3.

What does available data support regarding complications

in these pts

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aspects-of-platelet-transfusion-
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0781574&source=see_link#H323107

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 in the absence of bleeding or a required
invasive procedure.

Liver disease and DIC — Patients with liver disease and disseminated intravascular
coagulation (DIC) have a complex mixture of procoagulant and anticoagulant defects along with
thrombocytopenia, and therefore they are at risk for 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 "Clinical features, diagnosis, and treatment of disseminated intravascular coagulation in
adults", section on 'Prevention/treatment of bleeding' and "Hemostatic abnormalities in patients
with liver disease", section on 'Bleeding'.)

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e_link#H323107
COMPLICATIONS OF PLATELET TRANSFUSION (in general)— Platelet transfusion carries
several risks. The relative frequency of complications with apheresis versus whole blood-
derived, pooled platelets have 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 whole blood-derived platelets;
however, this was no longer significant after controlling for the use of leukoreduction [54]. A
2016 study involving almost 800,000 platelet transfusions in France 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 whole blood-derived platelets) [55]. In this
study, all platelets were leukoreduced (during collection for apheresis, and before storage for
whole blood-derived). However, comparison may be difficult due to the different size of
 apheresis versus pooled 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. (Seepla 'Dose' above.)

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growth-
factors?search=liver%20cirrhosis%20and%20platelet%20transfusion&source=sear
ch_result&selectedTitle=5~150&usage_type=default&display_rank=5#H31

IMPACT ON PLATELET TRANSFUSION — There was much early enthusiasm for using
thrombopoietin (TPO) in the acute treatment of thrombocytopenia in lieu of platelet transfusions
[106]. However, since none of the thrombopoietic molecules hastens megakaryocyte
fragmentation into platelets and all take five days to start to increase platelet production [9],
TPO will not replace platelet transfusions in this acute setting. Nevertheless, there remains
interest in developing another substance (eg, SDF-1) that might stimulate platelet shedding from
existing megakaryocytes and possibly reduce the need for acute platelet transfusions.

It is unlikely that TPO receptor agonists will have a major impact on the need for platelet
transfusions. The TPO receptor agonists may be useful in modestly reducing the incidence of
thrombocytopenia in nonmyeloablative chemotherapy. However, since this type of
thrombocytopenia is a rather uncommon event in routine oncology practice, there will probably
be little reduction in the overall use of platelet transfusions. For several newer chemotherapy
regimens (eg, use of bortezomib, lenalidomide, gemcitabine) in which thrombocytopenia is more
marked, thrombopoietic growth factors may be of greater, as yet untested, use.

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ch_result&selectedTitle=5~150&usage_type=default&display_rank=5#H31

SIDE EFFECTS AND RISKS — For any hematopoietic growth factor, potential adverse effects
must be carefully assessed. For the thrombopoietins a number of actual or potential toxicities
have been identified (table 3). Cost may also be limiting in some settings.

Potential adverse consequences of thrombopoietic growth factor

treatment
Thrombocytosis
Thrombosis

Stimulation of tumor cell growth

Stimulation of leukemia cell growth

Interactions with other cytokines

Autoantibody formation

Reduction in threshold for platelet activation

Increased bone marrow reticulin (positive reticulin stain)

Increased bone marrow collagen (positive trichrome stain)

Rebound worsening of thrombocytopenia upon stopping treatment

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Refractoriness to platelet transfusion therapy

Authors:

Dennis Goldfinger, MD

James D Burner, MD

Section Editor:

Arthur J Silvergleid, MD

Deputy Editor:

Jennifer S Tirnauer, MD

INTRODUCTION

Platelets play a vital role in the maintenance of normal hemostatic activity. Accordingly, for
patients with low platelet counts (thrombocytopenia) or impaired platelet function, platelet
transfusion can be of significant value in preventing and treating hemorrhage. (See "Overview of
hemostasis".)

Although many patients have an appropriate increase in platelet count when transfused with
platelets, less than adequate results tend to be common with 28 to 44 percent of platelet
transfusions failing to produce a satisfactory response [1-3]. In the hematology/oncology patient,
published reports have cited an incidence of refractoriness to platelet transfusion of 15 to 25
percent utilizing leukocyte-reduced blood products and even higher rates during the pre-
leukocyte-reduction era [2,4-6]. This poor response to platelet transfusion leads to an increased
risk of morbidity and mortality, as well as longer hospital stays and higher inpatient hospital
costs [7,8]. (See "Clinical and laboratory aspects of platelet transfusion therapy".)

The numerous factors associated with poor recovery and survival of transfused platelets (non-
immune and immune), and the diagnosis, management, and prevention of alloimmune
refractoriness to platelet transfusion will be reviewed here. General issues related to platelet
transfusion are discussed separately. (See "Clinical and laboratory aspects of platelet
transfusion therapy".)

ETIOLOGY

Refractoriness to platelet transfusion is often multifactorial and can be separated into non-
immune and immune causes (table 1).

●Approximately two-thirds of refractory episodes are due to non-immune causes, such

as sepsis/infection, fever (temperature >38.4°C), bleeding, splenomegaly, disseminated
intravascular coagulation (DIC), hepatic sinusoidal obstruction syndrome (hepatic veno-
occlusive disease), graft-versus-host disease (GVHD) and medications such as
vancomycin, amphotericin B and heparin [4,5,9]. (See 'Non-alloimmune causes' below.)

4. Can these complications be correlated to platelet count of the patient