eanm-logo eanm-logo
European Nuclear Medicine Guide
eanm-logo eanm-logo
European Nuclear Medicine Guide
Chapter 9.1

Blood / Platelet Survival Study

9.1.1 Radiopharmaceutical

  • 111In-(autologous)-platelets

9.1.2 Uptake mechanism / biology of the tracer

This examination aims to look at the in vivo survival of autologous platelets. For this purpose, venous blood is taken from the patient, and after a number of technical steps, platelets are isolated and labelled with 111In(most frequently [111In]In-oxinate, less frequently, [111In]In-tropolone) able to enter through the cell membrane and, hence, be retained intracellularly. Labelled platelets are reinjected into the patient, and their survival observed by both blood samples and γ scintigraphy. Since platelets harvested from venous blood already have a certain age, their survival is expected to be between 8-10 days. This is why 111In is used, because it has relatively long half-life which allows for procedures that can last up to 7 days. Interestingly, very little elution of 111Inform the labelled platelets occurs, and no plasma activity can be detected. Physiologically, platelets will eventually die, in the liver and spleen, and to a minor extent intravascularly. Therefore, looking at liver and spleen accumulation is of interest, whereas intravascular platelet destruction must be looked at using other (laboratory) techniques.

9.1.3 Indications

  • Identify reduced autologous platelet peripheral survival as a cause of thrombocytopenia;
  • Identify increased spleen platelet pooling, for instance in portal hypertension, as a cause of thrombocytopenia;
  • In selected cases (e.g. early myelodysplastic syndromes), demonstrate that the platelet production is insufficient;
  • Determine whether the liver or spleen are involved in platelet sequestration, in peripheral thrombocytopenia and in some patients who are refractory to platelet transfusions.

9.1.4 Contra-indications

  • Pregnancy;
  • Platelet counts lower than 25.000/µL shall result in poor labelling results; in selected cases compatible (ABO-Rh) platelets from a blood bank can be used;
  • The test is not useful in disseminated intravascular coagulation, as imaging does usually not allow to localize any site of platelet destruction except for the liver and spleen.

9.1.5 Clinical performances

The technique is unique in the indications described above because of its high selectivity; no comparator is available. Platelet survival studies are used to predict the response to splenectomy in immune thrombocytopenic purpura (ITP) and other autoimmune disorders. Increased spleen platelet sequestration predicts a good response in ~80% of the patients. However, even in patients with selective liver destruction, response to splenectomy can be observed in ~50% of the patients because the source of anti-platelet antibodies could be the spleen. The discovery of increased spleen pooling in portal hypertension (e.g. liver cirrhosis) is significant, since splenectomy will not result in any clinical benefit.

9.1.6 Activities to administer

The suggested activity to administer is:

  • 111In-platelets: 10-18.5 MBq

No recommendations are given for paediatric nuclear medicine.

9.1.7 Dosimetry

The effective dose for 111In-platelets is 0.39 mSv/MBq [109]. The organ with the highest absorbed dose is the spleen: 7.5 mGy/MBq (1).

The effective dose for 111In-platelets is: 3.9-7.2 mSv per procedure.

Caveat: “Effective Dose” is a protection quantity that provides a dose value related to the probability of health detriment to an adult reference person due to stochastic effects from exposure to low doses of ionizing radiation. It should not be used to quantify the radiation risk for a single individual associated with a particular nuclear medicine examination. It is used to characterize a certain examination in comparison to alternatives, but  it should be emphasized that if the actual risk to a certain patient population is to be assessed, it is mandatory to apply risk factors (per mSv) that are appropriate for the gender, the age distribution and the disease state of that population."

9.1.8 Interpretation criteria/major pitfalls

The following information should be reported:

  • T1/2 of the labelled platelets (N: 4 ± 0.5 d);
  • Labelled platelets’ survival (8-10 d);
  • Recovery in peripheral blood (which is inversely proportional to the spleen pooling and should normally be ~60% [accurate measurement of this requires a simultaneous measurement of plasma volume using 125I-human serum albumin]).

Platelet production can be estimated from the platelet count at the time of the test, the mean survival and the platelet recovery in peripheral blood. Beside poor labelling efficiency due to very low platelet counts or inadequate technique, two major pitfalls have to be kept in mind: recent interference due to the initiation of treatment just before the test (e.g. steroids), and alloimmunization in patients who have received many platelet transfusions in the past.

9.1.9 Patient preparation

No specific preparation. Check platelets counts the day before labelling (should be >25,000/µL). In case of use of homologous platelets, accurate determination of blood group is mandatory and should be confirmed when the platelets are delivered by the blood bank.

Clinicians should refrain, unless absolutely necessary, to start any immunosuppressive therapy before the test, especially in ITP or related immune thrombocytopenia (for instance systemic disorders).

9.1.10 Methods

After in vitro labelling (in appropriate sterility conditions [Class A vertical laminar air flow]), platelets are re-suspended in saline and reinjected as a slow bolus. An aliquot of the injected syringe is used to determine the total injected activity for subsequent whole blood activity measurements. Blood samples are taken at 3, 10, 20, 30, 45, 60 min and then 3, 24, 48, 72, and 96 h, actually until less than 50% of the 1h pi. activity remains in blood. Surface counts are performed using γ probes in coincidence or using a dual-head γ camera: counts are measured on the heart, liver, and spleen areas. From the decay-corrected organ and blood counts, TACs are created. Liver and spleen sequestration are estimated by the excess counts methods, i.e., the counts in an organ that are in excess of the counts that this specific organ would contain due to circulating blood.