Resuscitation
Along
with early excision and grafting, one of the central tenets of current
burn
care is fluid resuscitation of the burn victim. Many different methods have
been
proposed, all valid, but with no universal acceptance for one formula. They
vary
in their use of crystalloid and colloid components and are in continuing
evolution
as we understand the pathophysiology of the burn wound better. The
most
important principle in burn resuscitation is that any of these formulas are
only
guidelines and individual fluid requirements are to be judged by clinical and
hemodynamic
parameters as endpoints. Without adequate resuscitation, tissue
perfusion
suffers and the burn shock cascade is perpetuated. Delay to adequate
resuscitation
is one of the factors identified with increased mortality.
One
of the many functions of the skin is to maintain fluid and electrolyte
hemostasis.
After
burn injury, the integrity of skin is lost and leakage of plasma occurs.
This
is complicated by edema secondary to loss of endothelial integrity and
further
sequestration of fluid in tissues not directly affected by the burn itself.
Thermal
injuries of greater than 30% have been demonstrated to initiate a cascade
of
inflammatory mediators leading to capillary leak that lea ds to the anasarca
in
unburned areas and pulmonary edema. These mediators include histamine,
bradykinin,
and serotonin but the exact mechanism to initiate the cascade
has
not been elucidated. Attempts at modulation of the cascade are reported, but
have
not been successfully applied in a clinical setting. Adequate resuscitation
aims
to
counter these effects and reduce this process of postburn shock.
Intravenous
access should be established early in the initial evaluation of the
burn
patient after the airway has been secured according to standard trauma
protocols.
Peripheral,
large bore IVs provide excellent access and can actually administer
greater
volumes of fluid due to diminished resistance of the catheter secondary
to
a shorter length. Central venous access may be difficult to establish with the
crowding
of people around the torso of a newly arrived trauma victim, and also
carry
risks of pneumothorax or inability to control bleeding from inappropriate
placement.
In children it can be particularly difficult to establish intravenous access,
and
the intra-osseous route can be used emergently for fluids and medicines.
Calculations
of fluid requirements are based on the amount of body surface
involved
in second or third degree burns (not first-degree burns). The “Rule of
Nines”
has been used to estimate the body surface area burned (Fig. 3.1), but this
does
have limitations in the pediatric population where the head is proportionally
larger
than the body when compared to the adult. Modifications of this burn diagram
are
available (Fig 3.2) or nomograms are available as well (Fig 3.3) to calculate
body
surface area and percent burn. On a more practical note, knowing that
the patient’s palm (not the examiner’s) is
equal to 1% of total body surface, body
surface
area (BSA) burned can be estimated by “patting out” the burned areas
when
a quick evaluation is needed.
Resuscitation
Along
with early excision and grafting, one of the central tenets of current
burn
care is fluid resuscitation of the burn victim. Many different methods have
been
proposed, all valid, but with no universal acceptance for one formula. They
vary
in their use of crystalloid and colloid components and are in continuing
evolution
as we understand the pathophysiology of the burn wound better. The
most
important principle in burn resuscitation is that any of these formulas are
only
guidelines and individual fluid requirements are to be judged by clinical and
hemodynamic
parameters as endpoints. Without adequate resuscitation, tissue
perfusion
suffers and the burn shock cascade is perpetuated. Delay to adequate
resuscitation
is one of the factors identified with increased mortality.
One
of the many functions of the skin is to maintain fluid and electrolyte
hemostasis.
After
burn injury, the integrity of skin is lost and leakage of plasma occurs.
This
is complicated by edema secondary to loss of endothelial integrity and
further
sequestration of fluid in tissues not directly affected by the burn itself.
Thermal
injuries of greater than 30% have been demonstrated to initiate a cascade
of
inflammatory mediators leading to capillary leak that lea ds to the anasarca
in
unburned areas and pulmonary edema. These mediators include histamine,
bradykinin,
and serotonin but the exact mechanism to initiate the cascade
has
not been elucidated. Attempts at modulation of the cascade are reported, but
have
not been successfully applied in a clinical setting. Adequate resuscitation
aims
to
counter these effects and reduce this process of postburn shock.
Intravenous
access should be established early in the initial evaluation of the
burn
patient after the airway has been secured according to standard trauma
protocols.
Peripheral,
large bore IVs provide excellent access and can actually administer
greater
volumes of fluid due to diminished resistance of the catheter secondary
to
a shorter length. Central venous access may be difficult to establish with the
crowding
of people around the torso of a newly arrived trauma victim, and also
carry
risks of pneumothorax or inability to control bleeding from inappropriate
placement.
In children it can be particularly difficult to establish intravenous access,
and
the intra-osseous route can be used emergently for fluids and medicines.
Calculations
of fluid requirements are based on the amount of body surface
involved
in second or third degree burns (not first-degree burns). The “Rule of
Nines”
has been used to estimate the body surface area burned (Fig. 3.1), but this
does
have limitations in the pediatric population where the head is proportionally
larger
than the body when compared to the adult. Modifications of this burn diagram
are
available (Fig 3.2) or nomograms are available as well (Fig 3.3) to calculate
body
surface area and percent burn. On a more practical note, knowing that
the patient’s palm (not the examiner’s) is
equal to 1% of total body surface, body
surface
area (BSA) burned can be estimated by “patting out” the burned areas
when
a quick evaluation is needed.
The
modified Brooke and Parkland (Baxter) formulas are the most commonly
used
early resuscitation formulas at this time. They use 2-4 cc/kg/%BSA burn of
Lactated
Ringers solution respectively. The calculated needs are for the total fluids
to
be given over 24 h. Because of the previously mentioned fluid shifts in the
immediate
postburn period, one half of these calculated needs are given in the
first
8 h postinjury, and the remaining one half are administered in the next 16 h.
It
is important to remember that if resuscitation is delayed for a period that
“burn
time”
begins from the injury, not initiation of treatment, so it may be necessary to
administer
even larger volumes to catch up with needs. Again, these are only estimates
of
needs and fluid administration must be adjusted to maintain urine output
at 1/2-1 cc/kg/h.
For
example, a 70 kg person with a 50% TBSA burn resuscitated immediately
would
require between 7 and 14 liters of resuscitation fluid, at a rate of 437 cc/h-
875
cc/h for the first 8 h depending whether 2 or 4 cc/kg/%TBSA is chosen, respectively.
The
subsequent 16 h would need between 219 cc/h and 437 cc/h, again
based
on this same range. A more complex calculation, for a 60 kg person with a
75%
TBSA burn presenting 4 h postinjury resuscitated at 2 cc/kg/%TBSA would
require
1.125 liters/h for the first 4 h of resuscitation (the first 4.5 liters need to
be
given
over 8 h but because of the delay in instituting treatment, all of this volume
must
be given in the remaining 4 h of the initial segment of “burn time”).
Regardless,
clinical
condition and urine output must be the final determinants. Use of
albumin
in early resuscitation is currently not advocated with the understanding
that
increased capillary leak would allow the administered protein to pass to the
injured
tissues and actually increase osmotic pressure of the tissues and hence
edema.
Once endothelial integrity has been restored at 6-8 h postinjury, albumin
administration
may proceed to attempt to maintain plasma oncotic pressure. In
general,
minor burns (less than 15% BSA burn) do not require intravenous supplementation
and
can be managed with close attention to oral intake.
Continuing
fluid replacement must also take into account ongoing losses until
the
burn wounds and donor sites have healed as demonstrated by complete reepithelization.
After
the initial 24 h, approximate ongoing losses are 1 cc/kg/%BSA
burn
to be replaced in addition to standard maintenance fluids, again adjusted
based
on urine output and clinical evaluation. Electrolytes and protein will also
be
lost until the wound is closed and need appropriate replacement. Another
important
consideration
is the large volume of “insensible losses” burn patients suffer
secondary
to ventilators and the air-fluidized sand beds of up to one liter per
day.
Children
pose a special challenge to resuscitation efforts. Body composition of
a
child consists of relatively more free water compared to an adult and there is
also
a
relatively larger surface area per kilogram in a child, hence resuscitation
formulas
for
adults usually underestimate the needs of a child. Infants also have relatively
little
glycogen stores, so dextrose containing solutions must be added to
their
resuscitation fluids (D5LR). The Shriner’s Burns Institute-Galveston Branch
has
developed the resuscitation formula 5000 cc/m2 BSA
burn/24 h for resuscitation
and
2000 cc/m2 Total BSA maintenance fluids using Ringers lactate
solution;
again
one half of the resuscitation fluid is given in the first 8 h and the remainder
in
the subsequent 16 h. Monitor blood sugars and replace as necessary to keep
serum
glucose between 60 and 180 gm/dl. Subsequent fluid losses are replaced at
3750
cc/m2 BSA remaining open at any time and 1500 cc/m2 total
BSA for maintenance
fluids.
The
elderly and people with underlying cardiopulmonary dysfunction need
aggressive
monitoring with Swan-Ganz catheters to follow volume status. Inhalation
injuries
commonly require additional fluids to overcome additional evaporative
losses
from the respiratory tract, commonly as much as twice the estimated
needs
to resuscitate a similar pat ient without the respiratory component. In
addition
to the cutaneous manifestations of an
electrical burn injury, there is commonly
a
component of muscle injury with the release of nephrotoxic substances such as
myoglobin.
A positive urine dipstick for heme without visualization of intact red
cells
on microscopic exam points to diagnosis of this complication. To aid in
clearance
of
myoglobin, additional fluids, as well as to replace losses induced by diuretics
and
mannitol (an osmotic diuretic and free radical scavenger), may be needed
with
alkalinization of the urine. The formulas above include the use primarily of
Lactated
Ringers solution; however, in the setting of acute renal failure that results
from
inadequate resuscitation, the added potassium load becomes potentially
dangerous
and normal saline should b e substituted.
Despite
all attempts to control the edema formation postinjury, its occurrence
is
inevitable. Risk of associated complications need to be constantly monitored.
Delayed
airway compromise can occur as edema of the glottis forms, both from
inhalation
injury and the above-mentioned capillary leak. Previously soft compartments
in
burned extremities can develop elevated intracompartmental pressures
and
decreased tissue perfusion (compartment syndrome) requiring
escharotomies
at a later time as resuscitation proceeds.
Several
common electrolyte abnormalities occur during the initial postburn
period
and must be monitored and corrected. Calcium, magnesium and phosphorus
are
found to be low quite frequently, likely due to wound and renal losses
from
lowered levels of circulating albumin initially and subsequent altered bone
metabolism.
Changes in antidiuretic hormone (ADH) levels cause the body to
think
it is volume depleted, so the stimulation of thirst follows, leading to the
ingestion
of large amounts of free water. Unmonitored, this results in hyponatremia.
Hypernatremia
and hyperchloremia will result from overzealous use of normal
saline
(hypertonic) solutions. Hypokalemia results from ongoing renal losses,
while
hyperkalemia follows tissue loss and release of this intracellular ion as well
as
from renal failure.
It
cannot be overemphasized that any fluid resuscitation formula is only a
guideline
and
not a guarantee of adequate resuscitation. The principles of critical care,
correction
of any metabolic acidosis by improving tissue perfusion and good clinical
judgment should be the ultimate endpoints
of resuscitation.
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نوشته شده در تاریخ 1391/10/20 و در ساعت : 11:40 - نویسنده : departman-burn