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Platelet transfusion: Indications, ordering, and associated risks

Platelet transfusion: Indications, ordering, and associated risks
Shan Yuan, MD
Section Editor:
Steven Kleinman, MD
Deputy Editor:
Jennifer S Tirnauer, MD
Literature review current through: Dec 2022. | This topic last updated: Nov 11, 2022.

INTRODUCTION — Hemostasis depends on an adequate number of functional platelets, together with an intact coagulation (clotting factor) system. This topic covers the logistics of platelet use and the indications for platelet transfusion in adults. The approach to the bleeding patient, refractoriness to platelet transfusion, and platelet transfusion in neonates are discussed separately.

Evaluation of bleeding – (See "Approach to the adult with a suspected bleeding disorder".)

Refractoriness to platelet transfusion – (See "Refractoriness to platelet transfusion".)

Neonates – (See "Neonatal thrombocytopenia: Clinical manifestations, evaluation, and management", section on 'Platelet transfusion'.)

COLLECTION METHODS — There are two ways that platelets can be collected: by isolating and pooling platelets from units of donated whole blood or by collecting platelets via apheresis directly from a donor. Most platelets in the United States are collected by apheresis.

Apheresis (single donor) platelets – Platelets can also be collected from volunteer donors in a one- to two-hour apheresis procedure. Platelets are selectively removed along with some white blood cells (WBCs) and plasma, and most red blood cells (RBCs) and plasma are returned to the donor. Some systems will also remove the majority of WBCs, resulting in a leukodepleted product.

A typical apheresis platelet unit provides the equivalent of four to six units of platelets from whole blood (3 to 4 x 1011 platelets) [1]. It is common in larger donors with high platelet counts for an apheresis procedure to collect enough platelets to split the collection into two separate transfusable apheresis units ("doubles," or "splits"), and sometimes three separate units ("triples") can be obtained from a single donor, increasing the operational efficiency of the collection facility and the availably platelet supply.

Advantages of apheresis platelets are exposure of the recipient to a single donor rather than multiple donors, and the ability to match donor and recipient characteristics such as human leukocyte antigen (HLA) type, cytomegalovirus (CMV) status, and blood type. (See 'Ordering platelets' below.)

The effects of platelet apheresis on the donor are covered elsewhere. (See "Blood donor screening: Overview of recipient and donor protections", section on 'Complications of apheresis'.)

Whole blood derived (WBD) pooled platelets – A single unit of platelets can be isolated from a whole blood donation by centrifuging the blood within the closed collection system to separate the platelets from the red blood cells (RBCs). Two manufacturing methods are used.

The platelet rich plasma (RPR) method is the main method in use in the United States. It involves the centrifugation of the whole blood first under a sufficient g-force to pellet the RBCs (the "soft spin") but leaves most of the platelets in suspension in the RPR. The PRP is then centrifuged again in a second container at a higher g-force to pellet the platelets (the "hard spin"). The supernatant platelet-poor plasma is removed. The platelets are then resuspended in the residual plasma and stored.

The buffy coat method is used more commonly outside the United States (in the rest of the world). In this method, whole blood is first subjected to a hard spin to allow plasma to be expressed off the top and the sedimented RBCs to be expressed off the bottom, leaving behind the platelet-containing buffy coat. Several buffy coat units can then be pooled together with plasma or platelet additive solution, and the pool is subjected to a soft spin to sediment the residual RBCs. The pooled platelet concentrate is then expressed off the RBCs and stored.

The number of platelets per unit varies according to the platelet count of the donor and the manufacturing process. However, the Association for the Advancement of Blood & Biotherapies (AABB) requires each platelet concentrate unit to contain ≥5.5 x 1010 platelets/unit in 90 percent of units tested [2]. The Council of Europe requires each single unit equivalent to contain >6.0 x 1010 platelets; a yield of 7 x 1010 platelets is typical [3,4]. Since this number is inadequate to raise the platelet count in an adult recipient, four to six platelet units are pooled to allow transfusion of 3 to 4 x 1011 platelets per transfusion [1]. These units, produced by either the RPR or the buffy coat method, are called whole blood-derived (WBD) platelets or platelet concentrates; they were previously called random donor pooled platelets.

Advantages of WBD platelets include lower cost and ease of collection and processing (a separate donation procedure and apheresis equipment are not required). The major disadvantage of WBD platelets is recipient exposure to multiple donors in a single transfusion and the increased work of bacterial testing. In addition, it is more labor intensive and time consuming to perform the required bacterial testing. In the United States, commercial collection systems exist that allow the pooling, leukofiltration, and bacterial culture testing to be done by the blood collection agency in an integrated bag system, making prepared pools of platelets "transfusion ready" and easing the burden for the transfusion service.

Both WBD and apheresis platelets contain some WBCs that were collected along with the platelets. These WBCs can cause febrile nonhemolytic transfusion reactions (FNHTR), alloimmunization, or transfusion-associated graft-versus-host disease (TA-GVHD) in some patients. (See "Immunologic transfusion reactions", section on 'Febrile nonhemolytic transfusion reactions' and "Transfusion-associated graft-versus-host disease".)

Platelet products are suspended either in plasma or in platelet additive solution, which reduces the plasma volume by approximately one-third. Because of their plasma content, transfused platelets can cause adverse reactions including transfusion-related acute lung injury (TRALI) and anaphylaxis. (See "Immunologic transfusion reactions", section on 'Anaphylactic transfusion reactions' and "Transfusion-related acute lung injury (TRALI)".)

Several strategies are used to prevent the complications associated with the presence of WBCs and plasma in platelet products. (See 'Complications' below and 'Ordering platelets' below.)

Platelets concentrates also contain a small number of RBCs that express Rh antigens on their surface (platelets do not express Rh antigens). The small numbers of RBCs in apheresis platelets pose an extremely low, but non-zero risk of Rh alloimmunization in most patients [5]. However, transfusion medicine services avoid giving platelets from RhD-positive donors to RhD-negative females of childbearing potential because of the potential risk of RhD alloimmunization and subsequent hemolytic disease of the fetus and newborn (HDFN). (See "RhD alloimmunization in pregnancy: Overview".)


Room temperature storage — Platelets are routinely stored at room temperature, because cold induces clustering of von Willebrand factor (WVF) receptors on the platelet surface and morphological changes of the platelets, leading to enhanced clearance by hepatic macrophages and reduced platelet survival in the recipient [6-9].

All cells are more metabolically active at room temperature; platelets are stored in bags that allow oxygen and carbon dioxide gas exchange. Citrate is included to prevent clotting and maintain proper pH, and dextrose is added as an energy source [1].

The risk of bacterial infection from platelets increases with storage duration. The shelf-life of platelets stored at room temperature is generally only five days, which are counted starting from midnight on the day of collection. This short shelf-life contributes to the potential for low platelet inventory and platelet shortages. However, facilities can store platelets for up to seven days if they use a container cleared or approved for seven-day storage by the US Food and Drug Administration (FDA) and if the platelet unit(s) are subsequently tested for bacteria using a bacterial detection device cleared by the FDA and labeled for use as a "safety measure."

Cold storage (investigational) — Storage of platelets in the cold (refrigerator temperature; 2° to 6°C) is investigational.

Cold-stored platelets could potentially reduce the risk of bacterial growth. However, there are concerns about poorer recovery and reduced circulatory half-life of cold-stored platelets [6,10,11].

Small preliminary studies suggest that platelets stored in the cold have similar efficacy and safety as platelets stored at room temperature [12-14]. Data also suggest that cold-stored platelets may have superior hemostatic efficacy in patients with acute hemorrhage [15-17]. As such, the use of cold-stored platelets has expanded in military and trauma settings. However, the overall availability of cold-stored platelets is limited and typically reserved for patients with acute trauma [18].

Cryopreservation — Cryopreserved platelets have the potential to dramatically increase shelf-life (to years rather than days) and in turn to greatly improve inventory and availability as well as to reduce the risk of transfusion-transmitted bacterial infection. Cryopreserved platelets are not clinically available in the United States, but they have been used in military settings and are in use or development in some countries in Europe, Asia, and Australia [19].

The largest trial of cryopreserved platelets (the cryopreserved versus liquid platelet [CLIP-I] trial) randomly assigned 121 adults undergoing cardiac surgery to receive up to three units of cryopreserved or room temperature-stored (liquid) platelets if they needed a platelet transfusion [20]. The cryopreserved platelets were prepared from apheresis units from group O donors and frozen in DMSO as a preservative; after thawing they were reconstituted with AB or group-specific plasma. The control platelets (referred to as liquid storage) could be prepared from whole blood derived units or by apheresis (see 'Collection methods' above). All measures of blood loss, need for red blood cell (RBC) transfusion, and frequency of adverse events were similar between groups, and there were no thrombotic events associated with cryopreserved platelets. Compared with the control group, the group assigned to cryopreserved platelets had a lower platelet count increment (median platelet count on the first postoperative day, 150,000 in controls versus 112,000/microL for cryopreserved platelets); the cryopreserved platelet group also received more platelet transfusions.

A reduced platelet count increment with cryopreserved platelets versus controls was also seen in a trial in a small number of hematology-oncology patients who were transfused with platelets in the setting of bleeding and thrombocytopenia [21].

These results suggest that cryopreserved platelets are likely to be safe and effective in a surgical setting. Cryopreserved platelets could potentially be a useful way to augment blood inventories and improve product availability in settings such as combat, in remote locations, or to alleviate shortages in urban areas with high usage. However, additional trials are needed in other patient populations with other clinical indications. Considerable regulatory hurdles must also be addressed [22].

Another potential concern with cryopreserved platelets is the delay in obtaining the platelet unit due to thawing and reconstitution with plasma [22]. This delay is approximately 10 minutes if thawed plasma is available for reconstitution and 30 to 40 minutes if plasma is frozen and also has to be thawed [20].

STRATEGIES FOR REDUCING BACTERIA AND OTHER PATHOGENS — A disadvantage of room temperature storage (see 'Storage' above) is the increased growth of bacteria compared with blood products stored in the refrigerator or freezer. (See 'Complications' below.)

Strategies for reducing exposure to pathogens in the platelet product include:

Donor screening for bloodborne pathogens. (See "Blood donor screening: Laboratory testing", section on 'Infectious disease screening and surveillance' and "Blood donor screening: Overview of recipient and donor protections", section on 'Protection of the recipient'.)

Use of proper skin sterilization techniques during collection and diversion of the first 15 to 45 mL of blood collected, which is the most likely part of the collection to contain skin bacteria. (See 'Infection' below.)

Test on the platelet unit to screen for bacteria such as automated culture-based assays, and/or rapid point-of-issue tests. (See "Transfusion-transmitted bacterial infection", section on 'Platelet-specific guidance and requirements'.)

Using platelets that have been subjected to pathogen inactivation procedures. (See "Pathogen inactivation of blood products", section on 'Platelets'.)

In 2020 to 2021, the US Food and Drug Administration (FDA) provided updated guidance for strategies to reduce risk of bacterial transmission from platelets [23]. The guidance provides recommendations to control the risk of bacterial contamination using bacterial testing strategies (culture-based and rapid detection) and pathogen reduction technologies. Culture-based testing includes primary and secondary cultures and large volume delayed sampling (LVDS). Pathogen inactivation of platelets allows for 5 or 7 day storage [24]; details are presented separately. (See "Pathogen inactivation of blood products", section on 'Platelets'.)

INDICATIONS FOR PLATELET TRANSFUSION — By convention, most authors use the term "therapeutic transfusion" to refer both to transfusion of platelets to treat active bleeding and transfusion of platelets in preparation for an invasive procedure that could cause bleeding. The term "prophylactic transfusion" is used to refer to platelet transfusion given to prevent spontaneous bleeding.

Actively bleeding patient — Actively bleeding patients with thrombocytopenia should be transfused with platelets immediately to keep platelet counts >50,000/microL in most bleeding situations including disseminated intravascular coagulation (DIC), and >100,000/microL if there is central nervous system bleeding [25]. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Treatment' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Triage'.)

Other factors that could contribute to bleeding (either directly or indirectly) should also be addressed. These include:

Surgical or anatomic lesion


Infection or inflammation


Acquired or inherited platelet function disorder

The dose and frequency of platelet transfusions will depend on the platelet count and the severity of bleeding. (See 'Dose' below.)

Preparation for an invasive procedure — Platelets are transfused in preparation for an invasive procedure if the thrombocytopenia is severe, if there is insufficient time to use other therapies to raise the platelet count when indicated (eg, if there is insufficient time to administer intravenous immune globulin or glucocorticoids in an individual with immune thrombocytopenia [ITP]), and if the risks of bleeding are deemed high.

Most of the data used to determine bleeding risk come from retrospective studies of patients who are afebrile and have thrombocytopenia but not coagulopathy [26,27]. Typical recommended platelet count thresholds used for some common procedures are listed below. Platelet transfusion may be considered when the patient platelet count is below the threshold for the corresponding procedure.

Neurosurgery or ocular surgery – <100,000/microL

Most other major surgery – <50,000/microL

Endoscopic procedures – <50,000/microL for therapeutic procedures; 20,000/microL for low risk diagnostic procedures (see "Gastrointestinal endoscopy in patients with disorders of hemostasis")

Bronchoscopy with bronchoalveolar lavage (BAL) – <20,000 to 30,000/microL [28]

Central line placement – <20,000/microL [29]

Lumbar puncture – <10,000 to 20,000/microL in patients with hematologic malignancies and <40,000 to 50,000 in patients without hematologic malignancies; lower thresholds may be used in patients with immune thrombocytopenia (ITP) [30-32]

Neuraxial analgesia/anesthesia – <80,000/microL (see "Thrombocytopenia in pregnancy", section on 'Neuraxial anesthesia' and "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Neuraxial analgesia and low platelets')

Bone marrow aspiration/biopsy – <20,000/microL

Prevention of spontaneous bleeding — We use prophylactic platelet transfusion to prevent spontaneous bleeding in most afebrile patients with platelet counts <10,000/microL due to bone marrow suppression.

For patients with fever, infection, or inflammation, we generally transfuse at a platelet count ≤15,000 to 20,000/microL due to the increased risk of bleeding [33].

Patients with acute promyelocytic leukemia (APL) have a coexisting coagulopathy, and for them we transfuse at a platelet count ≤30,000 to 50,000/microL. (See 'Leukemia, chemotherapy, and HSCT' below.)

These and other scenarios are discussed below. (See 'Specific clinical scenarios' below.)

There are no ideal tests for predicting who will bleed spontaneously [34]. Studies of patients with thrombocytopenia suggest that patients can bleed even with platelet counts >50,000/microL [35]. However, bleeding is much more likely at platelet counts <5000/microL. Among individuals with platelet counts between 5000/microL and 50,000/microL, clinical findings can be helpful in decision-making regarding platelet transfusion.

The platelet count at which a patient bled previously can be a good predictor of future bleeding.

Petechial bleeding and ecchymoses are generally not thought to be predictive of serious bleeding, whereas mucosal bleeding and epistaxis (so-called "wet" bleeding) are thought to be predictive.

Coexisting inflammation, infection, and fever also increase bleeding risk.

The underlying condition responsible for a patient's thrombocytopenia also may help in estimating the bleeding risk. As an example, some patients with ITP often tolerate very low platelet counts without bleeding, while patients with some acute leukemias that are associated with coagulopathy (eg, acute promyelocytic leukemia) can have bleeding at higher platelet counts (eg, 30,000 to 50,000/microL). (See 'Specific clinical scenarios' below.)

Compared with adults, children with bone marrow suppression may be more likely to experience bleeding at the same degree of thrombocytopenia. In a secondary subgroup analysis of the PLADO trial, in which patients were randomly assigned to different platelet doses, children had more days of bleeding, more severe bleeding, and required more platelet transfusions than adults with similar platelet counts [36]. However, these findings do not suggest a different threshold for platelet transfusion in children, as the increased risk of bleeding was distributed across a wide range of platelet counts.

Tests for platelet-dependent hemostasis (ie, bleeding time, thromboelastography (TEG), and other point of care tests) are generally not used to predict bleeding in thrombocytopenic patients. (See "Platelet function testing", section on 'When to order platelet function testing' and "Platelet function testing", section on 'Tests not commonly used'.)

The findings from clinical trials support the use of prophylactic transfusion for patients with hematologic malignancies and hematopoietic stem cell transplant (HSCT), as discussed below. Standard practice has evolved to transfusion of platelets at a threshold platelet count of 10,000 to 20,000/microL for most patients with severe hypoproliferative thrombocytopenia due to hematologic malignancies, cytotoxic chemotherapy, and HSCT [37]. However, the risks and benefits of reserving platelet transfusion for active bleeding episodes in these patients continue to be evaluated [26,38-41]. (See 'Supporting evidence' below.)

Although withholding platelet transfusion until there is active bleeding may be safe for some adults undergoing autologous HSCT, such a strategy requires intensive monitoring and the ability to perform immediate imaging for suspected central nervous system (CNS) or ocular bleeding. We do not recommend withholding platelet transfusion until there is active bleeding in patients with HSCT outside of a clinical trial or a specific protocol in a highly specialized center with the ability to support this level of vigilance. (See 'Leukemia, chemotherapy, and HSCT' below.)

Supporting evidence — Several randomized trials have compared prophylactic platelet transfusion with no transfusion (or placebo transfusion), as reviewed in a 2022 meta-analysis [42]. The analysis included seven randomized controlled trials in hospitalized patients with hematologic malignancy or dengue fever. The trials were conducted over a period of 37 years and were clinically heterogeneous in several ways (patient populations, interventions, timing of outcome measurement, assessments, and definitions of clinically important bleeding). The conditions for platelet transfusions or interventions differed, with some trials administering prophylactic platelet transfusions in both groups prior to certain invasive procedures, and most transfusing platelets in both groups when bleeding occurred. The threshold for prophylactic platelet transfusion also varied among the different trials (10,000, 20,000, or 30,000/microL).

Overall, prophylactic transfusions resulted in lower risks of clinically important bleeding (relative risk [RR] 0.75, 95% CI 0.64-0.87), but there was not a statistically significant reduction in all-cause mortality (RR 0.99, 95% CI 0.58-1.68) [42]. Given the clinical and statistical heterogeneity, the overall certainty of evidence was low. The authors cautioned against drawing conclusions on the effects of prophylactic platelet transfusions on all-cause mortality. Furthermore, although the evidence suggested that prophylactic platelet transfusions may reduce clinically significant bleeding in hospitalized patients with hematologic malignancy or dengue fever, uncertainty remains, and additional studies are warranted to investigate the risks and benefits of prophylactic platelet transfusions in other thrombocytopenic patient populations.

Two of the largest trials were conducted in hematology/oncology patients:

A 2012 trial from Germany randomly assigned 400 patients with acute myeloid leukemia (AML; patients with APL were excluded) or undergoing autologous HSCT for hematologic malignancies to receive platelet transfusions for platelet counts ≤10,000/microL or only for active bleeding, and it found higher rates of major bleeding in the patients with AML assigned to the control arm (six cerebral, four retinal, and one vaginal bleed; two of the cerebral bleeds were fatal) [43]. The patients with AML in the prophylactic transfusion arm had four retinal hemorrhages. Patients undergoing HSCT also experienced more bleeding episodes when transfused only for active bleeding, but most of these were minor.

The 2013 TOPPS trial (Trial of Prophylactic Platelets) randomly assigned 600 patients with hematologic malignancies receiving chemotherapy, autologous HSCT, or allogeneic HSCT to receive platelet transfusion for a platelet count ≤10,000/microL or only for active bleeding, and it found a higher incidence of major bleeding in the control arm (50 versus 43 percent) and a shorter time to first bleed (1.2 versus 1.7 days) [44]. There were no differences in the duration of hospitalization and no deaths due to bleeding. In a predefined subgroup analysis, patients undergoing autologous (but not allogeneic) HSCT had similar rates of major bleeding whether they were transfused for a platelet count ≤10,000/microL or only for active bleeding (45 and 47 percent). However, this may reflect a shorter duration of severe thrombocytopenia in this population and more aggressive, early treatment of suspected bleeding in the context of a clinical trial, rather than an inherently different rate of bleeding.

SPECIFIC CLINICAL SCENARIOS — There are several common clinical scenarios that raise the questions of whether to transfuse patients prophylactically to prevent bleeding, and, if prophylactic transfusion is used, of what platelet count is the best threshold for transfusion.

Leukemia, chemotherapy, and HSCT — Patients with leukemia, or those being treated with cytotoxic chemotherapy or undergoing hematopoietic cell transplant (HSCT) have a suppressed bone marrow that often cannot produce adequate platelets. We use prophylactic transfusion in these settings, assuming the patient is hospitalized, afebrile, and without active infection. We generally use a threshold platelet count of 10,000/microL (transfuse for a platelet count <10,000/microL). An exception is acute promyelocytic leukemia (APL), for which the threshold is higher (transfuse for a platelet count of <30,000 to 50,000/microL) due to a higher bleeding risk. If fever, sepsis, or coagulopathy is present, or if the patient is not hospitalized and/or cannot be closely monitored, higher thresholds may be needed.

This approach is in line with the 2017 American Society for Clinical Oncology (ASCO) guidelines (table 1) and a 2015 practice guideline from the Association for the Advancement of Blood & Biotherapies (AABB) [45,46]. It is supported by randomized trials comparing prophylactic (ie, threshold-based) and therapeutic platelet transfusion, in which patients who did not receive prophylactic transfusion had more severe bleeding [43,47]. (See 'Supporting evidence' above.)

While the 2017 ASCO guideline suggests that some individuals undergoing autologous HSCT may omit prophylactic platelet transfusions if they are being treated in a highly specialized center, we do not believe there is sufficient evidence to support this approach in most practice settings and clinical scenarios, and we continue to use prophylactic transfusions in our practice unless the patient is enrolled in a clinical trial or is following a specific institutional protocol, as discussed above. (See 'Prevention of spontaneous bleeding' above.)

Acute myeloid leukemia (AML) – Patients with AML can have suppressed bone marrow from AML, chemotherapy, or HSCT. We use standard dose prophylactic transfusion of these patients at a threshold platelet count of 10,000/microL, and transfusion for any bleeding greater than petechial bleeding. (See 'Dose' below.)

Acute promyelocytic leukemia (APL) – Patients with APL differ from other patients with AML because they often have an associated severe coagulopathy that puts them at high risk for disseminated intravascular coagulation and bleeding. We prophylactically transfuse these patients at a platelet count of ≤30,000 to 50,000/microL. We treat any sign of bleeding, especially central nervous system bleeding, with immediate platelet transfusion. (See "Clinical manifestations, pathologic features, and diagnosis of acute promyelocytic leukemia in adults", section on 'Coagulopathy and APL' and "Initial treatment of acute promyelocytic leukemia in adults", section on 'Control of coagulopathy'.)

Acute lymphoblastic leukemia (ALL) – Patients with ALL have thrombocytopenia from bone marrow suppression. In addition, these patients are often treated with L-asparaginase, which causes severe hypofibrinogenemia. However, the risk of life-threatening bleeding is low. As an example, in over 2500 children with ALL, only two intracranial hemorrhages occurred, and they were associated with hyperleukocytosis in one case and intracerebral fungal infection in the other [30]. We transfuse adults with ALL at a threshold platelet count of 10,000/microL. The use of platelet transfusion in children with ALL is discussed separately. (See "Treatment of acute lymphoblastic leukemia/lymphoma in children and adolescents".)

Chemotherapy for solid tumors – Cancer chemotherapy often makes patients thrombocytopenic from bone marrow suppression. Randomized trials of platelet transfusion threshold in this population have not been performed. Observational studies support a prophylactic platelet transfusion threshold of 10,000/microL; a higher threshold, such as 20,000/microL, may be appropriate for patients with necrotic tumors [46].

Hematopoietic stem cell transplant (HSCT) – Chemotherapy and radiation therapy administered as part of the conditioning regimen for HSCT can be highly bone marrow suppressive, depending on the doses used. We use standard dose prophylactic platelet transfusion of these patients at a threshold platelet count of 10,000/microL, and therapeutic transfusion for any bleeding greater than petechial bleeding. As noted above, patients in the TOPPS trial who were undergoing autologous HSCT had similar rates of major bleeding whether they were transfused for a platelet count ≤10,000/microL or only for active bleeding; however, there are several caveats that limit the use of this approach in the vast majority of patients undergoing HSCT. (See 'Prevention of spontaneous bleeding' above and "Hematopoietic support after hematopoietic cell transplantation", section on 'Platelet transfusion'.)

Aplastic anemia – Patients with aplastic anemia do not have a malignancy, but they may have severe thrombocytopenia, and they may be candidates for HSCT. Issues related to platelet transfusion in these patients are discussed separately. (See "Treatment of aplastic anemia in adults" and "Treatment of acquired aplastic anemia in children and adolescents" and "Dyskeratosis congenita and other telomere biology disorders" and "Management and prognosis of Fanconi anemia".)

Immune thrombocytopenia (ITP) — Individuals with ITP produce antiplatelet antibodies that destroy circulating platelets and megakaryocytes in the bone marrow. Circulating platelets in patients with ITP tend to be highly functional, and platelet counts tend to be well above 30,000/microL. Bleeding is rare even in patients with severe thrombocytopenia (platelet count <30,000/microL). (See "Immune thrombocytopenia (ITP) in adults: Clinical manifestations and diagnosis", section on 'Pathogenesis'.)

Our general approach to platelet transfusion in patients with ITP is to transfuse for bleeding rather than at a specific platelet count. (See "Initial treatment of immune thrombocytopenia (ITP) in adults", section on 'Overview of decision-making'.)

TTP or HIT — Thrombotic thrombocytopenic purpura (TTP) and heparin-induced thrombocytopenia (HIT) are disorders in which platelet consumption causes thrombocytopenia and an increased risk of bleeding; the underlying platelet activation in these conditions also simultaneously increases the risk of thrombosis.

Platelet transfusions can be helpful or even life-saving in patients with these conditions who are bleeding and/or have anticipated bleeding due to a required invasive procedure (eg, placement of a central venous catheter), and platelet transfusion should not be withheld from a bleeding patient due to concerns that platelet transfusion will exacerbate thrombotic risk. However, platelet transfusions may cause a slightly increased risk of thrombosis in patients with these conditions; thus, we do not use prophylactic platelet transfusions routinely in patients with TTP or HIT.

Support for this approach comes from a large retrospective review of hospitalized patients with TTP and HIT, in which platelet transfusion was associated with a very slight increased risk of arterial thrombosis but not venous thromboembolism [48]. In contrast, the review found that patients with immune thrombocytopenia (ITP) had no increased risk of arterial or venous thrombosis with platelet transfusion. Of note, this was a retrospective study in which sicker patients were more likely to have received platelets, and the temporal relationships between platelet transfusions and thromboses were not assessed.

TTP – Of 10,624 patients with TTP in the large review mentioned above, approximately 10 percent received a platelet transfusion [48]. Bleeding occurred in 13.7 percent of individuals with TTP. Arterial thrombosis occurred in 1.8 percent of patients who received platelets, versus 0.4 percent of patients who did not (absolute increase, 1.4 percent; adjusted odds ratio [OR], 5.8; 95% CI, 1.3-26.6). The rate of venous thrombosis was not different in those who received platelets and those who did not (adjusted OR 1.1; 95% CI 0.5-2.2).

In contrast, a systematic review of patients with TTP who received platelet transfusions, which included retrospective data for 358 patients and prospective data for 54 patients, did not find clear evidence that platelet transfusions were associated with adverse outcomes [49].

HIT – Of 6332 patients with HIT in the large review mentioned above, approximately 7 percent received a platelet transfusion [48]. Arterial thrombosis occurred in 6.9 percent of patients who received platelets, versus 3.1 percent of patients who did not (absolute increase, 3.8 percent; adjusted OR, 3.4; 95% CI, 1.2-9.5). The rate of venous thrombosis was not different in those who received platelets and those who did not (adjusted OR 0.8; 95% CI 0.4-1.7).

In a series of four patients with HIT who received platelet transfusions, two of three with active bleeding had cessation of bleeding following platelet transfusion, and no thromboses occurred; a literature review was not able to identify any complications clearly attributable to platelet transfusion [50].

Management of TTP and HIT is discussed in detail separately. (See "Immune TTP: Initial treatment" and "Management of heparin-induced thrombocytopenia".)

Liver disease and DIC — Liver disease and disseminated intravascular coagulation (DIC) are two processes that can cause a complex mixture of abnormalities with procoagulant and anticoagulant effects, along with thrombocytopenia; patients with either of these disorders are at risk for both thrombosis and bleeding. There is no evidence to support the administration of platelets in these patients if they are not bleeding. However, platelet transfusion is justified in patients who have serious bleeding, are at high risk for bleeding (eg, after surgery), or require invasive procedures. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Prevention/treatment of bleeding' and "Hemostatic abnormalities in patients with liver disease", section on 'Bleeding'.)

Platelet function disorders — Platelet function disorders can be inherited or acquired, and may be associated with thrombocytopenia or a normal platelet count. Platelet transfusion in these settings is typically reserved for bleeding.

Inherited diseases – Platelet function is impaired in Wiskott-Aldrich syndrome, Glanzmann thrombasthenia, and Bernard-Soulier syndrome. Bleeding in patients with these conditions is treated with platelet transfusion, along with other hemostatic agents discussed below. (See 'Alternatives to platelet transfusion' below and "Congenital and acquired disorders of platelet function".)

Acquired conditions – Uremia, diabetes mellitus, myeloproliferative disorders, and other medical conditions can impair platelet function. Bleeding risk can be reduced by treating the underlying condition. Platelet transfusion is typically reserved for major bleeding in these conditions. (See "Congenital and acquired disorders of platelet function", section on 'Acquired platelet functional disorders'.)

Patients who are febrile or septic can have impaired platelet function. We transfuse these patients for bleeding. We may also provide prophylactic transfusions at a higher-than-usual platelet count when fever or sepsis coexist with thrombocytopenia (eg, in patients with leukemia). (See 'Leukemia, chemotherapy, and HSCT' above.)

Antiplatelet agents — Aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), dipyridamole, ADP receptor (P2Y12) inhibitors (clopidogrel, ticlopidine), and GPIIb/IIIa antagonists (abciximab, eptifibatide) are used to prevent thrombosis by interfering with normal platelet function. The antiplatelet effects of NSAIDs and aspirin are relatively weak compared with the other antiplatelet agents, but the inhibitory effects of aspirin are irreversible during the lifespan of the platelets. (See "Platelet biology", section on 'Drugs with antiplatelet actions'.)

Typically, the approach to treating mild bleeding in a patient taking an antiplatelet agent is to discontinue the drug, assuming a favorable risk-benefit ratio. For more severe bleeding or urgent surgical procedures, high quality evidence regarding the benefit of platelet transfusion is lacking, and some evidence suggests that platelet transfusion may be deleterious. These cases can be complex, however, and we favor an individualized approach based on the complete clinical picture.

Evidence suggesting platelet transfusion is not effective in some sites of severe bleeding comes from the following:

The 2016 PATCH trial (Platelet Transfusion in Cerebral Hemorrhage) randomly assigned 190 patients with intracerebral hemorrhage (ICH) in the setting of aspirin or another antiplatelet agent to receive platelet transfusion or standard care without platelet transfusions [51]. Compared with controls, patients who received platelet transfusions had a higher incidence of a composite outcome of death or shift toward a worse score on the modified Rankin Scale for functional independence. When analyzed separately, the increase in mortality did not reach statistical significance. Serious adverse events were greater with platelet transfusion (42 versus 29 percent); enlargement of the ICH was similar in both groups at approximately 15 percent. The authors did not identify a clear mechanism for the inferior outcomes with platelet transfusion but offered several hypotheses, including the possibility of concomitant ischemia, possible proinflammatory effects of platelets, or characteristics of the hemorrhage such as location or etiology. A subsequent reanalysis of the trial by the original authors suggested that the arms of the trial were not balanced at baseline (patients in the platelet transfusion arm had a larger ICH volume and more peri-hemorrhage edema), which might account for some portion of the difference in outcomes [52].

The management of ICH is discussed in detail separately. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)

A 2017 study retrospectively reviewed outcomes in 204 individuals with gastrointestinal bleeding associated with an antiplatelet agent who received platelet transfusion as part of their management with 204 matched controls who did not receive platelet transfusions [53]. None of the people in the study had thrombocytopenia. In a multivariate analysis, platelet transfusion was associated with a higher risk of death (adjusted odds ratio [OR] 5.6; 95% CI 1.5-27).

The role of platelet transfusion in the setting of urgent surgical procedures (eg, coronary artery bypass grafting, neurosurgical interventions, and others) is also not well defined. Some clinicians give prophylactic platelet transfusions to patients taking antiplatelet drugs who require major surgery, while other clinicians use platelet transfusion only to treat excessive surgical bleeding [54,55]. There is no compelling evidence to support platelet transfusions in such scenarios, especially when platelet counts are within normal range; at the same time, there are limitations of the studies cited above (associating platelet transfusions with no clear benefits and possibly harm), making it challenging to interpret and extrapolate the data. The AABB has noted the low quality of the evidence and does not recommend for or against platelet transfusion for patients receiving antiplatelet therapy who have traumatic or spontaneous intracranial hemorrhage [45]. This decision continues to be individualized according to the specific patient factors and the judgment of the treating clinician.

Other medications may impair platelet function. As an example, the Bruton tyrosine kinase (BTK) inhibitor ibrutinib inhibits platelet aggregation by interfering with activation signals. The role of platelet transfusion in patients with ibrutinib-associated bleeding despite a sufficient platelet count is unknown, and decisions are individualized according to the platelet count and the severity and site of bleeding. This association is discussed in more detail separately. (See "Treatment of relapsed or refractory chronic lymphocytic leukemia".)

Massive blood loss — Patients with massive blood loss from surgery or trauma are transfused with red blood cells (RBCs), resulting in partial replacement of the blood volume with a product lacking platelets and clotting factors. In this setting, we transfuse RBCs, fresh frozen plasma (FFP), and platelet units in a 1:1:1 ratio. As an example, a patient transfused with six units of RBCs would also receive a pooled whole blood derived (WBD) platelet product (containing four to six WBD platelet concentrates) or one apheresis unit (both of which provide approximately 3 to 4 x 1011 platelets) and six units of FFP. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient".)

Cardiopulmonary bypass — Patients who undergo prolonged cardiopulmonary bypass can have thrombocytopenia and impaired platelet function. The use of platelet transfusion in the cardiopulmonary bypass setting is discussed separately. (See "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Bleeding'.)

Neonates — This subject is discussed separately. (See "Neonatal thrombocytopenia: Clinical manifestations, evaluation, and management", section on 'Platelet transfusion'.)

ORDERING PLATELETS — When ordering platelets, the following factors may need to be considered depending upon hospital and blood collection policies:

Platelet dose

Whether to use apheresis versus whole blood derived (WBD) platelets, if both are available

Whether to request leukoreduced units (if not routinely provided by the blood collection agency)

Whether to request irradiated units

Whether platelets are suspended in plasma or in platelet additive solution (PAS)

Whether to request pathogen-reduced platelets (if available)

Whether cytomegalovirus (CMV)-negative platelets are required

Whether the ABO type of the donor and the recipient need to be identical

For individuals receiving multiple platelet transfusions, the transfusion service or blood bank may provide platelets that are matched for ABO and RhD type and/or human leukocyte antigen (HLA) antigens depending on the clinical setting (eg, ABO and RhD-matched platelets for individuals of childbearing potential, HLA-matched platelets for individuals with HLA alloimmunization and decreased platelet count increment [refractoriness to platelet transfusion]). (See "Refractoriness to platelet transfusion".)

Dose — A standard dose of platelets for prophylactic therapy in adults is approximately one WBD unit per 10 kg of body weight, which translates to four to six units of WBD platelets or one apheresis unit, both providing approximately 3 to 4 x 1011 platelets [1,45]. A standard pediatric dose is 5 to 10 mL/kg. For prophylactic transfusion, there is generally no reason to transfuse platelets more often than once a day. This platelet dosing is expected to raise the platelet count by approximately 30,000/microL within 10 minutes of the infusion. (See 'Platelet count increment' below.)

Clinical trials comparing standard platelet dosing with other doses have been limited to patients with hypoproliferative thrombocytopenia due to bone marrow suppression (eg, leukemia, hematopoietic cell transplant, or chemotherapy). Two large trials that evaluated the use of higher or lower platelet doses in these groups have conflicting results, as illustrated below.

In the PLAtelet DOse (PLADO) trial, 1272 patients with thrombocytopenia due to chemotherapy or hematopoietic stem cell transplant (HSCT) were randomly assigned to receive standard-dose (2.2 x 1011 platelets per m2), half-dose (1.1 x 1011 per m2), or double-dose (4.4 x 1011 per m2) platelet transfusions [35]. The primary endpoint of prolonged mucosal or deep bleeding was similar among all groups (67 to 69 percent). The half-dose group received more platelet transfusions during the 30-day study period (a median of five in the half-dose group versus three in the other groups) but received fewer platelets overall, as determined by platelet counts in the transfused units (9.25 × 1011 versus 11.25 × 1011 and 19.63 × 1011 in the standard- and double-dose groups, respectively).

In the Strategies for Transfusion of Platelets (SToP) trial, patients with hypoproliferative thrombocytopenia were randomly assigned to receive platelet transfusion at standard dose (3 to 6 x 1011 platelets) or half dose (1.5 to 3 x 1011 platelets) when platelet counts fell below a trigger value (most participating institutions used 10,000/microL) [56]. The trial was halted prematurely (at 119 patients) because of life-threatening bleeding or bleeding requiring transfusion in the low dose arm (3 of 58 patients versus none of 61 in the standard dose arm).

Additional findings from these trials are discussed above. (See 'Supporting evidence' above.)

Based on review of these and other trials, the Association for the Advancement of Blood & Biotherapies (AABB) recommends transfusions of up to a single standard-dose apheresis unit of platelets (or the equivalent) and states that "greater doses are not more effective, and lower doses are equally effective" [35,45,56-58]. However, given the burdens associated with more frequent platelet transfusions when low-dose units are used, and at times conflicting results from available studies, most centers continue to use standard-dose transfusion until further data become available.

In contrast to prophylactic transfusion, a higher dose or more frequent transfusions may be required for patients who are being transfused therapeutically (for active bleeding or in preparation for an invasive procedure).

Infusion rate — For an average-sized adult, six units of WBD platelets or one unit of apheresis platelets are transfused over approximately 20 to 30 minutes. Patients at risk for transfusion-associated circulatory overload (TACO) can be transfused at a slower rate as long as the transfusion is completed within four hours of issuance from the blood bank. (See "Transfusion-associated circulatory overload (TACO)", section on 'Prevention'.)

Whole blood derived (WBD) versus apheresis platelets — The platelet count increment and hemostatic effects of pooled WBD and apheresis platelets are comparable [59].

Apheresis platelets have the advantages of limiting the recipient exposure to a single donor, which potentially reduces the possibility of infection and alloimmunization; some centers use apheresis platelets exclusively. Many believe it is less burdensome to perform bacterial testing on apheresis platelets than on WBD platelets. (See 'Complications' below.)

Use of apheresis platelets also permits transfusion of platelets from specific donors selected based on HLA matching or platelet crossmatching, cytomegalovirus (CMV) status, and ABO blood group. Patients with confirmed alloimmune mediated platelet refractoriness due to anti-HLA antibodies should receive HLA-matched platelets, platelets negative for the corresponding antigen(s), or crossmatch compatible platelets; in other cases, either WBD or apheresis platelets can be used [60]. (See "Refractoriness to platelet transfusion".)

Leukoreduction — Leukoreduction is done by passing platelets through a filter that blocks passage of most white blood cells (WBCs). Apheresis platelets can be leukoreduced during collection, and WBD platelets can be leukoreduced shortly after collection (pre-storage leukoreduction) or at the bedside (post-storage) before transfusion. Pre-storage leukoreduction is standard practice in nearly all centers in the United States.

Leukoreduction removes most of the WBCs from the platelet transfusion and has the following demonstrated or potential benefits [61]:

Reduction of HLA alloimmunization

Reduction of CMV transmission

Reduction of febrile nonhemolytic transfusion reactions (FNHTR)

Post-storage leukoreduction is not optimal for reducing FNHTR because it does not remove cytokines released from WBCs during storage. (See "Immunologic transfusion reactions", section on 'Prevention of FNHTR'.)

While leukoreduction can reduce the risks of certain complications, it is not adequate to prevent transfusion-associated graft-versus-host disease (TA-GVHD), because some WBCs can pass through the leukoreduction filter. Irradiation must be used to prevent TA-GVHD. (See "Transfusion-associated graft-versus-host disease", section on 'Prevention'.)

The only drawback of leukoreduction is cost.

Irradiation — Platelet irradiation is used to prevent TA-GVHD, in which donor WBCs attack recipient tissues and cause serious, often fatal, outcomes. This is most likely to occur when the recipient is immunosuppressed (fetus, neonatal exchange transfusion, congenital cell-mediated immunodeficiency, hematopoietic stem cell transplant, Hodgkin disease, hematologic malignancies, fludarabine) or when there is partial HLA matching between donor and recipient such that the recipient's immune system does not recognize donor cells as foreign. (See "Transfusion-associated graft-versus-host disease", section on 'Risk factors'.)

Irradiation damages the deoxyribonucleic acid (DNA) of donor lymphocytes in the transfusion, so that they cannot proliferate and mount an immune response against the recipient. Platelets are anucleate, so their functions are unaffected by irradiation, although there may be a slight effect on platelet survival due to membrane damage [62]. Platelets are irradiated by exposing the bag to 25 Gy from a Cesium or radiography source. Platelets can be irradiated at any stage during storage and can be stored up to the normal shelf-life after irradiation.

Irradiation is not a substitute for leukoreduction, because lymphocytes inactivated by irradiation still express HLA on their surfaces and can elicit an anti-HLA antibody response from the recipient. Irradiation is also inadequate to kill certain pathogens.

Indications for irradiation are summarized in the table (table 2) [63].

Irradiation is not necessary if platelets have been subjected to pathogen inactivation methods that also prevent lymphocyte proliferation (eg, photochemical treatments) [64]. These methods, which have the added advantage of not requiring a radioactive source, are discussed separately. (See "Pathogen inactivation of blood products", section on 'Methods that damage nucleic acids'.)

CMV — Some cytomegalovirus (CMV) seronegative transfusion recipients (eg, immunosuppressed patients) are at greater risk of adverse outcomes from receiving CMV-positive blood products than the general population. The Association for the Advancement of Blood & Biotherapies (AABB) considers transfusion of platelets from CMV-negative donors and leukoreduction to be equivalent in reducing this risk.

ABO, Rh, and HLA matching — Platelets express ABO antigens and HLA class I antigens on their surface. They do not express Rh antigens (D, c, C, e, or E) or HLA class II antigens.

HLA compatible platelets are more likely to result in a greater platelet count increment in patients who have developed refractoriness to platelet transfusion due to alloimmunization to HLA antigens [35]. (See "Refractoriness to platelet transfusion", section on 'Management'.)

Although it is common and acceptable to transfuse non ABO-identical platelets due to inventory constraints, transfusion of ABO-non-identical platelets are associated with lower post-transfusion platelet increments when compared with transfusion of ABO-identical platelets, especially when there is major-ABO incompatibility between the recipient and the platelets (eg, group O recipient receiving group A platelets) [65-68]. However, despite the decreased absolute corrected post-transfusion increments, transfusion of ABO-non-identical platelets has no evidence demonstrating improved clinical outcomes, such as reduced bleeding, with ABO-identical or ABO-compatible platelets [69].

Clinically significant hemolytic transfusion reactions secondary to transfusion of minor ABO-incompatible platelet products with high amounts of plasma and or "high titers" of anti-A or anti-B (eg, group O platelets given to group A patient) are uncommon, but they do occur [70,71].

To limit such hemolytic reactions, some transfusion services monitor and limit the volume of ABO incompatible plasma given to a patient via platelet transfusions, or they volume-reduce or wash the ABO incompatible platelet products to reduce the plasma content. Some also screen platelet products for high anti-A or anti-B titers and give products with high titers only to group O patients. However, the critical threshold has not been determined for either the volume of incompatible plasma or the level of anti-A and anti-B titers. (See "Red blood cell antigens and antibodies", section on 'Blood component transfusion' and "Hemolytic transfusion reactions".)

The possibility of alloimmunization to red blood cell (RBC) antigens causing hemolytic disease of the fetus and newborn (HDFN) during pregnancy raises another important issue related to Rh matching of platelets [72]. Although platelets do not express Rh antigens, platelet products contain small numbers of RBCs, which could be Rh incompatible with the recipient. Thus, when an RhD-negative female of childbearing potential receives a platelet transfusion, platelets from an RhD-negative donor are used to prevent alloimmunization and HDFN. The Royal College of Obstetricians and Gynaecologists (RCOG) advises administration of anti-D immune globulin (also called Rho[D] immune globulin) in this setting [73].

Even if this is not done and platelets from an RhD-positive donor are used, the risk of alloimmunization remains low. This was illustrated in a retrospective analysis of 1014 RhD-negative patients who received 6043 platelet transfusions from RhD-positive donors (89 percent from pooled platelets) [74]. No patients who received only apheresis platelets developed anti-RhD antibodies, and 12 of 315 (3.8 percent) who received pooled platelets developed anti-RhD antibodies. However, in a series of 59 RhD-negative patients transfused with platelets from an RhD-positive donor for a non-hematologic condition such as pneumonia or surgery (typical dose, one to three units, given without anti-D immune globulin), alloantibodies to RhD were detected in eight (13.5 percent) [75].

To further reduce the risk of alloimmunization if only RhD-positive platelets are available, anti-D immune globulin can be coadministered with platelet transfusions. Each dose of anti-D immune globulin is considered sufficient to prevent alloimmunization for up to 15 mL of RhD-positive RBCs, and most units of platelets do not contain more than 0.5 mL of RBCs. Thus, a single dose of anti-D immune globulin is likely to be sufficient even if several units of platelets are transfused. If necessary, this can be repeated once every eight weeks (a similar interval to that used to prevent HDFN). (See "RhD alloimmunization in pregnancy: Overview" and "RhD alloimmunization: Prevention in pregnant and postpartum patients".)

WBCs present in HLA matched platelet products can cause transfusion-associated graft-versus-host disease (TA-GVHD), so all HLA-matched platelets must be irradiated. (See "Transfusion-associated graft-versus-host disease", section on 'Partial HLA matching'.)

Platelet additive solutions — After collection, platelets can be resuspended in one of several platelet additive solutions (PAS), as a substitute for a portion of the associated plasma. PAS consist of salts, buffers, and sometimes glucose [76]. Use of PAS platelets decreases but does not eliminate donor plasma exposure, and PAS may provide a less labor-intensive option for reducing allergic transfusion reactions than platelet washing or volume-reduction.

Decisions regarding when to use PAS platelets may depend on the incremental costs and expected benefits. Local availability of PAS platelets may vary, and institution-specific guidelines regarding their use should be followed. One strategy is to use PAS apheresis platelets, which contain less plasma, for patients without a coagulopathy and/or patients who have had minor allergic transfusion reactions [77].

A reduction in allergic transfusion reactions with PAS platelets has been demonstrated in two randomized trials using PAS available in Europe [78,79].

In one trial of patients receiving multiple platelet transfusions (324 transfusions in 21 patients), platelets resuspended in 65 percent PAS with 35 percent plasma were associated with fewer allergic reactions than platelets in 100 percent plasma (5 versus 12 percent) [79]. The platelet count increases following transfusion were slightly lower with PAS platelets than non-PAS platelets (corrected count interval [CCI] at 20 hours 10,000 versus 12,000/microL). (See "Refractoriness to platelet transfusion", section on 'Post-transfusion platelet count'.)

In a trial that randomly assigned 168 patients to PAS versus non-PAS platelets, mild transfusion reactions were seen less commonly with PAS compared with non-PAS platelets (2 versus 6 percent) [78]. CCI was slightly lower with PAS compared with non-PAS platelets in this trial as well (CCI at 24 hours 7000 versus 8000/microL).

Neither trial showed a difference in bleeding complications with PAS versus non-PAS platelets.

A large retrospective study (5078 patients) compared outcomes with apheresis platelets resuspended in a PAS solution approved by the US Food and Drug Administration (InterSol, 65 percent, with 35 percent plasma) versus 100 percent plasma [77]. The incidence of allergic transfusion reactions was reduced with PAS apheresis platelets (PAS AP) compared with non-PAS AP (1.01 versus 1.85 percent; relative risk [RR] 0.54; 95% CI 0.30-0.99). The incidence of febrile non-hemolytic transfusion reactions did not differ. Among individuals for whom paired PAS AP and non-PAS AP transfusions could be compared, there was no difference in the CCI at 12 to 24 hours, although PAS AP were associated with a slight reduction in CCI at four hours compared with non-PAS AP.

The use of PAS platelets may not be possible when HLA matched or CMV-negative products are needed. PAS platelets can be irradiated.

Other special modifications — Patients with known IgA deficiency who have a history of anaphylactic transfusion reactions or demonstrate anti-IgA antibodies can be transfused with platelets that have been washed to remove IgA-containing plasma or obtained from IgA deficient donors. (See "Selective IgA deficiency: Management and prognosis", section on 'Safe administration of blood products'.)

In addition, volume-reduced platelets can be used when exposure to ABO incompatible plasma needs to be limited, or for transfusion of volume-sensitive patients.

As noted above and separately, platelets can also be treated with a pathogen-inactivation method. (See 'Storage' above and "Pathogen inactivation of blood products", section on 'Platelets'.)

COMPLICATIONS — Platelet transfusion carries several risks including infection, transfusion reactions, alloimmunization, and post-transfusion purpura.

Complication rate with apheresis versus whole blood-derived (WBD) platelets — The relative frequency of complications with apheresis versus WBD platelets has not been studied in large randomized trials.

A 2008 systematic review and meta-analysis that evaluated several small randomized trials (mostly with fewer than 100 patients) found a greater incidence of reactions with WBD platelets; however, this was no longer significant after controlling for the use of leukoreduction [80].

A 2016 study involving almost 800,000 platelet transfusions found that apheresis platelets were associated with a greater frequency of adverse reactions (approximately 6 per 1000 for apheresis platelets versus 2 per 1000 for WBD platelets) [81]. In this study, all platelets were leukoreduced (during collection for apheresis, and before storage for WBD). However, comparison may be difficult due to the different size of apheresis versus WBD platelet units and the challenges of calculating the incidence per unit when multiple units are administered.

Additional data are needed before a clear conclusion on relative risk of complications can be made.

Infection — Donor screening procedures and pathogen inactivation do not completely eliminate the risk of bacterial and other bloodborne infections, and transfusion-transmitted bacterial infection from platelets represents a serious hazard of platelet transfusion that may be fatal [82-85]. This is because platelets are stored at room temperature, where bacteria can proliferate rapidly. (See 'Room temperature storage' above.)

Bacteria are more often cultured from platelets (approximately 1 in 2000) than red blood cells (RBCs) (approximately 1 in 30,000) [86,87]. A 2020 meta-analysis that included 22 studies (over 5 million platelet units) found a rate of 1:1961, with lower rates for apheresis units and platelet rich plasma collection versus buffy coat collection and a gradual decline in rates year over year [88].

Evaluation and management of septic transfusion reactions are discussed separately. (See "Transfusion-transmitted bacterial infection".)

Measures that reduce the presence of bacteria include enhancements to skin preparation technique, diversion of the first 15 to 45 mL of collected blood so that it is not transfused, culturing the product, and using pathogen-inactivation technologies.

A change to the skin preparation technique in 2012 in the United States was associated with a decrease from 4.2 instances of bacterial contaminants per year to 0.8 per year [89,90].

Culture of the product 24 to 36 hours after collection to identify and remove contaminated units was associated with a decrease from 492 to 82 septic transfusion reactions per million units [89].

Guidance from the US Food and Drug Administration (FDA) requires additional procedures to reduce infectious risks. (See 'Strategies for reducing bacteria and other pathogens' above.)

Alloimmunization — Platelets express Class I human leukocyte antigen (HLA) antigens, which can be recognized by the recipient's immune system as foreign. Production of anti-HLA antibodies can adversely affect the response to future platelet transfusions. The incidence of alloimmunization depends on the number of transfusions a patient has received. (See "Refractoriness to platelet transfusion", section on 'Alloimmunization' and 'Platelet count increment' below.)

Platelet products also contain small volumes of RBCs, and alloimmunization to RBC antigens can occur as a result. This is especially of concern in RhD-negative females of childbearing potential, who are at risk for hemolytic disease of the fetus and newborn (HDFN) if they have an RhD-positive pregnancy. Platelet transfusion to an RhD-negative recipient of childbearing potential is one of the settings in which it may be appropriate to use RhD-matched platelets and/or to administer anti-D immune globulin (also called Rho[D] immune globulin) when RhD-positive platelets are transfused, as a way to limit the risk of alloimmunization. (See 'ABO, Rh, and HLA matching' above.)

Transfusion reactions — Transfusion of any blood product, including platelets, can cause transfusion reactions including those listed here. An approach to distinguishing among acute transfusion reactions is presented separately. (See "Approach to the patient with a suspected acute transfusion reaction".)

Transfusion-related acute lung injury (TRALI) – Transfusion-related acute lung injury (TRALI) is a form of acute lung injury that causes respiratory distress following transfusion. The contemporary incidence of TRALI from platelet transfusion is unknown; it has decreased since institution of TRALI mitigation strategies in the late 2000s [91]. (See "Transfusion-related acute lung injury (TRALI)", section on 'Epidemiology'.)

Transfusion-associated circulatory overload (TACO) – Platelet transfusion introduces approximately 200 mL of intravascular volume per transfusion. The incidence of TACO is in the range of 1 percent of transfused recipients. The incidence is higher in patients predisposed to volume overload due to comorbidities such as congestive heart failure, kidney failure, respiratory failure, and positive fluid balance. (See "Transfusion-associated circulatory overload (TACO)".)

Allergic and anaphylactic reactions – Allergic reactions to platelet transfusion are relatively common. They are usually due to IgE directed against proteins in the donor plasma. Common symptoms include urticaria and pruritus in mild cases, and wheezing, shortness of breath and hypotension in more severe cases. (See "Immunologic transfusion reactions", section on 'Allergic reactions'.)

Patients with a history of allergic transfusion reactions who require additional platelet transfusions may benefit from platelets in additive solution (PAS), which contain less plasma than non-PAS platelets. Those who continue to have allergic reactions with PAS platelets may receive concentrated or washed platelets. (See 'Platelet additive solutions' above and 'Other special modifications' above.)

Anaphylactic reactions (ie, severe allergic reactions) are a very rare complication of platelet transfusion. These are associated with rapid onset of shock, angioedema, and respiratory distress. Some cases are due to the production of anti-IgA antibodies in recipients who are IgA deficient. (See "Immunologic transfusion reactions", section on 'Anaphylactic transfusion reactions'.)

Febrile non-hemolytic transfusion reactions (FNHTR) – These reactions are mediated by various inflammatory mediators and leukocytes and may manifest as fevers, chills, and rigors. (See "Immunologic transfusion reactions", section on 'Febrile nonhemolytic transfusion reactions'.)

TA-GVHD – Transfusion-associated graft-versus-host disease (TA-GVHD) can occur with any type of transfusion that contains lymphocytes, given the correct immunologic setting. Its incidence continues to drop due to irradiation of blood products for at-risk patients, such as patients with hematopoietic cell transplantation, immunodeficiency, or other types of immunosuppression. (See 'Irradiation' above.)

A second and potentially less obvious situation that can lead to TA-GVHD in immunocompetent recipients is partial HLA matching, as can occur in donations made by relatives and in genetically homogeneous populations [64]. In this case, the HLA antigens on the donor lymphocytes are seen by the recipient lymphocytes as self, so recipient lymphocytes do not attack the donor lymphocytes; however, recipient cells also express unique HLA antigens that the donor lymphocytes recognize as foreign. This can result in donor lymphocytes destroying the recipient's tissues, including bone marrow, skin and liver, which can be fatal. (See "Transfusion-associated graft-versus-host disease".)

Post-transfusion purpura — Post-transfusion purpura (PTP) is a rare transfusion reaction to any platelet-containing product, in which thrombocytopenia develops 5 to 10 days following transfusion. This can occur in the <2 percent of individuals who lack the platelet antigen PIA1, now known as human platelet antigen 1a (HPA-1a), and who have become previously sensitized to the antigen during pregnancy or prior transfusion. (See "Immunologic transfusion reactions", section on 'Post-transfusion purpura'.)

In PTP, transfused platelets are removed by an antibody-mediated mechanism; the patient's own HPA-1a-negative platelets are also destroyed by an incompletely understood process.

Treatment is with intravenous immune globulin (IVIG), with or without a glucocorticoid. HPA-1a-negative products should be used whenever possible if platelet transfusion is indicated.

PLATELET COUNT INCREMENT — Following a platelet transfusion, the platelet count should rise, with a peak at 10 minutes to one hour and a gradual decline over 72 hours. A general rule of thumb is that transfusion of a standard pool of whole blood derived (WBD) platelets or one apheresis unit should increase the platelet count by approximately 30,000/microL in an adult of average size.

Platelet count increment is typically measured within 24 hours in patients given prophylactic platelet transfusions. For patients undergoing invasive procedures, it is prudent to check that the desired platelet count was achieved before performing the procedure, which can be done within 10 minutes of the transfusion. For actively bleeding patients, cessation of bleeding is a more important clinical endpoint than the post-transfusion platelet count.

The length of time platelets have been stored has a modest effect on their survival in the recipient. As an example, compared with platelets stored for two or three days, platelets stored for five days produce a smaller increment in platelet count. This information is not usually factored into assessment of a patient's response to platelet transfusion.

Many patients who receive platelet transfusions reproducibly show a less-than-expected increase in platelet count. The definition of platelet refractoriness and its management are discussed separately. (See "Refractoriness to platelet transfusion", section on 'Monitoring and evaluation' and "Refractoriness to platelet transfusion".)

ALTERNATIVES TO PLATELET TRANSFUSION — There are no substitutes for platelet transfusion to rapidly increase the platelet count in a bleeding patient. Reversal of thrombocytopenia due to autoimmune platelet destruction, platelet consumption, or bone marrow suppression can take days to weeks, depending on the underlying cause.

Patients with ongoing bleeding not responsive to platelet transfusion and other interventions can also be given procoagulant bypass agents, such as prothrombin complex concentrates or recombinant factor VIIa [60]. (See "Medical management of the dialysis patient undergoing surgery", section on 'Bleeding diathesis' and "Uremic platelet dysfunction", section on 'Acute life-threatening bleeding'.)

In some settings, fibrinolytic inhibitors such as tranexamic acid have been effective. (See "Coagulopathy in trauma patients", section on 'Pharmaceutical hemostatic agents' and "Managing an episode of acute uterine bleeding", section on 'Tranexamic acid'.)

Stimulation of bone marrow megakaryocytes with thrombopoietin receptor agonists can take up to seven days (ie, the time it takes for new platelets to form). This might be appropriate for selected indications for preventing bleeding. (See "Clinical applications of thrombopoietic growth factors", section on 'Use of TPO receptor agonists'.)

Investigational approaches such as the use of human leukocyte antigen (HLA)-deleted platelets generated from induced pluripotent stem cells (iPSCs) (see "Genetics: Glossary of terms", section on 'Induced pluripotent stem cell (iPSC)') or the use of platelet substitutes (eg, synthetic or acellular biological materials that could replace the primary hemostatic function of platelets) have not reached clinical trials [92-95].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Immune thrombocytopenia (ITP) and other platelet disorders" and "Society guideline links: Transfusion and patient blood management".)


Means of collection and content of a unit – A unit of whole blood derived (WBD) platelets contains approximately 7 x 1010 platelets, and four to six of these units are typically pooled for transfusion. Apheresis platelets are collected from a single donor and contain approximately 3 to 4 x 1011 platelets (the equivalent of a pool of four to six WBD units). (See 'Collection methods' above.)

Storage – Platelets are stored at room temperature; consequently, their shelf-life is only five days (though it may be extended to seven days if additional requirements are met). Cold storage of platelets and cryopreservation are under study. (See 'Storage' above.)


Bleeding – Platelet transfusion can be lifesaving in bleeding patients with thrombocytopenia or reduced platelet function. Platelets should be transfused in any patient who is bleeding with a platelet count <50,000/microL (100,000/microL for central nervous system or ocular bleeding), or in any patient with an acquired or inherited platelet function disorder, regardless of platelet count. Platelet transfusion may also be indicated in thrombocytopenic patients undergoing invasive procedures, depending on the procedure and the platelet count. (See 'Actively bleeding patient' above and 'Preparation for an invasive procedure' above.)

Other conditions that impair hemostasis (coagulopathy, fever, infection, anatomic lesions) should be corrected in thrombocytopenic patients when possible, to reduce active bleeding and lessen the risk of spontaneous bleeding. (See 'Actively bleeding patient' above.)

Prophylaxis – For most hospitalized afebrile patients with platelet counts ≤10,000/microL due to bone marrow suppression, we suggest prophylactic platelet transfusion rather than reserving transfusions only for bleeding (Grade 2C). Centers that use lower thresholds or only transfuse for bleeding should ensure that experienced clinicians are present who can rapidly identify bleeding and administer platelet transfusions.

Some individuals may require transfusion at higher platelet counts. For patients with fever, infection, or inflammation, we generally transfuse at a platelet count ≤15,000 to 20,000/microL due to the increased risk of bleeding. For patients with acute promyelocytic leukemia (APL), which is associated with a severe coagulopathy, we transfuse at a platelet count of ≤30,000 to 50,000/microL. (See 'Prevention of spontaneous bleeding' above and 'Specific clinical scenarios' above.)

Platelet consumption disorders – Patients with platelet consumption disorders, including immune thrombocytopenia (ITP), thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT), disseminated intravascular coagulation (DIC), liver disease, as well as those with platelet function disorders, are typically transfused only for bleeding or selected invasive procedures. Platelets should not be withheld in bleeding patients with these conditions due to fear of "fueling the fire" of thrombosis. (See 'Specific clinical scenarios' above.)

Complications – Platelet transfusion has risks, including sepsis/infection, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), alloimmunization, allergic and anaphylactic transfusion reactions, febrile non-hemolytic transfusion reactions (FNHTR), transfusion-associated graft-versus-host disease (TA-GVHD), and post-transfusion purpura (PTP). The US Food and Drug Administration (FDA) issued guidance to reduce the risk of transfusion-transmitted infections from platelet products. (See 'Complications' above and 'Strategies for reducing bacteria and other pathogens' above.)

Refractoriness – (See "Refractoriness to platelet transfusion".)

Dosing and modifications – When ordering platelets, one should consider the appropriate dose; whether to use apheresis versus WBD platelets; and whether to request leukoreduction, irradiation, a pathogen-inactivated product, or a CMV-negative product; and whether to match for ABO, RhD type, and human leukocyte antigen (HLA) type. (See 'Ordering platelets' above.)

Alternatives to platelet transfusion – Limited alternatives to platelet transfusion exist for thrombocytopenia-associated bleeding. Longer term alternatives include discontinuation of anti-platelet drugs, treatment of underlying conditions, and medications to increase platelet production. (See 'Actively bleeding patient' above and 'Alternatives to platelet transfusion' above and 'Platelet function disorders' above.)

ACKNOWLEDGMENT — We are saddened by the death of Dennis Goldfinger, MD, who passed away in September 2021. The UpToDate editorial staff acknowledges Dr. Goldfinger's past work for many years as an author for this topic.

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