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massive blood transfusions


  • many health services have created a massive transfusion protocol (MTP) to help expedite timely and appropriate administration of blood and adjuncts to patients in need of massive blood transfusions.
  • the administration of one unit of RBCs at 4deg C will reduce the core temperature of a 70kg patient approximately 0.25deg C
  • cold blood infused faster than 100mL/min has been reported to cause cardiac arrest.
  • use of a blood warmer is advised for adults receiving infusion of blood at rates >50ml/kg/hour

complications of massive transfusions

  • hypothermia which may cause:
    • impaired haemostasis
    • slower metabolism of citrate
    • increased Hb-oxygen affinity
    • reduced myocardial function
    • cardiac arrest if sudden drop in cardiac temperature
    • massive transfusion of units containing increased potassium may lead to hyperkalemia – adding to elevated potassium levels caused by severe shock, renal dysfunction and muscle necrosis
    • patients with chronic renal failure may require special products such as freshly collected (< 7 days) RBC or washed blood.
  • paradoxical hypokalaemia
    • some patients may experience a paradoxical hypokalemia resulting from metabolism of citrate to bicarbonate and increased urinary excretion of potassium
  • metabolic alkalosis
    • metabolic alkalosis (MA) is the most common pH abnormality after massive blood transfusions
    • results as citrate & lactate in the transfusion convert to bicarbonate in the liver
    • 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.
  • citrate toxicity
    • may cause a temporary reduction in ionized calcium levels
      • can cause muscle tremor, increased myocardial irritability and decreased cardiac output.
    • hypocalcaemia should not occur unless the rate of transfusion exceeds 1 mL/kg per minute or about 1 unit of blood per 5 minutes in an average-sized adult.
    • citrate is metabolized by the liver – severe hypotension, hypothermia, hepatic injury or pre-existing liver disease increases the risk of citrate toxicity.
  • coagulopathy
    • 18-30% of massively transfused patients develop a coagulopathy
    • develops as a consequence of the replacement of shed whole blood with factor and platelet-poor fluids like crystalloids, colloids and stored red blood cells.
    • dilutional coagulopathy
      • level of fibrinogen falls first – the critical level of 1.0 g/L is likely to be reached after 150% blood loss
      • clinical coagulopathy from dilution doesn’t usually occur until replacement >1 blood volume or INR and APTT >1.5 times normal
    • dilutional thrombocytopenia with platelets < 50 x 109/L - usually occurs once > 2 units RBCs are transfused
    • hypothermic coagulopathy
  • transfusion reactions:
    • ABO incompatibility haemolytic reactions - usually related to human error
    • febrile non-haemolytic reactions
  • blood group cross-over:
    • those who have received > 4 units of uncrossmatched Group O blood may develop admixture of blood type, thus once more than 10-12 units have been given, they should not be given their own ABO type blood until tests confirm absence of significant titres of anti-A or anti-B antibodies.
  • microaggregates /RBC dysfunction:
    • Storage of red blood cells is associated with a progressive decrease in intracellular ATP and 2,3-DPG with a resultant left shifting of the O2-Hb dissociation curve.
    • The cell’s deformability may also be limited which restricts it’s ability to pass through the microcirculation.
    • This capability is dependant on cellular ATP - special additive solutions used in the preparation of red cell concentrates have reduced the loss of ATP from that seen in whole blood
  • infection risk:
  • fluid overload and acute pulmonary oedema (APO)
  • transfusion-associated graft vs host disease
    • may develop during the course of a massive blood transfusion, although its cause is most likely to be related to the underlying reason for transfusion, such as hypovolaemic shock, trauma or obstetric complications, rather than the transfusion itself.

clinical management


  • oxygen
  • large bore iv access x 2
  • avoid excessive crystalloid
  • tolerate permissive hypotension (systolic BP 80-100mmHg) until bleeding controlled (unless traumatic head injury is present)
  • do not use Hb alone as a trigger for transfusion need
  • start blood transfusion ASAP once blood sent for Xmatch - initially may need uncross-matched Group O RBCs (Rh neg. if woman of child bearing age or unknown Rh group)
  • identify cause of bleeding
  • attempt to control bleeding - compression, tourniquet, packing
  • early surgical assessment +/- angiography
  • consider use of intra-operative cell salvage where appropriate
  • avoid hypothermia, institute active warming


  • oxygenation
  • cardiac output
  • tissue perfusion
  • metabolic state

monitor every 30-60min:

  • blood count
  • coagulation screen
  • ionised calcium
  • blood gases


  • temp > 35deg C
  • arterial pH > 7.2
  • base excess < -6
  • lactate < 4mmol/L
  • ionised calcium > 1.1 mmol/litre
  • platelets > 50 x 109/L (if head injury, aim for > 100 x 109/L)
  • PT, APTT < 1.5 x normal
  • INR < 1.5
  • fibrinogen > 1.0 g/L (> 1.5g/L for pregnant women)

criteria for activating MTP

  • actual or anticipated 4 units RBCs within 4 hours, + haemodynamically unstable, +/- anticipated ongoing bleeding, or,
  • severe thoracic, abdominal, pelvic or multiple long bone trauma, or,
  • major obstetric, GIT or surgical bleeding
blood_massive.txt · Last modified: 2018/08/11 17:33 (external edit)