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PLATELET TRANSFUSIONS IN CLINICAL MEDICINE

R.N. Makroo* and Pushkar Kumar***Director, **Registrar, Department of Transfusion Medicine, Indraprastha Apollo Hospitals, Sarita Vihar,

New Delhi 110 076, India.

Correspondence to Dr. R.N. Makroo, Director, Department of Transfusion Medicine,Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi 110 076, India.

e-mail: makroo@apollohospitals.com

Whole blood transfusion is becoming a practice of the past very speedily. Use of various components of bloodis the order of the day. Platelet transfusion has gained significant importance in recent times, and there is nozero risk blood despite carrying out various safety tests.

Key words: Thrombocytopenia, random donor platelets, single donor platelets

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INTRODUCTION

THE value of platelet transfusions for thrombocytopeniawas first reported in 1910,when Duke described threepatients with bleeding due to thrombocytopenia, each ofwhom showed improvement with transfusions of fresh,whole blood containing platelets [1]. When tissue injuryoccurs, platelets initiate haemostasis, help promotecoagulation, contribute to clot retraction and to theformation of the haemostatic plug that is critical inachieving haemostasis. Platelets also store and transportseveral chemicals, including serotonin, epinephrine andhistamine. Platelets, the cellular component of blood, arevery small (1-2 0 μm) in diameter and comprises of lessthan 1% of the total blood volume. The normal plateletcount is 150,000-450,000/cumm. Platelet transfusion isan important tool for the prevention and treatment ofhaemorrhage caused by insufficient platelet productionor defective platelet function[2].

DESCRIPTION OF COMPONENTS

Platelets are prepared in blood bank either by PlateletRich Plasma (PRP) method or by buffy coat method andare called Random Donor Platelets (RDP). Platelets arealso prepared by apheresis procedure called SingleDonor Platelets (SDP). A single unit of random donorplatelets (RDP) contains a minimum of 5.5 × 1010

platelets suspended in 50 mL-70 mL of plasma. Singledonor platelets (SDP) are collected by apheresis andcontain a minimum of 3.0 × 1011 platelets suspended in200-350 mL of plasma. Platelet products may be storedfor 5 days with continuous agitation at 22ºC+ 2ºC.The

day of collection is considered as zero day.

COMPATIBILITY

Platelets transfusions are given according to theABO and Rh grouping. ABO identical or compatibleunits are preferred, but not required. In adults, ABOincompatible platelets may be used because the volumeof plasma in the product is usually not clinicallysignificant. Apheresis units may contain 200-300 mL ofplasma, but passive transfer of antibodies rarely resultsin hemolysis. Cross matching is not necessary becausethe volume of RBCs is less than 0.5 mL in each plateletcomponent. However, one mL of RBCs is capable ofcausing alloimmunization to the D antigen. Rhcompatibility is therefore recommended in women ofchildbearing age to prevent iso-immunization in casethere is RBC contamination.

DOSAGE

Random Donor Platelets (RDP) is given in a dose ofone unit per 10 kg of body weight. Stable patients whoare not refractory to platelet transfusions can beexpected to have a platelet count increase between5,000-7,000 per unit in a 70 kg adult[3]. Single DonorPlatelets (SDP) provides an adequate dose for an adultfrom one transfusion.

INDICATIONS

Platelet transfusion is indicated in several conditionssuch as acute myeloid leukemia and other malignantdiseases, aplastic anaemia, disseminated intravascular

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coagulation (DIC), dilutional thrombocytopenia e.g.,massive transfusion with stored blood, Glanzmannthrombasthenia, storage pool disease, Wiskott-Aldrichsyndrome, Chediak Higashi Syndrome, Gray Plateletsyndrome, hypersplenism, uraemia, paraproteinemiaetc. The currently accepted threshold for platelettransfusion was derived from a 1962 study by Gaydos,et al., in which gross haemorrhage in patients withleukaemia became more frequent as platelet count ofless than 20,000 per cumm[4]. Platelet transfusions areindicated to control or prevent bleeding associated withthrombocytopenia or platelet dysfunction. Guidelinesfor transfusing patients with thrombocytopenia include:Patients with platelet counts <10,000/mL, patients withplatelet counts <20,000/mL associated with minorbleeding, fever or splenomegaly, patients with plateletcounts <50,000/mL with significant bleeding orundergoing an invasive procedure, patients withdocumented platelet function abnormalities. A numberof studies have been performed to assess bleeding riskat varying platelet counts, the risk does not increase inpatients with an intact vascular system until the plateletcount is <10000/cumm[5].

Platelet transfusion is also indicated in viral diseasesincluding viral haemorrhagic fevers e.g., dengue fever(DF). Dengue virus destroys the platelets and mega-karyocytes (the precursor of the platelet) by immunemechanism and thereby reduces their number. Thereduced number of megakaryocytes produces lessnumber of platelets and hence the condition ofthrombocytopenia arises in the dengue patients. Oncethe number of platelets becomes less than 50,000/cummthe patients are judged to be at the risk of haemorrhagicsymptoms and if the count is very low i.e., less than10,000/cumm, the patients may even bleed. Bleeding indengue is one of the dreaded complications. Clinicalmanifestations of bleed are highly variable from simpleskin bleeds like petechiae or purpura to severe bleedslike bleed from puncture site, gastro-intestinal bleeds,fatal intracranial bleed and bleed from viscera. Bleedingduring DHF may result from a combination of factorssuch as thrombocytopenia, coagulation defect andvasculopathy.

In a study conducted at Indraprastha ApolloHospitals on 225 serologically confirmed dengue casesin 2005, the prevalence of thrombocytopenia (count lessthan 100,000/cumm) was 84.88% on admission andbleeding was recorded in 22 (9.7%) patients[6] Ninety-six (42.6%) patients of dengue cases received platelettransfusion. Among them 47 (20.88 %) patients had a

platelet count <20,000/cumm, 43(19.11%) had a plateletcount in the range of 21-40,000/cumm while 6 (2.66%)patients had the platelet count in between 41-50,000/cumm. Out of 49 patients with a platelet count>20,000/cumm, 18 (8.0%) patients had haemorrhagicmanifestations like petechiae, gum bleeding, epistaxisetc. which necessitates the use of platelet transfusion.However, 31(13.77%) patients received inappropriateplatelet transfusion.

CONTRAINDICATIONS AND PRECAUTIONSFOR PLATELET TRANSFUSIONS

In thrombotic thrombocytopenic purpura, hemolyticuremic syndrome, heparin induced thrombocytopenia,platelet count >100,000/mL without evidence of plateletdysfunction, idiopathic thrombocytopenic purpura(unless bleeding is life threatening) and prophylacticallyfollowing routine cardiac surgery.

COMPLICATIONS OF TRANSFUSION

A febrile non-hemolytic transfusion reaction(FNHTR) is the most common complication of platelettransfusion. FNHT reactions occur in approximately 1%of all transfusion reactions. This increases to as much as30% in patients who have multiple transfusions. This isdue to either recipient antibodies to donor WBCs orcytokines, i.e., IL-1, IL-6, IL-8 and TNF in the plateletcomponents that are released from the WBCs duringstorage[7]. Symptoms include an increase intemperature, chills/rigors, tachycardia, and dyspnea.The reaction generally subsides within 30 minutes ofstopping the transfusion.

Allergic reactions occur in approximately 1% ofplatelet transfusions. These reactions are generallymild and respond to antihistamines. Rare reactions toplatelets include bacterial sepsis, transfusion relatedacute lung injury (TRALI) and transfusion associatedgraft vs. host disease. Fever and chills may be thepresenting symptoms of acute hemolysis, bacterialsepsis, or FNHTR. Therefore, it is important to stopthe transfusion and follow hospital policy for reportingtransfusion reactions to the blood bank so thatan investigation can determine the cause of thereaction. Since a temperature of 22ºC facilitatesbacterial proliferation, any contamination of theplatelets either due to asymptomatic donor bacteremiaor the phlebotomy site not being meticulously cleanedproperly can lead to sepsis which can provefatal [8].

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MANAGEMENT OF PLATELETREFRACTORINESS

Patients repeatedly exposed to foreign plateletantigens may develop alloantibodies that cause plateletimmune refractoriness or alloimmunization. Previousexposure occurs through pregnancy or transfusion.Alloimmuni-zation is most often due to patientantibodies against donor HLA class I antigens on theplatelet surface. The risk of alloimmunization is greatlyreduced by leukoreduction, with no difference in riskbetween leukoreduced RDP and SDP. To assess plateletresponse, a one-hour post-platelet count is necessary.Patients having fever, sepsis, bleeding, or splenomegalyusually show poor platelet increment.+ Such patientsmay benefit from larger doses or more frequent platelettransfusions. A one hour post-platelet count increment of<10,000-15,000/mL after SDP, on two separateoccasions, reflects a poor platelet response. This may bedue to immune-mediated platelet destruction.

FUTURE CONSIDERATIONS

The use of leucodepleted blood products is gainingimportance because of the scientific evidence thatfiltered blood products to remove leucocytes prior totransfusion prevent or reduce the incidence and severityof a number of adverse transfusion effects like FebrileNon Hemolytic Transfusion Reaction, sensitization toblood products (HLA alloimmunization), refractivenessto platelet therapy and prevention against lymphotropicviruses including CMV. Leucoreduction is advantageousin neonates; transplant patients and patients ofleukaemia and aplastic anemia. The incidence ofFNHTR has considerably decreased with the use ofrandom donor platelets concentrate prepared by buffycoat method using top and bottom blood collection bagsfrom Baxter since it provide one log leucoreduced blood

components. To prevent the risk of alloimmunization &transmission of lymphotrophic viruses like CMV bloodcollection bags with integrated leucocyte filters are used.

Although transmission of infectious disease throughblood transfusion has been markedly reduced, a smallrisk remains despite rigorous donor screening andimproved viral screening assays. The residual risk is theimpetus for the development of virally inactivated bloodcomponents and blood substitutes. Even with all thesafety features included, there is no zero risk bloodinspite of all testing.

REFERENCES

1. Duke WW. The relation of blood platelets to hemorrhagicdisease. JAMA 1910; 55:1185-1192.

2. Slichter SJ. Principles of platelet transfusion therapy. InHoffman R Benz. EJJr, Shattil SJ, Furie B, Cohen HJ(eds): Haematology. Basic principles and practice.Churchill Livingstone, New York, 1991, 1610-1622.

3. Makroo RN. Compendium of Transfusion Medicine. 1999;134-135.

4. Gaydos LA, Freireich EJ, Mantel N. The quantitativerelation between platelet count & hemorrhage in patientswith acute leukaemia. N Engl J Med 1962; 266: 905-909.

5. Navarro JT, Hernandez JA, Ribera JM, Sancho JM, OriolA, Pujol M, Milla F, Feliu E: Prophylactic platelettransfusion threshold during therapy for adult acutemyeloid leukaemia: 10000/cumm versus 20000/cumm.Haematologica 1998; 83: 998-1000.

6. Makroo RN. Role of Platelet Transfusion in theManagement of Dengue patients in a tertiary carehospital. Vox Sanguinis 2006; 91(Suppl. 3): 554.

7. Heddle NM, Klama L, Singer J, et al. The role of theplasma from platelet concentrates in transfusionreactions. N Engl J Med 1994; 331: 625-628.

8. Sazama K. Reports of 355 transfusion associated deaths:1976 through 1985. Transfusion 1990; 30: 583-590.