PLT
Platelets (thrombocytes, PLT) are small cell fragments that stop bleeding: within seconds of a vessel injury they stick to the wound, clump together and form the first plug, on which a fibrin clot is then built. Too few platelets (thrombocytopenia) lead to bruising and bleeding; too many (thrombocytosis) can signal inflammation, iron deficiency or a bone-marrow disease and may increase the risk of thrombosis.
What platelets are
Platelets are not complete cells. They are disc-shaped fragments, 2–3 µm across, that bud off from giant bone-marrow cells called megakaryocytes; one megakaryocyte releases thousands of platelets. Production is controlled mainly by the hormone thrombopoietin, made in the liver. A platelet lives 7–10 days, and about one-third of all platelets are normally held in the spleen as a reserve.
Although they have no nucleus, platelets are packed with granules containing clotting factors, calcium, ADP, serotonin and growth factors, and their surface carries receptors that recognise damaged vessel walls and other platelets.
How platelets stop bleeding
This is why both the number and the function of platelets matter. A normal count with poor function (for example after aspirin, in kidney failure or in von Willebrand disease) can still cause bleeding, while a very high count of abnormal platelets in a myeloproliferative neoplasm can cause both clotting and bleeding.
Reference values
| Platelet count (×10⁹/L) | Category | Typical clinical meaning |
|---|---|---|
| > 1000 | Extreme thrombocytosis | Risk of both thrombosis and bleeding (acquired von Willebrand syndrome); urgent evaluation |
| 450–1000 | Thrombocytosis | Usually reactive; persistent values require haematology work-up |
| 150–400 (450) | Normal | — |
| 100–149 | Mild | Usually no symptoms; find the cause |
| 50–99 | Moderate | Bleeding mainly with surgery or injury |
| 20–49 | Severe | Easy bruising, petechiae, gum and nose bleeds |
| < 20 (especially < 10) | Critical | Risk of spontaneous serious bleeding, including intracranial |
Low platelets — thrombocytopenia
Thrombocytopenia has three basic mechanisms: the marrow makes too few platelets, platelets are destroyed or consumed too fast, or they are trapped in an enlarged spleen.
| Mechanism | Examples |
|---|---|
| Reduced production | Vitamin B12 or folate deficiency, alcohol, viral infections, chemotherapy and radiotherapy, aplastic anaemia, leukaemia, myelodysplastic syndromes, bone-marrow infiltration by cancer |
| Immune destruction | Immune thrombocytopenia (ITP); HIV, hepatitis C, Helicobacter pylori; lupus; drug-induced (e.g. heparin-induced thrombocytopenia, quinine, some antibiotics) |
| Consumption | Disseminated intravascular coagulation (DIC) in sepsis or trauma, thrombotic thrombocytopenic purpura (TTP), haemolytic uraemic syndrome, HELLP syndrome in pregnancy |
| Sequestration | Liver cirrhosis with portal hypertension and enlarged spleen |
| Physiological / artefact | Gestational thrombocytopenia (mild, late pregnancy); pseudothrombocytopenia — platelets clump in EDTA tubes and are falsely counted low |
Signs of low platelets
- Petechiae — tiny red-purple dots on the skin, often on the legs
- Bruising after minor knocks
- Bleeding gums, nosebleeds, prolonged bleeding from cuts
- Heavy menstrual periods
- Blood in urine or stools
Situations that need immediate attention
- A new, sudden fall in platelets during heparin treatment (possible HIT — paradoxically causes clots)
- Low platelets with fever, confusion, anaemia or kidney problems (possible TTP)
- Low platelets with severe infection or bleeding from several sites (possible DIC)
- Any count below 20 ×10⁹/L, or headache and vomiting with low platelets
High platelets — thrombocytosis
In about 80–90 % of people with a raised platelet count the cause is reactive (secondary): the marrow responds to cytokines such as interleukin-6. Common causes are iron deficiency, infection, chronic inflammation (for example rheumatoid arthritis or inflammatory bowel disease), recovery after bleeding or surgery, removal of the spleen and some cancers. Reactive thrombocytosis usually does not raise the risk of clots by itself and resolves when the cause is treated.
Primary thrombocytosis arises in the bone marrow: essential thrombocythaemia (with mutations in JAK2, CALR or MPL), polycythaemia vera, primary myelofibrosis and chronic myeloid leukaemia. These conditions carry a real risk of arterial and venous thrombosis — and, at very high counts, of bleeding — and need specialist care.
Pitfalls and related indices
- Pseudothrombocytopenia: in about 1 in 1000 people platelets clump in EDTA tubes. If a low count does not fit the clinical picture, the laboratory should check a blood smear or repeat the test in a citrate tube.
- Giant platelets (some inherited disorders) may not be counted as platelets by analysers.
- MPV (mean platelet volume): a high MPV with low count suggests increased destruction with active production (as in ITP); a low MPV suggests reduced production.
- Medicines such as aspirin, clopidogrel and NSAIDs do not change the count but reduce platelet function.
When to see a doctor
platelets are below 20 ×10⁹/L, or a low count is accompanied by bleeding that does not stop, blood in vomit, urine or stools, a severe headache, confusion or fever. Seek urgent care also if a very high count is accompanied by chest pain, sudden weakness, speech problems or a painful swollen leg.
the count is repeatedly below 150 or above 450 ×10⁹/L. Your doctor will review medicines and infections, check iron, vitamin B12, liver function and a blood smear, and refer you to a haematologist if no clear cause is found.
References
- Stasi R. How to approach thrombocytopenia. Hematology Am Soc Hematol Educ Program. 2012;2012:191–197. doi:10.1182/asheducation-2012.1.191
- Neunert C, Terrell DR, Arnold DM, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia. Blood Adv. 2019;3(23):3829–3866. doi:10.1182/bloodadvances.2019000966
- Kaufman RM, Djulbegovic B, Gernsheimer T, et al. Platelet transfusion: a clinical practice guideline from the AABB. Ann Intern Med. 2015;162(3):205–213. doi:10.7326/M14-1589
- Schafer AI. Thrombocytosis. N Engl J Med. 2004;350(12):1211–1219. doi:10.1056/NEJMra035363
- Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391–2405. doi:10.1182/blood-2016-03-643544
This article is for general information and does not replace a consultation with a doctor. Do not stop prescribed antiplatelet or anticoagulant medicines without medical advice.
Published on 2 June 2019