PLATELECOUNT REPORT SCRIPT

Platelets are very small non-nucleated, membrane-bound cell fragments only 2 to 4

micrometers in diameter and originate from separation from the ends of cytoplasmic processes
extending from giant polypoid bone marrow cells called megakaryocytes.

The normal platelet count is 150,000 to 450,000 per microliter.

Platelets promote blood clotting and helps repair minor tears or leaks in the walls of blood
vessels, preventing loss of blood from the microvasculature.

Platelets circulate with an average lifespan of 7-10 days.

The total platelet count as a part of the complete blood count can tell us about whether there is
an existing disorder of the platelets. One’s platelet count can either be high, normal, or low

Theoretically, thrombocytosis is an excess of platelets typically beyond 400 or 450 thousand

per microliter. Just because one’s platelet is beyond this value doesn’t necessarily mean that
he or she will develop an increased propensity to developing a thrombus. In fact, patients with
markedly elevated platelet counts like over 1.5 million per cubic millimeter, usually seen in the
setting of a myeloproliferative disorder, have an increased risk of bleeding.

Thrombocytosis can either be primary (AKA essential) or secondary (AKA reactive). Primary
thrombocytosis is usually one of the myeloproliferative disorders found in the elderly and is due
to CML, polycythemia vera, among others. On the other hand, secondary thrombocytosis is
more common in adults and is the body’s reaction to certain derangements such as iron
de ciency, in ammation, cancer or infection.

On the other end of the spectrum is a condition of decreased platelet count called
thrombocytopenia wherein platelets are below the normal lower limit of 150,000 per cubic
millimeter. It should be kept in mind that in the evaluation of a patient with a thrombocytopenia,
a key step is to rst rule out pseudothrombocytopenia, particularly in a patient without an
apparent cause for the thrombocytopenia.. Pseudothrombocytopenia is an in vitro articfact
resulting from platelet agglutination via antibodies when the calcium content is reduced due to
the EDTA anticoagulant in blood collection tubes during extraction. If a low platelet count is
obtained in blood collected using EDTA-coated tubes, a blood smear should be evaluated and
a platelet count determined in blood collected into sodium citrate or heparin, or a smear of
freshly obtained anti-coagulated blood, such as from a nger stick can be examined.

Thrombocytopenia results from one or more of these three processes: (1) decreased bone
marrow production, (2) sequestration usually in an enlarged spleen, or (3) increased platelet
destruction. Except in inherited disorders, decreased platelet production usually results from
bone marrow disorders that also a ect RBC and/or WBC production, and thus it is wise to
check these parameters as well. In a patient presenting with isolated thrombocytopenia who
are older than 60 years, the bone marrow should be examined nonetheless because
myelodysplasia can present with isolated thrombocytopenia. We also have to carefully probe
into the patient’s history as to whether there is any drug, even the nonprescription and herbal
ones, that could be causing the condition since thrombocytopenia can be drug induced, since
drugs are the most common cause of decreased platelet counts. We also have to document if
there is any presence of splenomegaly determined during the physical exam, as well as any
signs of bleeding into the skin, such as petechiae, and into the mucous membranes, such as
wet purpuras in the mouth.

It is also prudent to note that many viral and bacterial infections result in thrombocytopenia and
they are the most common noniatrogenic cause of it. Again, in patients with thrombocytopenia
in which an apparent cause cannot be determined, all drugs should be suspect as it could be a
drug-induced low platelet count.

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Heparin-induced thrombocytopenia is a type of drug-induced thrombocytopenia but unlike the
ones that seen with other drugs, the thrombocytopenia is not usually severe and IS NOT
associated with bleeding and instead predisposes the patient to THROMBOSIS due to anti-
heparin/PF4 antibody complex that activates the endothelial cells.

The idiopathic thrombocytopenic purpura (ITP) is also associated with infection presenting
acutely after an infection especially in children and chronically in adults, and is characterized by
mucocuteneous bleediong a a very low platelet count.

Thrombotic thrombocytopenic microangiopathies including TTP and HIS both present with
microangiopathic hemolytic anemias wherein fragmented RBCs are seen as well as renal
failure. TTP is due to a de ciency to ADAMTS13 leading to VWF remaining uncleaved and
ultra-large and causes platelet adhesion and aggregation, whereas HUS is closely tied to an E
Coli infection.

DIC can also cause decreased platelets as the process consumes clotting factors and platelets
later on in its course, as well as chemotherapy which can damage the bone marrow and its
capabilities in producing the blood cells including platelets.

Mean platelet volume (MPV) is a measurement of the average size

of platelets found in blood. Since the average platelet size is larger when
the body is producing increased numbers of platelets, the MPV test results
can be used to make inferences about platelet production in bone
marrow or platelet destruction problems

MPV may be higher when there is destruction of platelets. This may be

seen in immune thrombocytopenic purpura (ITP), myeloproliferative
diseases and Bernard–Soulier syndrome. It may also be related to pre-
eclampsia and recovery from transient hypoplasia.[2]
Abnormally low MPV values may correlate with thrombocytopenia when it
is due to impaired production of megakaryocytes in the bone marrow, such
as in aplastic anemia. A low MPV may indicate in ammatory bowel
disease (IBD), such as Crohn's disease and ulcerative colitis.[3] In addition,
low MPV may correlate with abnormally small platelet size, sometimes a
symptom of a spectrum referred to as Wiskott–Aldrich syndrome (WAS),
[4] caused by a genetic mutation of the WAS gene
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