Fluid resuscitation burns 2009


Published on

Published in: Health & Medicine, Technology
1 Like
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Fluid resuscitation burns 2009

  1. 1. Fluid Resuscitationof the ThermallyInjured PatientRobert Cartotto, MD, FRCS(C)a,b,* KEYWORDS Burns Fluid resuscitation Fluid creep Burn shock Parkland formulaAcute fluid resuscitation is fundamental to modern IMPORTANT HISTORICAL DEVELOPMENTSburn care. Plastic surgeons in many parts of theworld are involved in the acute care of thermally Before the 1940s patients with moderate and largeinjured patients and as such should have an up- burns commonly developed hypovolemic shock,to-date understanding of the current approaches which resulted in acute renal failure and eventuallyto acute fluid resuscitation. For decades, fluid death in many cases. Two mass casualty fires inresuscitation has been progressively streamlined North America, the Rialto Theater fire in 1921into a relatively ‘‘routine’’ process of using and the Cocoanut Grove Nightclub fire in 1942,a formula to derive a weight and burn size adjusted led to important advances in the understandingvolume of fluid, which is then infused into the of the burn shock process, and the need to treatacutely burned patient, aiming to optimize a variety this with early provision of intravenous fluid basedof somewhat loosely defined end points led chiefly on burn size and weight of the patient.2,3 A host ofby urinary output (UO). In recent years, however, formulas, which varied in the type of crystalloid,there has been an important shift in the under- the proportion of colloid administered, and thestanding of and approach to fluid resuscitation, fu- timing of administration of these fluids, subse-eled largely by increasing recognition that modern quently followed4–6 and culminated in the Parklandcrystalloid resuscitation frequently provides formula proposed by Baxter and Shires in 1967.7substantial volumes of fluid, often in excess of The Parkland formula, which is the dominantthat predicted by current formulas, resulting in burn resuscitation strategy in North Americanumerous edema-related complications (Fig. 1). today, was derived from empiric experiments onThis phenomenon, coined ‘‘fluid creep’’ by Pruitt,1 burned dogs, and subsequent testing amongis now a topic that dominates most current discus- several hundred human burn patients.7–9sion of fluid resuscitation. It is increasingly recog- Baxter explicitly stated that most burn patientsnized that fluid resuscitation is anything but could be successfully resuscitated by providinga rote, standardized process, and that there is an fluid within the relatively narrow range of 3.7 tourgent need for re-evaluation of existing resuscita- 4.3 mL/kg/% total body surface area (TBSA).10tion approaches to avoid fluid creep. This article After more than four decades of acceptance offamiliarizes plastic surgeons with current concepts the Parkland formula as a cornerstone of burnin burn shock and edema formation physiology care, and despite the fact that this approach hasand current resuscitation strategies. An important provided effective resuscitation that has markedlytheme throughout this article is the understanding reduced the incidence of burn shock-inducedof why fluid creep is so prevalent, and what strat- acute renal failure,11,12 several reports have plasticsurgery.theclinics.comegies can be used to minimize it. recently surfaced that show that modern burn a Department of Surgery, University of Toronto, Toronto, Canada b Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Room D712, 2075 Bayview Avenue, Toronto, Canada M4N 3M5 * Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Room D712, 2075 Bayview Avenue, Toronto, Canada M4N 3M5. E-mail address: robert.cartotto@sunnybrook.ca Clin Plastic Surg 36 (2009) 569–581 doi:10.1016/j.cps.2009.05.002 0094-1298/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
  2. 2. 570 Cartotto hand-in-hand with development of edema of the soft tissues. Significant edema is the hallmark of moderate to large burn injuries, and is worsened by fluid resuscitation itself. Fluid resuscitation may produce acute weight gains of as much as 20%, purely on the basis of retained resuscitation fluid.20,21 Most of the edema fluid is found in and surrounding the burn wound within the interstitial space of the skin and subcutaneous soft tissue planes, and to a lesser extent within the cells of these tissues. Intracellular edema is seen in combination with accumulation of sodium within cells and a drop in the transmembrane electrical potential of these cells.22 Although incompletely understood, a circulating shock factor may be partly responsible for the intracellular accu- Fig. 1. An elderly patient recently treated demon- mulation of water and sodium and reduction of strating ‘‘fluid creep.’’ The patient had a 25% TBSA transmembrane potential.23 When burn size full-thickness burn but no smoke inhalation 16 hours approaches 25% TBSA or greater, edema also previously. The patient had been managed without endotracheal intubation initially. At 15 hours post- forms in the nonburned soft tissues distant from burn he had received 7901 mL of cumulative fluid, the burn wound, including the lung, muscles, and which was 62% greater than what the Parkland intestines. The amount of edema in the nonburn formula would have predicted to this time point, tissues is directly proportional to the burn size.24,25 despite UO averaging only 48 mL/h (0.7 mL/kg/h) Direct thermal damage is partly responsible for over this time period. He began to develop early signs the alterations in the burn wound that are of edema-related upper airway obstruction and described next. Locally released inflammatory required prophylactic intubation. mediators, however, play an even more significant role. Discussion of the complex interactions of the clinicians are providing volumes that are substan- inflammatory mediators is beyond the scope of tially in excess of Baxter’s original recommenda- this article but suffice it to say that neutrophils, tions.13–18 Not surprisingly, as a consequence of oxygen-free radicals, prostaglandins and leukotri- these large resuscitation volumes, complications enes, kinins, serotonin, and histamine are all impli- related to edema formation led chiefly by cated in the pathogenesis of edema formation secondary abdominal compartment syndrome postburn injury.19 (ACS), have also appeared. Current research in fluid resuscitation now concentrates on approaches to minimize fluid creep, including tighter control of fluid Normal Starling Forces infusion rates, earlier and more liberal use of The normal forces that control the movement of colloids, and the use of hypertonic saline (HTS). fluid across the capillary membrane were originally elucidated by the physiologist Starling in 1896.26 Subsequent refinements of his observations PATHOPHYSIOLOGY OF BURN SHOCK resulted in the well-known Starling equation: AND EDEMA FORMATION À Á À Á Q 5 Kf Pcap À Pi 1s pp À pi Familiarity with the pathophysiology of burn shock and edema formation is necessary to understand At the outset this formula usually seems daunt- current fluid resuscitation guidelines and the ing to most readers, but it can easily be under- possible causes and correction of fluid creep. stood by breaking it down into its five main This section reviews the normal forces that control components (Fig. 2). movement of fluid across the capillary membrane, Q is the fluid filtration rate and is simply the rate and how these are altered following thermal injury. at which fluid moves (or ‘‘fluxes’’) from the vascular An excellent review of this topic has recently been space, across the capillary membrane, into the published by Demling.19 interstitial space. Under normal circumstances Burn shock is a form of hypovolemic shock that any fluid entering the interstitium is equally arises as a result of the translocation of isotonic removed by the lymphatics, so that edema does protein-containing fluid from the vascular space not form. into the interstitial space, resulting in edema.19 Kf is the fluid filtration coefficient, which is The contraction of the intravascular space goes a measure of how easily fluid is able to move
  3. 3. Fluid Resuscitation 571Fig. 2. Diagram summarizing forces acting across the capillary membrane. Pcap-Pi is the capillary hydrostatic pres-sure gradient; pcap-pi is the colloid osmotic pressure gradient; Kf is the fluid filtration coefficient; s is the reflec-tion coefficient.across the capillary membrane and into the inter- protein within the plasma relative to that in thestitial space. This depends on the properties of interstitial space. The pp – pi counterbalancesthe capillary membrane itself, especially the the opposing hydrostatic gradient (Pcap – Pi), sosurface area of the capillary membrane surface in that edema does not normally develop. If ppquestion (ie, larger areas facilitate movement), were to decrease significantly (eg, as in hypopro-and the actual compliance of the interstitium.19 In teinemic states) then pp – pi decreases leavingthe case of the skin and surrounding soft tissue the hydrostatic gradient (Pcap – Pi) unopposed,planes the compliance depends on the structural which allows increased fluid flux (Q) into the inter-integrity of the collagen fibers and the hyaluronic stitial space.19acid linkages between them and the density and s is the reflection coefficient and represents thehydration of the ground substance in which these degree of capillary membrane permeability. Anmolecules are embedded. If the collagen frame- impermeable membrane has a s of 1, whereaswork is destroyed and the ground substance a freely permeable membrane has a s of 0. Normalbecomes more hydrated (eg, by burn injury fol- dermal capillaries have a s of 0.9.19lowed by early edema formation), complianceincreases and the ease of fluid movement into Altered Starling Forces in the Burn Woundthe interstitium increases.27,28 Pcap – Pi is the gradient in hydrostatic pressure Q is dramatically increased immediately, mostbetween the capillary pressure (Pcap) and the inter- notably in the first 1 to 2 hours postinjury, butstitial hydrostatic pressure (Pi). The gradient is generally reaches a plateau by 24 hours, andnormally 10 to 12 mm Hg in dermis19 and is in then although remaining elevated above normala direction favoring fluid movement out of the gradually declines over the next few days.19,21,29capillary into the interstitium. A higher gradient s increases significantly in the microcirculation(eg, caused by an elevation of Pcap or a reduction within and surrounding the burn wound and isin Pi) pushes more fluid out and increases Q. Were here the most important cause of edema. Theit not for an opposing force (the colloid osmotic capillary membrane becomes permeable topressure gradient, described next), fluid would many plasma proteins including albumin andcontinually seep out of the capillary into the small-to-moderate sized globulins. In the dermisinterstitium. s drops numerically from 0.9 (nearly impermeable) pp – pi is the colloid osmotic pressure gradient to 0.3 (highly permeable). This increase in capillaryrepresenting the difference between the plasma permeability is most profound acutely and maycolloid osmotic pressure (pp) and the interstitial remain elevated for several days postburn. Thecolloid osmotic pressure (pi). This gradient is also severity and duration of the leak is directly propor-normally 10 to 12 mm Hg in the dermis but is in tional to the extent of the burn.19,25,29–31the direction favoring fluid retention within the Kf increases following a burn injury, whichcapillary because of the higher concentration of means that fluid can more easily cross the capillary
  4. 4. 572 Cartotto membrane into the interstitial space. Of particular immediately following the burn, allowing fluid and importance is that the compliance of the interstiti- plasma proteins to move from the vascular space um itself increases. This probably is related to into the interstitial space, reducing the colloid destruction of the collagen framework and osmotic pressure gradient, which normally helps surrounding matrix, which normally restricts fluid to retain fluid within the vascular space. Simulta- influx. Furthermore, as edema progresses, hydra- neously, an increase in the hydrostatic pressure tion of the matrix increases the compliance gradient, produced in part by a transient but because the swelling mechanically disrupts bonds powerful ‘‘sucking’’ force, displaces fluid from between various macromolecules. A self-perpetu- the vascular space into the interstitium. Finally, ating cycle is created in which edema leads to breakdown of the collagen framework of the inter- more edema formation, allowing large increases stitium and progressive hydration of its matrix as in interstitial volume with relatively little edema develops make the interstitium more corresponding increase in hydrostatic compliant facilitating entry of even more fluid into pressure.19,29,32,33 this space, perpetuating edema generation. Pcap – P i, the hydrostatic pressure gradient, increases meaning that there is an increased Alteration of Starling Forces in Nonburn hydrostatic force moving fluid out of the vascular Soft Tissues space and into the interstitium. This is partly When the burn size approaches 25% to 30% caused by a small and transient increase in Pcap TBSA or larger, edema in the unburned skin and immediately following the burn, but more impor- soft tissues develops.24 Acutely, within the first tantly by a profound (albeit transient) decrease in few hours postburn, there is an increase in capil- Pi from its usual value of À2 to 12 mm Hg to as lary permeability (s), which may be caused by low as À20 to À40 mm Hg. This is believed to the systemic dissemination of inflammatory medi- occur because the collagen and hyaluronic acid ators.35–37 The change in s is transient and capil- are held in the dermis in a dense, tightly packed lary permeability soon returns to normal, but coiled configuration. Burn and inflammation-medi- edema continues to develop in the nonburn ated collagen denaturation allows an unraveling of tissues for at least 24 to 36 hours postinjury. The this framework and produces fragmentation of the most important alteration is the loss of plasma molecules into osmotically active particles. The colloid osmotic pressure and resultant decrease end result is that, much like a compressed sponge in the colloid osmotic pressure gradient (pp – pi) that is allowed to expand, the interstitium draws as a consequence of the hypoproteinemic state fluid into itself by creating a negative ‘‘sucking’’ that develops with burns greater than or equal to or ‘‘vacuum’’ force, lowering Pi and dramatically 25% to 30% TBSA. Correction of the hypoprotei- increasing the hydrostatic gradient Pcap – nemic state with infusions of albumin or plasma Pi.19,29,34 As fluid expands the interstitium, Pi hinders the development of nonburn soft tissue begins to rise again and returns to a slightly posi- edema.25,38 tive value within a few hours. As described previ- ously, however, because of the increased Hemodynamic Consequences interstitial compliance, interstitial pressures do of the Fluid Shifts not rise with this volume increase to the degree that happens in the normal state.19 The most important consequence of the afore- pp – pi, the osmotic pressure gradient, is nor- mentioned fluid shifts is a reduction in circulating mally 10 to 12 mm Hg but begins to decrease plasma volume. Cardiac output (CO) falls, largely following burn injury, which means that there is because of hypovolemia and reduced preload, less osmotic force to hold fluid within the intravas- but interestingly in larger burns (R40% TBSA), cular space. An important force that normally an immediate fall in CO has been repeatedly neutralizes the hydrostatic pressure gradient is observed before any measurable decrease in the eliminated. This occurs as a result of decreasing plasma volume, suggesting that depressed plasma protein concentration caused by leakage myocardial contractility plays a role. Earlier litera- of protein across the now highly permeable ture suggested that an uncharacterized ‘‘myocar- plasma membrane (hence pp decreases), and by dial depressant factor’’ was responsible,39–42 and a gradual increase in pi as plasma proteins and it is now thought that inflammatory mediators other osmotically active particles accumulate in from the burn wound, distributed systemically, the interstitium.19,28 are responsible.43,44 Further supporting the likeli- To summarize, the following takes place within hood of direct myocardial depression is the fact and surrounding the burn wound. The capillary that CO has been observed to remain temporarily membrane becomes highly permeable depressed despite restoration of plasma volume
  5. 5. Fluid Resuscitation 573with fluid resuscitation. Simultaneous with the used only as a guideline to determine an initialacute reductions in plasma volume and CO, rate of fluid infusion. The resuscitation rate andsystemic vascular resistance increases because volume must be continually adjusted based onof sympathetic-mediated peripheral vasoconstric- the response of the patient (see Fig. 3). A secondtion and the effects of increased viscosity of the important principle of Parkland-based crystalloidblood because of hemoconcentration. The eleva- resuscitation, which is frequently ignored bytion in systemic vascular resistance is an addi- modern burn clinicians but which was emphasizedtional factor that contributes to the acute in two important consensus conferences,10,46,47 isdepression of CO.45 Organ perfusion, particularly that resuscitation should use the least amount ofrenal blood flow, is compromised as a result of fluid (ie, somewhere between 2 and 4 mL/kg/%the hypovolemic state, depressed CO, and periph- TBSA) necessary to achieve adequate UO anderal vasoconstriction, especially if fluid resuscita- prevent early organ failure and avoid later compli-tion is delayed. As resuscitation proceeds, CO cations. What exactly qualifies as ‘‘adequate’’ UOslowly climbs back to normal and in patients with is open to some debate. Unfortunately, in severalmajor burn injuries, a hyperdynamic picture with of Baxter’s publications on the Parkland formula,supranormal CO develops by 36 to 72 hours post- ‘‘recommended’’ UO fluctuated between 50 andburn as part of the hypermetabolic response. 70 mL/h,9 50 and 100 mL/h,22 greater than 40 mL/h,9 The intended goal of fluid resuscitation is to and 40 to 70 mL/h.46 One question that has notre-expand the plasma volume, restore CO, and been completely resolved is whether the desiredimprove organ and tissue perfusion. It should be UO of 0.5 to 1 mL/kg/h should be based on actualevident from the foregoing discussion that crystal- body weight or predicted body weight. The issueloid resuscitation fluids, although necessary to of what constitutes optimum UO is highly importantachieve the goal of restoring tissue perfusion, are because more fluid delivery is needed to drive thealso subject to the altered Starling forces and as UO to the higher end of any desired range, whichsuch, large amounts of the resuscitation fluid also results in increased edema formation. Thenecessarily end up as interstitial and cellular body mass index of the average North Americanedema fluid. has been steadily increasing over the past several decades48 and one wonders if this may be partlyCRYSTALLOID RESUSCITATION responsible for fluid creep, as clinicians try to achieve higher and higher weight-based hourlyIn North America, resuscitation based on use of UO. Currently, some experts recommend mainte-crystalloids during the first 24 hours postburn has nance of UO of 30 to 50 mL/h in adults and 1 tobeen the dominant strategy for several decades. 2 mL/kg/h in children weighing less than 30 kg,49Most clinicians continue to base early fluid resusci- whereas current Practice Guidelines of the Amer-tation on the Parkland formula for the initial 24-hour ican Burn Association advise maintenance of UOperiod (4 mL of Ringer’s lactate (RL) per kilogram at approximately 0.5 to 1 mL/kg/h in adults andbody weight per percent TBSA burn with half the 1 to 1.5 mL/kg/h in children.50volume given in the first 8 hours postburn). The During the second 24-hour period postburn,rationale behind the use of RL (Na 130 mEq/L, Baxter22 recommended that 20% to 60% of thephysiologic pH 7.4) and no colloid in the first calculated plasma volume be restored by adminis-24 hours is based on two observations. First, the tration of colloid, in the form of plasma. Additionalfluid leaving the intravascular space, which then fluid in the form of dextrose and water would beaccumulates in the interstitial space as edema fluid, used to maintain UO. The amount of colloidis isotonic relative to the plasma with a similar pH required varied between 0.3 and 0.5 mL/kg/%and ratio of sodium to potassium as plasma.7 TBSA burn.46 Baxter22 argued that this amount isSecond, the acute increase in capillary perme- sufficient to re-expand the plasma volume inability (s) within and around the burn wound allows most patients where the capillary leak would bemost plasma proteins to leave the vascular space sealed by 24 hours, but recognized that inand enter the interstitium during the first 24 hours, a minority of patients colloid may not be effectiveso that the protein concentration of the edema fluid until 36 hours postburn because of ongoing capil-begins to approach that of plasma.19,28 lary leak between 24 and 36 hours postburn.22 The The Parkland formula seems to suggest that provision of colloid after 24 hours postburn isa fixed amount of 4 mL/kg/%TBSA burn should frequently underemphasized in descriptions ofbe administered and that a static rate of infusion modern crystalloid fluid resuscitation strategies.follows a series of stepwise cuts at 8 and 24 hours With the re-emergence of interest in use of colloids(Fig. 3). The single most important principle in using as a fluid-sparing strategy to limit fluid creep (dis-the Parkland formula, however, is that it should be cussed later), this often forgotten component of
  6. 6. 574 Cartotto Fig. 3. Chart showing hourly resuscitation data from a 40-year-old man weighing 100 kg with a 74% TBSA flame burn. The actual fluid volume delivered is consistently above the Parkland prediction, which theoretically suggests a static infusion rate with a prescribed cut at 8 hours postburn (top panel). Note that the hourly infusion rate is continually adjusted to keep UO between 0.5 and 1 mL/kg/h (bottom panel). This patient survived. the Parkland formula may take on greater impor- Unpredictable Scenarios and Fluid Creep tance in the future. The more pressing problem for the modern burn clinician is fluid creep, which is the unpredictable DIVERGENCE OF ACTUAL AND PREDICTED FLUID trend toward provision of larger and larger resusci- VOLUMES DURING CRYSTALLOID RESUSCITATION tation fluid volumes to burn patients who do not fit Predictable Scenarios into the well-defined subgroups identified previ- In a variety of predictable situations, resuscitation ously. A number of recent studies have found volumes are significantly greater than anticipated that crystalloid fluid resuscitation volumes for the by the Parkland formula. These situations include initial 24 hours postburn among burn patients delayed resuscitation,51 high voltage electrical have ranged between 4.8 and 6.7 mL/kg/ burns, coincident alcohol intoxication,52 extensive %TBSA,13–18 in many instances independent of deep burns,14 advanced age,53 and the presence the presence of a documented inhalation injury. of smoke inhalation injury.53–57 The increased fluid The consequences of this increased fluid adminis- requirements when burn injury is combined with tration are similarly well characterized, and include inhalation injury have been well characterized airway swelling requiring prophylactic intubation58 and repeatedly demonstrated among human (see Fig. 1), secondary ACS,59 soft tissue edema burn plus smoke inhalation patients to range in the extremities necessitating more frequent between 35% and 65% greater than burn injury escharotomies and even fasciotomies,58 elevated alone.54–57 In practice, however, this does not intraocular pressures,60 and an overall increased mean that a higher value than 4 mL/kg/%TBSA risk of death.18 burn should be used to calculate the initial infusion The development of intra-abdominal hyperten- rate. Rather, the clinician should initiate fluids sion (IAH) and the ACS deserve special mention using the Parkland formula, but should anticipate because these are perhaps the most dangerous giving more fluid than predicted (again, titrated and frequently reported consequences of fluid based on the patient’s response), and importantly, creep in association with massive burn resuscita- not to reduce fluids to ‘‘run the patient dry’’ out of tion (Fig. 4).59,61–64 The most recent Consensus concern for the pulmonary injury. These patients Guidelines define IAH as an intra-abdominal pres- require increased volumes of crystalloid fluid to sure (obtained by transduction of bladder pres- avoid burn shock. sure) greater than or equal to 12 mm Hg and
  7. 7. Fluid Resuscitation 575Fig. 4. A patient with 65% TBSA full-thickness burnsand smoke inhalation who developed ACS and Fig. 5. Extension of abdominal escharotomies torequired decompressive laparotomy. This patient did control rising intra-abdominal pressures. These es-not survive. charotomies may be extended further (dotted lines) in a ‘‘checkerboard pattern’’ as needed.ACS as an intra-abdominal pressure greater than20 mm Hg with evidence of new organ dysfunction tissues and organs, and with more severe ACS,(typically manifested as oliguria, impaired particularly with massive burn injury, definitivemechanical ventilation with high peak airway pres- treatment by decompressive laparotomy maysures, worsening metabolic acidemia, and hemo- be required.59,67,68 Mortality following surgicaldynamic instability).65 ACS is considered decompression for ACS is reported to be betweensecondary when there is no demonstrable intra- 50% and 100%.59,63,66,68abdominal pathology,65 as in the case of a burnwhere bowel and mesenteric edema andincreased peritoneal fluid are the cause of the Why is fluid creep happening?raised intra-abdominal pressures. Left untreated, One observation is that clinicians treating burnACS is invariably fatal, and probably was the patients do not devote adequate attention to thecause of early ‘‘death due resuscitation failure’’ careful titration (and in particular the downwardbefore formal recognition of the syndrome. Ivy titration) of fluids to keep UO within a tightlyand colleagues62 prospectively followed burn controlled range, ideally at the lower end of thepatients with intra-abdominal pressure greater accepted range.69 In some of the studies thatthan 25 mm Hg and developed a score that indi- described resuscitation volumes in excess ofcated that cumulative resuscitation volumes Parkland predicted range, mean UOs during thegreater than or equal to 250 mL/kg were associ- first 24 hours postburn exceeded 1 mL/kg/h inated with IAH and a high risk of ACS.62,66 When most patients.13,14,16,17 Similarly, Cancio andcumulative volumes reach 250 mL/kg or more colleagues15 from the US Army Burn Center foundintra-abdominal pressure measurements (by that in the face of high UO (50 mL/h or 1 mL/kg/h)bladder pressure transduction) should be per- over 2 consecutive hours during burn resuscita-formed every 2 hours and conservative measures tion, the treating clinicians appropriately reducedto reduce intra-abdominal pressure should be the RL infusion only 33% of the time. Finally,considered.62,66 These include use of neu- excessive fluid provision in the pre–burn centerromuscular relaxants and increased sedation in setting by well-meaning emergency personnelmechanically ventilated patients; extension of es- may be a source of excessive fluids. In one studycharotomies on any anterior trunk burns (Fig. 5); burn patients had received a mean of 2.5 L of RLand possible judicious use of diuretics if adequate within the mean delay of 2.8 hours between injuryintravascular volume can be confirmed by place- and arrival to the burn center.14 Althoughment of a pulmonary artery catheter, which adequate early fluid provision is important,demonstrates pulmonary capillary wedge pres- aggressive fluid infusion is not necessarily better.sures greater than 18 mm Hg.62,66,67 Studies in Clinician inattention, however, cannot entirelya limited number of patients have found that in account for the phenomenon of fluid creep. Othersome instances, IAH and possibly early ACS may studies that have reported 24-hour resuscitationbe reversed by the insertion of peritoneal dialysis volumes in excess of 4 mL/kg/% TBSA alsocatheters to remove peritoneal fluid, but this reported that the mean 24-hour UOs in these patientsdoes not treat the edema of the intra-abdominal fell within the range of 0.5 to 1 mL/kg/h,15,18
  8. 8. 576 Cartotto suggesting that fluid creep may develop even with Harborview Burn Center in Seattle. Opiates do appropriate titration of the resuscitation. have important cardiovascular effects, such as Another consideration is that the original popu- hypotension, which could lead to increased fluid lation of patients treated with the Parkland formula administration during acute burn resuscitation. and reported in Baxter’s original studies may not As with the previously described mechanisms, be representative of current practice, where opioid creep is likely not the sole cause but one greater numbers of patients with larger and more of several contributory factors. extensive burn injuries routinely survive resuscita- tion.69 In many of these massive injuries, resusci- END POINTS AND MONITORING DURING tation volumes greatly exceed 4 mL/kg/% TBSA. CRYSTALLOID RESUSCITATION Significant associations between both the burn size15,17 and burn depth14 and an excessive resus- Hourly urine output is still the cornerstone of citation volume have been demonstrated in recent monitoring of burn resuscitation despite the emer- studies. Volumes above the Baxter range may be gence in the past decade of more sophisticated the necessary cost of successfully resuscitating approaches, such as the use of malperfusion larger and deeper burns. markers (arterial base deficit and serum lactate); The trend toward abandonment of colloids over cardiac index determinations; measurements of the past two or three decades may also have oxygen delivery and uptake variables; and intratho- contributed to the subtle advance of fluid creep.69 racic blood volume estimations. The fluid infusion Baxter’s original approach included use of plasma rate should be adjusted to achieve a UO of 0.5 to at 24 hours, and two well-conducted randomized 1 mL/kg/h in adults and 1 to 1.5 mL/kg/h in chil- prospective studies both demonstrated that early dren.50 It has never been specified whether this use of colloids significantly reduced 24-hour should be based on actual or predicted weight, resuscitation volumes, compared with use of crys- but in heavier and obese patients, aiming for a UO talloids alone.70,71 at the lower end of the range seems to make sense An intriguing theory on fluid creep has been to use the least amount of fluid possible. described by Saffle,69 who suggests that fluid The arterial base deficit and serum lactate are creep may be a physiologically based phe- well-recognized markers of tissue malperfusion nomenon in which excessive fluid in the early that have been used to monitor resuscitation in postburn period, combined with the altered trauma and critically ill populations. More recently, derangements in the Starling forces described several investigators have demonstrated that previously, may perpetuate a self-repeating these are also important markers during burn cycle of edema-genesis and escalating volume resuscitation and that their elevation or failure to requirements. Under this theory, excessive fluid correct over time are associated with increased early on could increase the capillary hydrostatic morbidity (eg, increased fluid requirements, multi- pressure (Pcap) and drive more and more fluid organ dysfunction, and acute respiratory distress into the interstitial space, causing edema, loos- syndrome73,74) and predict increased mortality.75–77 ening interstitial structure, and increasing its Unfortunately, it is not known yet how to use these compliance, allowing more and more edema to markers to guide resuscitation, and more impor- form. Simultaneously, this process lowers the tantly whether resuscitation directed at their plasma colloid osmotic pressure (pp) allowing correction improves outcome. more fluid flux out of the vascular space and re- The use of invasive cardiovascular monitoring sulting in a vicious cycle characterized by wors- during burn resuscitation has been investigated ening edema formation and an escalating need by several groups.78–80 The principle is to use for more and more crystalloid resuscitation fluid. fluids and inotropes to optimize in a goal-directed This might explain a paradoxic observation from fashion a variety of end points, such as serum the author’s institution that resuscitation volumes lactate, base deficit, cardiac index, and oxygen are relatively close to predicted during the first delivery and uptake. Although one study found 8 hours postinjury (where one expects capillary that a goal-directed resuscitation improved leak to be most severe), but then severely survival,78 other studies have failed to show any deviate above predicted during the second and obvious benefit to this approach,79,80 and impor- third 8-hour periods postburn.14 tantly demonstrated that ‘‘optimization’’ of cardiac A final mechanism, referred to as ‘‘opioid index and oxygen uptake required liberal provision creep,’’ may also contribute to fluid creep.69,72 of crystalloid fluid, well above Parkland predic- Sullivan and colleagues72 identified a correlation tions.79,80 It is noteworthy that nearly 40 years between elevated resuscitation volumes and ago Baxter and others45 observed that crystalloid increased dosages of opioid analgesics at the resuscitation did not normalize preload, CO, or
  9. 9. Fluid Resuscitation 577pH for at least 24 to 48 hours. One wonders if and early edema formation. Whether this mightattempts to normalize these variables more translate to other benefits, such as improvedaggressively and earlier in resuscitation by using survival, is unknown at this time. It is also impor-high fluid infusion volumes may be another tant to point out that use of fresh frozen plasmacontributory cause of fluid creep.69 as the early colloid is not generally recommended outside of an approved research protocol,COLLOID RESUSCITATION because this colloid is a limited and expensive blood bank resource, and because of the potentialAlthough original resuscitation strategies, such as for viral disease transmission and induction ofthe Evans and Brooke formulas, provided colloids transfusion-related acute lung injury.81 Use ofduring the first 24 hours, concern about the loss 5% albumin is an acceptable alternative, and atof capillary membrane integrity and leakage of the author’s institution they begin an infusion ofdelivered proteins into the interstitial space 50 to 100 mL/h of 5% albumin at 8 to 12 hoursprogressively led to avoidance of colloids in the first postburn in burns greater than 40% or as a form24-hour period and reliance on a pure crystalloid of ‘‘colloid rescue’’ when crystalloid volumes areapproach for the first 24 hours. At the present deviating significantly above predicted.time, burn clinicians generally fall into three groups To a lesser extent, the use of nonprotein colloidwith respect to colloid provision: (1) some believe it solutions, such as Dextran, Pentastarch, orshould not be used before 24 hours, because of the Hetastarch, in burn resuscitation has also beenloss of capillary integrity, which could allow accu- described. Over two decades ago Demling andmulation of the administered protein (and water) colleagues,38 in an animal model, demonstratedin the interstitium, particularly the lung;70 (2) others that burn resuscitation with Dextran 40 (low-molec-advocate immediate colloids (albumin) on the basis ular-weight Dextran) maintained hemodynamicthat these help to maintain intravascular volume;4 variables and UO with significantly less fluid andand (3) a third group takes an intermediate significantly less nonburn tissue edema, than withapproach and gives colloids at 8 to 12 hours post- RL alone. This was caused by an increase ininjury arguing that normal capillary permeability is the colloid osmotic pressure gradient by therestored in nonburn soft tissues by 8 to 12 hours low-molecular-weight Dextran. Human studiesand that hypoproteinemia is the major cause of involving small numbers of patients suggest thatongoing edema formation at this time.25,38 starches are comparable volume expanders when Two randomized prospective studies have compared with albumin during the first 24 hourscompared crystalloids with early colloid in the first of resuscitation.82 Until more data and experience24 hours postburn. Goodwin and colleagues70 in are accumulated with these substances, however,1983 randomized adult burn patients to resuscita- their routine use cannot be recommended.tion with RL, or a 2.5% albumin in RL solution, bothtitrated to achieve a UO of 30 to 50 mL/h. The HYPERTONIC SALINE RESUSCITATIONalbumin-treated group achieved the desired UOend point and had significantly higher echocardi- The appeal of HTS in burn resuscitation stemsography-measured cardiac index, with significantly from its ability to shift water from the intracellularless resuscitation fluid than the crystalloid-only space into the extracellular compartment, and ingroup. The albumin group, however, had signifi- so doing, expand the intravascular space. Thecantly greater late lung water accumulation after obvious benefits to the burn patient are the needresuscitation. In a more recent study, O’Mara for less fluid administration, and less generationand colleagues71 randomized adult burn patients of tissue edema. Indeed, the pioneers of HTSto resuscitation with a RL infusion or to 2000 mL burn resuscitation, Monafo and Moylan, demon-of RL infused over 24 hours combined with an strated that hypertonic salt solutions wereadjustable infusion 75 mL/kg of fresh frozen effective volume expanders that resulted inplasma, with infusions in both groups titrated to acceptable resuscitation with less fluid volumeachieve an hourly UO between 0.5 and 1 mL/kg/ and edema formation than when isotonic solutionsh. The colloid group required significantly less were used.83–85 Subsequent studies have mostlyresuscitation fluid to achieve the UO end point, confirmed these early findings.86–89 A consensuswhich resulted in significantly lower peak intra- on the most appropriate use of HTS during burnabdominal and airway pressures in that group, resuscitation has not been reached because ofpresumably on the basis of less edema formation the wide variations in the timing (bolus versusin that group. From these two studies, it can be continuous infusion), composition (HTS versussafely concluded that early colloid provision HTS plus colloid), and concentration of the hyper-reduces overall resuscitation volume requirements tonic solutions that have been reported.86,88–91
  10. 10. 578 Cartotto Hyperosmolarity and hypernatremia are ever- burn patient carefully to review the extent of burn present dangers with use of this strategy, and with first providers. Similarly, repeated communi- serum sodium concentrations must be frequently cation with the emergency room to review fluid and carefully monitored to avoid complications, infusion rates and UO is important when transfer such as organ failure and death related either to to a burn center is delayed beyond a few hours. excessive or prolonged hyperosmolarity, or too rapid correction of the hyperosmolar state. Serum Titrate, Titrate, Titrate sodium levels should be maintained at less than Rigid adherence to a fluid infusion rate prescribed 160 mEq/L.49 The ultimate dangers in HTS resus- by a formula is potentially harmful. Rather, the citation are described in the study by Huang and clinician should continually adjust the infusion colleagues,92 who reported a fourfold increase in rate based on the patient’s response. Practically, the incidence of acute renal failure associated this is based on evaluation of the UO at 1- to 2- with HTS resuscitation. Marked and sustained hour intervals. A protocol, such as that described elevations in serum sodium were the hallmarks of by Saffle,69 is one of several ways to achieve this patients who developed acute renal failure in that goal. In this strategy, an hour of UO less than study. Current practice guidelines of the American 15 mL calls for an increase in the infusion rate by Burn Association recommend that HTS resuscita- 20% or 200 mL/h, whichever is greater; an hour tion should be used by experienced burn clinicians with UO 15 to 30 mL gets an increase of 10% or and should be accompanied by meticulous moni- 100 mL/h, whichever is greater; and hour with toring of serum sodium concentrations. UO 30 to 50 mL prompts no change in the infusion rate. Conversely, for UO greater than 50 mL/h the PRACTICAL POINTERS FOR OPTIMIZING BURN infusion rate for the next hour is decreased by 10% RESUSCITATION AND MINIMIZING FLUID CREEP or 100 mL/h, whichever is greater. Within this Pay Close Attention to Pre–burn Center particular protocol, persistent oliguria or esca- Fluid Administration lating fluid infusion rates are managed by institu- tion of albumin, described next. Overzealous fluid administration combined with overestimation of burn size by prehospital and Contemplate Colloids emergency room personnel can contribute to fluid creep (Table 1). It is incumbent on the plastic Colloids do seem to reduce the overall volume surgeon who is involved in the early care of the requirements compared with use of crystalloid Table 1 Summary of practical pointers for the plastic surgeon involved in early resuscitation of a patient with major burn injuries Principle Interventions When to resuscitate? % TBSA second- or third-degree burns are R20% Where to start? Calculate 4 mL/kg/%TBSA, with half this volume administered in the first 8 hours From the time of injury Must include any fluids already administered Attention to pre–burn center fluids Ensure correct TBSA estimation Review formula, infusion rate, urinary output regularly Titration Use formulas to determine starting infusion rate only Monitor UO q 1–2 h Consider bolus or increase in infusion rate for oliguria Reduce infusion by approximately 10% or 100 mL/h (whichever is greater) for UO 50 mL/h Colloids Consider 5% albumin when cumulative fluids reach 120%–200% of predicted Monitor edema Repetitive bedside examination of edema, airway pressure, and tidal volume trends Bladder pressure measurements when cumulative fluids 200–250 mL/kg or 500 mL/h Abbreviations: TBSA, total body surface area; UO, urinary output.
  11. 11. Fluid Resuscitation 579alone.70,71 Colloids may be instituted according to 11. Tremblay R, Ethier J, Querin S, et al. Veno-venousthe original recommendations of the Parkland continuous renal replacement therapy for burnedformula by administering approximately 0.3 to patients with acute renal failure. Burns 2000;26:0.5 mL/kg/%TBSA of 5% albumin during the 638–43.second 24 hours of resuscitation. One of my 12. Chrysopoulo MT, Jeschke M, Dziewulski P, et al.approach is to administer colloids as a ‘‘rescue’’ Acute renal dysfunction in severely burned adults.technique when crystalloid requirements become J Trauma 1999;46:141–4.excessive. Yowler and Fratienne93 start albumin 13. Engrav LH, Colescott PL, Kemalyan N, et al. Aat 12 hours postburn if fluid needs are greater biopsy of the use of the Baxter formula to resuscitatethan 120% predicted; Saffle’s69 protocol calls for burns or do we do it like Charlie did? J Burn Carealbumin for persisting oliguria or infusion rates Rehabil 2000;21:91–5.more than twice the calculated rate for greater 14. Cartotto R, Innes M, Musgrave MA, et al. How wellthan 2 hours; and Chung and colleagues94 recom- does the Parkland formula estimate actual fluidmend 5% albumin if a patient, at 12 to 18 hours resuscitation volumes? J Burn Care Rehabil 2002;postburn, has a projected 24-hour requirement 23:258–65.that exceeds 6 mL/kg/%TBSA. 15. Cancio L, Chavez S, Alvarado-Ortega M, et al. Pre- dicting increased fluid requirements during theMonitor Edema, Especially resuscitation of thermally injured patients. J Traumain the Abdominal Compartment 2004;56:404–14. 16. Friedrich JB, Sullivan SR, Engrav LH, et al. Is supra-Serial bedside assessments of the evolution of the Baxter resuscitation in burn patients a new phenom-patient’s soft tissue edema, particularly in the enon? Burns 2004;30:464–6.abdominal compartment, combined with regular 17. Klein MB, Hayden D, Elson C, et al. The associationmeasurement of bladder pressures are important between fluid administration and outcome followingadjuncts when burns are extensive; when oliguria major burn: a multicenter study. Ann Surg 2007;persists; or when volume requirements become 245:622–8.excessive (eg, cumulative volume 200–250 mL/kg 18. Blumetti J, Hunt JL, Arnoldo BD, et al. The Parklandor 500 mL/h). formula under fire: is the criticism justified? J BurnREFERENCES Care Res 2008;29:180–6. 19. Demling RH. The burn edema process: current 1. Pruitt BA. Protection from excessive resuscitation: concepts. J Burn Care Res 2005;26:207–27. pushing the pendulum back. J Trauma 2000;49: 20. Brouhard BH, Carvajal HF, Linares HA. Burn edema 567–8. and protein leakage in the rat: relationship to size of 2. Underhill F. The significance of anhydremia in exten- injury. Microvasc Res 1978;15:221–8. sive superficial burns. JAMA 1930;95:852–7. 21. Carvajal HF, Linares HA, Brouhard BH. Relationship 3. Cope O, Moore F. The redistribution of body water of burn size to vascular permeability changes in and the fluid therapy of the burned patient. Ann rats. Surg Gynecol Obstet 1979;149:193–202. Surg 1947;126:1010–45. 22. Baxter CR. Fluid volume and electrolyte changes in 4. Evans EI, Purnell OJ, Robinett PW, et al. Fluid and the early post burn period. Clin Plast Surg 1974;1: electrolyte requirements in severe burns. Ann Surg 693–709. 1952;135:804–17. 23. Evans JA, Darlington DN, Gann DS. A circulating 5. Reiss E, Stirman JA, Artz CP, et al. Fluid and electro- factor mediates cell depolarization in hemorrhagic lyte balance in burns. JAMA 1953;152:1309–13. shock. Ann Surg 1991;213:549–57. 6. Moyer CA, Margraf HW, Monafo WW. Burn shock 24. Kramer GC, Lund T, Herndon DN. Pathophysiology and extravascular sodium deficiency: treatment of burn shock and burn edema. In: Herndon DN, with Ringers solution with lactate. Arch Surg 1965; editor. Total burn care. 2nd edition. Philadelphia: 90:799–811. Saunders Co; 2003. p. 78–87. 7. Baxter CR, Shires T. Physiological response to crys- 25. Demling RH, Kramer GC, Harms B. Role of thermal talloid resuscitation of severe burns. Ann N Y Acad injury induced hypoproteinemia on fluid flux and Sci 1968;150:874–94. protein permeability in burned and nonburned 8. Baxter CR, Marvin J, Curreri PW. Fluid and electro- tissue. Surgery 1984;95:136–44. lyte therapy of burn shock. Heart Lung 1973;2: 26. Starling E. On the absorption of fluids from the 707–13. connective tissue spaces. J Physiol 1896;19: 9. Baxter CR. Problems and complications of burn shock 312–26. resuscitation. Surg Clin North Am 1978;58:1313–22. 27. Guyton AC, Coleman TG. Regulation of interstitial10. Baxter CR. Guidelines for fluid resuscitation. fluid volume and pressure. Ann N Y Acad Sci J Trauma 1981;21:687–9. 1968;150:537–47.
  12. 12. 580 Cartotto 28. Harms BA, Kramer GC, Bodai BI, et al. Effect of hy- 45. Pruitt BA, Mason AD, Moncrief JA. Hemodynamic poproteinemia on pulmonary and soft tissue edema changes in the early postburn patient: the influence formation. Crit Care Med 1981;9:503–8. of fluid administration and of a vasodilator (hydral- 29. Lund T, Onarkeim H, Reed R. Pathogenesis of azine). J Trauma 1971;11:36–46. edema formation in burn injuries. World J Surg 46. Baxter CR. Fluid resuscitation, burn percentage, 1992;16:2–9. and physiologic age. J Trauma 1979;19:864–5. 30. Cope O, Moore F. A study of capillary permeability in 47. Pruitt BA. Fluid resuscitation for extensively burned experimental burns and burn shock using radioactive patients. J Trauma 1981;21:690–2. dyes in blood and lymph. J Clin Invest 1944;23:241–9. 48. Ford ES, Zhao G, Li C, et al. Trends in obesity and 31. Bert J, Bowen B, Reed R, et al. Microvascular abdominal obesity among hypertensive and non- exchange during burn injury: fluid resuscitation hypertensive adults in the United States. Am J model. Circ Shock 1991;37:285–97. Hypertens 2008;21:1124–8. 32. Granger HJ. Role of the interstitial matrix and 49. Warden GD. Fluid resuscitation and early manage- lymphatic pump in regulation of transcapillary fluid ment. In: Herndon DN, editor. Total burn care. 3rd balance. Microvasc Res 1979;18:209–16. edition. Philadelphia: Saunders Elsevier Inc; 2007. 33. Leape L. Initial changes in burns: tissue changes in p. 107–18. burned and unburned skin of rhesus monkeys. 50. Pham TN, Cancio L, Gibran NS. American Burn J Trauma 1970;10:488–92. Association practice guidelines: burn shock resusci- 34. Lund T, Wiig H, Reed R, et al. A new mechanism for tation. J Burn Care Res 2008;29:257–66. edema formation: strongly negative interstitial fluid 51. Wolf SE, Rose JK, Desai MH, et al. Mortality determi- pressure causes rapid fluid flow into thermally nants in massive pediatric burns: an analysis of 103 injured skin. Acta Physiol Scand 1987;129:433–5. children with R80% TBSA burns (R70% full thick- 35. Arturson G, Jakobsson OR. Oedema measurements ness). Ann Surg 1997;225:554–65. in a standard burn model. Burns 1985;1:1–7. 52. Warner P, Connolly JP, Gibran NS, et al. The meth- 36. Arturson G. Microvascular permeability to macro- amphetamine burn patient. J Burn Care Rehabil molecules in thermal injury. Acta Physiol Scand 2003;24:275–8. 1979;463:111–22. 53. Pruitt BA. Fluid and electrolyte replacement in the 37. Harms B, Kramer GC, Bodai B, et al. Microvascular burned patient. Surg Clin North Am 1978;58: fluid and protein flux in pulmonary and systemic 1291–311. circulations after thermal injury. Microvasc Res 54. Dai NT, Chen TM, Cheng TY, et al. The comparison 1982;23:77–86. of early fluid therapy in extensive flame burns 38. Demling RH, Kramer GC, Gunther R, et al. Effect of between inhalation and non inhalation injury. Burns nonprotein colloid on postburn edema formation in 1998;24:671–5. soft tissue and lungs. Surgery 1984;95:593–602. 55. Darling GE, Keresteci MA, Ibanez D, et al. Pulmo- 39. Baxter CR, Cook WA, Shires GT. Serum myocardial nary complications in inhalation injuries with associ- depressant factor of burn shock. Surg Forum 1966; ated cutaneous burns. J Trauma 1996;40:83–9. 17:1–3. 56. Herndon DN, Barrow RE, Linares HA, et al. Inhala- 40. Hilton JG, Marullo DS. Effects of thermal trauma on tion injury in burned patients: effects and treatment. cardiac force of contraction. Burns Incl Therm Inj Burns Incl Therm Inj 1988;14:349–56. 1986;12:167–71. 57. Navar PD, Saffle JR, Warden GD. Effect of inhalation 41. Papp A, Uusaro A, Parvianen I, et al. Myocardial injury on fluid resuscitation requirements after function and hemodynamics in extensive burn thermal injury. Am J Surg 1985;150:716–20. trauma: evaluation by clinical signs, invasive 58. Zak AL, Harrington DL, Barillo DJ, et al. Acute respi- monitoring, echocardiography, and cytokine ratory failure that complicates the resuscitation of concentrations. A prospective clinical study. Acta pediatric patients with scald injuries. J Burn Care Anesthesiol Scand 2003;47:1257–63. Rehabil 1999;20:391–9. 42. Adams HR, Baxter CR, Izenberg SD. Decreased 59. Hobson KG, Young KM, Ciraulo A, et al. Release of contractility and compliance of the left ventricle as abdominal compartment syndrome improves complications of thermal trauma. Am Heart J 1984; survival in patients with burn injury. J Trauma 2002; 108:1477–87. 53:1129–34. 43. Horton J, Maass D, White DJ, et al. Effect of aspira- 60. Sullivan SR, Ahmadi AJ, Singh CN, et al. Elevated tion pneumonia: induced sepsis on post burn orbital pressure: another untoward effect of massive cardiac inflammation and function in mice. Surg resuscitation after burn injury. J Trauma 2006;60: Infect (Larchmt) 2006;7:123–35. 72–6. 44. Huang YS, Yang ZC, Yan BG, et al. Pathogenesis of 61. Greenhalgh DG, Warden GD. The importance of in- early cardiac myocyte damage after severe burns. traabdominal pressure measurements in burned J Trauma 1999;46:428–32. children. J Trauma 1994;36:685–90.
  13. 13. Fluid Resuscitation 58162. Ivy ME, Possenti PP, Kepros J, et al. Abdominal prediction of mortality after burn injury. J Burn Care compartment syndrome in patients with burns. Res 2006;27:289–96 [discussion: 296–7]. J Burn Care Rehabil 1999;20:351–3. 78. Schiller WR, Bay CR, Garren RL, et al. Hyperdynamic63. Oda J, Ueyama M, Yamashita K, et al. Effects of resuscitation improves survival in patients with life escharotomy as abdominal decompression on threatening burns. J Burn Care Rehabil 1997;18:10–6. cardiopulmonary function and visceral perfusion in 79. Barton RG, Saffle JR, Morris SE. Resuscitation of abdominal compartment syndrome with burn thermally injured patients with oxygen transport patients. J Trauma 2005;59:369–74. criteria as goals of therapy. J Burn Care Rehabil64. Jensen AR, Hughes WB, Grewal H. Secondary 1997;18:1–9. abdominal compartment syndrome in children with 80. Holm C, Mayr M, Tegeler J, et al. A clinical random- burns and trauma: a potentially lethal combination. ized study on the effects of invasive monitoring on J Burn Care Res 2006;27:242–6. burn shock resuscitation. Burns 2004;30:798–807.65. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. 81. Higgins S, Fowler R, Callum J, et al. Transfusion Results from the international conference of experts related acute lung injury in patients with burns. on intra-abdominal hypertension and abdominal J Burn Care Res 2007;28:57–64. compartment syndrome. 1. Definitions. Intensive 82. Waters LM, Christensen MA, Sato RM. Hetastarch: Care Med 2006;32:1722–32. an alternative colloid in burn shock management.66. Ivy ME, Atweh NA, Palmer J, et al. Intra-abdominal J Burn Care Rehabil 1989;10:11–5. hypertension and abdominal compartment syndrome 83. Monafo WW, Halverson JD, Schechtman K. The role of in burn patients. J Trauma 2000;49:387–91. concentrated sodium solutions in the resuscitation of67. Hershberger RC, Hunt JL, Arnoldo BD, et al. patients with severe burns. Surgery 1984;95:129–34. Abdominal compartment syndrome in the severely 84. Monafo WW. The treatment of burn shock by the burned patient. J Burn Care Res 2007;28:708–14. intravenous and oral administration of hypertonic68. Latenser BA, Kowal-Vern A, Kimball D, et al. A pilot lactated saline. J Trauma 1970;10:575–86. study comparing percutaneous decompression with 85. Moylan JA, Reckler JM, Mason AD. Resuscitation decompressive laparotomy for acute abdominal with hypertonic lactate saline in thermal injury. compartment syndrome. J Burn Care Rehabil Am J Surg 1973;125:580–4. 2002;23:190–5. 86. Caldwell FT, Bowser BH. Critical evaluation of hyper-69. Saffle JR. The phenomenon of fluid creep in acute tonic and hypotonic solutions to resuscitate severely burn resuscitation. J Burn Care Res 2007;28: burned children. Ann Surg 1979;189:546–52. 382–95. 87. Jelenko C, Williams JB, Wheeler ML, et al. Studies in70. Goodwin C, Dorethy J, Lam V, et al. Randomized shock and resuscitation. I: use of a hypertonic trial of efficacy of crystalloid and colloid resuscita- albumin containing fluid demand regimen(HALFD) tion on hemodynamic response and lung water in resuscitation. Crit Care Med 1979;7:157–65. following thermal injury. Ann Surg 1983;197:520–8. 88. Shimazaki H, Yukioka T, Matuda H. Fluid distribution71. O’Mara MS, Slater H, Goldfarb W, et al. A prospec- and pulmonary dysfunction following burn shock. tive randomized evaluation of intra-abdominal pres- J Trauma 1991;31:623–8. sures with crystalloid and colloid resuscitation in 89. Oda J, Ueyama M, Yamashita K, et al. Hypertonic burn patients. J Trauma 2005;58:1011–8. lactated saline resuscitation reduces the risk of72. Sullivan SR, Freidrich JB, Engrav LH. Opioid creep abdominal compartment syndrome in severely is real and may be the cause of fluid creep. Burns burned patients. J Trauma 2006;60:64–71. 2004;30:583–90. 90. Elgjo GI, Traber DL, Hawkins HK, et al. Burn resus-73. Kaups KL, Davis JW, Dominic WJ, et al. Base deficit as citation with two doses of 4 ml/kg hypertonic saline an indicator of resuscitation needs in patients with dextran provides sustained fluid sparing: a 48 hour burn injuries. J Burn Care Rehabil 1998;19:346–8. prospective study in conscious sheep. J Trauma74. Cartotto R, Choi J, Gomez M, et al. A prospective 2000;49:251–65. study on the implication of a base deficit during fluid 91. Milner SM, Kinsky MP, Guha C, et al. A comparison of resuscitation. J Burn Care Rehabil 2003;24:75–83. two different 2400 mOsm solutions for resuscitation of75. Cochrane A, Edelman LS, Saffle JR, et al. The relation- major burns. J Burn Care Rehabil 1997;18:109–15. ship of serum lactate and base deficit in burn patients 92. Huang PP, Stucky FS, Dimick AR, et al. Hypertonic to mortality. J Burn Care Res 2007;28:231–40. sodium resuscitation is associated with renal failure76. Jeng JC, Jablonski K, Bridgeman A, et al. Serum and death. Ann Surg 1995;221:543–7. lactate not base deficit rapidly predicts survival after 93. Yowler CJ, Fratienne RB. Current status of burn major burns. Burns 2002;28:161–6. resuscitation. Clin Plast Surg 2000;27:1–10.77. Cancio LC, Galvez E, Turner CE, et al. Base deficit 94. Chung KK, Blackbourne LH, Wolf SE, et al. Evolution and alveolar-arterial gradient during resuscitation of burn resuscitation in operation Iraqi Freedom. contribute independently but modestly to the J Burn Care Res 2006;27:606–11.