MASSIVE BLOOD TRANSFUSION
Ileana Lopez-Plaza, M.D.
Introduction
Massive blood transfusion is defined as the replacement of at least one
blood volume (³ 10 units red cells) within a 24-hour period.
General Concepts
The most frequent indication for massive blood transfusion is
hypovolemic shock secondary to blood loss (hemorrhagic shock), most often seen in the
setting of trauma, ruptured aortic aneurysm, massive GI hemorrhage and liver
transplantation.
The initial resuscitation in hemorrhagic shock should begin with
crystalloid infusion to restore intravascular volume followed by infusion of red cells to
restore adequate oxygen delivery to tissues. Isotonic salt solutions (normal saline or
Ringers lactate) are the most common crystalloid solutions used. Colloid solutions
(pentastarch or albumin) should be limited to a secondary agent for fluid resuscitation.
Normal saline is the only salt solution that may be mixed directly with blood components.
It is important to keep in mind that, most frequently, in the massive transfusion setting,
primary surgical treatment is required to achieve hemostasis. The transfusion of blood
components is usually a supportive, rather than primary therapeutic intervention for
hemostasis.
Regardless of the emergency, the patients identity should be
checked against the patient compatibility tag attached to the blood bag to be infused. All
blood products must be transfused through a standard blood infusion filter. Massive blood
transfusion metabolic effects are not unpredictable. Therefore, baseline laboratories,
including hematocrit/ hemoglobin, platelet count, prothrombin time, partial thromboplastin
time, fibrinogen, arterial blood gases, electrolytes and electrocardiogram should be
performed. Follow-up laboratories should be repeated as clinically indicated, prior to
correction of symptoms.
Associated Potential Acute
Metabolic Effects:
Metabolic Derangements: The patients
underlying condition and rate of blood administration will have the greatest effect on the
developments of the most commonly observed derangements: hypothermia, coagulation
abnormalities, citrate toxicity, and hyperkalemia.
Hypothermia: Hypothermia is often present, mostly
as a consequence of shock due to loss of thermal regulation but compounded by
intravascular infusion of cold fluids and a cold environment. Warming of crystalloid
solutions may be supplemented with blood warming when blood is rapidly infused through a
central line and/or when infusion rate is faster than 50 ml/kg/hour (60 mL/min in an
adult). Acidosis and coagulopathy are most likely to develop secondary to hypoperfusion
and hypothermia and not to the massive blood replacement.
Citrate Toxicity: By chelating calcium, citrate
prevents clotting in blood products during storage. During massive transfusion, the dose
of citrate infused is influenced primarily by the type of blood component and by the rate
of administration. The infused citrate is rapidly metabolized and excreted by the liver
and kidneys, respectively with bicarbonate being the end product. Citrate toxicity can be
manifested by hypocalcemia, neuromuscular or cardiac abnormalities. Laboratory evaluations
for acid-base status and ionized calcium are strongly recommended prior to initiation of
pharmacological therapy, as calcium overtreatment is associated with significant morbidity
or mortality.
Hyperkalemia: Potassium leaks out of the red cell during storage
(contents of 4-8-mEq content of potassium per red cell unit in a 250-300mL volume). This
extracellular potassium load is only a transient effect, because once infused, potassium
is taken up by red cell, and/or eliminated by urinary excretion secondary to the
bicarbonate production of the citrate metabolism. Most often recipients of massive
transfusion become hypokalemic and may require potassium supplementation.
Transfusion-associated hyperkalemia may be observed in patients with renal failure with
already elevated potassium levels or in neonates receiving rapid or large volume
transfusions. In these situations the removal of the extracellular potassium in the blood
product might be helpful, but more important is the correction of the underlying clinical
condition causing the patients hyperkalemia.
Coagulation Abnormalities
After one blood volume replacement, 37% of the patients blood
remains and sufficient coagulation factor activity and platelets remain to maintain
hemostasis. Dilution and consumption are the major causes of microvascular bleeding (onset
of oozing from multiple sites). Dilutional thrombocytopenia is the major cause of
microvascular bleeding, rarely observed with less than 1.5 - 2 blood volume replacements.
Coagulation factor deficiency bleeding is more likely caused by consumption coagulopathy.
Thrombocytopenic bleeding is not observed routinely with platelet counts >50,000/m L unless platelets are dysfunctional. Hemostatic levels of
coagulation factors are maintained with levels of PT/PTT<1.5 times normal. In a
non-bleeding patient, prophylactic transfusion of platelets, plasma, or cryoprecipitate is
unlikely to prevent microvascular bleeding. For the correction of coagulopathy, platelet
count, PT, PTT, and fibrinogen assays should be repeated as necessary to guide transfusion
therapy.
| Fluid Resuscitation In Hemorrhagic Shock |
1.
Infuse crystalloid solution (use colloid solutions only if necessary). |
2.
Obtain and send sample for type and screen to the blood bank. |
3.
Infuse uncrossmatched O positive RBC, if indicated (O negative RBC for females <50
years or children <18 years). |
4.
Obtain baseline platelet count, PT, PTT, and fibrinogen levels. |
5.
Determine blood component therapy. |
Blood Component Therapy
Packed Red Blood Cells: Red cell transfusions
initially may be achieved with uncrossmatched type O red cells. By limiting the use of O
negative red cells to children and women of child bearing age, a valuable and scarce
resource will be preserved. If a patients blood type has been determined, ABO and Rh
specific red cells can be used. Every effort should be made to establish the blood type of
a patient prior to transfusion to preserve type O red cell availability and accurately
determine the patients blood type.
Platelets: Platelet transfusion therapy after
massive transfusion is an accepted intervention in the presence of microvascular bleeding
prior to documentation of thrombocytopenia. The platelet transfusion dose recommended is 1
unit per 10 kg body weight for platelet counts <50,000 or when platelet dysfunction is
suspected.
Plasma: Plasma transfusion therapy should be
instituted after laboratory confirmation of coagulation factor deficiencies. The
recommended dose is 10-15 mL/kg body weight for PT/PTT>1.5 normal range.
Cryoprecipitate: Cryoprecipitate therapy should be
instituted for the correction of laboratory evidence of hypofibrinogenemia (fibrinogen
<100 mg/dL). Dosing will depend on the degree of hypofibrinogenemia and the
patients weight. For an average size adult, 6-unit pool for fibrinogen levels
between 50-100 mg/dL; 12-unit pool for fibrinogen levels <50 mg/dL.
Copyright ã 1998, Institute For Transfusion
Medicine
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