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• W2156983984 abstract "Br J Anaesth 2000; 84: 446–55 Br J Anaesth 2000; 84: 446–55 Coagulation problems may be broadly divided into disorders of haemostasis and disorders of thrombosis, although there is a small intermediate group which involves both disorders. The special requirements of such patients in the peri-operative period will be discussed in the setting of the underlying condition. A broad classification of the inherited disorders of haemoplasm is set out in Table 1.Table 1Inherited disorders of haemostasisDisorderPathophysiology (deficiency or defect)InheritanceIncidence per millionHaemophilia AFactor VIIIX-linked recessive100Haemophilia B (Christmas disease)Factor 1XX linked recessive20Haemophilia CFactor X1Autosomal dominant or recessive5% Ashkenazi Jews (others rare)Von Willebrand's diseaseVon Willebrand factorAutosomal dominant or recessive>100Factor X deficiencyFactor XAutosomal recessive1Factor V deficiencyFactor VAutosomal recessive1Factor VII deficiencyFactor VIIAutosomal rececessive1Prothrombin deficiencyFactor IIAutosomal rececessive1AfibrinogenaemiaFactor I1Factor XIII deficiencyFactor XIII1Factor V plus VIII deficiency1DysfibrinogenaemiaFactor IAutosomal dominant1 Open table in a new tab The haemophilias are characterized by a deficiency of coagulant factor which leads to increased bleeding at surgery and in the postoperative period. In the absence of platelet dysfunction, the bleeding time is normal. Haemophilia A, the most common of the haemophilias, is associated with deficiency of factor VIII coagulant protein. Haemophilia B (Christmas disease) is caused by deficiency of factor IX coagulant protein. Both these conditions have sex-linked recessive inheritance, affected males being born to carrier females, although up to 50% of cases appear de novo as a result of new mutations. The clinical severity of bleeding relates directly to the degree of deficiency. Spontaneous bleeding, classically haemarthroses, occur in severe cases (<2% coagulant factor VIII) while the moderately deficient (2–10% coagulant factor VIII) and those mildly affected (>10% coagulant factor VIII) may be expected to bleed excessively only after trauma or surgery. Some of the carrier females have significantly reduced coagulation factors and may behave clinically as mild cases themselves. This is particularly important in obstetric practice and in the peri-operative period, when specific replacement therapy may be required. Over the last 50 yr, there has been progressive refinement in the provision of specific coagulant factor replacement therapy from fresh whole blood to the plasma-free recombinant products which have become available in the last 10 yr. In the intervening period, coagulation factor concentrates were obtained by fractionation from human plasma pooled from several thousand donations. Before the introduction of viral inactivation in 1985, the vast majority of patients treated with concentrate, which was thus derived from pooled plasma, contracted transfusion-transmitted hepatitis C (HCV) and half of those in the UK with severe haemophilia also acquired the human immunodeficiency virus (HIV). In view of this history, therapeutic strategies to replace coagulation factors are also designed to minimize exposure to plasma components wherever possible.47United Kingdom Haemophilia Centre Directors Organisation Executive Committee Guidelines on therapeutic products to treat haemophilia and other hereditary coagulation disorders.Haemophilia. 1997; 3: 63-77Crossref PubMed Scopus (53) Google Scholar Recommended therapeutic products are described in Table 2. For major surgery, a target concentration of 100% factor VIII is set to be maintained for the first 5–7 postoperative days, whereas minor procedures may be adequately covered by concentrations of 50% after the first day. Doses of factor VIII required to meet these targets are listed in Table 3. Many patients with moderate or mild haemophilia A produce a 2- to 4-fold increase in factor VIII in response to 1-deamino-8-d-arginine vasopressin (DDAVP), which will be adequate to cover minor surgery. Where higher concentrations are required, recombinant coagulant factor concentrate is the recommended replacement for all new patients and for children under 16 yr with haemophilia A and haemophilia B. For those over 16 yr, already established on treatment, high-purity coagulant factor replacement may be used. Since 1985, all such plasma products have been subjected to viral inactivation by heat treatment or a solvent detergent method to kill viruses with a lipid envelope (e.g. hepatitis B virus, HCV and HIV). More recently, an additional terminal filtration step has been introduced by some manufacturers to prevent the transmission of viruses which lack a lipid envelope, such as human parvovirus B19 and hepatitis A, by their products.Table 2Therapeutic materials for the treatment of haemophiliaMaterialFactor VIIIVon Willebrand factorAdvantagesDisadvantagesDDAVP−−No risk infectionOnly effective in mild cases TachyphylaxisIntermediate-purity factor VIII concentrate20–50 IU ml−120–50 IU ml−1Non-factor VIII proteins present Plasma-derivedHigh-purity factor VIII concentrate= 5000 IU mg−1 before addition of albumin carrier−ConveniencePlasma-derived ExpensiveRecombinant factor VIII= 5000 IU mg−1 before addition of albumin carrier−PureNo risk of infectionVery expensive Limited supply Open table in a new tab Table 3Plasma levels of factor VIII to achieve haemostasisClinical indicationPlasma factor VIII target(IU dl−1)Dose of factor VIII(IU kg−1)Early haemarthrosis or muscle bleed15–208–10Minor trauma or more severe bleeding30–5015–25Surgery, major trauma or head injury80–12040–60 Open table in a new tab Factor XI deficiency29Lee CA, Bolton-Maggs P. Guidelines for the management of factor XI deficiency. Prepared in February 1998 on behalf of UKHCDOGoogle Scholar is sometimes know as haemophilia C, despite its different mode of inheritance and clinical features. It is an autosomal recessive condition, particularly common in Ashkenazi Jews. Homozygotes usually have factor XI concentrations less than 4% whereas heterozygotes have a wide range of concentrations (between 15 and 65%), but the bleeding diathesis may not correlate well with factor concentrations. Factor XI has a long half-life and replacement therapy may be required only infrequently after operation. A plasma-derived, virally inactivated factor XI concentrate is available for use but is recognized to be thrombogenic in some individuals. Where factor XI is used, the target concentration should not exceed 70% for this reason. Fresh-frozen plasma contains adequate amounts of factor XI46UK Transfusion Services. Information sheet on fresh frozen plasma, 25 July 1997.Google Scholar, and now that this product is available in a virally inactivated form some clinicians prefer to use it to minimize thrombotic complications. The basic defect in this condition is abnormal production of von Willebrand factor (vWF), a long protein monomer produced from the Weible Palade bodies of endothelial cells and from the alpha granules of platelets. vWF functions primarily in platelet adhesion to the subendothelial layers at high shear rates and, in addition, acts as a carrier molecule for factor VIII coagulant protein in the circulation. Hence, the clinical presentation is characterized by mucosal bleeding and easy bruising in association with a prolonged bleeding time in the majority of kindreds, where inheritance is autosomal dominant. It is the commonest of the inherited bleeding disorders, and it has been suggested that it might be present in as many as 20% of women with menorrhagia. Very rarely, the condition occurs in a severe form with autosomal recessive inheritance, very low concentrations of vWF and clinical features more like classical haemophilia, spontaneous haemarthroses occurring as well as mucosal bleeding. Von Willebrand's disease is diagnosed48Von Willebrand Working Party. Guidelines for the diagnosis and management of von Willebrand's disease. Prepared in 1995 on behalf of the United Kingdom Haemophilia Centre Directors OrganisationGoogle Scholar by measuring factor VIII coagulant protein (VIIIc), vWF antigen (vWFAg) and platelet activity as an estimate of binding to platelet glycoprotein with ristocetin as cofactor (vWRiCof), all of which will be reduced to 40% or less, giving rise to a prolonged bleeding time in the presence of a normal platelet count. These assays are, however, measuring labile factors which are influenced by stress and the results may therefore be variable and require repetition to confirm the diagnosis. It is usually possible to avoid the use of blood components to control haemorrhage in the majority of cases of von Willebrand's disease. The antifibrinolytic agent tranexamic acid reduces minor bleeding, e.g. menorrhagia or epistaxis, and is prescribed in the postoperative period. DDAVP administered 90 min before operation at a dose of 0.3 μg kg−1 may be expected to increase concentrations of vWFAg and factor VIII coagulant protein to normal (>100 IU ml−1) in the majority who have a quantitative defect of vWFAg. Although further doses may be given postoperatively, the effect is maximal on first administration of DDAVP in any treatment episode as tachyphylaxis is well recognized. In a small proportion of cases, namely those with a qualitative defect of vWFAg or with the more severe autosomal recessive type, a plasma product will be required to supplement vWFAg and VIIIc together. Haemate P (Centeon) and 8Y (BPL) are two intermediate-purity factor VIII concentrates which fulfil these criteria and are licensed for use in the UK. These are uncommon conditions. Inherited thrombocytopenia of clinical significance will usually be diagnosed in childhood and platelet concentrates are required to support surgery. The better-defined thrombocytopathias (platelet function defects) are also very rare. Glanzmann's thrombaesthenia is characterized by the absence of platelet glycoprotein IIb/IIIa, which binds fibrinogen and is the site of the platelet-specific HPA 1a antigen. Platelet transfusion35Norfolk DR Ancliffe PJ Contreras M Hunt BJ Machin SJ Murphy WG et al.Synopsis of background papers from the Consensus Conference on Platelet Transfusion at the Royal College of Physicians of Edinburgh, 27–28 November 1997.Br J Haematol. 1998; 101: 609-617Crossref PubMed Scopus (118) Google Scholar in patients with Glanzmann's thrombaesthenia is therefore associated with the development of anti-HPA 1a antibodies, necessitating the selection of donors lacking this antigen. Sometimes, HLA selection may be required in addition. This is associated with a defect of platelet binding to collagen, demonstrated by absent aggregation on exposure to ristocetin. Glycoprotein Ib/IX, which is the platelet-binding site for collagen, is not, however, associated with a platelet-specific antigen site, and patients may usually, therefore, be repeatedly transfused with platelet concentrate35Norfolk DR Ancliffe PJ Contreras M Hunt BJ Machin SJ Murphy WG et al.Synopsis of background papers from the Consensus Conference on Platelet Transfusion at the Royal College of Physicians of Edinburgh, 27–28 November 1997.Br J Haematol. 1998; 101: 609-617Crossref PubMed Scopus (118) Google Scholar without acquiring specific antibodies. Far more common, but with less well-defined causes, are the platelet storage pool defects, many of which are reversed by administration of DDAVP. Where this agent fails to correct a prolonged bleeding time, transfusion with platelet concentrate will be required to cover surgery. Since the introduction of universal leukodepletion of platelet concentrate in the UK in 1998, the incidence of febrile transfusion reactions and development of HLA antibodies has been significantly reduced.8British Committee for Standards in Haematology Blood Transfusion Task Force Guidelines on the clinical use of leucodepleted blood components.Transfusion Med. 1998; 8: 59-71Crossref PubMed Scopus (105) Google Scholar 34Norfolk DR Williams LM Leucodepletion of blood products by filtration.Blood Rev. 1995; 9: 7-14Abstract Full Text PDF PubMed Scopus (32) Google Scholar The consumptive coagulopathies are a spectrum of disorders characterized by inappropriate and widespread small vessel thrombosis, associated with generalized bleeding as a result of the consumption of coagulation factors and excessive fibrinolysis. Very often, a microangiopathic haemolytic anaemia ensues as red cells are damaged passing through blood vessels distorted by thrombosis. Although several distinct syndromes are described, the first line of management is to diagnose and treat the underlying cause. DIC is the most common consumptive coagulopathy, often with a prodromal thrombocytopenia giving way to hypofibrinogenaemia as a result of excessive fibrinolysis, the latter demonstrated by increased fibrin(ogen) degradation products and d-dimers. In the absence of sepsis or obstetric causes, extensive endothelial damage with collagen exposure may initiate the process. The main causes of DIC are listed in Table 4.Table 4Aetiology of disseminated intravascular coagulationConditionExamplesInfectionSepticaemia, e.g. meningococcaemiaViraemiaProtozoa, e.g. malariaMalignancyMetastatic carcinomaHaematological (especially acute promyelocytic leukaemia)Obstetric disordersSeptic abortionPlacental abruptionPre-eclampsia (pregnancy-induced hypertension)Amniotic fluid embolismPlacenta praeviaShockTraumaBurnsHeat strokeLiver diseaseCirrhosisAcute hepatic necrosisTransplantationTissue necrosisExtracorporeal circulationCardiopulmonary by passIntravascular haemolysisABO incompatible blood transfusionSnakebite Open table in a new tab In this condition, there is rarely an underlying immune cause, and transfusion support should be guided by clinical signs and coagulation results to include platelet concentrate,35Norfolk DR Ancliffe PJ Contreras M Hunt BJ Machin SJ Murphy WG et al.Synopsis of background papers from the Consensus Conference on Platelet Transfusion at the Royal College of Physicians of Edinburgh, 27–28 November 1997.Br J Haematol. 1998; 101: 609-617Crossref PubMed Scopus (118) Google Scholar fresh frozen plasma,46UK Transfusion Services. Information sheet on fresh frozen plasma, 25 July 1997.Google Scholar 52Working Party of the Blood Transfusion Task Force for the British Committee for Standards in Haematology Guidelines for the use of fresh frozen plasma.Transfusion Med. 1992; 2: 57-63Crossref PubMed Scopus (154) Google Scholar cryoprecipitate (as a source of fibrinogen) and red cells. During 1999, component preparation was modified to ensure that all red cells, as well as platelet concentrate produced within the UK, are leukodepleted at source to minimize febrile reactions and HLA sensitization. A number of other agents have been advocated in certain specific situations.38Riewald M Reiss H Treatment options for clinically recognised disseminated intravascular coagulation.Semin Haemost Thromb. 1998; 24: 53-59Crossref PubMed Scopus (34) Google Scholar Antithrombin III12Eisele B Lamy M Clinical experience with antithrombin III concentrates in critically ill patients with sepsis and organ failure.Semin Haemost Thromb. 1998; 24: 71-80Crossref PubMed Scopus (41) Google Scholar concentrate may reverse the DIC process in septicaemia, with notable success in meningococcal infection. It has been suggested that protein C concentrate42Smith OP White B Vaughan D Rafferty M Claffey L Lyons B et al.Use of protein C concentrate heparin and haemodiafiltration in meningococcal-induced purpura fulminans.Lancet. 1997; 350: 1590-1593Abstract Full Text Full Text PDF PubMed Scopus (217) Google Scholar may be equally effective in paediatric practice, but comparative data are difficult to evaluate in view of the extensive therapeutic support which is required to achieve a successful outcome in such patients. Where platelet activation is thought to be the primary cause, prostacyclin has been tried. Aprotonin may be helpful where the original problem is thought to be fibrinolysis. The use of antifibrinolytic agents may, however, be complicated by the formation of permanent clot in undesirable sites such as small renal blood vessels. The prescription of heparin is controversial,13Feinstein DI Diagnosis and management of disseminated intravascular coagulation: the role of heparin therapy.Blood. 1982; 60: 284-287PubMed Google Scholar with reports of benefit in amniotic fluid embolism,23Hull RD Pineo GF Stein P Heparin and low-molecular weight heparin for venous thromboembolism: the twilight of anticoagulant monitoring.Int Angiol. 1998; 17: 213-224PubMed Google Scholar but is a brave course to take in the haemorrhagic patient. In acute promyelocytic leukaemia, however, where disseminated intravascular coagulation is a frequent association, heparin and platelet support may be used to advantage to cover remission induction1Avvisati G Ten Cate JW Mandelli F Acute promyelocytic leukaemia.Br J Haematol. 1992; 81: 315-320Crossref PubMed Scopus (46) Google Scholar 22Hoyle CF Swirsky DM Freedman L Hayhoe FGJ Beneficial effects of heparin in the management of patients with APL.Br J Haematol. 1998; 68: 283-289Crossref Scopus (80) Google Scholar and sometimes an antifibrinolytic agent may be helpful, depending on the coagulation profile. Less common are the microangiopathies, which are thought to be immune in origin and in which platelet transfusion is contraindicated. Thrombotic thrombocytopenic purpura (TTP). In TTP, there is a predominantly neurological deficit caused by thrombosis in small cerebral vessels in association with fever and thrombocytopenia, and there is often evidence of an underlying immune disorder. Recently, it has been shown that there is an increase in very large molecular weight multimers of vWF as a result of the formation of an antibody to their cleaving metalloprotease. Haemolytic uraemic syndrome (HUS). By contrast, HUS features renal dysfunction with thrombocytopenia, often after an infection, particularly with enteric pathogens which produce a verotoxin in children. In both HUS and TTP, thrombocytopenia is the predominant haematological feature, in association with microangiopathic haemolysis. The treatment for both conditions is total plasma exchange (1½ volumes), replacing with cryoprecipitate supernatant2Bell WR Braine HG Ness P Kickler TS Improved survival in thrombocytopenic purpura–haemolytic uraemic syndrome: clinical experience in 108 cases.N Engl J Med. 1991; 325: 398-403Crossref PubMed Scopus (717) Google Scholar 39Rock G Shumak KH Sutton DMC Buskard NA Nair RC Cryosupernatant as replacement fluid for plasma exchange in thrombotic thrombocytopenic purpura.Br J Haematol. 1996; 94: 383-386Crossref PubMed Scopus (165) Google Scholar plasma, which is deficient in high molecular weight von Willebrand multimers. Platelet transfusion must be avoided. The main causes of autoimmune thrombocytopenias are described in Table 5. Their prognosis and management varies according to their causative antibody and presentation.15George JN El-Harake MA Raskob E Chronic idiopathic thrombocytopenic purpura.N Engl J Med. 1994; 331: 1207-1211Crossref PubMed Scopus (264) Google Scholar 16George JN Woolf S H Raskob G E Wasser JS Aledort LM Ballem P J et al.Idiopathic thrombocytopenia purpura: a practice guideline developed by explicit methods for the American Society of Haematology.Blood. 1996; 88: 3-40PubMed Google Scholar 25Karpatkin S Autoimmune (idiopathic) thrombocytopenic purpura.Lancet. 1997; 349: 1531-1535Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar An acute thrombocytopenia caused by IgM antibodies is the commonest form in childhood, commonly following a viral illness and usually recovering spontaneously with no need for therapeutic intervention.Table 5Classification of autoimmune thrombocytopeniaAIdiopathic (primary)A diagnosis of exclusion of secondary causesBSecondaryDrug-induced Drug-dependent Drug-independent Autoimmune systemic disorders Organ-specific, e.g. thyroid Haematological, e.g. Evans syndrome Generalized, e.g. systemic lupus erythematosusMalignant disease Non-Hodgkin's lymphoma Chronic lymphocytic leukaemia CarcinomaPostinfective Childhood virusImmunodeficiency Post-transplant Chemotherapy, radiotherapy HIV Open table in a new tab Adults, by contrast, are more likely to acquire an IgG-mediated disorder which runs a chronic course and requires immunosuppressant therapy. Although some individuals remit on steroids, many relapse when treatment is stopped, and in this group splenectomy offers a 50% chance of cure. The platelet count may be improved in preparation for surgery using a course of i.v. immunoglobulins at a dose of 0.4 mg kg−1 daily for 5 days, a target platelet count of 80–100 × 109 litre−1 being considered adequate to secure haemostasis at operation. The introduction of laparoscopic technology to perform splenectomy has reduced the morbidity of the procedure significantly.3Bernard T Rhodes M Turner GE Wimperis ZE Deane AM Laparoscopic splenectomy: single centre experience of a district general hospital.Br J Haematol. 1999; 106: 1065-1067Crossref PubMed Scopus (10) Google Scholar The permanent risk of overwhelming postsplenectomy infection remains. Vaccination against pneumococcal pneumonia should be administered before operation in the form of Pneumovax and pneumococcal antibodies quantitated every 5–10 yr, with booster immunization as necessary. To obtain an optimal response, immunization should start 2–3 months before surgery. In addition, vaccination against Haemophilus influenzae B and the meningococcal strains A and C should be provided, with a recommendation for lifelong oral prophylaxis against encapsulated organisms with daily penicillin V or erythromycin.33McMullin M Johnstone G Long-term management of patients after splenectomy.Br Med J. 1993; 307: 1372-1373Crossref PubMed Scopus (59) Google Scholar In view of the rebound thrombocytosis which usually occurs immediately after operation, such individuals are at increased risk of venous thromboembolism in the peri-operative period and require adequate anticoagulant prophylaxis until they are fully mobile. Unfortunately, about one-quarter of cases of chronic thrombocytopenia fail to respond to these measures and must then be managed on the basis of their haemorrhagic risk. Other treatment strategies include alternative immunosuppressants, e.g. azathioprine, cyclosporin, vincristine and synthetic hormones, e.g. danazol. Special consideration must be given to the management of thrombocytopenia in pregnancy.32Maternal and Neonatal Haemostasis Working Party of the Haemostasis and Thrombosis Task Force of the British Society for Haematology Guidelines on the Investigations and Management of Thrombocytopenia in Pregnancy and Neonatal Alloimmune Thrombocytopenia.Br J Haematol. 1996; 95: 21-26PubMed Google Scholar Maternal thrombocytopenia is a frequent occurrence in pregnancy, the causes of which are set out in Table 6. The platelet count tends to fall in a normal pregnancy. Although mild thrombocytopenia (120–150 × 109 litre−1) is not uncommon, it is important that more serious underlying disease is excluded.Table 6Causes of maternal thrombocytopenia in pregnancySpurious‘Benign’ gestational thrombocytopenia of pregnancyAutoimmune thrombocytopenia Idiopathic Drug-related HIV–associatedPre-eclampsia; HELLP syndromeDisseminated intravascular coagulation (DIC)Haemolytic uraemic syndrome (HUS)/thrombotic thrombocytopenia purpura (TTP)Severe folate deficiencyOthers (rare) Congenital, e.g. May–Hegglin, Bernard–Soulier Hypersplenism Coincidental marrow disease Open table in a new tab Having eliminated the apparent thrombocytopenia associated with platelet clumping in the anticoagulant EDTA, the commonest cause is ‘benign’ gestational thrombocytopenia, which occurs in up to 7% of pregnancies. The platelet count rarely falls below 80 × 109 litre−1 and no intervention is, therefore, necessary as the condition is reversible after delivery. When autoimmune thrombocytopenia is present in pregnancy, management is directed at maintaining a maternal platelet count above 50 × 109 litre−1 to minimize peripartum haemorrhage and prevent spontaneous fetal haemorrhage. Evidence of associated autoimmune disorders, such as the antiphospholipid syndrome, should be sought. In many cases, no intervention is necessary and vaginal delivery proceeds uneventfully, although epidural anaesthesia is contraindicated if the platelet count falls below 80 × 109 litre−1. If the platelet count falls below 50 × 109 litre−1, specific measures are required to prevent bleeding at delivery. Treatment options are corticosteroids and high-dose i.v. immunoglobulin (0.4 g kg−1 daily for 5 days) Where these modalities fail, consideration should be given to high-dose methylprednisolone and other immunosuppressants, such as azathioprine. Splenectomy should be a last resort in the presence of a gravid uterus, but is best performed before 28 weeks with the support of platelet transfusion. The neonates of such severely affected mothers require careful surveillance for the first few days after delivery, as the nadir in the platelet count occurs from the second to the fifth day of postnatal life as the splenic circulation is established. The thrombocytopenia and disseminated intravascular coagulation of obstetric complications such as pre-eclampsia will require specific transfusion support in line with the results of serial monitoring of the coagulation profile, with urgent delivery of the fetus to secure early resolution. More rarely, recovery may be delayed until a few days after the baby is delivered in the presence of maternal haemolysis with elevated liver enzymes and low platelets (HELLP) syndrome. Thrombocytopenia as a feature of thrombotic thrombocytopenic purpura and the haemolytic uraemic syndrome is a rare event in pregnancy and the post-partum period. Additional features include microangiopathic haemolytic anaemia with fluctuating neurological signs and deteriorating renal function. Evidence of DIC is absent and prompt delivery does not expedite clinical resolution. Furthermore, platelet transfusion is contraindicated and urgent plasma exchange is required, replacing with fresh frozen plasma. Massive transfusion involves the replacement of circulating blood volume within 24 h and often much more quickly. Stored red cells are deficient in functional platelets and plasma reduction effectively removes coagulation factors. Transfused red cells serve to dilute out the patient's native coagulation reserves.7British Committee for Standards in Haematology Blood Transfusion Task Force Transfusion for massive blood loss.Clin Lab Haematol. 1988; 10: 265-267Crossref PubMed Scopus (30) Google Scholar These effects are exacerbated by the infusion of dextrans and/or starch. Specific transfusion of coagulation factors in the form of fresh frozen plasma52Working Party of the Blood Transfusion Task Force for the British Committee for Standards in Haematology Guidelines for the use of fresh frozen plasma.Transfusion Med. 1992; 2: 57-63Crossref PubMed Scopus (154) Google Scholar and platelet concentrate35Norfolk DR Ancliffe PJ Contreras M Hunt BJ Machin SJ Murphy WG et al.Synopsis of background papers from the Consensus Conference on Platelet Transfusion at the Royal College of Physicians of Edinburgh, 27–28 November 1997.Br J Haematol. 1998; 101: 609-617Crossref PubMed Scopus (118) Google Scholar should be guided by the results of the coagulation profile, which must be repeated until haemostasis is achieved. Each unit of blood is collected from the donor in 63 ml of anticoagulant (citrate phosphate dextrose with adenine), and higher volumes transfused lead to citrate toxicity with associated hypocalcaemia. In emergency situations, when blood is transfused rapidly, cooled red cells may also contribute to the patient's falling pH. Care must be exercised in the use of blood-warmers and pumps to ensure their proper function, in order to avoid haemolysis of red cells for transfusion. Potassium toxicity rarely presents problems in this situation except in neonates. Widely used for many years in cardiopulmonary bypass procedures, other extracorporeal techniques, such as intraoperative cell salvage, may now contribute to the support of various operative procedures. When platelets are exposed to large areas of inert material, some are retained there, rendering the patient thrombocytopenic. Reduced temperatures inhibit the production of thromboxane A2 in some platelets, while others aggregate spontaneously and prematurely. Those platelets which do return to the patient's circulation may thus have been injured on their journey, for early sequestration in the spleen. For these reasons, the bleeding patient may benefit from platelet transfusion, irrespective of the postoperative platelet count after bypass procedures. Anticoagulation administered to facilitate cardiopulmonary bypass procedures may also be associated with postoperative bleeding. Heparin is reversed by protamine sulphate,9British Committee for Standards in Haematology Haemostasis and Transfusion Task Force The use and monitoring of heparin.J Clin Pathol. 1993; 46: 97-103Crossref PubMed Scopus (41) Google Scholar which, in excess, gives rise to a consumptive coagulopathy. If neutralization is incomplete, active heparin may reappear in the circulation 2–6 h after operation as it is released from heparin–protamine complexes in the extravascular compart" @default.
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