Blood loss, Hypothermia and Transfusion in the Burn O'R'

1
Blood loss, Hypothermia and Transfusion in the
Burn O.R.

• Roy R. Danks, DO
• Assistant Professor of Surgery
• Trauma/Burns/Critical Care
• Director, Burn Unit

2
Objectives

• Review the pathophysiology of the burn wound
• Understand the changes in skin anatomy that make
  blood loss in the burn O.R. a reality
• Review resuscitation end-points
• Review indications for transfusion in the burn
  O.R.

3
Pathophysiology of the burn wound

• Thermal and chemical injuries cause drastic
  changes in the inherently protective properties
  of the skin
• Loss of skin integrity due to deep burns results
  in
• Ongoing fluid losses (evaporative losses)
• Attenuation of thermal control
• Increased risk of infection
• Hypercatabolism

4
Burn Wound Edema

• Burn wound edema occurs as a result of several
  factors
• Direct thermal injury to dermal vessels
• Inflammatory response by capillaries, resulting
  in capillary leak syndrome
• Ischemic zones near zones of coagulation/necrosis
• JV Kf Pc Pif) s (pp - pif)

5
Burn Wound Edema

• The edema of burn wounds is maximal at
  approximately 8 hrs post-burn (but may extend to
  24 hrs)
• In burns gt25 TBSA, edema occurs in non-burned
  tissues
• This results in massive fluid shifts
• Other tissue beds can become compromised because
  of this edema
• The gut, in particular, is at risk and bowel
  edema can result in abdominal compartment
  syndrome (ACS)
• At 24 hrs post-burn, capillaries leak less and
  fluids begin to mobilize
• This is dependent on several factors
• Burn size
• Adequacy of initial resuscitation
• Degree of inflammatory response

6
Burn Wound Edema

• JV Kf Pc Pif) s (pp - pif)
• JV ? Capillary filtrate
• Kf ? Capillary filtration coefficient
• Pc Pif ? capillary hydrostatic pressure and
  interstitial fluid hydrostatic pressure
• s ? osmotic reflection coefficient
• pp pif ? plasma (p) and interstitial fluid (if)
  colloid osmotic pressure

7
Fluid Resuscitation First 24 hrs

• Burn shock resuscitation should follow a
  predictable course
• Using the concensus formula, half of the
  calculated fluid is given over the first 8 hrs
  (when burn wound edema maximizes) and the other
  half over the next 16 hrs
• The formula, formerly known as the Parkland
  Formula, combines two well known formulas and
  allows for some variability based on the patients
  physiology and burn size

8
Fluid Resuscitation First 24 hrs

• Brooke Formula 2 mL/kg/TBSAB
• Parkland Formula 4 mL/kg/TBSAB
• Consensus Formula
• 2-4 mL/kg/TBSA Burn
• So 75 kg, 55 burn will need 16,500 mL in 24
  hrs or 8,250 mL over 8 hrs which is 1030 mL/hr
• This fluid rate is meant to MATCH the fluid being
  lost to the interstitium
• Giving more than this will contribute to a more
  negative Pif and thus will generate more wound
  edema without improving intravascular fluid
  volume
• Giving boluses will cause a rapid washout of
  the crystalloid into the interstitium again,
  intravascular volume will not be restored

9
Vascular changes in the burn wound bed

• Numerous vascular changes occur in burned skin
• Direct thermal injury results in the loss of
  millions of capillary beds? this contributes to a
  significant loss of RBC mass
• Indirect injury (collateral damage) to arterioles
  and venules occurs in the zone of ischemia
• Adequate resuscitation in the early injury phase
  can significantly reduce this phenomenon
• As wound healing begins, marked hypervascularity
  of the burn wound also begins the result is a
  rich vascular network? this network is in
  existance beneath the burn eschar

10
Early excision and grafting

• Prior to 1974 (or so), burn wounds were treated
  in an expectant manner
• Wounds were cared for with daily or every other
  day dressing changes
• The eschar was allowed to separate from the wound
  bed (this, through the activity of bacterial
  collagenases)
• Once separated, formal excision was under taken
  and grafting was completed
• This process would take several weeks
• Blood loss in this manner of treatment was low,
  but outcomes were extremely poor
• Significant scars, infectious and septic
  complications were rampant

11
Early excision and grafting

• In 1972 (in the U.S.), the concept of early
  excision and grafting was pioneered
• It was found that the earlier a burn was excised,
  the less infectious complications there would be
  and a better the cosmetic outcome was realized
• Early excision occurs at a time when the vascular
  supply to the wound bed is controlled
• Early excision ideally occurs prior to
  significant over-population of bacteria in the
  eschar
• In some institutions, early excision takes place
  within 24 hrs of admission? this significantly
  reduces blood loss
• Generally, early excision means within 72 hrs of
  burn injury
• Pt must be resuscitated and well perfused first

12
Loss of Red Cell Mass

• In burns of 15-40 BSA, FT, 12 of the red cell
  mass will be lost in the first 6 hrs post burn
  and as much as 18 in the first 24 hrs
• Severe burns will loose 1-2 of their red cell
  mass per day until the burn is healed

13
Why the loss of red cells?

• Acute red cell destruction (thermal injury)
• Burn-induced intrinsic and extrinsic alterations
  to the erythrocytes
• Morphology of red cells in non-burned circulation
  is altered
• Osmotic fragility and loss of membrane
  deformability
• Red cell lysis may lead to acute hemoglobinuria

14
Prediction of blood loss

• The amount of blood lost can be estimated using
  several known data points
• Age of the burn
• Size of the burn
• Depth of the burn
• Technique of excision
• Surface area to be excised
• Location (skin depth)

15
Prediction of blood loss
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How much can we afford to lose?

• Can be estimated using pre-operative values of
  Hematocrit and the estimation of blood volume
• Equation
• Acceptable losses Hct now Hct allowed X
  EBV
• Mean Hct

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Prevention of blood loss

• Early (within 24 hrs) excision
• Infiltration and tumescence
• Excision of extremities under tourniquet
• Topical agents
• Thrombin spray
• Fibrin spray
• Vasoconstrictor (phenylephrine and epi)

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Excision With Tourniquet
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End-points of resuscitation

• Relying on intra-operative hemoglobin levels as a
  transfusion trigger may be dangerous
• Hgb/Hct values lag behind actual losses
• Blood loss in any O.R. situation should be viewed
  as an ongoing resuscitation situation
• Efforts should focus on
• Limiting losses (the surgeon)
• Proactive resuscitation (anesthesia) AND, most
  importantly COMMUNICATION between the surgeon
  and the anesthesiologist/CRNA

20
End-points of resuscitation

• Traditional end-points of fluid resuscitation
  are
• Urine output
• Heart rate
• Blood pressure (SBP and MAP)
• CVP

21
End-points of resuscitation

• Traditional end-points of fluid resuscitation
• Using these traditional end-points presents
  several problems
• When these parameters are abnormal, uncompensated
  shock is present
• However, even after normalization of these
  parameters, up to 85 of severely injured trauma
  patients still have evidence of inadequate tissue
  oxygenation based on the findings of inadequate
  tissue oxygenation, ongoing metabolic acidosis or
  evidence of gastric mucosal ischemia
• This condition is best termed compensated
  shock numbers look good, but the cells remain
  hypoxic

22
End-points of resuscitation

• Newer end-points
• Base deficit and pH
• Serum lactate

23
End-points of resuscitation

• Base deficit, serum lactate and pH
• Sensitive predictor of tissue perfusion
• Readily obtained
• Easily repeated (ERMA in burn unit)
• Has repeatedly been shown to predict outcome in
  acutely injured patients
• Can be used to watch trends in blood loss during
  the case
• A persistent acidosis in the face of ongoing
  blood loss indicates ill-perfused tissue
• The response to this should be volume infusion
  and replacement of lost RBC volume
• Packed red cells, FFP and crystalloids all have a
  role in replacement

24
Acidosis

• This is the most prominent physiologic defect
  arising from persistent hypo-perfusion
• It is a metabolic derangement
• When the oxygen debt occurs, the cell shifts from
  aerobic to anaerobic metabolism
• Lactic acid is produced
• Severity of lactic acidosis can be used to
  predict outcome in critically ill patients

25
Lactic Acid
26
Lactate in Acidosis

• Correlation of serum lactate and outcome
• Lactate levels of gt4.4 mmol/L are associated with
  a 75 mortality in critically ill patients
• Of patients who clear their lactate in 24 hrs,
  100 survive
• Patients who fail to clear their lactate in 48
  hrs have only a 14 survival rate

27
BD vs Lactate

• Base deficit
• Normal values -3 to 3 mmol/L
• Test is expedient and sensitive
• Measures the degree and duration of inadequate
  perfusion
• May remain abnormal when a hyperchloremic
  acidosis is present

• Serum Lactate
• Normal is lt 2 mmol/L
• Not available in all labs
• Slow to clear with hepatic insufficiency
• Very good predictor of outcome

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Burn Resuscitation and BD

• J Burn Care Rehabil. 1998 Jul-Aug19(4)346-8.
• Base deficit as an indicator or resuscitation
  needs in patients with burn injuries.Kaups KL,
  Davis JW, Dominic WJ.Department of Surgery,
  UCSF/Fresno, University Medical Center, USA.The
  utility of base deficit (BD) as a marker of shock
  and as an indicator of resuscitation requirements
  has been recognized in the trauma population.
• Base deficit in thermally injured patients has
  not been closely examined..
• Parkland estimated fluid requirements
  underestimated actual volume requirements, but
  Parkland-calculated fluid requirements were
  related (p lt 0.01) to actual volume requirements.
  
• BD had a better correlation to actual volume
  requirements, and a BD of -6 or less correlated
  with larger burn size (23 /- 2 vs 47 /- 9
  total body surface area), and markedly increased
  mortality rate (9 vs 72, p lt 0.001).

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BD and Transfusion

• J Trauma 1996 Davis et al
• Admission Base Deficit Predicts Transfusion
  Requirements and Risk of Complications
• Retrospective review of 2,954 trauma patients at
  a Level I center
• Found that, as admission BD increases (becomes
  more negative), transfusion becomes more likely
  and ICU and hospital LOS is increased
• Pts with a BD of lt/ -6 should undergo type and
  cross-match rather than screen

30
BD and Transfusion

• BD and PRBC usage
• Normal BD? ave 0.5 units/first 24 hrs, 1.4 total
• Mild (-3 to -5)? ave 1.4 units/first 24 hrs, 2.6
  total
• Moderate (-6 to -9)? 3.8 units/first 24 hrs, 5.3
  total
• Severe (-10 or worse)? 8.3 units/first 24 hrs and
  9.7 units total

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Hypothermia The Problem

• Hypothermia in the thermally injured patient
  begins in the field and continues to be a problem
  until the patients wounds are completely closed
• Hypothermia in the O.R. is a preventable problem
• Hypothermia results in physiologic abberations
  which contribute to blood loss and ill-perfusion

32
Hypothermia

• Thermal regulation is maintained by three
  mechanisms
• Resetting of the hypothalamic set point
• Vasoconstriction (cold) and vasodilation (hot)
• These are skin level controls which are lost in
  large burns
• Shivering
• This mechanism of rewarming is lost in the
  chemically paralyzed burn patient

33
Thermoregulation in Burn Patients

• Three components to regulation
• Afferent limbs
• Central regulatory limbs
• Efferent limbs
• Ad C Fibers
• Present in the skin and most other tissues of the
  body (including deep tissues)
• Loss of insulation

34
Thermoregulation in Burn Patients

• Burn pts perceive changes in ambient temp as well
  as controls
• An increase in gradient ambient temp to skin temp
  results in radiant heat loss which results in the
  sensation of cold
• Metabolic rate changes based on the sensation of
  cold
• Burn pts will respond with a brisk increase in
  heat generation and metabolic rate during these
  periods of perceived cold discomfort
• Their metabolic losses can exceed 3,500 kcal/day
• They cannot retain the heat generated because of
  loss of insulation

35
Threshold

• In normal individuals, the threshold range for
  set point is 36.5-37.5C
• In burn patients this is higher and is
  proportional to the size of the burn
• Caldwell, et al showed that the threshold
  increases by 0.03 C per TBSA burn

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Prevention of Hypothermia

• This begins in the Burn Unit with ambient
  temperature control
• A cold burn patient leaving the burn unit, will
  be colder on arrival in the cold O.R.
• Increasing the room temperature is the single
  most important step in preventing ongoing
  heat-loss
• Administration of warm fluids will help to
  maintain body temperature
• Warm fluids alone will not significantly raise
  body temperature

37
Prevention of Hypothermia

• Keeping room temp up is especially important in
  the pediatric burn OR

38
Modalities to Re-warm
39
Effects of Hypothermia Coagulation

• The enzymes of coagulation are significantly
  temperature dependent
• Platelets, too, require a narrowly maintained
  temperature range in order to function properly
• The coagulopathy of hypothermia results from
• Slowing of enzyme kinetics, despite normal levels
  of the factors
• Reversible platelet dysfunction
• Vascular dynamics
• Clotting factor activation

40
Hypothermia

• First recognized in association with hypothermia
  in cardiopulmonary bypass patients (Harker, et
  al, 1980)
• Enzymatic reactions of coagulation are well known
  to be temperature dependent
• The most likely clotting factor involved is
  thromboxane B2 (from platelets) which has a
  temperature-dependent function curve.
  Thromboxane synthetase is probably inhibited by
  hypothermia.
• Skin cooling causes a reversible platelet
  dysfunction

41
Combining the Insults

• Hypothermia, Acidosis and Coagulopathy
• The Triad of Death
• Is well appreciated in the critically injured
  trauma patient
• Is well established in the burn O.R.
• This lethal combination results in a downward
  spiral from which poor outcomes result

42
The Bloody Viscious Cycle
43
Outcomes in Cold patients

• A single, prospective, randomized human subject
  trial has been published
• 57 hypothermic (lt34.5C) critically injured
  patients were randomized to
• Continuous arteriovenous rewarming (n29)
• Standard rewarming (n28)
• Primary outcomes First 24-hr blood product and
  fluid resuscitation requirements

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Results

• 2 (7) of the CAVR patients failed to rewarm to
  36C both died
• 12 of 28 patients undergoing standard re-warming
  failed to rewarm to 36 C all 12 died
• CAVR patients required less total fluid
• 24,702 mL vs 32,540 mL
• Is Hypothermia in the Victim of Major Trauma
  Protective or Harmful? Gentilello, et al. Ann
  Surg. 1997226439-449

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Coagulopathy

• In trauma patients and hemorrhaging surgical
  patients, the coagulopathic state is caused by 4
  factors
• Dilution of plasma (with crystalloids)
• Consumption of coagulation products in clot
  formation and early DIC
• Hypothermia
• Massive blood transfusion

46
Prevent and Treat the Vicious Cycle

• Warm fluids
• Warm room
• LR instead of Normal saline
• Hyperchloremia has been shown to decrease renal
  blood flow and glomerular filtration rate in an
  isolated kidney model, suggesting that large
  volumes of NS could have an adverse effect on
  renal function

47
Transfusion

• Massive transfusion of red blood cells (RBCs)
  plus crystalloid has been associated with a
  transient but significant hypocoagulable state
  due to dilution of platelets and coagulation
  factors
• American Society of Anesthesiologists guidelines
  indicate that transfusion is rarely necessary at
  a hgb of 10 g/dL (or greater) and is almost
  always indicated at a Hgb of 6 g/dL or less

48
Transfusion in Burns

• Blood loss during the excision of large burns is
  a given
• The amount to be lost, based on burn sized being
  excised and amount that can be lost is easily
  calcuated
• Replacement of blood loss with crystalloids is a
  temporizing measure
• PRBCs are not good volume expanders, however
• Combining crystalloids, colloids and PRBCs will
  help to replace losses

49
Proposed Transfusion Protocol

• In an effort to decrease volume of crystalloid
  administered
• Maintain normal coagulation profile
• Replenish lost plasma volume
• Administer at a ratio of 11
• PRBCsFresh Frozen Plasma

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Summary

• Hypothermia is a common problem in burn patients
  and is caused by several preventable and
  unpreventable mechanisms
• Hypothermia results in coagulopathy due to
  platelet and clotting enzyme dysfunction
• Ill-perfused tissue beds results in acidosis and
  this contributes to the vicious cycle that
  results in coagulopathy and ongoing blood loss
• Keeping the pt warm from the beginning, keeping
  up with losses and properly resuscitating during
  OR will improve outcomes