Judicious Use of Blood Components
Utilization of blood components requires an objective and judicious approach. In blood transfusion, one comes across varied presentations and problems. There are some situations that one may confront with only occasionally, yet it is worth having a proper knowledge about them. This way one can arm oneself with proper insight to tackle it, if it happens unexpectedly. Further, there is room to modify our routines in daily transfusion practice.
In our set up, whole blood is still the most commonly used despite the fact that it has a marginal place in modern transfusion practice. The only true indication for whole blood transfusion is hypovolemia with hypoxemia. This situation is encountered in acute blood loss, be it a road traffic accident, ante-partum haemorrhage, post-partum haemorrhage or other situations associated with loss of 30-40% of blood volume. Volume overload and exposure to multiple antigens are a few of the mentionable hazards of whole blood transfusion. Citrate intoxication is also likelihood when large amount of whole blood is transfused.
Occasionally we come across a demand of fresh blood. Freshness of blood is determined by its ability to deliver oxygen. Blood refrigerated for at least 5 days has the same oxygen carrying capacity as the fresh blood. So, blood refrigerated upto 5 days is considered as fresh. The concentration of 2, 3-DPG falls with storage. However, once transfused, the red cells restore their concentration of 2, 3-DPG, in vivo, in about 24 hours. The indications for the transfusion of fresh blood are intrauterine transfusion and exchange transfusion.
In preoperative preparation the attendants are very frequently asked to arrange one pint of blood, without assessing the expected blood loss and the haemoglobin status of the patient. Single unit red cells or whole blood transfusion does not raise white cells count, platelets count, plasma proteins or serum immunoglobulins. It raises haemoglobin by about 1.0 gram/ dl and oxygen carrying capacity of blood by about 7%. All these benefits are marginal and insignificant therapeutically. Volume overload, exposure to antigens and transmission of diseases are potential risks. Arranging one unit of whole blood to combat a possible loss of one unit of blood intra-operatively is also unnecessary as one unit loss will not lead to significant hypovolemia. Volume depletion of 10% (loss of one unit of blood) can be safely treated by infusion of crystalloid solution. Even loss of two units whole blood does not disturb homeostasis to any appreciable degree and can be managed by crystalloids with or without colloid infusion. Exceptionally, in severely anaemic child with marked hypotension and elderly patients with anaemic heart failure, single unit transfusion may be life saving. American Association of Blood Banks has commented that requests for single unit of blood be taken to indicate the need for the education of the requesting physicians.
It is ideal to give leuco-depleted blood, to transfusion dependent individuals. By definition a unit of blood (or red blood cells) from which at least 70% of leucocytes are removed is labelled as leucocytes depleted blood. This leuco-depletion can be achieved by centrifugation with subsequent removal of plasma and buffy coat, red cells washing, red cells sedimentation, filtration of blood by using specific leucocytes depleting filters and by freezing and thawing. Leucocytes depleted blood is usually, required for the prevention of non- haemolytic febrile transfusion reaction (NHFTR) caused by antibodies to leucocytes and HLA antigens in sensitized patients receiving multiple transfusions or those who are transfusion dependent. Leucocytes depleted blood is also required in the potential recipients of tissue transplants, to prevent sensitization.
In cases of autoimmune haemolytic anaemia blood transfusion is often necessary for patients with severe symptomatic anaemia. If the specificity of antibody is known, red cell concentrate negative for this antigen should be transfused. The presence of alloantibodies resulting from previous transfusions has to be excluded. Because of the presence of alloantibodies it is often difficult to find compatible blood. Hence, the least incompatible blood is transfused with informed consent and adequate monitoring. Some physicians request for plasmapheresis; however, the IgG antibody can be present in very high concentration in tissues, so it is not cleared by plasmapheresis.
If emergency transfusion is required, then uncrossmatched O positive (for males) and O negative (for female) will be released. If there is time to determine ABO and Rh type, then uncrossomatched group specific blood will be released. Rapid spin cross match to determine ABO compatibility between donor (cells) and recipient (plasma) can be performed if time permits.
Indications, dosage and response to platelets concentrates needs a critical appraisal. Under normal physiological states, platelets survive in the peripheral blood for a period of eight days. Immunological derangements, platelet pooling, platelet consumption, external loss and many other factors can reduce platelets survival. In ITP, platelets usually survive in the recipient’s blood for less than 12 hours. Similarly in thrombotic thrombocytopenic purpura, haemolytic uremic syndrome and disseminated intravascular coagulation, platelets survival is drastically reduced. Splenic pooling, viral infections, increased platelet utilization associated with wound healing, some drugs and septicemias also shorten platelet survival to a variable extent.
In Idiopathic thrombocytopenic purpura (ITP) platelets are hypergranular and functionally more effective, hence patients with platelets count as low as 30,000/ul tend not to bleed seriously. As there are antibodies against platelets, so transfused platelets are likely to meet the same fate, i.e., they will be destroyed. Not only that the platelet transfusion will not produce any rise in platelet count, it may actually aggravate the situation by providing more antigenic meal. At times in ITP platelet transfusions have a role. For emergency splenectomy in a case of ITP, platelets may be transfused to severely thrombocytopenic patients at the time of splenectomy to ensure hemostasis at the very outset. To tide over a haemorrhagic crisis, when bleeding takes place in critical areas like brain, eyes, etc it is recommended to transfuse large number of platelets, in conjunction with immunosuppressive therapy. It can mop-up most of the free antibody.
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Editorial
Nadeem Ikram
Rawalpindi Medical College |
There is no fixed platelet count at which platelets are to be transfused. One has not to treat the platelet numbers; rather the issue is to combat the symptoms. Platelet count as low as 100,000/ul is equally efficacious. Below this level there is a linear relationship between haemorrhagic tendencies and platelet count. If there is associated platelet dysfunction (aspirin or NSAID ingestion, chronic renal failure, platelet function defects), then bleeding may become manifest at higher platelet counts.
The main indications for platelet concentrates administration are thrombocytopenic and thromobocytopathic bleeding. Long term platelet concentrates administration warns against emergence of “platelet refractoriness”. Prophylactic trigger for platelet administration is a count less than 50,000/ul in operative cases, less than 20,000/ul in patients who are under active chemotherapeutic regimens and less than 5,000/ul in all situations.
In manually prepared platelet concentrate, from multiple donors; the incidence of the formation of anti-platelet antibodies is far higher, as compared to single unit platelet concentrates prepared from one donor. One unit of platelet concentrate harvested by aphaeresis is, for the purpose of calculating dose, equivalent to five units of platelet concentrates obtained manually. One unit of manually prepared platelet concentrate contains 50X10 9/l platelets and is likely to increase platelets count by 1X10 9/l. One unit of platelet concentrate prepared by cell separator contains 200-600 X10 9/l and is likely to increase the platelet count by 50X10 9/l.
Neonatal Alloimmune thrombocytopenia (NAIT) is the most important cause of thrombocytopenia in an otherwise healthy infant. It is a serious disorder resulting from platelets antigen incompatibility between the mother and the fetus. Pathogenesis of NAIT is similar to erythroblastosis fetalis, except that 50% cases occur during first pregnancy. Plasma depleted and irradiated maternal platelets are recommended. Ideal is to give HPA-1a/5b negative platelets.
Advances in blood safety have greatly reduced the risk of transfusion-associated infectious disease transmission. As a result, non-infectious hazards of transfusion have came to the forefront, and transfusion associated acute lung injury (TRALI) is an important entity in this group. If, within two to six hours after transfusion, there is development of rigors, non- productive cough, breathlessness, fever, bilateral pulmonary infiltrates without cardiac enlargement (on X- ray chest), hypoxemia and oxygen saturation of less than 90%, then the findings are most likely consistent with TRALI. It is a severe transfusion reaction. It has been associated with leucocyte antibodies in donor plasma, which activate leucocytes leading to pulmonary endothelial cell injury. Blood donors most likely implicated in TRALI are multiparous women in whom maternal alloantibody formation occurred after exposure of alloantigens on the fetal cells entering maternal circulation during pregnancy.
Transfusion associated graft versus host disease (TA-GVHD) is also a rare but under appreciated complication of blood transfusion. It is associated with an extremely high mortality rate. Immunodeficient and immunocompromised patients are at risk. In a typical case of TA-GVHD the patient presents, usually after eight to ten days after the blood transfusion with fever, maculopapular rash and pancytopenia. In severe cases the rash may progress to generalized erythroderma and desquamation. It results from the engraftment of immunocompetent donor T-lymphocytes into recipient whom immune system is unable to reject. Donor T lymphocytes are stimulated by the recipient tissues, and undergo clonal proliferation and differentiation. Different HLA antigens are presented to donor T cells by host macrophages, with subsequent donor T cell activation Activated donor T cells release cytokines, which induce further T cell expansion and activate effecter cell population including cytotoxic T lymphocytes. The recipient’s B cells, T cells, epithelial cells and bone marrow stem cells are the main target. The pancytopenia reflects stem cell injury. Majority of the patients die within a few days to weeks due to marrow failure. The treatment of TA-GVHD is ineffective. The preventive approach is focused on means to reduce or inactivate donor T lymphocytes. This objective can be achieved by using leucocytes filters and blood irradiation (by using X-ray or Caesium source)
Although blood transfusion is life saving, yet one can not have the liberty of its liberal use. Standardization and uniform utilization of blood components is lacking through out the country. People usually have to go through an exhaustive hunt for platelet concentrates, fresh frozen plasma, cryoprecipitates and other blood components, even though they are going down the drain, untapped, in whole blood transfusions: paucity in midst of plenty. Blood is a precious commodity with a perplexed and paradoxical scenario of its over utilization some where, with underutilization elsewhere.
Bibliography
- Moinuddin. Blood component therapy. Publication of Baqai Institute of Haematology, 1995. 1 – 41
- Brozovic B, Brozovic M. Manual of clinical blood transfusion, 1987. Churchill Livingstone. 1-90
- Ayyub M. Case based handbook of transfusion medicine. Armed Forces Institute of Transfusion, 2007.1 – 79
- Triulzi DJ. Transfusion – related acute lung injury; An update. Hematology, 2006: American society of hematology education program book. Florida. 497 - 500
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