Massive Transfusion 848th FST

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Massive Transfusion848th FST
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-The lethal factor in shock is the irreversible
anoxic cellular injury that kills a critical mass
of cells.-Inadequate cellular oxygen delivery
via the microcirculation leads to this
irreversible cellular damage.-Successful
resuscitation requires restoration of cellular
oxygenation via increasing blood flow to
microcirculation
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Introduction

• The lethal factor in shock is the irreversible
  anoxic cellular injury that kills a critical mass
  of cells
• Inadequate cellular oxygen delivery via the
  microcirculation leads to this irreversible
  cellular damage
• Successful resuscitation requires restoration of
  cellular oxygenation via increasing blood flow to
  microcirculation

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Hemorrhage (Hemorrhagic shock)

• Most common form of shock to affect trauma
  patients.
• Due to inadequate blood flow for tissue
  oxygenation.
• Caused by
• External blood loss
• Occult blood loss
• Inadequate resuscitation
• Aortic or great vessel injury

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Hemorrhagic shock

• Diagnosed by
• Tachycardia
• Hypotension
• Cool clammy skin
• Decreased loc
• Low urine output

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Classification of HemorrhageAmerican College of
Surgeons Committee on TraumaAdvanced Trauma Life
Support Program (1989)

• Class I hemorrhage Loss as much as 15 of blood
  volume minimal physiologic change
• Class II hemorrhage 15-30 blood volume loss
  associated with modest elevation in heart rate
  and decreases in pulse pressure as diastolic
  pressures rise and systolic pressures tend to
  maintain
• Capillary refill time tend to me slightly
  retarded
• Urinary output mildly decreased (lt.5ml/kg/hr)
• Slightly orthostatic, anxious, hostile

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Classification of hemorrhage

• Class III hemorrhage 30-40 blood volume loss
• Tachycardia, systolic and diastolic hypotension,
  delayed capillary refill ( gt2 seconds), reduced
  urinary output, and clouded sensorium
• Class IV hemorrhage gt40 blood lossfrank shock
• Skin cool, diaphoretic, ashen. Tachycardia,
  hypotension, unobtainable BP, anuria, decreased
  LOC

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Treatment

• Class I hemorrhage rapidly infuse 1-2 liters of
  crystalloids then maintenance fluids
• Class II hemorrhage rapidly infuse 2 liters of
  crystalloids then re-evaluate
• Continue replacement as necessary
• Class III hemorrhage rapidly infuse 2 liters of
  crystalloids re-evaluate, replace blood losses
  with 31 crystalloids or 11 blood products
• Keep U.O.gt.5ml/kg/hr.
• Class IV hemorrhage rapidly infuse 2 liters of
  crystalloids re-evaluate, replace blood losses
  initially with 31 crystalloids or 11 blood
  products
• Keep U.O.gt.5ml/kg/hr.
• Restore oxygen delivery with blood products to
  keep consumption gt 100ml/min/m2

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Treatment

• Class III IV hemorrhage patients require
  immediate IV fluid resuscitation in order to
  survive
• Class IV hemorrhage patients will require blood
  transfusion
• Hematocrits 20-25 may be acceptable as long as
  an otherwise healthy patient is adequately volume
  resuscitated
• Studies have shown Hct. 28-30 is optimal for
  oxygen carrying ability and viscosity

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Blood Blood ProductMassive Transfusions

• Well over 50 of homologous blood and the
  majority of autologous blood transfused is
  administered to surgical patients
  intraoperatively
• Blood transfusions may be the most common
  non-pain relieving therapy performed by
  anesthesia providers

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Blood type

• 1900 Carl Landsteiner discovered the ABO red
  blood cell (RBC) groups
• gt600 antigen groups have been discovered since
  this time
• No blood is ever perfectly matched due to the
  antigen grouping
• Rh type refers to the presence or absence of
  the Rh0D antigen
• Rh(-) recipients, 80 will be immunized by a
  single unit of Rh() transfusion

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Type Screen

• Determine ABO-Rh for more commonly found
  antibodies
• ABO-Rh typing has a 99.8 chance of a compatible
  transfusion
• Cross-matching with antibodies increases to
  99.94
• Universal donor O-negative
• Can use O-positive in an emergency
• Consider Rhogam if Rh(-) female of child bearing
  age is transfused with Rh() blood
• Rhogam 300mcg IM

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Preferential order of blood transfusion

• ABO type specific, partially cross-matched
• ABO type specific, uncross-matched
• O(-), uncross-matched

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Storage of blood

• Shelf life of 35-42 days
• Decreases in stored blood
• pH
• 2-3 DPG
• Platelets
• RBCs (lyses)
• Factor V VIII
• Only K will increase minimally

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Citrate Phosphate Dextrose(CPD)

• Maintains 70 RBC survival for 28 days (FDA
  approval for 21 days)
• Citrate ions bind with Calcium to prevent
  clotting (anticoagulant)
• Dextrose allows the RBCs to continue glycolysis
  and maintain ATP
• Phosphate has a pH of 5.5 and acts as a buffer
• Storage at 1-6 deg. C. slows the rate of
  glycolysis about 40 times
• CPD with Adenine (CPDA-1) preservative with
  anticoagulant
• Prolongs storage to 35 days
• Adenine allows RBCs to resynthesize ATP
• Contains 25 more glucose

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Massive Transfusions

• Transfusing 1 blood volume replacement (10-20
  units for most adults) in less than a 24 hour
  period or as an acute administration of more than
  ½ the patients EBV per hour
• Main objective is to improve and maintain
  adequate oxygen carrying capabilities,
  hemostasis, oncotic pressure, and biochemistry
• Multiple studies show 18-30 of massively
  transfused patients develop a coagulopathy
• There is debate whether or not to
  prophylactically replace platelets and
  coagulation factors or wait until there is
  abnormal micro vascular bleeding and laboratory
  evidence of coagulation factor deficiencies

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Complications of Transfusion

• Metabolic acidosis is uncommon unless there is
  inadequate resuscitation
• Blood pH is 6.9 after 21 days of storage, due to
  continued RBC metabolism of glucose to lactate
  and pyruvate and bags are impermeable to CO2.
  Preservative CDPA-1 pH 6.9 after 21 days and 6.71
  after 35 days
• Metabolic alkalosis (MA) is the most common pH
  abnormality after massive blood transfusions
• Progressive MA results as citrate lactate in
  the transfusion convert to bicarbonate in the
  liver
• MA most likely to occur in patients with renal
  dysfunction since kidneys are responsible for
  HC03 elimination.
• If alkalosis occurs, there is a left shift for O2
  affinity, and a possibility for cellular hypoxia.
  There is also a decrease in 2,3 DPG for a left
  shift of O2
• Compensation for these abnormalities by
  increasing CO2 and increase O2 delivery

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Thrombocytopenia

• Dilutional thrombocytopenia is inevitable
  following massive transfusion
• Platelet function declines to 0 after only a few
  days of storage
• Studies have shown that 1.5 blood volumes are
  necessary for this to become problematic
  clinically
• However this can occur with smaller transfusions
  if DIC occurs or pre-existing thrombocytopenia

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Coagulation Factor Depletion

• Stored blood contains all coagulation factors
  except V VIII
• Products of these factors increases with the
  stress of trauma
• Therefore only mild changes in coagulation are
  due to transfusion
• DIC is more likely be responsible for disordered
  hemostasis
• DIC is a consequence of delayed or inadequate
  resuscitation

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Hyperkalemia

• Plasma K concentration of stored blood may be
  over 30mmol/l. Hyperkalemia is generally not a
  problem unless very large amounts of blood are
  given quickly
• Hypokalemia is more common as red cells begin
  active metabolism, and intracellular uptake of K
  restarts

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Hypocalcemia

• Each unit of blood contains approx. 3g. of
  citrate, this binds with ionized calcium
• Healthy adult liver will metabolize 3g. citrate
  every 5 min. Transfusion rates higher than this
  or impaired liver function, may lead to citrate
  toxicity and hypocalcemia
• Hypocalcemia clinically doesnt affect
  coagulation, but may transiently exhibit tetany
  and hypotension
• Calcium should only be given if there is a
  biochemical, clinical, or EKG evidence of
  hypocalcaemia

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Hypothermia

• Leads to reduction in citrate and lactate
  metabolism (leading to hypocalcaemia and MA),
  increased affinity for HGB to O2
• Impairment of RBC deformability
• Platelet dysfunction
• Increased tendency for cardiac dysrythmias

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Adult Respiratory Distress Syndrome (ARDS)

• Exact etiology unknown
• Over and under transfusions have been associated
  with increased risk of ARDS
• Albumin lt 30g/l also implicated
• Blood filters recommended for massive
  transfusions except with giving fresh whole blood

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Blood Bank Arrangements

• Routine procedures followed until apparent that
  massive transfusion is likely
• Inform blood bank as soon as possible.
• O group blood supplied first then switched to
  type specific as soon as possible to not deplete
  the blood supply of O-type
• Continue this until cross matched blood is
  available from original serum sample
• If antibody screen is negative and more than one
  blood volume has been administered there is no
  point in attempting compatibility tests except to
  exclude ABO mismatches

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Monitoring

• During massive transfusion, regular monitoring
  of
• HGB
• Platelets
• PT/INR, PTT
• Fibrinogen levels to guide component replacement

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Components

• Component replacement should occur only in the
  presence off active bleeding or if interventional
  procedures are to be undertaken
• Platelet concentrates (1pack/10kg) are given if
  platelet count lt50. each platelet concentrate
  also provides around 50ml of fresh plasma
• FFP (12 ml/kg) is administered if PT or PTT are
  running higher than 1.5 times control levels
• Cryo 1-1.5 packs/10kgs is given for fibrinogen
  levels lt0.8g/L

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Massive Transfusion continued

• For massive uncontrolled traumatic hemorrhage,
  maintenance of full haemostatic ability is
  usually unrealistic
• Priority is for definitive surgical arrest of
  hemorrhage from major vessels
• Combinations of stored whole blood, packed cells,
  colloids crystalloids are given to maintain
  blood volume or pressure at adequate levels and
  HGB at or around 7g/dl or HCT at 25
• Conserve limited supplies of fresh blood, plasma
  or platelets until the bleeding is controlled

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References

• Seaman, D. M. J., Park, G. R.Trauma.org,
  resuscitation Transfusion for Massive Blood
  Loss.
• Massoli, K. L. Lecture Blood Component
  Therapy and Massive Transfusion, Jan., 2003.
• Stene, J. K., Grande, C. M. Trauma Anesthesia.
  Williams Wilkins, 1991, Baltimore, Maryland.

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Questions
Jim Malson, CPT