Fluid resuscitation burns 2009

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


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


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


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.


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
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