thrombosis incidence of 3.2% and central-line-associated bloodstream infection rate of 6.9% with PICCs in burns ^[17]. Austin et al. reported a symptomatic upper-extremity deep vein thrombosis rate of 5.5% and a central-line-associated bloodstream infection rate of 4.3% (2.72 infections per 1000 line days) in burn-unit PICCs ^[16].

The resuscitation-formula landscape

The ideal burn resuscitation formula does not exist ^[21]. Whichever formula is used, the patient must be monitored closely and fluid resuscitation individualized to clinical response ^[21]. The dominant historical formulas estimate first-24-hour crystalloid in the 2–4 mL/kg/%TBSA range ^[2]. The 2024 ABA guideline recommends initiating resuscitation at the lower end of that range, 2 mL/kg/%TBSA, to reduce total volumes ^[1]. Chung et al. compared military casualties resuscitated with the modified Brooke formula versus the Parkland formula and reported that the modified Brooke group received significantly lower 24-hour volumes (3.8 vs 5.9 mL/kg/%TBSA on average), with a lower proportion exceeding the Ivy index of 250 mL/kg (29% vs 57%), and no differences in measured outcomes ^[23]. Hansen's historical review notes that monumental advances in burn resuscitation have led to dramatically decreased mortality and virtually eliminated post-burn renal failure, but regardless of which formula is used, continuous individual titration of volume according to clinical response is required to avoid the complications of both over- and under-resuscitation ^[25].

Adherence matters. Mankowski et al. reported that patients managed under provincial burn resuscitation guidelines received 3.2 mL/kg/%TBSA in the first 24 hours, while non-adherent care averaged 4.4 mL/kg/%TBSA, and in-hospital mortality was significantly lower with guideline adherence (2.7% vs 16.2%, P = 0.04) ^[27]. Pediatric formulas calculated against body surface area rather than body weight remove the systematic over-prediction that weight-based formulas produce in small children: Carvajal observed that when fluid and sodium needs of pediatric age groups are calculated using BSA as the indexing factor, age-related differences in requirement disappear ^[36]. The [[fluid-resuscitation-in-burns]] page treats formula choice (Parkland, modified Brooke, BSA-based pediatric formulas, fixed-volume protocols, restrictive plus-FFP variants) in protocol detail.

Adjuncts overview

Several adjuncts have been tested. The 2024 ABA guideline is unable to make recommendations on high-dose vitamin C (ascorbic acid), fresh frozen plasma (FFP), early continuous renal replacement therapy, or vasopressors as adjuncts during acute burn shock resuscitation ^[1].

High-dose ascorbic acid is the most thoroughly studied adjunct. Tanaka et al.'s 2000 RCT in patients with burns of 30% TBSA or greater reported that high-dose ascorbic acid attenuated post-burn lipid peroxidation, reduced 24-hour fluid volumes (3.0 ± 1.7 vs 5.5 ± 3.1 mL/kg/%TBSA, P < 0.01), and reduced edema generation; the ascorbic acid group also showed a shorter duration of mechanical ventilation (12.1 ± 8.8 vs 21.3 ± 15.6 days, P < 0.05) ^[42]. A 2011 systematic review by Edgar et al. concurred that continuous ascorbic acid in acute burn resuscitation reduces local wound edema and systemic fluid retention with large effect sizes, while flagging that each outcome was based on a small single-facility study ^[43].

Vasopressor and inotrope use is contested. A 2022 systematic review concluded that there is a lack of evidence regarding the benefits and harms of using vasoactive or inotropic drugs in addition to fluids during early resuscitation of major burns; vasopressor use was associated with increasing age, Baux score, and %TBSA burned, with more frequent dialysis and increased mortality, though the direction of causality is unclear ^[44]. In Winter et al.'s cohort of severely burned norepinephrine-dependent patients, the median fluid requirement of survivors could be significantly reduced, and survivors achieved significant norepinephrine reduction whereas non-survivors required significant norepinephrine increases ^[45]. Methylene blue has been described as a salvage agent for vasoplegia that persists despite adequate fluid resuscitation and treatment with norepinephrine, vasopressin, and steroids ^[46]. Inotropic support with dobutamine and careful titration of volume infusion according to end-diastolic volume indices has been used to improve right-ventricular function in severely burned patients with concomitant inhalation injury ^[38].

Therapeutic plasma exchange has been described as a salvage option in patients who fail conventional volume therapy. Mosier et al.'s literature review concluded that therapeutic plasma exchange shows persistent clinical benefits and reduced morbidity and mortality in toxic epidermal necrolysis, burn shock, and sepsis ^[47].

Transfusion-threshold frameworks

Burn resuscitation rarely requires acute blood transfusion in the first 24 hours; the early problem is plasma volume, not red-cell mass. Whole-blood use in burn shock did not increase hemoconcentration or viscosity in a 2630-patient series and was reported to improve anemia, oncotic pressure, hypoproteinemia, acid-base balance, oxygenation, hemodynamics, and myocardial contractility, with renal failure, pulmonary edema, and gastrointestinal bleeding incidence of 0.9%, 0.4%, and 0.6% respectively in that cohort ^[63]. Routine albumin supplementation to maintain a serum albumin level above 20 g/L did not improve SOFA scores, hospital length of stay, ventilator duration, or mortality in Melinyshyn et al.'s comparison, at more than four times the daily cost of the control approach ^[48]. The role of fresh frozen plasma as a primary resuscitation fluid is treated at [[ffp-resuscitation-in-burns]]; the role of albumin at [[albumin-resuscitation-in-burns]].

Complications

The complications of burn resuscitation cluster around two failure modes.

Over-resuscitation. Saffle's 2007 review documented that modern burn patients routinely receive far more resuscitation fluid than predicted by the Parkland formula, a phenomenon termed "fluid creep," consisting largely of progressive edema formation in unburned areas after the first 8 hours post-burn and linked to abdominal compartment syndrome and other serious complications ^[22]. Bacomo and Chung observed that under-resuscitation of patients with severe burns is now relatively uncommon and that over-resuscitation, or "fluid creep," has emerged as one of the most important problems during the initial phases of burn care ^[24]. Sullivan et al. reported that patients in a contemporary cohort received a significantly higher mean opioid equivalent than a historical cohort (26.5 ± 12.3 vs 3.9 ± 2.2 in the first 24 hours, P < 0.001), and that higher opioid agonist doses may have hemodynamic consequences that contribute to increased fluid volumes ^[54]. Faraklas et al. demonstrated that fluid creep is not explained by nursing-level protocol deviation: under a tight single-institution protocol, more seriously injured patients still exceeded Parkland prediction despite excellent adherence ^[56]. Payne et al. found that dexmedetomidine exposure during acute resuscitation increased first-24-hour fluid requirements (4.2 ± 1.7 vs 3.6 ± 1.1 mL/kg/%TBSA, P = 0.03), independently associated with fluid creep ^[55].

Abdominal compartment syndrome. Ivy et al. documented that intra-abdominal hypertension occurs commonly in major burn patients and that abdominal compartment syndrome (ACS) is seen regularly in patients with burns greater than 70% TBSA; they recommended bladder pressure measurement after infusion of more than 0.25 L/kg during acute resuscitation and for peak inspiratory pressures greater than 40 cm H2O ^[28]. Oda et al. reported that patients requiring more than 300 mL/kg in the first 24 hours developed ACS at 18.3 ± 4.9 hours, with a significant correlation between intra-bladder pressure, peak inspiratory pressure, and resuscitation volume ^[29]. O'Mara et al. demonstrated that the intra-abdominal pressure rise was significantly greater with crystalloid than with plasma resuscitation (26.5 vs 10.6 mmHg, P < 0.0001), and plasma-resuscitated patients maintained intra-abdominal pressures below the threshold for ACS complications ^[58]. The [[fluid-resuscitation-in-burns]] page treats ACS-prevention strategy in detail.

Orbital compartment syndrome. Mai et al. identified TBSA burned, resuscitation above the Ivy index of 250 mL/kg, and Parkland-calculated volumes as risk factors for elevated intraocular pressures in patients resuscitated with the Parkland formula; orbital congestion can develop within the first 24 hours of admission when resuscitation volumes are greatest ^[30]. Vrouwe et al. described orbital compartment syndrome as a rare but devastating complication of over-resuscitation that may lead to permanent visual loss; intraocular pressure was routinely measured by only 23% of survey respondents during acute burn resuscitation, despite cases occurring even at relatively modest mL/kg/%TBSA volumes when cumulative liters/kg was high ^[31]. Makarewicz et al.'s 2024 systematic review found that orbital compartment syndrome occurred most frequently within 24 hours post-burn, with a mean TBSA of 58.7%, a mean 24-hour resuscitation volume of 6.01 mL/kg/%TBSA, and periorbital burns in 86.5% of cases; the threshold for surgical decompression remains conflicted, but intraocular pressure greater than 30–40 mmHg warrants intervention ^[32]. The 2024 ABA guideline recommends selective monitoring of intra-abdominal and intraocular pressure during burn shock resuscitation ^[1].

Pulmonary edema and ARDS. Edgar et al.'s systematic review reported that management of acute major burn resuscitation including colloid increases lung edema (MD 0.04 mL/mL alveolar volume; 95% CI 0.03–0.04; P < 0.00001) and mortality (RR 3.67; 95% CI 1.16–11.58; P = 0.03) ^[43]. Clark et al. found that the increase in wet-to-dry lung weight ratio was 2% in uninjured controls, 28% with smoke alone, and 42% with smoke plus fluid resuscitation, consistent with pulmonary edema in the combined-insult group; reduced oncotic pressure was not the explanation, with microvascular pressure changes, endothelial and epithelial damage, and surfactant inactivation contributing ^[37].

Under-resuscitation: acute kidney injury and shock. Untreated hypovolemia progresses to inadequate organ perfusion, lactic acidosis, and acute tubular necrosis; the Day-0 lactate signal (survival 68% with 24-hour clearance to normal versus 32% with persistent supra-normal lactate) operationalizes the cost of under-resuscitation ^[9]. Hypertonic sodium resuscitation, an older strategy for fluid restriction, was associated with a fourfold increase in renal failure (40.0 vs 10.1%, P < 0.001) and twice the mortality of lactated Ringer's controls (53.8 vs 26.6%, P < 0.001) in Huang et al.'s comparison; hypertonic sodium solution did not reduce total resuscitation volume and was an independent risk factor for renal failure by logistic regression ^[53]. Pre-hospital and training advances have made under-resuscitation relatively uncommon in modern practice; over-resuscitation now dominates the complication spectrum ^[24].

Special Considerations

Pediatric burns

Pediatric resuscitation differs from adult resuscitation across multiple dimensions. Urine output targets are 1.0–1.5 mL/kg/h in children, with the adult target of 0.5–1.0 mL/kg/h ^[2]. Maintenance of hourly urine outputs of 30–50 mL in adults and 1–2 mL/kg/% burn in children is the long-standing endpoint cited in foundational reviews; the failure rate for adequate initial volume restoration in expert hands is less than 5% even for burns greater than 85% TBSA ^[35]. Carvajal observed that when fluid and sodium needs of pediatric age groups are calculated using body surface area as the indexing factor rather than body weight, age-related differences in requirement disappear; children under 3 years require significantly more fluid and sodium when body weight is the indexing factor ^[36].

Resuscitation timing is a load-bearing pediatric outcome. Barrow et al. reported that the incidence of sepsis, renal failure, non-survival with cardiac arrest, and overall mortality was significantly higher in burned children whose fluid resuscitation was delayed by 2 hours or more compared with children resuscitated within 2 hours; fluid resuscitation given within 2 hours of thermal injury may be one of the most important steps in preventing multi-organ failure and mortality ^[34]. Müller Dittrich et al.'s pediatric RCT of early albumin versus later albumin reported a reduction in the need for crystalloid infusion during resuscitation, significantly fewer cases of fluid creep (4.3% vs 56.5%), and shorter median hospital length of stay (14 vs 18 days, P = 0.004) ^[50]. The [[pediatric-burn-care]] and [[fluid-resuscitation-in-burns]] subtopic pages treat pediatric protocol detail.

Elderly

Young and elderly patients show greater diminution of burn-induced cardiac contractile function than adult subjects, related to differences in intracellular calcium availability ^[60]. Resuscitation in older adults requires individual attention to pre-existing cardiopulmonary disease, which is one of the modifiers Robins identified for tailoring fluid therapy ^[4]. Wolf et al. identified time to intravenous access as an independent predictor of mortality in children with massive burns, underlining how access-related delays compound the resuscitation problem at the extremes of age ^[20].

Inhalation injury

Inhalation injury raises predicted fluid requirements. The 2008 ABA guideline notes that increased volume requirements can be anticipated in patients with full-thickness injuries, inhalation injury, and delay in resuscitation ^[2]. Inoue et al. observed that combined inhalation and cutaneous injury reduced circulating blood volume below that seen with severe cutaneous burns alone, which contributes to the increased fluid requirement ^[14]. Clark et al. demonstrated experimentally that the smoke-injured lung loses the ability to protect itself when challenged with fluid, with the increase in wet-to-dry lung weight ratio rising from 28% with smoke alone to 42% with smoke plus fluid resuscitation ^[37]. Schultz et al. reported that severely burned patients with concomitant inhalation injury showed severely compromised right ventricular function (increased end-diastolic volumes, decreased ejection fractions, low stroke work indices, and increased pulmonary vascular resistances), and that inotropic support with dobutamine combined with volume titration improved hemodynamics ^[38]. The [[inhalation-injury-pulmonary]] page treats the airway and ventilator-management intersection.

Pre-hospital and transport

Pre-hospital resuscitation has historically been a vulnerable link in the chain. Baack et al. concluded that helicopter transport within a 180-mile radius in a non-hospital-based system was not appreciably faster than ambulance transport and did not clinically benefit most burn patients; their criteria for fluid resuscitation in transit included a surface area large enough to require formal resuscitation, suspected inhalation injury, or possible need for escharotomy ^[39]. Mitra et al. reported that the Alfred pre-hospital fluid formula increased median pre-hospital fluid volume from 0.14 to 0.35 mL/kg/%TBSA without changes in physiological endpoints, and that 24-hour total volumes were not significantly higher than the pre-formula period ^[40]. Lairet et al. reported that in a combat zone, 50% of casualties had pre-hospital vascular access obtained, 58.3% received no pre-hospital fluid resuscitation, and most of those who did receive fluid received volumes in excess of ABA and Tactical Combat Casualty Care guideline recommendations ^[41]. The 2008 ABA guideline applies regardless of setting: titration to urine output 0.5–1.0 mL/kg/h adults and 1.0–1.5 mL/kg/h children is the operative endpoint ^[2].

Electrical and chemical injury

High-voltage electrical injury produces deep tissue damage with myoglobinuria and an elevated risk of acute kidney injury requiring dialysis. Culnan et al. identified urine output as the primary endpoint in adult high-voltage electrical injury, with a goal of 1 mL/kg/h, and noted that continuous venovenous hemofiltration is a well-supported adjunct to clear the myoglobin load that hemodialysis cannot ^[33]. Chemical-injury resuscitation principles diverge by agent and are deferred to dedicated content (this page covers the umbrella concept that endpoint-titrated resuscitation applies, but pigment-clearance and chemical-specific decontamination details are outside scope).

Outcomes

Resuscitation quality is measurable and predictive. Chung et al. demonstrated that exceeding the Ivy index of 250 mL/kg in 24 hours is an independent predictor of death on multivariate analysis in severely burned military casualties ^[23]. Mankowski et al. reported that adherence to a burn resuscitation guideline was associated with significantly lower in-hospital mortality (2.7% vs 16.2%, P = 0.04) and lower first-24-hour volumes compared with non-adherent practice ^[27]. Greenhalgh et al.'s ABRUPT multicenter prospective trial reported that first-24-hour volumes in 2023 were at or above Parkland prediction across North American centers, and that albumin use was associated with older age, larger and deeper burns, higher SOFA scores at presentation, and worse organ dysfunction; this likely reflects selection of the sicker subgroup for albumin rescue rather than a harm signal from albumin itself ^[26].

Day-0 lactate and lactate clearance are independent mortality predictors: survival 68% when lactate clears to normal within 24 hours versus 32% with persistent supra-normal lactate ^[9]. Base deficit less than -6 mmol/L tracks with downstream organ failure and ARDS ^[10]. From cholera to fluid creep, monumental advances in burn resuscitation have produced dramatically decreased mortality and have virtually eliminated post-burn renal failure as a cause of death in modern burn centers ^[25]. The 2024 ABA guideline framework operationalizes the modern outcome literature: starting at 2 mL/kg/%TBSA, considering albumin in larger burns, monitoring intra-abdominal and intraocular pressure, and avoiding transpulmonary thermodilution variables as resuscitation targets ^[1].

Controversies and Evidence Gaps

The field has several active controversies.

Optimal starting dose. The shift from a 4 mL/kg/%TBSA Parkland-formula starting point to a 2 mL/kg/%TBSA modified Brooke-formula starting point reflects two decades of fluid-creep observation and Chung et al.'s military comparison data, but the 2024 ABA recommendation for the lower starting dose rests on observational and retrospective evidence rather than a multicenter prospective RCT ^[1,23]. The ABRUPT trial documented that contemporary practice still tends to deliver first-24-hour volumes at or above Parkland prediction ^[26].

Colloid timing and choice. Whether to deploy colloid early, late, or only as rescue for established fluid creep is unsettled. The 2024 ABA guideline conditionally recommends considering human albumin solution, especially in patients with larger burns, to lower resuscitation volumes and improve urine output ^[1]. A 2017 systematic review and meta-analysis by Eljaiek et al. found no significant benefit of albumin on mortality (RR 1.6; 95% CI 0.63–4.08) but reported reduced total volume of fluid infusion during the resuscitation phase (-1.00 mL/kg/%TBSA; 95% CI -1.42 to -0.58); the pooled estimate demonstrated a neutral effect on mortality ^[51]. The 2024 ABA guideline does not make a recommendation on fresh frozen plasma as an adjunct ^[1]. Kahn et al.'s 2025 series reported that patients receiving 2 mL/kg + FFP received significantly less fluid than 3 or 4 mL/kg protocols (1.7 vs 3.3 vs 4.15 mL/kg/%TBSA) with significantly less mortality, mechanical ventilation, tracheostomy, and hemodialysis, suggesting FFP as a glycocalyx-restoring adjunct that is not yet standard of care despite increasing evidence of benefit ^[49]. The [[albumin-resuscitation-in-burns]] and [[ffp-resuscitation-in-burns]] subtopic pages treat each colloid in depth.

Hydroxyethyl starch. Béchir et al.'s double-blind RCT of balanced HES 130/0.4 (6%) plus lactated Ringer's versus lactated Ringer's alone in severe burns found no volume-sparing effect and no advantage on ARDS incidence or ICU length of stay; the authors concluded balanced HES could not be considered superior to lactated Ringer's alone ^[52]. Regulatory action and the lack of demonstrated superiority have removed HES from active clinical practice in burns.

High-dose vitamin C definitiveness. Despite Tanaka et al.'s 2000 RCT data and Edgar et al.'s 2011 systematic review supporting volume reduction and edema reduction with continuous high-dose ascorbic acid ^[42,43], confirmatory multicenter trial data are lacking, and the 2024 ABA guideline cannot make a recommendation ^[1].

Endpoints beyond urine output. Whether ITBV-guided or other hemodynamic-monitor-guided resuscitation improves outcomes compared with urine-output titration is contested. The 2014 systematic review found that the apparent survival benefit of hemodynamic monitoring was driven by non-randomized studies and disappeared when analysis was restricted to RCTs ^[11]. Holm et al. observed that ITBV-guided resuscitation administered significantly larger crystalloid volumes than Parkland prediction ^[12]. Jiang et al. reported in a non-randomized single-center study that PiCCO-guided rehydration shortened ICU stay but used larger total volumes ^[57]. The 2024 ABA guideline explicitly does not recommend transpulmonary thermodilution-derived variables for routine use ^[1].

Vasopressor and inotrope use. A 2022 systematic review concluded that evidence is insufficient to support routine vasoactive or inotropic adjuncts during early major-burn resuscitation; vasopressor use is associated with markers of higher injury severity and with increased mortality, though direction of causality is not established ^[44]. The 2024 ABA guideline does not make a recommendation ^[1].

Tonicity and volume-reduction strategies. Gigengack et al. compared a Dutch Burn Society pre/post change from 4 mL/kg/%TBSA hypertonic solution to 3 mL/kg/%TBSA isotonic solution and reported no differences in renal function, renal replacement therapy, urinary output, AKI incidence, or mortality, supporting volume and tonicity reduction without adverse renal effect in their population ^[59]. The wider hypertonic-saline debate remains unsettled, with Huang et al.'s older renal-failure-and-mortality signal still informing reluctance to use hypertonic resuscitation routinely ^[53].

Plasmapheresis. Mosier et al.'s literature review documented persistent clinical benefits and reduced morbidity and mortality with therapeutic plasma exchange in toxic epidermal necrolysis, burn shock, and sepsis ^[47], but the technique is not in widespread routine use for burn resuscitation and is generally reserved for salvage.

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