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Post-Transfusion Thrombocytopenia: Its Duration in Splenic and Asplenic Individuals
Abstract
Previous work in our department showed that after blood transfusion, the platelet count often falls to levels which are clinically significant. The probable site of platelet sequestration was identified as the spleen, and post-transfusion thrombocytopenia was prevented by blood filters which remove microaggregate debris from the donor blood. Since the duration of the thrombocytopenia has not been investigated, the purpose of the present study was to establish the rate of onset and duration of post-transfusion thrombocytopenia following packed red blood cell transfusions. In addition, the effect of spleen size, patients' diagnosis and post-transfusion history were examined. These observations provide interesting new data on the mechanisms involved in this phenomenon.
... Leucocyte depleted 20 27´2 26´1 À 1´1 6´1 À 0´81 0´43 (9±50) (5±48) (À 8 to 12) Non-leucocyte depleted 10 28´2 25´5 À 2´7 3´4 2´5 0´03 (15±48) (9±44) (À 7 to 2) (a) Red cells-OAS 6 32´8 28´8 À 4´0 1´79 À 5´5 0´003 only (20±48) (13±44) (À 7 to 0) (b) Red cells-OAS 4 21´3 20´5 À 0´8 5´2 À 0´29 0´79 combined with LD (15±29) (9±31) (À 6 to 2) and/or BCD splenic sequestration of platelets, and they suggested that this was probably a result of adherence to microaggregate debris. Observations in another study supported this conclusion; it was found that post-transfusion platelet counts continued to drop for 3 days before returning to pretransfusion levels after 4 days, and the fall in platelet count did not occur in asplenic patients (Hart et al, 1990). ...
Platelet counts were measured before and after red cell transfusions in 30 patients with anaemia and severe thrombocytopenia resulting from haematological diseases. There was a mean reduction of 1.1 x 109/l (P = 0.43) in the platelet count after transfusions of 2-3 units of leucocyte-depleted red cell concentrates (20 patients). However, there was a mean reduction of 2.7 x 109/l (P = 0.03), approximately 10%, in the platelet count after transfusions of non-leucocyte-depleted red cell concentrates (10 patients). The findings suggest that the forthcoming introduction of universal leucocyte depletion of red cell concentrates will minimize the worsening of thrombocytopenia that occurs in severely thrombocytopenic patients receiving standard non-leucocyte-depleted red cell concentrates.
... Thrombocytopenia following blood transfusions can occur after less than a five unit transfusion 29 . The fall in platelet count is greatest at 72 hours after transfusion 29 and can be only partially be explained by the dilutional effect [29][30][31] . Lim et al 32 found that the fall in platelet count decreased tenfold if microfilters were used. ...
The use of various types of filters in anaesthesia and intensive care seems ubiquitous, yet authentication of the practice is scarce and controversies abound. This review examines evidence for the practice of using filters with blood and blood product transfusion (standard blood filter, microfilter, leucocyte depletion filter), infusion of fluids, breathing systems, epidural catheters, and at less common sites such as with Entonox inhalation in non-intubated patients, forced air convection warmers, and air-conditioning systems. For most filters, the literature failed to support routine usage, despite this seemingly being popular and innocuous. The controversies, as well as guidelines if available, for each type of filter, are discussed. The review aims to rationalize the place of various filters in the anaesthesia and intensive care environment.
The von Willebrand factor (vWf) activity, as measured by the ristocetin co-factor (vWf:RCo) and collagen binding (vWf:CBA) assays, declined progressively in standard blood units stored at 4°C after a 2-day storage period. This loss of activity was accompanied by a loss and degradation of high molecular weight (HMW) vWf multimers. In studies using a paired design, filtration of blood with a high efficiency leucocyte-removal filter, prior to storage at 4°C, led to significantly improved maintenance of vWf:RCo and vWf:CBA compared with unfiltered units (P, < 0·01 after 8 days). Loss and degradation of HMW vWf decreased when blood was filtered prior to 4°C storage. Filtration had no effect on vWf-associated activities when blood was stored at 22°C for 10 days.
These results indicate that part of the storage lesion of vWf in banked blood is due to leucocyte-mediated removal and degradation of HMW vWf. This has implications when specifying plasma for the production of vWF concentrates and may also play a role in the haemostatic lesion associated with massive transfusion of stored blood.
Blood filters have been available since the 1930s. In this review we evaluate the role of microaggregate filters (MF) in certain transfusion complications, namely non-haemolytic febrile transfusion reactions (NHFTR), pulmonary injury, thrombocytopenia, fibronectin depletion and histamine release. We review the latest generation of leucocyte depleting filters and discuss their role in preventing alloimmunisation, immunosuppression and CMV transmission. Finally, we provide a rationale for the role of blood microfiltration in the present day practice of intensive care medicine.
The von Willebrand factor (vWf) activity, as measured by the ristocetin co-factor (vWf:RCo) and collagen binding (vWf:CBA) assays, declined progressively in standard blood units stored at 4 degrees C after a 2-day storage period. This loss of activity was accompanied by a loss and degradation of high molecular weight (HMW) vWf multimers. In studies using a paired design, filtration of blood with a high efficiency leucocyte-removal filter, prior to storage at 4 degrees C, led to significantly improved maintenance of vWf:RCo and vWf:CBA compared with unfiltered units (P < 0.01 after 8 days). Loss and degradation of HMW vWf decreased when blood was filtered prior to 4 degrees C storage. Filtration had no effect on vWf-associated activities when blood was stored at 22 degrees C for 10 days. These results indicate that part of the storage lesion of vWf in banked blood is due to leucocyte-mediated removal and degradation of HMW vWf. This has implications when specifying plasma for the production of vWF concentrates and may also play a role in the haemostatic lesion associated with massive transfusion of stored blood.
To determine the incidence of thrombocytopenia (< 100 platelets x 10(3)/mm3) and potential risk factors, including medications, associated with the development of thrombocytopenia in critically ill trauma patients.
Prospective, observational study.
A 20-bed trauma intensive care unit (ICU) at a university hospital.
Sixty-three critically ill trauma patients without baseline thrombocytopenia admitted to the trauma ICU for at least 48 hours.
Patients were followed for up to 14 days. Platelet counts were determined daily. The following data were collected and analyzed as potential risk factors for the development of thrombocytopenia: medications, age, sex, race, trauma score, mode and type of injury, alcohol history, units of packed red blood cells (PRBC) and platelets transfused, surgical procedures, duration of ICU stay, and the development of systemic inflammatory response syndrome or disseminated intravascular coagulation.
Thrombocytopenia occurred in 26 (41%) of the patients. Among risk factors studied, nonhead injury, age, trauma score, duration of ICU stay, and the number of PRBC transfusions were significantly associated with the development of thrombocytopenia (p < 0.05). However, nonhead injury, age, and trauma score were useful variables in predicting the development of thrombocytopenia by using multivariate analysis. Medications were not associated with the development of thrombocytopenia.
The type of injury sustained, the quantity of platelet-deficient, transfusions, and age are the greatest risk factors associated with the development of thrombocytopenia in critically ill trauma patients. Drug-induced thrombocytopenia appears to play a minor role in the development of thrombocytopenia; therefore, medications should not be automatically discontinued or substituted when thrombocytopenia occurs.
Blood component therapy has enabled us to successfully support the increasing demands for treatment of haematological abnormalities. Continuous efforts are made to minimize or prevent immediate side effects of transfusion but the long-term effects of component therapy will remain unknown for some time. There is always a need for products with special qualities (i.e. no CMV, no HLA immunization etc.) however when considering adverse effects it is important to look for alternative strategies which produce minimal alteration in the cellular and fluid components of blood while maintaining optimal clinical efficacy. Continuous education of clinicians and laboratory scientists is needed so that the best possible products are provided reliably and with consistency. This review focused on some of the important debatable issues on the laboratory/microbiology aspects and clinical practice. It is clear that the presence of leucocytes is associated not only with reduced quality, based on the morphological and functional integrity of blood components but also reduced post-transfusion response in some specified cases.
11 patients with anaemia and thrombocytopenia due to bone marrow failure each received 2 sets of red-cell transfusions. They were randomised to receive 1 blood transfusion through a standard 170-micron giving set filter and another through a 40 micron micro-aggregate filter. After transfusion, the mean fall in platelet count was 15 x 10(9)/l (41.7%) and 1.4 x 10(9)/l (4.6%), respectively (p less than 0.01). The results confirm the findings of a previous study which showed that micro-aggregate filters prevent a post-transfusional decrease in platelet counts. In addition, this new study shows that this is clinically relevant in patients who are thrombocytopenic at the time of their blood transfusion.
The mean fall in the platelet count following 23 routine transfusions of 3-5 units packed cells for anaemia was 32.5%. This was significantly reduced to 12.5% in 15 similar transfusions through a 40 microns microaggregate filter (P less than 0.01) and to 4.6% following five transfusions through a polyester fibre filter (P less than 0.005). In 10 transfusions with frozen or polyester fibre filtered, washed red cells, the decrease in platelet count was 4.2% (P less than 0.001). A study of 111In-oxine labelled autologous platelets in nine patients indicated that the fall in platelet count was due to increased splenic sequestration. Since thrombocytopenia following routine transfusion is reduced by procedures which filter the packed cells, the decrease in platelets is probably caused by their adherence to infused microaggregate debris causing their premature removal from the circulation. Patients with preexisting thrombocytopenia who receive red cell transfusions for anaemia, should therefore receive blood products depleted of microaggregate debris in order to avoid exacerbation of thrombocytopenia and haemorrhagic complications.
Deleterious effects of transfused red cell products on platelet counts in thrombocytopenic patients
- Schifano J.
- Galligan B.
- Ernst P.
- Bernvil S.
Deleterious effects of transfused red cell products on platelet counts in thrombocytopenic patients
- Schifano J.