Resuscitation burn

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.