MASSIVE BLOOD TRANSFUSION
Ileana Lopez-Plaza, M.D.
Massive blood transfusion is defined as the replacement of at least one blood volume (³ 10 units red cells) within a 24-hour period.
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.
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.
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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