What makes platelets clump

How can we estimate these counts? Or, should we break our estimates into more ranges to give physicians more valuable information? What can we do to provide a count? Some of the first steps recommended include vortexing the sample for 2 minutes to break up platelet clumps, then re-analyzing. Warming samples may also help to resolve platelet clumps, particularly in samples with cold agglutinins or that have had a delay in testing and have been transported or stored at room temperature or below.

If clumps persist and recollecting the sample still yields platelet clumping, then pre-analytical error can be ruled out an EDTA induced pseudothrombocytopenia may be suspected.

Many labs will have an alternate tube drawn or use another method to help resolve the clumping. These antibodies bind to platelet membrane glycoproteins in presence of EDTA. EDTA induces and enhances this binding by exposing these glycoproteins to the antibodies. Geok Chin Tan, Though it is an in vitro phenomenon, patients with certain conditions, such as malignant neoplasms, chronic liver disease, infection, pregnancy, and autoimmune diseases, do have increased risk of EDTA-PTCP.

Zhang, What are some alternate methods to help resolve EDTA induced platelet clumping challenges? Probably the most common is to redraw the sample in a Na Citrate tube. Because of the volume of the anticoagulant in the Na Citrate tube you must also apply the dilution factor of 1.

If you wish to use a different anticoagulant, the method must be validated in your laboratory. In addition, anticoagulant induced thrombocytopenia is not limited to EDTA. It can also occur with citrate and heparin.

In fact, researchers have found, and we have found in our own validations, that some samples that do not clump in EDTA actually DO clump in Na Citrate. Thus, alternate tubes may not resolve all platelet clumping.

Geok Chin Tan, Using this method, the EDTA tube and ACD must be run in parallel and a conversion factor applied, reflecting the difference in sample dilution in the 2 tubes. A parameter such as the RBC must be chosen to make this comparison. CAP Today, Some sources have recommended ACD tubes because the incidence of clumping with Na Citrate can be frustratingly high.

Manthorpe, Less commonly used tubes are CTAD trisodium citrate, theophylline, adenosine, dipyridamole and heparin. CTAD acts directly on platelets and inhibits platelet factor 4 thus minimizing platelet activation. Downsides to CTAD tubes are that they are light sensitive and must be stored in the dark, and can be costly. Heparin tubes are less commonly found to be beneficial in resolving platelet clumping issues because heparin can active platelets.

Amikacin should be added to the EDTA tube within 1 hour after draw and testing is stable for up to 4 hours at room temperature. Results of a study done in showed that the addition of amikacin to the EDTA tube produced rapid dissociation of the platelet clumps with little or no effect on morphology or indicies. Femoral-Patellar Syndrome. Flu influenza. Folic acid and erythrocyte folates. Free Kappa and Lambda. Free T3. Free T4. Free Testosterone.

G G6PD Quantitative. Gamma globulins. Glucose routine urine test. Granular Casts. Grass Mix 1. Growth Hormone. Gynecological Cytology. H Hallux valgus. HDL Cholesterol. Heel spur. Helicobacter pylori Breath Test. Helicobacter pylori Serology.

Hemochromatosis Genotype. Hemoglobin Electrophoresis. Hepatitis B. Hepatitis C IgG. Herniated disc. Hiatal hernia. HLA B Hot zone.

Howell-Jolly Body. HS Troponin T. Hyaline Casts. I Icterus. IGF 1. Iliotibial Band Friction Syndrome. Immunity and herd immunity. Inhibin B. Insomnia acute or chronic. Ionized Calcium.

Iron profile. Irritable bowel syndrome. K Karyotype. Ketones routine urine test. Kidney Cells. Kidney Disease nephropathy. L Lactiferous ducts. Lateral epicondylitis. LDL Cholesterol. Leflunomide Metabolite. Leukocytes esterase. Leukocytes routine urine test. Liver profile. Lumbar Facet Syndrome. Lumbar osteoarthritis. Lumbar sprain.

Lying Aldosterone. Lying Renin. Lyme Disease. Lymphogranuloma venereum. M Macadamia Nuts. Maintenance of Wakefulness Test. Mean Corpuscular Hemoglobin. Mean Corpuscular Volume. Mean Platelet Volume. Medial epicondylitis. Meniscal lesion. Microbiological stool analysis by PCR. Mixed Casts. There is a condition called pseudothrombocytopenia, spuriously low platelet count due to a laboratory artefact, in which the platelets clump together.

In such instances the instrument does not count these clumps of platelets and gives the platelet count as factitiously low. This can be confirmed by examining a peripheral blood smear in which many clumps of platelets will be seen suggesting that the platelet count is normal. Sometimes, changing the anticoagulant in which the blood is collected from EDTA to citrate or heparin may solve the problem but rarely, platelets may clump on being exposed to any anticoagulant. If a platelet count is still required in such cases, a manual platelet count is done using finger-prick blood and directly collecting the blood into the diluting fluid.

Pseudothrombocytopenia may also be seen in some patients who are taking certain drugs. The anticoagulant or drug affects the membrane of platelets causing a conformational change in them because of which they bind to non-specific circulating antibodies in the blood and clump together.

Further coagulation work-up revealed low von Willebrand factor antigen and ristocetin cofactor activity, and molecular testing confirmed vWD type 2B [ 3 ]. The latter is an in vivo consumption of platelet, which results in true thrombocytopenia. This morphologic observation may help further separate the two conditions presumptively upon examination of PB smear; refer to Figure 2 for morphologic comparison and Table 2 for comparative features.

Other possible preanalytical factors to consider upon investigating platelet clumps include the collection method, that is, capillary venous or line draws.

Capillary collections are prone to clotting and formation of platelet clumps. Viral infection, drugs, and medications, especially chemotherapeutic agents, are all possible inducers of platelet clumping [ 5 , 6 ]. Clumping can also be due to a combination of more than one of the above factors, and it is possible that a transient viral infection was a confounding cause in our patient note the atypical lymphocyte suggestive of a viral infection seen in Figure 1 and the CBC results listed in Table 1 showing the fluctuation in WBC, RBC, and Hgb levels coinciding with episodes of clumping and returning to normal levels along with the platelet count.

From a practical laboratory point of view, investigation of platelet clumping may include the following steps until a nonclumping smear is obtained, noting that Steps 3 and 4 are reserved for the rare instances, where Steps 1 and 2 do not resolve the platelet clumping. Step 1. Verify method of blood draw e. Step 2. Test a blood sample collected in sodium citrate.

Step 3. Test a sample collected in heparin. If Step 3 is not possible, proceed to Step 4. Step 4. Obtain a sample in ammonium oxalate, and count platelets utilizing a hemocytometer grid, if available, as per described methods [ 4 ]. Reporting platelet counts on samples that show platelet clumps can be a challenge. The authors declare that there are no competing interests regarding the publication of this paper.