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Fluid Resuscitation
of the Thermally
Injured Patient
Robert Cartotto, MD, FRCS(C)a,b,*

 KEYWORDS
  Burns  Fluid resuscitation  Fluid creep
  Burn shock  Parkland formula



Acute fluid resuscitation is fundamental to modern         IMPORTANT HISTORICAL DEVELOPMENTS
burn care. Plastic surgeons in many parts of the
world are involved in the acute care of thermally          Before the 1940s patients with moderate and large
injured 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 eventually
to acute fluid resuscitation. For decades, fluid           death in many cases. Two mass casualty fires in
resuscitation has been progressively streamlined           North America, the Rialto Theater fire in 1921
into 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 understanding
volume of fluid, which is then infused into the            of the burn shock process, and the need to treat
acutely burned patient, aiming to optimize a variety       this with early provision of intravenous fluid based
of somewhat loosely defined end points led chiefly         on burn size and weight of the patient.2,3 A host of
by 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 the
standing 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 Parkland
crystalloid resuscitation frequently provides              formula proposed by Baxter and Shires in 1967.7
substantial volumes of fluid, often in excess of           The Parkland formula, which is the dominant
that predicted by current formulas, resulting in           burn resuscitation strategy in North America
numerous edema-related complications (Fig. 1).             today, was derived from empiric experiments on
This phenomenon, coined ‘‘fluid creep’’ by Pruitt,1        burned dogs, and subsequent testing among
is now a topic that dominates most current discus-         several hundred human burn patients.7–9
sion of fluid resuscitation. It is increasingly recog-        Baxter explicitly stated that most burn patients
nized that fluid resuscitation is anything but             could be successfully resuscitated by providing
a rote, standardized process, and that there is an         fluid within the relatively narrow range of 3.7 to
urgent need for re-evaluation of existing resuscita-       4.3 mL/kg/% total body surface area (TBSA).10
tion approaches to avoid fluid creep. This article         After more than four decades of acceptance of
familiarizes plastic surgeons with current concepts        the Parkland formula as a cornerstone of burn
in burn shock and edema formation physiology               care, and despite the fact that this approach has
and current resuscitation strategies. An important         provided effective resuscitation that has markedly
theme throughout this article is the understanding         reduced the incidence of burn shock-induced
of why fluid creep is so prevalent, and what strat-        acute renal failure,11,12 several reports have
                                                                                                                  plasticsurgery.theclinics.com




egies 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.
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
Fluid Resuscitation              571




Fig. 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 the
stitial space. This depends on the properties of               interstitial space. The pp – pi counterbalances
the capillary membrane itself, especially the                  the opposing hydrostatic gradient (Pcap – Pi), so
surface area of the capillary membrane surface in              that edema does not normally develop. If pp
question (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 leaving
the 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.19
acid linkages between them and the density and                    s is the reflection coefficient and represents the
hydration of the ground substance in which these               degree of capillary membrane permeability. An
molecules are embedded. If the collagen frame-                 impermeable membrane has a s of 1, whereas
work is destroyed and the ground substance                     a freely permeable membrane has a s of 0. Normal
becomes more hydrated (eg, by burn injury fol-                 dermal capillaries have a s of 0.9.19
lowed by early edema formation), compliance
increases and the ease of fluid movement into
                                                               Altered Starling Forces in the Burn Wound
the interstitium increases.27,28
   Pcap – Pi is the gradient in hydrostatic pressure           Q is dramatically increased immediately, most
between the capillary pressure (Pcap) and the inter-           notably in the first 1 to 2 hours postinjury, but
stitial hydrostatic pressure (Pi). The gradient is             generally reaches a plateau by 24 hours, and
normally 10 to 12 mm Hg in dermis19 and is in                  then although remaining elevated above normal
a direction favoring fluid movement out of the                 gradually declines over the next few days.19,21,29
capillary 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 is
in Pi) pushes more fluid out and increases Q. Were             here the most important cause of edema. The
it not for an opposing force (the colloid osmotic              capillary membrane becomes permeable to
pressure gradient, described next), fluid would                many plasma proteins including albumin and
continually seep out of the capillary into the                 small-to-moderate sized globulins. In the dermis
interstitium.                                                  s drops numerically from 0.9 (nearly impermeable)
   pp – pi is the colloid osmotic pressure gradient            to 0.3 (highly permeable). This increase in capillary
representing the difference between the plasma                 permeability is most profound acutely and may
colloid osmotic pressure (pp) and the interstitial             remain elevated for several days postburn. The
colloid 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.19,25,29–31
the direction favoring fluid retention within the                 Kf increases following a burn injury, which
capillary because of the higher concentration of               means that fluid can more easily cross the capillary
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
Fluid Resuscitation            573



with fluid resuscitation. Simultaneous with the          used only as a guideline to determine an initial
acute reductions in plasma volume and CO,                rate of fluid infusion. The resuscitation rate and
systemic vascular resistance increases because           volume must be continually adjusted based on
of sympathetic-mediated peripheral vasoconstric-         the response of the patient (see Fig. 3). A second
tion and the effects of increased viscosity of the       important principle of Parkland-based crystalloid
blood because of hemoconcentration. The eleva-           resuscitation, which is frequently ignored by
tion in systemic vascular resistance is an addi-         modern burn clinicians but which was emphasized
tional factor that contributes to the acute              in two important consensus conferences,10,46,47 is
depression of CO.45 Organ perfusion, particularly        that resuscitation should use the least amount of
renal 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 and
eral 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’’ UO
slowly climbs back to normal and in patients with        is open to some debate. Unfortunately, in several
major 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 and
burn 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 not
re-expand the plasma volume, restore CO, and             been completely resolved is whether the desired
improve organ and tissue perfusion. It should be         UO of 0.5 to 1 mL/kg/h should be based on actual
evident from the foregoing discussion that crystal-      body weight or predicted body weight. The issue
loid resuscitation fluids, although necessary to         of what constitutes optimum UO is highly important
achieve the goal of restoring tissue perfusion, are      because more fluid delivery is needed to drive the
also subject to the altered Starling forces and as       UO to the higher end of any desired range, which
such, large amounts of the resuscitation fluid           also results in increased edema formation. The
necessarily end up as interstitial and cellular          body mass index of the average North American
edema fluid.                                             has been steadily increasing over the past several
                                                         decades48 and one wonders if this may be partly
CRYSTALLOID RESUSCITATION                                responsible for fluid creep, as clinicians try to
                                                         achieve higher and higher weight-based hourly
In 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 to
been the dominant strategy for several decades.          2 mL/kg/h in children weighing less than 30 kg,49
Most 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 UO
period (4 mL of Ringer’s lactate (RL) per kilogram       at approximately 0.5 to 1 mL/kg/h in adults and
body weight per percent TBSA burn with half the          1 to 1.5 mL/kg/h in children.50
volume 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 the
physiologic 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. Additional
fluid leaving the intravascular space, which then        fluid in the form of dextrose and water would be
accumulates in the interstitial space as edema fluid,    used to maintain UO. The amount of colloid
is 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 is
Second, the acute increase in capillary perme-           sufficient to re-expand the plasma volume in
ability (s) within and around the burn wound allows      most patients where the capillary leak would be
most plasma proteins to leave the vascular space         sealed by 24 hours, but recognized that in
and enter the interstitium during the first 24 hours,    a minority of patients colloid may not be effective
so 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 is
a fixed amount of 4 mL/kg/%TBSA burn should              frequently underemphasized in descriptions of
be 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
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
Fluid Resuscitation           575




Fig. 4. A patient with 65% TBSA full-thickness burns
and smoke inhalation who developed ACS and             Fig. 5. Extension of abdominal escharotomies to
required 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 than
20 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, definitive
mechanical ventilation with high peak airway pres-     treatment by decompressive laparotomy may
sures, worsening metabolic acidemia, and hemo-         be required.59,67,68 Mortality following surgical
dynamic instability).65 ACS is considered              decompression for ACS is reported to be between
secondary when there is no demonstrable intra-         50% and 100%.59,63,66,68
abdominal pathology,65 as in the case of a burn
where bowel and mesenteric edema and
increased peritoneal fluid are the cause of the        Why is fluid creep happening?
raised intra-abdominal pressures. Left untreated,      One observation is that clinicians treating burn
ACS is invariably fatal, and probably was the          patients do not devote adequate attention to the
cause of early ‘‘death due resuscitation failure’’     careful titration (and in particular the downward
before formal recognition of the syndrome. Ivy         titration) of fluids to keep UO within a tightly
and colleagues62 prospectively followed burn           controlled range, ideally at the lower end of the
patients with intra-abdominal pressure greater         accepted range.69 In some of the studies that
than 25 mm Hg and developed a score that indi-         described resuscitation volumes in excess of
cated that cumulative resuscitation volumes            Parkland predicted range, mean UOs during the
greater than or equal to 250 mL/kg were associ-        first 24 hours postburn exceeded 1 mL/kg/h in
ated with IAH and a high risk of ACS.62,66 When        most patients.13,14,16,17 Similarly, Cancio and
cumulative volumes reach 250 mL/kg or more             colleagues15 from the US Army Burn Center found
intra-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 reduced
to 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 center
romuscular relaxants and increased sedation in         setting by well-meaning emergency personnel
mechanically ventilated patients; extension of es-     may be a source of excessive fluids. In one study
charotomies on any anterior trunk burns (Fig. 5);      burn patients had received a mean of 2.5 L of RL
and possible judicious use of diuretics if adequate    within the mean delay of 2.8 hours between injury
intravascular volume can be confirmed by place-        and arrival to the burn center.14 Although
ment 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 entirely
a limited number of patients have found that in        account for the phenomenon of fluid creep. Other
some instances, IAH and possibly early ACS may         studies that have reported 24-hour resuscitation
be reversed by the insertion of peritoneal dialysis    volumes in excess of 4 mL/kg/% TBSA also
catheters to remove peritoneal fluid, but this         reported that the mean 24-hour UOs in these patients
does not treat the edema of the intra-abdominal        fell within the range of 0.5 to 1 mL/kg/h,15,18
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
Fluid Resuscitation            577



pH for at least 24 to 48 hours. One wonders if             and early edema formation. Whether this might
attempts to normalize these variables more                 translate to other benefits, such as improved
aggressively 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 plasma
contributory 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 potential
Although original resuscitation strategies, such as        for viral disease transmission and induction of
the Evans and Brooke formulas, provided colloids           transfusion-related acute lung injury.81 Use of
during the first 24 hours, concern about the loss          5% albumin is an acceptable alternative, and at
of capillary membrane integrity and leakage of             the author’s institution they begin an infusion of
delivered proteins into the interstitial space             50 to 100 mL/h of 5% albumin at 8 to 12 hours
progressively led to avoidance of colloids in the first    postburn in burns greater than 40% or as a form
24-hour period and reliance on a pure crystalloid          of ‘‘colloid rescue’’ when crystalloid volumes are
approach 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 colloid
with respect to colloid provision: (1) some believe it     solutions, such as Dextran, Pentastarch, or
should not be used before 24 hours, because of the         Hetastarch, in burn resuscitation has also been
loss of capillary integrity, which could allow accu-       described. Over two decades ago Demling and
mulation of the administered protein (and water)           colleagues,38 in an animal model, demonstrated
in 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 hemodynamic
that these help to maintain intravascular volume;4         variables and UO with significantly less fluid and
and (3) a third group takes an intermediate                significantly less nonburn tissue edema, than with
approach and gives colloids at 8 to 12 hours post-         RL alone. This was caused by an increase in
injury arguing that normal capillary permeability is       the colloid osmotic pressure gradient by the
restored in nonburn soft tissues by 8 to 12 hours          low-molecular-weight Dextran. Human studies
and that hypoproteinemia is the major cause of             involving small numbers of patients suggest that
ongoing 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 hours
compared crystalloids with early colloid in the first      of resuscitation.82 Until more data and experience
24 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, both
titrated to achieve a UO of 30 to 50 mL/h. The             HYPERTONIC SALINE RESUSCITATION
albumin-treated group achieved the desired UO
end point and had significantly higher echocardi-          The appeal of HTS in burn resuscitation stems
ography-measured cardiac index, with significantly         from its ability to shift water from the intracellular
less resuscitation fluid than the crystalloid-only         space into the extracellular compartment, and in
group. The albumin group, however, had signifi-            so doing, expand the intravascular space. The
cantly greater late lung water accumulation after          obvious benefits to the burn patient are the need
resuscitation. In a more recent study, O’Mara              for less fluid administration, and less generation
and colleagues71 randomized adult burn patients            of tissue edema. Indeed, the pioneers of HTS
to 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 were
adjustable infusion 75 mL/kg of fresh frozen               effective volume expanders that resulted in
plasma, with infusions in both groups titrated to          acceptable resuscitation with less fluid volume
achieve an hourly UO between 0.5 and 1 mL/kg/              and edema formation than when isotonic solutions
h. The colloid group required significantly less           were used.83–85 Subsequent studies have mostly
resuscitation fluid to achieve the UO end point,           confirmed these early findings.86–89 A consensus
which resulted in significantly lower peak intra-          on the most appropriate use of HTS during burn
abdominal and airway pressures in that group,              resuscitation has not been reached because of
presumably on the basis of less edema formation            the wide variations in the timing (bolus versus
in that group. From these two studies, it can be           continuous infusion), composition (HTS versus
safely 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
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.
Fluid Resuscitation              579



alone.70,71 Colloids may be instituted according to           11. Tremblay R, Ethier J, Querin S, et al. Veno-venous
the original recommendations of the Parkland                      continuous renal replacement therapy for burned
formula 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. A
at 12 hours postburn if fluid needs are greater                   biopsy of the use of the Baxter formula to resuscitate
than 120% predicted; Saffle’s69 protocol calls for                burns or do we do it like Charlie did? J Burn Care
albumin 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 well
than 2 hours; and Chung and colleagues94 recom-                   does the Parkland formula estimate actual fluid
mend 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 the
Monitor Edema, Especially                                         resuscitation of thermally injured patients. J Trauma
in 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 association
measurement of bladder pressures are important
                                                                  between fluid administration and outcome following
adjuncts 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 Parkland
or 500 mL/h).
                                                                  formula under fire: is the criticism justified? J Burn
REFERENCES                                                        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 interstitial
10. 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.
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.
Fluid Resuscitation              581


62. 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. Hyperdynamic
63. 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 Rehabil
64. 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 of
67. 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 hypertonic
68. 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 in
70. 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 distribution
71. 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 of
72. 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 Trauma
74. 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 of
75. 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 failure
76. 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.

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Fluid resuscitation burns 2009

  • 1. Fluid Resuscitation of the Thermally Injured Patient Robert Cartotto, MD, FRCS(C)a,b,* KEYWORDS Burns Fluid resuscitation Fluid creep Burn shock Parkland formula Acute fluid resuscitation is fundamental to modern IMPORTANT HISTORICAL DEVELOPMENTS burn care. Plastic surgeons in many parts of the world are involved in the acute care of thermally Before the 1940s patients with moderate and large injured 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 eventually to acute fluid resuscitation. For decades, fluid death in many cases. Two mass casualty fires in resuscitation has been progressively streamlined North America, the Rialto Theater fire in 1921 into 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 understanding volume of fluid, which is then infused into the of the burn shock process, and the need to treat acutely burned patient, aiming to optimize a variety this with early provision of intravenous fluid based of somewhat loosely defined end points led chiefly on burn size and weight of the patient.2,3 A host of by 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 the standing 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 Parkland crystalloid resuscitation frequently provides formula proposed by Baxter and Shires in 1967.7 substantial volumes of fluid, often in excess of The Parkland formula, which is the dominant that predicted by current formulas, resulting in burn resuscitation strategy in North America numerous edema-related complications (Fig. 1). today, was derived from empiric experiments on This phenomenon, coined ‘‘fluid creep’’ by Pruitt,1 burned dogs, and subsequent testing among is now a topic that dominates most current discus- several hundred human burn patients.7–9 sion of fluid resuscitation. It is increasingly recog- Baxter explicitly stated that most burn patients nized that fluid resuscitation is anything but could be successfully resuscitated by providing a rote, standardized process, and that there is an fluid within the relatively narrow range of 3.7 to urgent need for re-evaluation of existing resuscita- 4.3 mL/kg/% total body surface area (TBSA).10 tion approaches to avoid fluid creep. This article After more than four decades of acceptance of familiarizes plastic surgeons with current concepts the Parkland formula as a cornerstone of burn in burn shock and edema formation physiology care, and despite the fact that this approach has and current resuscitation strategies. An important provided effective resuscitation that has markedly theme throughout this article is the understanding reduced the incidence of burn shock-induced of why fluid creep is so prevalent, and what strat- acute renal failure,11,12 several reports have plasticsurgery.theclinics.com egies 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. 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. Fluid Resuscitation 571 Fig. 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 the stitial space. This depends on the properties of interstitial space. The pp – pi counterbalances the capillary membrane itself, especially the the opposing hydrostatic gradient (Pcap – Pi), so surface area of the capillary membrane surface in that edema does not normally develop. If pp question (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 leaving the 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.19 acid linkages between them and the density and s is the reflection coefficient and represents the hydration of the ground substance in which these degree of capillary membrane permeability. An molecules are embedded. If the collagen frame- impermeable membrane has a s of 1, whereas work is destroyed and the ground substance a freely permeable membrane has a s of 0. Normal becomes more hydrated (eg, by burn injury fol- dermal capillaries have a s of 0.9.19 lowed by early edema formation), compliance increases and the ease of fluid movement into Altered Starling Forces in the Burn Wound the interstitium increases.27,28 Pcap – Pi is the gradient in hydrostatic pressure Q is dramatically increased immediately, most between the capillary pressure (Pcap) and the inter- notably in the first 1 to 2 hours postinjury, but stitial hydrostatic pressure (Pi). The gradient is generally reaches a plateau by 24 hours, and normally 10 to 12 mm Hg in dermis19 and is in then although remaining elevated above normal a direction favoring fluid movement out of the gradually declines over the next few days.19,21,29 capillary 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 is in Pi) pushes more fluid out and increases Q. Were here the most important cause of edema. The it not for an opposing force (the colloid osmotic capillary membrane becomes permeable to pressure gradient, described next), fluid would many plasma proteins including albumin and continually seep out of the capillary into the small-to-moderate sized globulins. In the dermis interstitium. s drops numerically from 0.9 (nearly impermeable) pp – pi is the colloid osmotic pressure gradient to 0.3 (highly permeable). This increase in capillary representing the difference between the plasma permeability is most profound acutely and may colloid osmotic pressure (pp) and the interstitial remain elevated for several days postburn. The colloid 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.19,25,29–31 the direction favoring fluid retention within the Kf increases following a burn injury, which capillary because of the higher concentration of means that fluid can more easily cross the capillary
  • 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. Fluid Resuscitation 573 with fluid resuscitation. Simultaneous with the used only as a guideline to determine an initial acute reductions in plasma volume and CO, rate of fluid infusion. The resuscitation rate and systemic vascular resistance increases because volume must be continually adjusted based on of sympathetic-mediated peripheral vasoconstric- the response of the patient (see Fig. 3). A second tion and the effects of increased viscosity of the important principle of Parkland-based crystalloid blood because of hemoconcentration. The eleva- resuscitation, which is frequently ignored by tion in systemic vascular resistance is an addi- modern burn clinicians but which was emphasized tional factor that contributes to the acute in two important consensus conferences,10,46,47 is depression of CO.45 Organ perfusion, particularly that resuscitation should use the least amount of renal 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 and eral 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’’ UO slowly climbs back to normal and in patients with is open to some debate. Unfortunately, in several major 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 and burn 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 not re-expand the plasma volume, restore CO, and been completely resolved is whether the desired improve organ and tissue perfusion. It should be UO of 0.5 to 1 mL/kg/h should be based on actual evident from the foregoing discussion that crystal- body weight or predicted body weight. The issue loid resuscitation fluids, although necessary to of what constitutes optimum UO is highly important achieve the goal of restoring tissue perfusion, are because more fluid delivery is needed to drive the also subject to the altered Starling forces and as UO to the higher end of any desired range, which such, large amounts of the resuscitation fluid also results in increased edema formation. The necessarily end up as interstitial and cellular body mass index of the average North American edema fluid. has been steadily increasing over the past several decades48 and one wonders if this may be partly CRYSTALLOID RESUSCITATION responsible for fluid creep, as clinicians try to achieve higher and higher weight-based hourly In 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 to been the dominant strategy for several decades. 2 mL/kg/h in children weighing less than 30 kg,49 Most 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 UO period (4 mL of Ringer’s lactate (RL) per kilogram at approximately 0.5 to 1 mL/kg/h in adults and body weight per percent TBSA burn with half the 1 to 1.5 mL/kg/h in children.50 volume 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 the physiologic 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. Additional fluid leaving the intravascular space, which then fluid in the form of dextrose and water would be accumulates in the interstitial space as edema fluid, used to maintain UO. The amount of colloid is 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 is Second, the acute increase in capillary perme- sufficient to re-expand the plasma volume in ability (s) within and around the burn wound allows most patients where the capillary leak would be most plasma proteins to leave the vascular space sealed by 24 hours, but recognized that in and enter the interstitium during the first 24 hours, a minority of patients colloid may not be effective so 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 is a fixed amount of 4 mL/kg/%TBSA burn should frequently underemphasized in descriptions of be 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. 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. Fluid Resuscitation 575 Fig. 4. A patient with 65% TBSA full-thickness burns and smoke inhalation who developed ACS and Fig. 5. Extension of abdominal escharotomies to required 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 than 20 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, definitive mechanical ventilation with high peak airway pres- treatment by decompressive laparotomy may sures, worsening metabolic acidemia, and hemo- be required.59,67,68 Mortality following surgical dynamic instability).65 ACS is considered decompression for ACS is reported to be between secondary when there is no demonstrable intra- 50% and 100%.59,63,66,68 abdominal pathology,65 as in the case of a burn where bowel and mesenteric edema and increased peritoneal fluid are the cause of the Why is fluid creep happening? raised intra-abdominal pressures. Left untreated, One observation is that clinicians treating burn ACS is invariably fatal, and probably was the patients do not devote adequate attention to the cause of early ‘‘death due resuscitation failure’’ careful titration (and in particular the downward before formal recognition of the syndrome. Ivy titration) of fluids to keep UO within a tightly and colleagues62 prospectively followed burn controlled range, ideally at the lower end of the patients with intra-abdominal pressure greater accepted range.69 In some of the studies that than 25 mm Hg and developed a score that indi- described resuscitation volumes in excess of cated that cumulative resuscitation volumes Parkland predicted range, mean UOs during the greater than or equal to 250 mL/kg were associ- first 24 hours postburn exceeded 1 mL/kg/h in ated with IAH and a high risk of ACS.62,66 When most patients.13,14,16,17 Similarly, Cancio and cumulative volumes reach 250 mL/kg or more colleagues15 from the US Army Burn Center found intra-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 reduced to 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 center romuscular relaxants and increased sedation in setting by well-meaning emergency personnel mechanically ventilated patients; extension of es- may be a source of excessive fluids. In one study charotomies on any anterior trunk burns (Fig. 5); burn patients had received a mean of 2.5 L of RL and possible judicious use of diuretics if adequate within the mean delay of 2.8 hours between injury intravascular volume can be confirmed by place- and arrival to the burn center.14 Although ment 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 entirely a limited number of patients have found that in account for the phenomenon of fluid creep. Other some instances, IAH and possibly early ACS may studies that have reported 24-hour resuscitation be reversed by the insertion of peritoneal dialysis volumes in excess of 4 mL/kg/% TBSA also catheters to remove peritoneal fluid, but this reported that the mean 24-hour UOs in these patients does not treat the edema of the intra-abdominal fell within the range of 0.5 to 1 mL/kg/h,15,18
  • 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. Fluid Resuscitation 577 pH for at least 24 to 48 hours. One wonders if and early edema formation. Whether this might attempts to normalize these variables more translate to other benefits, such as improved aggressively 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 plasma contributory 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 potential Although original resuscitation strategies, such as for viral disease transmission and induction of the Evans and Brooke formulas, provided colloids transfusion-related acute lung injury.81 Use of during the first 24 hours, concern about the loss 5% albumin is an acceptable alternative, and at of capillary membrane integrity and leakage of the author’s institution they begin an infusion of delivered proteins into the interstitial space 50 to 100 mL/h of 5% albumin at 8 to 12 hours progressively led to avoidance of colloids in the first postburn in burns greater than 40% or as a form 24-hour period and reliance on a pure crystalloid of ‘‘colloid rescue’’ when crystalloid volumes are approach 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 colloid with respect to colloid provision: (1) some believe it solutions, such as Dextran, Pentastarch, or should not be used before 24 hours, because of the Hetastarch, in burn resuscitation has also been loss of capillary integrity, which could allow accu- described. Over two decades ago Demling and mulation of the administered protein (and water) colleagues,38 in an animal model, demonstrated in 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 hemodynamic that these help to maintain intravascular volume;4 variables and UO with significantly less fluid and and (3) a third group takes an intermediate significantly less nonburn tissue edema, than with approach and gives colloids at 8 to 12 hours post- RL alone. This was caused by an increase in injury arguing that normal capillary permeability is the colloid osmotic pressure gradient by the restored in nonburn soft tissues by 8 to 12 hours low-molecular-weight Dextran. Human studies and that hypoproteinemia is the major cause of involving small numbers of patients suggest that ongoing 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 hours compared crystalloids with early colloid in the first of resuscitation.82 Until more data and experience 24 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, both titrated to achieve a UO of 30 to 50 mL/h. The HYPERTONIC SALINE RESUSCITATION albumin-treated group achieved the desired UO end point and had significantly higher echocardi- The appeal of HTS in burn resuscitation stems ography-measured cardiac index, with significantly from its ability to shift water from the intracellular less resuscitation fluid than the crystalloid-only space into the extracellular compartment, and in group. The albumin group, however, had signifi- so doing, expand the intravascular space. The cantly greater late lung water accumulation after obvious benefits to the burn patient are the need resuscitation. In a more recent study, O’Mara for less fluid administration, and less generation and colleagues71 randomized adult burn patients of tissue edema. Indeed, the pioneers of HTS to 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 were adjustable infusion 75 mL/kg of fresh frozen effective volume expanders that resulted in plasma, with infusions in both groups titrated to acceptable resuscitation with less fluid volume achieve an hourly UO between 0.5 and 1 mL/kg/ and edema formation than when isotonic solutions h. The colloid group required significantly less were used.83–85 Subsequent studies have mostly resuscitation fluid to achieve the UO end point, confirmed these early findings.86–89 A consensus which resulted in significantly lower peak intra- on the most appropriate use of HTS during burn abdominal and airway pressures in that group, resuscitation has not been reached because of presumably on the basis of less edema formation the wide variations in the timing (bolus versus in that group. From these two studies, it can be continuous infusion), composition (HTS versus safely 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. 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. Fluid Resuscitation 579 alone.70,71 Colloids may be instituted according to 11. Tremblay R, Ethier J, Querin S, et al. Veno-venous the original recommendations of the Parkland continuous renal replacement therapy for burned formula 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. A at 12 hours postburn if fluid needs are greater biopsy of the use of the Baxter formula to resuscitate than 120% predicted; Saffle’s69 protocol calls for burns or do we do it like Charlie did? J Burn Care albumin 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 well than 2 hours; and Chung and colleagues94 recom- does the Parkland formula estimate actual fluid mend 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 the Monitor Edema, Especially resuscitation of thermally injured patients. J Trauma in 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 association measurement of bladder pressures are important between fluid administration and outcome following adjuncts 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 Parkland or 500 mL/h). formula under fire: is the criticism justified? J Burn REFERENCES 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 interstitial 10. 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. 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. Fluid Resuscitation 581 62. 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. Hyperdynamic 63. 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 Rehabil 64. 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 of 67. 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 hypertonic 68. 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 in 70. 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 distribution 71. 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 of 72. 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 Trauma 74. 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 of 75. 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 failure 76. 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.