Platelet transfusion refractoriness: Difference between revisions

Latest revision as of 19:05, 22 March 2025

A condition where patients do not respond adequately to platelet transfusions

Platelet Transfusion Refractoriness[edit]

Platelet transfusion refractoriness is a clinical condition in which patients exhibit an inadequate response to platelet transfusions. This condition is of particular concern in patients who require frequent platelet transfusions, such as those undergoing treatment for hematological malignancies or those with severe thrombocytopenia.

Causes[edit]

Platelet transfusion refractoriness can be caused by a variety of factors, which are generally categorized into immune and non-immune causes.

Immune Causes[edit]

Immune-mediated refractoriness is often due to the development of alloantibodies against human leukocyte antigens (HLA) or human platelet antigens (HPA). These antibodies can develop after exposure to foreign antigens through previous transfusions, pregnancy, or transplantation. The presence of these antibodies leads to rapid destruction of transfused platelets, resulting in poor post-transfusion platelet increments.

Non-Immune Causes[edit]

Non-immune causes of refractoriness include factors such as splenomegaly, fever, sepsis, disseminated intravascular coagulation (DIC), and the use of certain medications. These conditions can lead to increased platelet consumption or destruction, independent of immune mechanisms.

Diagnosis[edit]

The diagnosis of platelet transfusion refractoriness is typically made by measuring the post-transfusion platelet count increment. A corrected count increment (CCI) of less than 5,000 to 7,500 per microliter at 10 to 60 minutes post-transfusion on at least two occasions is indicative of refractoriness.

Management[edit]

Management of platelet transfusion refractoriness involves identifying and addressing the underlying cause. For immune-mediated refractoriness, strategies may include:

For non-immune causes, treatment focuses on managing the underlying condition, such as controlling infections or discontinuing medications that may contribute to platelet destruction.

Prevention[edit]

Preventive strategies for platelet transfusion refractoriness include:

Limiting exposure to allogeneic platelets by using leukoreduced blood products
Using single-donor apheresis platelets instead of pooled random donor platelets
Implementing transfusion protocols that minimize unnecessary platelet transfusions

Related Pages[edit]

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-'''Platelet transfusion refractoriness''' is the repeated failure to achieve the desired level of [[blood platelet]]s in a patient following a platelet [[blood transfusion|transfusion]]. The cause of refractoriness may be either [[immune system|immune]] or non-immune. Among immune-related refractoriness, antibodies against [[Human leukocyte antigen|HLA antigens]] are the primary cause.  Non-immune causes include [[splenomegaly]] (enlargement of the spleen), [[fever]], and sepsis.<ref>
+{{Short description|A condition where patients do not respond adequately to platelet transfusions}}
-{{Citation
- | last = Colman
- | first = Robert W.
- | last2 = Marder
- | first2 = Victor J.
- | last3 = Clowes
- | first3 =Alexander W.
- | last4 = George
- | first4 = James N.
- | last5 = Goldhaber
- | first5 = Samuel Z.
- | date = 2005
- | title = Hemostasis and Thrombosis: Basic Principles and Clinical Practice
- | edition = 5th
- | publisher = Lippincott Williams & Wilkins
- | page = 1195
- | isbn = 978-0-7817-4996-1
-}}
-</ref><ref name=":0">{{Cite journal|last=Stanworth|first=Simon J.|last2=Navarrete|first2=Cristina|last3=Estcourt|first3=Lise|last4=Marsh|first4=Judith|date=2015|title=Platelet refractoriness – practical approaches and ongoing dilemmas in patient management|journal=British Journal of Haematology|language=en|volume=171|issue=3|pages=297–305|doi=10.1111/bjh.13597|pmid=26194869|issn=1365-2141}}</ref>
-==Cause==
+==Platelet Transfusion Refractoriness==
-Platelet refractoriness can be due to immune causes or non-immune causes.<ref name=":1">{{Cite web|url=http://hospital.blood.co.uk/media/2130/d5795605-7d36-40ce-8fb9-8c77254e24c6.pdf|title=Guidelines for the management of platelet transfusion refractoriness|last=|first=|date=|website=hospital.blood.co.uk|archive-url=|archive-date=|dead-url=|access-date=2018-12-28}}</ref> Non-immune causes account for over 80% of cases of platelet refractoriness, and sepsis is one of the most common non-immune causes.<ref name=":0" /><ref name=":1" /><ref name=":2">{{Cite web|url=https://transfusion.com.au/transfusion_practice/platelet_refractoriness|title=transfusion.com.au|website=transfusion.com.au|language=en|access-date=2018-12-28}}</ref><ref name=":3">{{Cite journal|last=Hod|first=Eldad|last2=Schwartz|first2=Joseph|date=2008|title=Platelet transfusion refractoriness|journal=British Journal of Haematology|language=en|volume=142|issue=3|pages=348–360|doi=10.1111/j.1365-2141.2008.07189.x|pmid=18510692|issn=1365-2141}}</ref> [[Human leukocyte antigen|HLA]] [[alloimmunization]] is the commonest immune cause of platelet refractoriness.<ref name=":0" /><ref name=":1" /><ref name=":2" /><ref name=":3" />
-===Non-immune causes===
+'''Platelet transfusion refractoriness''' is a clinical condition in which patients exhibit an inadequate response to platelet transfusions. This condition is of particular concern in patients who require frequent platelet transfusions, such as those undergoing treatment for hematological malignancies or those with severe thrombocytopenia.
-==== Patient-related ====
+==Causes==
-*[[Sepsis]]
+Platelet transfusion refractoriness can be caused by a variety of factors, which are generally categorized into immune and non-immune causes.
-*Fever
+===Immune Causes===
-*[[Disseminated intravascular coagulation]]
+Immune-mediated refractoriness is often due to the development of [[alloantibodies]] against human leukocyte antigens ([[HLA]]) or human platelet antigens ([[HPA]]). These antibodies can develop after exposure to foreign antigens through previous transfusions, pregnancy, or transplantation. The presence of these antibodies leads to rapid destruction of transfused platelets, resulting in poor post-transfusion platelet increments.
-*[[Splenomegaly]]
+===Non-Immune Causes===
-*Treatment of infection, antibiotics (vancomycin), antifungals (amphotericin B)
+Non-immune causes of refractoriness include factors such as [[splenomegaly]], [[fever]], [[sepsis]], [[disseminated intravascular coagulation]] (DIC), and the use of certain medications. These conditions can lead to increased platelet consumption or destruction, independent of immune mechanisms.
-*[[Graft-versus-host disease]]
-*[[Hepatic veno-occlusive disease]]
-*Bleeding
-==== Platelet component-related ====
-* Age of platelet component<ref name=":9">{{Cite journal|last=Slichter|first=Sherrill J.|last2=Granger|first2=Suzanne|last3=Kaufman|first3=Richard M.|last4=Hess|first4=John R.|last5=Ness|first5=P. M.|last6=Strauss|first6=Ronald G.|last7=Assmann|first7=Susan F.|last8=Triulzi|first8=Darrell J.|date=2012-06-07|title=The impact of platelet transfusion characteristics on posttransfusion platelet increments and clinical bleeding in patients with hypoproliferative thrombocytopenia|journal=Blood|language=en|volume=119|issue=23|pages=5553–5562|doi=10.1182/blood-2011-11-393165|issn=1528-0020|pmc=3369689|pmid=22496156}}</ref><ref name=":10">{{Cite book|url=https://professionaleducation.blood.ca/en/transfusion/guide-clinique/platelet-transfusion-alloimmunization-and-management-platelet|title=Chapter 18: Platelet Transfusion, Alloimmunization and Management of Platelet Refractoriness|last=Petraszko|first=Tanya|last2=Zeller|first2=Michelle|publisher=Canadian Blood Services|year=2018|isbn=|location=|pages=}}</ref>
-* ABO mismatch between platelet component and recipient<ref name=":9" /><ref name=":10" />
-* Number of platelets within the component if platelet increment (PI) is used to calculate platelet refractoriness<ref name=":9" />
-* Pathogen-reduced platelet component<ref>{{Cite journal|last=Estcourt|first=Lise J|last2=Malouf|first2=Reem|last3=Hopewell|first3=Sally|last4=Trivella|first4=Marialena|last5=Doree|first5=Carolyn|last6=Stanworth|first6=Simon J|last7=Murphy|first7=Michael F|date=2017-07-30|title=Pathogen-reduced platelets for the prevention of bleeding|journal=Cochrane Database of Systematic Reviews|volume=7|pages=CD009072|doi=10.1002/14651858.cd009072.pub3|issn=1465-1858|pmc=5558872|pmid=28756627}}</ref>
-===Immune causes===
-*Alloantibodies to platelet antigens
-**[[Human leukocyte antigen|Human leucocyte antigen (HLA)]] antibodies
-**Human platelet antigen (HPA) antibodies
-*[[Immune complex|Immune complexes]]
-*Other antibodies
-**Drug-related antibodies
 ==Diagnosis==
-Platelet transfusion refractoriness can be defined in several different ways. All measures of platelet refractoriness are defined by the timing of the post-transfusion platelet count, usually 1 hour post transfusion or 24 hours post transfusion or both.<ref name=":0" /><ref name=":4">{{Cite journal|last=Rebulla|first=Paolo|date=2005|title=A mini-review on platelet refractoriness|journal=Haematologica|volume=90|issue=2|pages=247–253|issn=1592-8721|pmid=15710579}}</ref>
-===Platelet increment (PI)===
-This is the simplest method, and only requires data on the platelet count before and after the transfusion.<ref name=":4" /> The platelet increment is also known as the '''absolute count increment''' and '''count increment'''.<ref name=":6" /><ref name=":3" />
-PI = post-transfusion platelet count - pre-transfusion platelet count
-However, it is affected by the number of platelets given in the transfusion (platelet dose) and the patient’s blood volume. Larger patients and smaller platelet doses decrease the platelet increment.<ref name=":0" /><ref name=":4" /> These factors are adjusted for in the other methods of defining platelet refractoriness.<ref name=":0" /><ref name=":1" /><ref name=":4" />
-A 1 hour post-transfusion PI of less than 5 to 10 x 10<sup>9</sup>/l is considered evidence of platelet refractoriness.<ref name=":3" /><ref name=":6" /> Due to lack of data on platelet dose this is often the only measure of platelet refractoriness that can be performed in routine clinical practice.<ref name=":3" />
-===Percentage platelet recovery (PPR)===
-Requires data on the platelet increment (PI), the patient’s total blood volume (TBV) - estimated using the patient’s weight multiplied by 0.075, and the number of platelets transfused (platelet dose)<ref name=":5">{{Cite journal|last=Rebulla|first=P.|date=1993|title=Formulae for the definition of refractoriness to platelet transfusion|journal=Transfusion Medicine|language=en|volume=3|issue=1|pages=91–92|doi=10.1111/j.1365-3148.1993.tb00108.x|issn=1365-3148}}</ref><ref name=":6">{{Cite journal|last=Pavenski|first=Katerina|last2=Freedman|first2=John|last3=Semple|first3=J. W.|date=2012|title=HLA alloimmunization against platelet transfusions: pathophysiology, significance, prevention and management|journal=Tissue Antigens|volume=79|issue=4|pages=237–245|doi=10.1111/j.1399-0039.2012.01852.x|issn=1399-0039|pmid=22385314}}</ref>
-PPR = ((PI x TBV)/PD) x 100
-At 1 hour post-transfusion, a PPR < 20% is considered evidence of platelet refractoriness.<ref name=":3" /><ref name=":6" /> At 16 hours post-transfusion a PPR < 10% is considered evidence of platelet refractoriness.<ref name=":6" />
-===Percentage platelet increment (PPI)===
-PPI is very similar to the percentage platelet recovery (PPR) but the patient’s total blood volume is estimated using the patient’s weight multiplied by 0.07, and there has been an additional adjustment for splenic pooling of platelets (multiplied by 2/3)<ref name=":5" /><ref name=":3" />
-PPI = ((PI x TBV x 0.67)/PD) x 100
-===Corrected count increment (CCI)===
-This requires data on the platelet increment (PI), the patient’s [[Body surface area]] (BSA), and the number of platelets transfused (PD).<ref name=":5" /><ref name=":3" /><ref name=":6" />
-CCI = ((PI x BSA)/PD
+The diagnosis of platelet transfusion refractoriness is typically made by measuring the post-transfusion platelet count increment. A corrected count increment (CCI) of less than 5,000 to 7,500 per microliter at 10 to 60 minutes post-transfusion on at least two occasions is indicative of refractoriness.
-At 1 hour post-transfusion a CCI greater than 7500 indicates a sufficient post-transfusion increment, whereas a CCI less than 7500 is considered diagnostic of platelet refractoriness.<ref name=":6" /> At 24 hours post transfusion a CCI less than 5000 suggests platelet refractoriness.<ref name=":6" />
+==Management==
-===Platelet dose===
+Management of platelet transfusion refractoriness involves identifying and addressing the underlying cause. For immune-mediated refractoriness, strategies may include:
-Some blood banks maintain records of the estimated number of platelets in each unit.<ref name=":3" /> Current requirements in the US stipulate that a unit of apheresis platelets must contain at least 3.0 x10<sup>11</sup> platelets.<ref>{{cite book|last=AABB|title=Standards for Blood Banks and Transfusion Services|date=2014|publisher=AABB|isbn=9781563958878}}</ref> In England only 1% of adult platelet components are tested to check the number of platelets meet the minimum required standard of 2.4 x 10<sup>11</sup> platelets. <ref name=":7">{{Cite web|url=https://www.transfusionguidelines.org/red-book/chapter-7-specifications-for-blood-components/7-10-platelets-apheresis-leucocyte-depleted|title=Platelets, Apheresis, Leucocyte Depleted|website=www.transfusionguidelines.org|access-date=2018-12-29}}</ref><ref name=":8">{{Cite web|url=https://www.transfusionguidelines.org/red-book/chapter-7-specifications-for-blood-components/7-11-platelets-in-additive-solution-and-plasma-leucocyte-depleted|title=Platelets, Pooled, Buffy Coat Derived, in Additive Solution and Plasma, Leucocyte Depleted|website=www.transfusionguidelines.org|access-date=2018-12-29}}</ref> Only components that contain fewer than 1.6 x 10<sup>11</sup> platelets are discarded.<ref name=":7" /><ref name=":8" /> This means that there can be a lot of variability in the number of platelets contained within each transfusion.<ref name=":3" />
-== Treatment ==
+* Using [[HLA-matched platelets]]
-This depends on the underlying cause.
+* Using [[cross-matched platelets]]
+* Using [[HPA-matched platelets]]
-Non-immune causes are usually treated by treating the underlying cause e.g. [[sepsis]].<ref name=":1" /><ref name=":11">{{Cite journal|last=Nahirniak|first=Susan|last2=Slichter|first2=Sherrill J.|last3=Tanael|first3=Susano|last4=Rebulla|first4=Paolo|last5=Pavenski|first5=Katerina|last6=Vassallo|first6=Ralph|last7=Fung|first7=Mark|last8=Duquesnoy|first8=Rene|last9=Saw|first9=Chee-Loong|date=2015|title=Guidance on platelet transfusion for patients with hypoproliferative thrombocytopenia|journal=Transfusion Medicine Reviews|volume=29|issue=1|pages=3–13|doi=10.1016/j.tmrv.2014.11.004|issn=1532-9496|pmid=25537844}}</ref>
+For non-immune causes, treatment focuses on managing the underlying condition, such as controlling infections or discontinuing medications that may contribute to platelet destruction.
-If there is no obvious non-immune cause, a first step can be to use platelet components that are likely to produce the greatest platelet increment (less than 3 days old and ABO-matched), while further investigations are performed (testing for HLA antibodies).<ref name=":1" /><ref name=":2" />
+==Prevention==
-If an immune cause is suspected and  HLA antibodies are detected, then HLA-selected platelet components can be used.<ref name=":1" /><ref name=":2" /> Although HLA-selected platelets lead to improved platelet increments at 1 hour post-transfusion,<ref name=":12">{{Cite journal|last=Pavenski|first=Katerina|last2=Rebulla|first2=Paolo|last3=Duquesnoy|first3=Rene|last4=Saw|first4=Chee Loong|last5=Slichter|first5=Sherrill J.|last6=Tanael|first6=Susano|last7=Shehata|first7=Nadine|date=2013|title=Efficacy of HLA-matched platelet transfusions for patients with hypoproliferative thrombocytopenia: a systematic review|journal=Transfusion|language=en|volume=53|issue=10|pages=2230–2242|doi=10.1111/trf.12175|pmid=23550773|issn=1537-2995}}</ref> there is currently insufficient evidence to demonstrate their clinical effectiveness at preventing bleeding.<ref name=":12" />
+Preventive strategies for platelet transfusion refractoriness include:
-If HLA antibodies are not detected, and HPA antibodies are detected, then HPA-selected or crossmatched platelet components can be used.<ref name=":1" /><ref name=":10" /><ref name=":11" />
+* Limiting exposure to allogeneic platelets by using leukoreduced blood products
+* Using single-donor apheresis platelets instead of pooled random donor platelets
+* Implementing transfusion protocols that minimize unnecessary platelet transfusions
-HLA and HPA-selected components should not be used if no HLA or HPA antibodies are detected.<ref name=":11" />
+==Related Pages==
-== References ==
+* [[Thrombocytopenia]]
-{{reflist}}
+* [[Blood transfusion]]
+* [[Hematology]]
+* [[Immunohematology]]
-[[Category:Transfusion reactions]]
+[[Category:Hematology]]
-[[Category:Coagulopathies]]
 [[Category:Transfusion medicine]]
-{{blood-disease-stub}}
-{{dictionary-stub1}}
-{{No image}}