Burn - Fluid ResuscitationAlamsyah Ambo Ala Husain

ObjectivesIdentify post-burn fluid requirementsList common complications of burn injury and resuscitation therapyIdentify patients requiring special fluid managementList the burn injuries that require a referral to a burn center.

Fluid ResuscitationGoal of Fluid ResuscitationThe goal of fluid resuscitation is to maintain tissue perfusion and organ function while avoiding the complications of inadequate or excessive fluid therapy.

PathophysiologyPlasma loss and vascular responsesIntravascular volume lossDiminished tissue perfusionRelease of vasoactive agentsCapillary semipermiability LostMoving of fluids and substances like proteins from the intravascular to interstitial spaceHyperemiaHypovolemia

Hemodynamic changes Lessened circulating blood volume results in decreased cardiac output initially and increased pulse rate. There is a decreased stroke volume as well as a marked rise in peripheral resistance (due to constriction of arterioles and increased hemoviscosity). This results in inadequate tissue perfusion, which may in turn cause acidosis, renal failure, and irreversible burn shock.

Hemodynamic Electrolyte imbalance may also occur. Hyponatremia usually occurs during the 3rd to 10th day due to fluid shift. The burn injury also causes hyperkalemia initially due to cell destruction, followed by hypokalemia as fluid shifts occur and potassium is not replaced.

Classification of burn injuries. Available at www.burn-recovery.org/injuries.htm.Accessed September 4, 2008.Classification made by size & depth of injuryMagnitude of injury based on size/depth of burn & patients prior health statusof great importance in the overall plan of care Care management & appropriate referral to a burn center based on this assessment Patient age & size of burn are principal survival determinants. Most at risk: < 2, > 60 y.o.multiple traumapreexisting co-morbidities

Classification of Burn Depth

Circulatory Management

Assess extent, depth of burnvarying degrees of tissue damage, cellular impairment, fluid shifts < 20% TBSA, actions usually limited to the burn siteTBSA > 20%, local response becomes systemicFluid resuscitation calculated for estimated TBSA of burnplasma volume loss hypovolemia shock potentialParkland formula a commonly used guidelineAdjust fluid replacement type/volume to the patients response adequate when HR and BP within normal limits for ageurine output = 0.5 ml/kg/hr for adults;1 -1.5 ml/kg/hr for infants

Fluid ResuscitationFluid resuscitation needs are estimated needs based on the body size and extent of the burn injury.After using a established fluid resuscitation guide to start the resuscitation you must adjust the infusion rates based on the patients response.

Fluid Therapy1 or 2 large bore IV linesFluid replacement based on: size/depth of burnage of pt.individualized considerations.

options- RL, D5NS, dextam, albumin, etc.there are formulas for replacement: Parkland formula Brooke formula

Fluid TherapyBurns < 15% can be resuscitated orally (unless patient has an electrical injury or associated trauma)Burns 15-40% need at least one large bore IV line in upper extremityBurns > 40% need two large bore IV lines in upper extremities

Fluid ResuscitationParkland Burn FormulaAdults Ringers Lactate 2-4 cc X Kg of body weight X percent burn (2nd and 3rd)Children - Ringers Lactate 3-4 cc X Kg of body weight X percent burn (2nd and 3rd)

First : over 1st 8 hours post burnSecond : over next 16 hours post burn

FormulaFluid in First 24 HoursCrystalloid in Second 24-Hours Colloid in Second 24-HoursParklandRL at 4 mL/kg per percentage burn20-60% estimated plasma volumeTitrated to urinary output of 30 mL/hEvans (Yowler, 2000)NS at 1 mL/kg per percentage burn, 2000 mL D5W*, and colloid at 1 mL/kg per percentage burn50% of first 24-hour volume plus 2000 mL D5W50% of first 24-hour volumeSlater (Yowler, 2000)RL at 2 L/24 h plus fresh frozen plasma at 75 mL/kg/24 hBrooke (Yowler, 2000)RL at 1.5 mL/kg per percentage burn, colloid at 0.5 mL/kg per percentage burn, and 2000 mL D5W50% of first 24-hour volume plus 2000 mL D5W50% of first 24-hour volumeModified BrookeRL at 2 mL/kg per percentage burnMetroHealth (Cleveland)RL solution with 50 mEq sodium bicarbonate per liter at 4 mL/kg per percentage burnHalf NS titrated to urine output1 U fresh frozen plasma for each liter of half NS used plus D5W as needed for hypoglycemiaMonafo hypertonic Demling250 mEq/L saline titrated to urine output at 30 mL/h, dextran 40 in NS at 2 mL/kg/h for 8 hours, RL titrated to urine output at 30 mL/h, and fresh frozen plasma 0.5 mL/h for 18 hours beginning 8 hours postburnOne-third NS titrated to urine output

Fluid ResuscitationPediatric PatientsPedi patients have a greater surface area in relation to body mass so they require greater amounts of fluid resuscitation, relatively speaking, BUT, this same surface area to body mass ratio reflects a smaller intravascular volume to surface area burned.

This makes the burned child more susceptible to fluid overload and hemodilution.

Fluid ResuscitationPediatric PatientsHypoglycemia may occur if the limited glycogen stores of the burned child are rapidly exhausted by the early post-burn elevation of circulating levels of steroids and catecholamines.

Monitor blood glucose levelsMaintenance solutions should contain glucose such as D5 NS or D5 NS.

Fluid ResuscitationMonitoring of Fluid ResuscitationRemember it is easier during resuscitation to infuse additional fluid as needed than to remove excess fluid.Goal is to minimize both volume and salt loading, prevent acute renal failure, pulmonary and cerebral edema while infusing enough volume to maintain tissue perfusion and organ function.

Fluid ResuscitationMonitoring Fluid ResuscitationFrequent assessment of the patients mental status (anxiety and restlessness are early signs of hypovolemia and hypoxemia)Frequent assessment of the patients urinary output (at least hourly)

Fluid ResuscitationHourly Urinary Output

Adults: 0.5 cc per Kg per hour (30-50cc/hr)Children

Fluid ResuscitationManagement of OliguriaOliguria, in association with an elevation of systemic vascular resistance and reduction in cardiac output is most frequently the result of inadequate fluid administration.Increase the fluid infusion rate!!

Fluid ResuscitationManagement of Hemochromogenuria(Red Pigmented Urine)Results from significant amounts of myoglobin and hemoglobin in the urine.Increase the fluid rate to maintain a UO of 1-1.5cc/Kg/hr (adult-approx 75-100cc/hr)Last resort add 12.5 gms of Mannitol to each liter of fluid Hourly UO no longer reliable for measure of resuscitation.

Fluid ResuscitationManagement of Hemochromogenuria(Red Pigmented Urine)Causes:High voltage electrical burn with associated soft tissue injuryCompartment SyndromeSince heme pigments are more soluble in an alkaline medium, sodium bicarbonate can be added to your resuscitation fluids to maintain a slightly alkaline urine.

Fluid Resuscitation

Are Blood Pressure and Heart Rate reliable indices of fluid resuscitation for the burn patient?

Fluid ResuscitationNO!BP can be misleading in the burned limb in which progressive edema formation occurs. Increasing edema = diminishing signal which can cause a misinterpretation of the BP.How about the HR?

Fluid ResuscitationNO!HR is also of limited usefulness in monitoring fluid therapy in the burn patient.A tachycardia of 100-120 is common in adult burn patients who are adequately hydrated. The level of tachycardia in pediatric patients depend upon their normal heart rate.

Fluid ResuscitationH & H (Hematocrit and Hemoglobin) and Serum Chemistries should be obtained as a baseline but remember that during the first 24 hours post burn the H & H levels are not a reliable guide to resuscitation. Blood infusions should only be considered for pre-existing conditions or blood loss from associated trauma at the time of the injury.

Fluid ResuscitationBaseline serum chemistries should be obtained in burn patients with serial chemistries done to measure the patients response to treatment.

Treat hyperkalemia and any other electrolyte abnormalities as needed.

SummaryUse the rule of 9s to accurately approximate the TBSA and use an established fluid resuscitation formula to calculate the fluid needs for the first 24 hoursInfants and young children will need maintenance fluids that have dextrose in addition to the resuscitation fluid calculated above

SummaryFrequent monitoring and observation of the burn patient for:Hourly urine outputThe patients general condition, including mental statusBaseline determination of hemaocrit, hemoglobin, serum chemistries and ABGs. Repeat studies as indicatedThe fluid infusion rate should be increased or decreased by 1/3 if the UO falls below or exceeds the desired level by more than 1/3 for 2-3 hours.

Burn Center Treatment ReferralPartial thickness burns 10% of total body surface area (TBSA)Full-thickness burns, any age group Burns of face, hands, feet, major joints, perineum, genitalia that can result in cosmetic/functional disabilityElectrical burns, lightning injuryChemical burnsInhalation injury

Partial-thickness hydrofluoric acid burn(Urden et al., 40.4, 2006)

Burn Center ReferralPatients with preexisting conditions that increase risk of death cardio/pulmonary, diabetes, renalBurn injury accompanied by other trauma Burned children in facility lacking qualified pediatric practitioners/equipment Patients who require special social, emotional, or long-term rehabilitative intervention

Flame burns on child (Evans, 18.3, 2007)

Care of B U R N SB - breathingU - urine outputR - rule of nines resuscitation of fluidN - nutritionS - shock silvadene

Questions?

*******A burn is an injury resulting in tissue loss or damage. Injury to tissue can be caused by exposure to thermal, electrical, chemical, and/or radiation sources. The temperature or causticity of the burning agent and duration of tissue contact with the source determine the extent of tissue injury. Tissue damage can occur at varying temperatures, usually between 40 and 44 C and above. The burn wound itself is responsible for both the local and systemic effects seen in the burned patient.[5] Tissue damage is caused by enzyme malfunction and denaturation of proteins. Prolonged exposure or higher temperatures can lead to cell necrosis and a process known as protein coagulation. The areas extending outward from this central area of injury sustain varying degrees of damage and are identified by zones of injury.[5]

Patient Age and History Age and history are significant determinants of survival. Patients considered most at risk are those younger than 2 years and those older than 60 years. History of inhalation injury and electrical burns, and all burns complicated by trauma and fractures, considered major injuries, significantly increase mortality. Obtaining a past medical history is important, particularly a history relating to cardiac, pulmonary, and renal disorders, as well as diabetes and central nervous system disorders.

(Urden et al., 2006). **The body responds to the burn injury with varying degrees of tissue damage, cellular impairment, and fluid shifts. A brief decrease in blood flow to the affected area is followed by a marked increase in arteriolar vasodilation. Damaged tissues release mediators that initiate an inflammatory response. Histamine, serotonin, prostaglandin derivatives, and the complement cascade are all activated. Release of proinflam-matory mediators combined with vasodilation causes increased capillary permeability, then intravascular fluid loss and wound edema. For burn injuries less than 20% TBSA, these actions are usually limited to the burn site. As the affected TBSA goes beyond 20%, local response becomes systemic. Hypoproteinemia resulting from increased capillary permeability aggravates edema in nonburned tissue. Basal metabolic rate increases from insensible fluid loss, which along with fluid shift produces hypovolemia. Capillary permeability increases for 2 to 3 weeks with the most significant changes occurring in the first 24 to 36 hours.[2] [,6] [,10] [,11]

Initially blood viscosity increases when hematocrit rises secondary to vascular fluid shifts into the interstitium. Because of a marked increase in peripheral resistance, decreased intravascular fluid volume, and increased blood viscosity, cardiac output falls. Capillary leak and depressed cardiac output can depress central nervous system function, causing restlessness, followed by lethargy, and finally coma. Decreased cardiac output, blood volume, and intense sympathetic response decrease perfusion to the skin, viscera, and renal perfusion. Levels of thromboxane A2, a potent vaso-constrictor, have been shown to be significantly increased in burned patients and contribute to mesenteric vasoconstric-tion and decreased splanchnic blood flow. Decreased flow can convert a zone of stasis to zone of coagulation, which increases depth of the burn. Decreased circulating plasma with increased hematocrit can cause hemoglobinuria, which can lead to renal failure. Immediate hemolysis of red cells occurs, with the life span of remaining red cells reduced by approximately 30% of normal. Platelet count and platelet survival time initially drop drastically then continue to decrease for 5 days after injury. This period is followed by a rebound increase in platelets over the next 2 to 3 weeks.[2] [,6] [,10] [,11] Cardiovascular changes begin immediately after a burn; their extent varies with burn size and presence of additional injuries. Patients with an uncomplicated burn less than 15% TBSA can usually be treated with oral fluid resuscitation. Burns that surpass 20% TBSA have massive shifts of fluid and electrolytes from the intravascular to extravascular space. This shift begins to resolve in 18 to 36 hours; however, normal extracellular volume is not completely restored until 7 to 10 days after the burn. If intravascular volume is not replenished, hypovolemic shock occurs. If untreated the patient dies of cardiovascular collapse. Inadequate treatment also leads to renal failure from acute tubular necrosis.TBSA burns 40%: Major burn injury can compromise all major body systems. Intravascular volume depletion as a result of major burn injury favors development of hypo-perfusion of burned areas and renal vasculature. Severe volume depletion leads to shock and may contribute to ARDS. Over-hydration aggravates edema and can lead to electrolyte disturbances. Over-hydration in the patient with cardiac disease can cause abdominal compartment syndrome, CHF, cerebral edema, and even death. Excess fluid cannot be compensated for by decreasing the IV rate in subsequent hours because the fluid is already out of the vascular space. (UCD Rx)************************Scar contracture is the primary cause of functional deficits in the patient with a burn. A contracture is essentially a shortening of a scar over a joint surface, limiting joint mobility ( Leman and Ricks, 1994 ). During the acute/wound care phase of recovery, the patient with a burn can experience intense pain, which inhibits movement. The patient tends to assume a comfortable position, usually flexed, which may predispose the new collagen fibers in wounds to fuse together in a shortened length ( Johnson, 1994 ). Early splinting, ROM exercises, positioning, and use of pressure garments with flexible inserts over joint surfaces aid in the development of parallel fibers and maintaining soft-tissue length ( Helm and Fisher, 1998 ). When a contracture does develop, serial casting and dynamic splints that exert a constant stretch on the joint can help reverse the problem. Some contractures will require surgical release to restore functional mobility ( Leman and Ricks, 1994 ).The location, extent, and depth of the injury are factors that affect the presence and extent of burn scar contractures. Specific anticontracure positions are used to align the extremities, neck, and trunk ( Figure 18-3 )***