Massive Transfusion

Chapter 160 Massive Transfusion





INTRODUCTION


Patients sustaining exsanguinating injuries as a result of trauma, coagulopathy, neoplasia, or surgery often require massive volume replacement during the resuscitation and perioperative periods. Massive transfusion, the term coined for this clinical entity, has traditionally been defined as the transfusion of a volume of whole blood or blood components that is greater than the patient’s estimated blood volume (90 ml/kg in the dog and 66 ml/kg in the cat) within a 24-hour period. Other definitions for massive transfusion have included the replacement of half the estimated blood volume in 3 hours or the administration of 1.5 ml/kg/min of blood products over a period of 20 minutes, reflecting an increased risk of adverse effects with rapid administration rates.1,2 As advancements have been made in the field of human transfusion medicine, the criteria for defining massive transfusion have evolved in some studies to include transfusions of more than 20 to 50 units of blood products.3-5


Massive transfusion imposes an incredible drain on blood banking resources. In veterinary clinics where blood products frequently are stored in limited quantities, a massively transfused patient may deplete most or all of the hospital’s blood supply, making this commodity unavailable to other patients in need. This type of expenditure is also associated with significant cost to pet owners.


Given the severity of injuries that cause near exsanguination, it should not be surprising that massive transfusion has been associated with a high mortality rate, and this has led some to question whether massive transfusion may be futile or wasteful. However, reports in the human literature have identified survival rates of between 25% to 60% following massive transfusion, and in one study of massively transfused dogs, 4 of 15 (27%) survived to discharge.4-8 Complications following massive transfusions are numerous, however, and may include electrolyte disturbances, coagulation defects, hypothermia, alterations in acid-base status, immunosuppression, acute lung injury, other immunologic transfusion reactions, and transmission of infectious diseases.



ELECTROLYTE DISTURBANCES


Stored blood undergoes changes in both the concentration and availability of various electrolytes. Recipients of massive transfusions may therefore develop electrolyte disturbances, with hypocalcemia, hypomagnesemia, and hyperkalemia most commonly reported.6,9 Hypocalcemia and hypomagnesemia result from the citrate that is added to blood products as an anticoagulant. Once in the body, citrate binds rapidly to both calcium and magnesium with equal affinity, resulting in decreases in ionized calcium and magnesium levels. In one veterinary study, ionized hypocalcemia was documented in 100% of cases following massive transfusion, with severe hypocalcemia (<0.7 mmol/L) noted in 20%.8 Changes in ionized magnesium concentration in this study tended to parallel those of ionized calcium. Ionized hypocalcemia has been reported to resolve quickly once perfusion is restored, because citrate is metabolized rapidly by the liver.10 Treatment with calcium gluconate is indicated in cases of severe hypocalcemia or when clinical signs such as hypotension, muscle tremors, arrhythmias, or prolonged QT interval manifest.


Potassium levels in stored (human) blood rise over time because of inactivation of the sodium-potassium ATPase pump by the cold storage temperatures. Humans receiving large volumes of stored blood products may therefore develop hyperkalemia. Most dogs, with the exception of Akitas and Shiba Inus, lack significant intracellular quantities of potassium in their red blood cells and, as a result, increased potassium levels are not observed in stored canine blood.11,12 Although this would suggest that hyperkalemia in massively transfused canine patients should theoretically be less of a concern, hyperkalemia was identified in 20% of dogs in one study, a prevalence similar to that reported in human patients.8 Hyperkalemia in these cases may have resulted from other factors related to their underlying injuries or illnesses, including potassium leakage into the bloodstream from damaged tissues, extracellular potassium shift secondary to acidosis, and reduced potassium excretion associated with oliguria.



HEMOSTATIC DEFECTS


Hemostatic defects are commonly seen in the massively transfused patient, with thrombocytopenia, hypofibrinogenemia, and dilutional coagulopathy most frequently reported. Thrombocytopenia following massive transfusion is believed to result primarily from blood loss and dilution. Blood products become devoid of platelets after 2 days of storage because the cold storage temperatures cause cell oxidation and death. Administering large volumes of these platelet-free blood products, especially after aggressive fluid resuscitation, can result in a dilutional thrombocytopenia. Thrombocytopenia resulting from dilution is generally less severe than the level that would have been predicted by the degree of dilution (i.e., the loss and replacement of 50% of a patients blood volume does not result in a 50% decrease in platelet count), because platelets are released from stores in the lungs and spleen.13


In studies of human patients wounded in war, nonhemostatic platelet counts of less than 50,000 cells/μl were noted only after transfusion of more than 2 blood volumes.14 Similarly, in 15 massively transfused dogs, moderate thrombocytopenia developed in all dogs for which posttransfusion platelet counts were available, but none developed platelet counts below 50,000 cells/μl.8


Dilution alone, however, does not account for all of the clinical observations regarding platelet counts. Blunt trauma, shock, sepsis, or systemic inflammation associated with the underlying injuries may also result in disseminated intravascular coagulation, leading to consumption of platelets and clotting factors. Platelet dysfunction resulting from acidosis or hypothermia is another well-documented phenomenon following massive transfusion and may be as important as platelet numbers in determining likelihood of bleeding.15


When large quantities of intravenous fluids and packed red blood cells are administered to replace massive blood loss, the dilutional effects may result in prolongation of prothrombin time (PT) and activated partial thromboplastin time (aPTT). Clotting factor consumption secondary to tissue injury may further exacerbate dilutional coagulopathy. Hemostasis is generally maintained as long as clotting factors are at least 30% of normal, and PT and aPTT values are not prolonged above 1.5 times normal.16 Exchange transfusion models predict that loss and replacement of 1 blood volume removes slightly less than 70% of circulating factors in the plasma, so theoretically transfusions of up to 1 blood volume should not be associated with abnormal bleeding tendencies.16 In human patients with war wounds, coagulopathy developed only after transfusion of more than 2 blood volumes.14 Coagulopathy was identified in 70% of dogs following massive transfusion, although a correlation with transfused volumes could not be made because of the retrospective nature of the study.8


Human trauma centers have traditionally employed empiric formulas for plasma and platelet replacement (e.g., giving 10 units of platelet concentrates and 5 units of plasma per 10 units of packed red blood cells administered) in an effort to prevent dilutional coagulopathy. However, formula replacement has not been shown to prevent coagulopathy or to reduce transfusion requirements. Instead, serial monitoring of coagulation parameters has been recommended, with blood components administered as needed to maintain the PT and aPTT under 1.5 times normal and the platelet count greater than 50,000 cells/μl.7,17

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Massive Transfusion

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