Configuraci´ on gr´ afica de Samba, interfaz SWAT

The quantity of platelets to be transfused depends on the source of the platelets, the cause and degree of thrombocytope- nia, and the observed response to transfusions. The usual ini- tial amount transfused is 6–8 units of random-donor platelets or 1 unit of single-donor apheresis product. Platelet packs should contain a minimum of 5.5 × 109_{platelets per unit.}

The response to platelet transfusions should be deter- mined by obtaining a platelet count 1 hour after transfusion and daily thereafter and by observing the effect on control of bleeding. The 1-hour count should increase by about 5000–10,000 per unit of random-donor platelets or 30,000–50,000 per unit of single-donor platelets. Stored homologous platelets survive about 3 days in thrombocy- topenic patients. The 1-hour count and subsequent platelet survival will be reduced in patients with increased destruc- tion or hypersplenism. These measurements will help to determine the magnitude of the benefit to be expected from subsequent transfusions. If only a minimal response occurs, or if the platelet rise is short-lived, subsequent prophylactic transfusions should be withheld. However, in patients with severe thrombocytopenia owing to destruction or hyper- splenism who have serious bleeding, platelet transfusions may be warranted. In any patient, if clinical bleeding does not improve despite platelet transfusion, other causes of bleeding should be evaluated and the utility of subsequent platelet transfusions in such patients reassessed.

The underlying cause of thrombocytopenia or platelet dysfunction should be determined so that specific therapy to reverse the process can be given if available. Alternatives to platelet transfusions in bleeding patients with thrombo- cytopenia or platelet dysfunction are set forth in Table 3–2.

Plasma

Plasma products available are listed in Table 3–1. Fresh frozen plasma (FFP) is prepared by separating plasma from red blood cells (after collection of whole blood or during plasmapheresis) and freezing it within 6 hours after collec- tion at –18°C or colder. It can be stored for up to 1 year and is thawed over 20–30 minutes prior to administration. Activities of coagulation factors are adequate for 24 hours after thawing. Fresh plasma and plasma recovered from out- dated blood products are used for preparation of plasma

derivatives (eg, immunoglobulin, cryoprecipitate, albumin, coagulation factor concentrates). Fresh plasma may be used as an alternative to FFP for replacement of coagulation fac- tors other than factors VIII and V.

Cryoprecipitate-poor plasma is the supernatant plasma remaining after preparation of cryoprecipitate and contains adequate quantities of all coagulation factors except fibrino- gen, factors VIII and XIII, and von Willebrand factor. Solvent-detergent treatment of plasma (S/D plasma) inac- tivates lipid-enveloped viruses and has been licensed recently by the Food and Drug Administration (FDA) to minimize the risk of transfusion-transmitted infections and allergic reactions in the management of coagulopathies and thrombotic thrombocytopenic purpura (TTP). The highest-molecular-weight von Willebrand factor multimers are reduced in S/D plasma, enhancing its efficacy in the

treatment of TTP, but protein S and plasmin inhibitor levels are also variably reduced, potentially causing venous throm- boembolism (low protein S) or excessive bleeding (low plas- min inhibitor). Numerous other derivatives of plasma are now available;Table 3–3outlines some of these products and their therapeutic uses.

Alternative Possible Indications

High-dose IgG Life-threatening bleeding in immune- mediated thrombocytopenia (ITP). Anti-D immune

globulin

Treatment of bleeding in ITP in Rh-positive patients.

Desmopressin (DDAVP)

Bleeding associated with platelet dysfunction, uremia, von Willebrand’s disease.

Antifibrinolytic agents (eg, aminocaproic acid)

Excessive bleeding without evidence of throm- botic diathesis or hematuria.

Estrogens Bleeding associated with uremic platelet dysfunction.

Red cell transfusions Severe anemia associated with thrombocy- topenia or platelet dysfunction. Erythropoietin Bleeding in anemic, uremic patients. Corticosteroids ITP, possibly thrombotic thrombocytopenic

purpura-hemolytic uremic syndrome (TTP-HUS). Splenectomy Refractory ITP, severe hypersplenism,

possibly TTP. Immunosuppressives, chemotherapy, danazol, vinca alkaloids, interferon alpha, protein-A immunoadsorption, rituximab Refractory ITP. Plasma infusion or exchange TTP-HUS.

Table 3–2. Alternatives to platelet transfusions.

Table 3–3.Therapeutic products derived from plasma.

Plasma Derivative Therapeutic Use

Fibrin glue (human fibrinogen combined with bovine thrombin)

Prevent surgical oozing with topical use

Albumin (heat-treated) Hypoalbuminemia in nephrotic syndrome

Plasma-derived factor VIII concentrate

Hemophilia A* Humate-P von Willebrand’s disease Prothrombin complex concentrate Coagulation inhibitors, factor X

and prothrombin deficiencies Activated factor IX concentrates

(Autoplex, FEIBA)

Factor VIII inhibitors Plasma-derived factor IX

concentrate

Hemophilia B* Fibrinogen concentrate Hypofibrinogenemia Factor VII concentrate Factor VII deficiency Factor XI concentrate Factor XI deficiency Factor XIII concentrate Factor XIII deficiency Antithrombin III concentrate Thrombosis in antithrombin III

deficiency C1 esterase inhibitor concentrate Angioedema α1-Antitrypsin concentrate Prevent lung damage in

α1-antitrypsin deficiency Protein C and S concentrate Severe protein C or S deficiency Intravenous immunoglobulin Immunodeficiency states; immune

cytopenias, Kawasaki syndrome, Guillain-Barré syndrome, dermatomyositis

Immune serum globulin Passive immunization against hep- atitis A, measles, poliomyelitis, varicella, rubella

*Recombinant products are available as an alternative to plasma- derived product; see Chapter 17.

Indications

The major indication for plasma transfusion is correction of coagulation factor deficiencies in patients with active bleeding or in those who require invasive procedures. Isolated congen- ital factor deficiencies (eg, factor II, V, VII, X, XI, or XIII) may be treated with plasma (FFP for factor V deficiency, FFP or fresh plasma for the remainder) if factor-specific concentrate is unavailable. Multiple acquired factor deficiencies compli- cating severe liver disease and disseminated intravascular coagulation (DIC) and, if associated with significant bleed- ing, may be treated with FFP. However, excessive volume expansion or decreased survival of coagulation factors may decrease the usefulness of FFP in these conditions. Vitamin K deficiency and warfarin therapy result in a functional defi- ciency of factors II, VII, IX, and X, and parenteral vitamin K administration will reverse these deficiencies within about 24 hours. If immediate correction is necessary because of active bleeding, plasma can be given. Massively bleeding patients requiring transfusion of red blood cells greater than 100% of normal blood volume in less than 24 hours may become deficient in multiple coagulation factors, and plasma is indicated if a demonstrable coagulopathy develops follow- ing massive transfusion and bleeding continues. However, bleeding in such patients is more often due to thrombocy- topenia than coagulation factor deficiencies, so prophylactic administration of plasma usually is not indicated.

Other indications for treatment with plasma include antithrombin III deficiency in patients at high risk for throm- bosis or who are unresponsive to heparin therapy, severe protein-losing enteropathy in infants, severe C1 esterase inhibitor deficiency with life-threatening angioedema, and TTP-HUS.

Plasma exchange therapy, with removal of undesirable plasma substances and reinfusion of normal plasma, appears to be effective alone or as an adjunct in the manage- ment of TTP-HUS, cryoglobulinemia, Goodpasture’s syn- drome, Guillain-Barré syndrome, homozygous familial hypercholesterolemia, and posttransfusion purpura. Plasma exchange may be of value in some patients with chronic inflammatory demyelinating polyneuropathy, cold agglu- tinin disease, autoimmune thrombocytopenia, rapidly pro- gressive glomerulonephritis, and systemic vasculitis. Rarely, patients with alloantibodies, pure red blood cell aplasia, warm autoimmune hemolytic anemia, multiple sclerosis, or maternal-fetal incompatibility may benefit from therapeutic plasma exchange.

Plasma should not be administered for reversal of volume depletion or to counter nutritional deficiencies (except severe protein-losing enteropathy in infants) because effective alter- natives are available. Purified human immunoglobulin has replaced plasma in the treatment of humoral immunodefi- ciency. Patients with coagulation factor deficiencies who are not bleeding or not in need of invasive procedures likewise should not be treated with plasma. Patients with mild coagu- lation factor deficiencies (ie, prothrombin time <16–18 s,

partial thromboplastin time <55–60 s) are unlikely to have bleeding in the absence of an anatomic lesion, and even with surgery or other invasive procedures, these patients may not have excessive bleeding. Therefore, prophylactic administra- tion of plasma should be discouraged in such patients.