Test
Method of action
Current use
PFA-100 (closure time)
Mimics a bleeding time by forcing whole blood at high shear through holes in a membrane coated with collagen and either epinephrine or ADP. The time taken for the platelet plug to stop flow is measured
Screening assessment of bleeding risk and quality of platelet concentrates; limitations at low platelet counts. Automated, relatively easy to perform but affected by vWF and haematocrit
Aggregometry
Assesses the ability of various agonists to activate platelets and induce platelet aggregation
Light transmission aggregometry often considered the gold standard but technically challenging, and variability in methodology between laboratories
Flow cytometry
Quantification of membrane glycoproteins
Specialist laboratories
Thromboelastograph (TEG)
Viscoelastic – a sample of blood is placed in a rotating cup; as fibrin forms it applies torque to a pin suspended in the cup; the rotation of the pin is converted to an electrical signal. This produces a graph representing clot formation and lysis
Screening: provides limited information on specific platelet function
Use in surveillance of cardiac surgery patients, trauma patients
Rotational thromboelastography (ROTEM)
Viscoelastic – similar principle to TEG, but cup is stationary and the pin rotates
As per TEG
Other tests
Impedance platelet aggregometry (IPA), e.g. multiplate system
Assessing antiplatelet therapy
Difficulties standardisation
Free oscillation rheometry
Uses oscillation to measure clotting time and changes in clot elasticity
Recent technology, under evaluation
Thrombolux
Tests platelet quality
Recent technology, under evaluation
13.2 Factors Affecting Platelets in Critical Care Patients
Platelet disorders result from a variety of conditions, both congenital (rare) and acquired (Table 13.2). In critically unwell patients, platelet disorders are usually multifactorial in nature and are frequently accompanied by disorders of other elements of normal haemostasis (such as clotting factors or fibrinogen deficiency).
Table 13.2
Disorders of platelets: some causes
Condition | Mechanism |
|---|---|
Inherited | |
Mostly rare conditions (giant platelet disorders, Wiskott-Aldrich syndrome etc.) [3] | |
Acquired | |
Drugs | |
Aspirin | Irreversible inhibition of cyclooxygenase (COX) |
Dipyridamole | Unclear |
P2Y12 receptor antagonists, e.g. clopidogrel, ticagrelor | Direct inhibition of ADP receptor or P2Y12 receptor |
Glycoprotein IIb/IIIa receptor antagonists, e.g. abciximab, tirofiban | Blockade of the GPIIb/IIIa receptor |
Nitrates | Nitric oxide mediated |
Calcium channel blockers, e.g. nifedipine | Reduced adhesion and aggregation |
Heparin | Reduced adhesion. Reduction in numbers in heparin induced thrombocytopenia |
Metabolic (hypothermia, acidaemia) | Reduction in platelet function |
Liver disease | Reduction in platelet numbers and function |
Uraemia | Reduction in platelet function |
Trauma | Reduction in platelet function (as part of the coagulopathy of trauma) and numbers (in major haemorrhage) |
Sepsis | Reduction in platelet production and increased platelet consumption |
Cardiopulmonary bypass | Reduction in platelet numbers and function |
Dysproteinaemia (e.g. multiple myeloma) | Reduction in platelet function |
Myeloproliferative disorders | Reduction in platelet function |
13.3 How Common Is Thrombocytopenia and What Are the Clinical Consequences of Thrombocytopenia?
Platelet abnormalities (often in the absolute number of platelets or in platelet function) may manifest with features of abnormal primary haemostasis such as petechiae, mucosal bleeding or rapid oozing from small cuts, but the exact nature of the relationship between severity of thrombocytopenia and bleeding risk is far from clear and varies considerably between patients. Of potential concern in critically unwell patients is occult bleeding that is not visible externally, such as into a viscus or an enclosed space (e.g. intracranially).
Thrombocytopenia is common in critically ill adult patients. A recent systematic review showed that it is present in 8–68 % of adult patients on admission to the intensive care unit (ICU) and acquired by 13–44 % of patients during their ICU stay [1]. Thrombocytopenia also complicates critical illness in younger age groups: 20–50 % of critically ill neonates develop thrombocytopenia, including 5–10 % with platelet counts less than 50 × 109/L [2].
Thrombocytopenia has been independently linked to death in ICU patients, but this association does not establish causality and therefore cannot be used to help guide platelet transfusion [1].
13.4 What Are Platelet Transfusions?
13.4.1 What Is a Bag of Platelets?
Platelets for transfusion are prepared either by centrifugation of whole blood donations or by aphaeresis. An adult equivalent dose is a pool of four platelet donations in the UK. Platelets can be stored for up to 5 days on an agitator at 22° or longer with a process of bacterial screening. One adult pack of platelets has a volume of 250–350 mL. The usual adult (therapeutic) dose is 1 unit (aphaeresis) or 1 pool (pooled). Each pack costs around 250 euros.
13.4.2 What Is the Effect of Platelet Transfusion on Platelet Count?
The effect of platelet transfusion on platelet count is often assessed by changes in platelet count. In five observational studies in critically ill adults [2, 4–7], platelet transfusion resulted in a median increment of 15 × 109/L. However, results vary considerably across patients [3, 4]. Of note, sustained correction of thrombocytopenia to a count above 100 × 109/L was rarely achieved. The increment in platelet count may be short lived because of the short life span of transfused platelets and coexisting consumptive causes, e.g. hypersplenism. What is less clear is how platelet functions impacts clinical outcomes, such as bleeding risk. No one would disagree with the use of platelet transfusions to treat major bleeding in association with thrombocytopenia. The more common practice of transfusing platelets in non-bleeding patients with thrombocytopenia, however, is more debatable.
13.5 Risks of Platelet Transfusions
The use of platelets is increasing worldwide. In the UK alone, around 266,000 doses (or aphaeresis equivalent units) were transfused in 2010. Platelets for transfusion are biological components, which are a scarce and costly resource. Nonhaemolytic febrile reactions and mild allergic reactions are common with an estimated incidence of 2 and 4 %, respectively. Anaphylaxis occurs rarely (1:20,000–1:50,000 of transfusions) but accounts for ~40 % of the serious adverse events reported [10]. As with all blood components, there is a risk of transfusion-transmitted infection. The rate of viral transmission (HIV, HBV, HCV) appears extremely low. Of more concern is the risk of bacterial infection. Transfusion-transmitted bacterial infection (TTBI) has an estimated incidence of 1:10,000 platelet transfusions. The risk of bacterial contamination is higher than for other blood products because, unlike other blood components, platelets are processed and stored at room temperature. Bacterial screening has been introduced to reduce the risk of TTBI. Transfusion-associated lung injury (TRALI) is a life-threatening complication following platelet transfusion and may be recognised more commonly in the ICU. Platelets are more commonly implicated in TRALI than red blood cells.
The hazards of platelet transfusion are well documented. The 2012 Annual Serious Hazards of Transfusion (SHOT) report featured a total of 2,767 incidents, with platelet transfusions implicated in 55 cases (Table 13.3).
Nature of incident | Number of incidents |
|---|---|
Bacterial infection | 8 |
Viral infection (hepatitis B) | 1 |
Transfusion-associated lung injury | 1 |
Anaphylaxis | 43 |
Posttransfusion purpura | 2 |
Total | 55 |
13.6 Current Evidence for Platelet Transfusions
13.6.1 Platelet Transfusions in Adults Who Are Not Critically Ill: Prophylactic Transfusion
In non-bleeding, non-ICU patients, current practice for prophylactic platelet transfusions is derived largely from data in haematology patients with chemotherapy-associated thrombocytopenia. A transfusion trigger of 20 × 109/L was widely used, but other studies comparing 10 × 109/L versus 20 × 109/L as thresholds for platelet transfusion showed no increased bleeding risk when 10 × 109/L was used as the trigger. Indeed, several very recent randomised trials have now tested whether a no-prophylaxis policy can be safely followed in selected low-risk patients with haematological malignancies and severe thrombocytopenia. These findings taken together suggest a limited role for platelet transfusions to reduce bleeding risk, even at counts under 10 × 109/L [11].
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