Back To Search Results

Normal and Abnormal Platelet Count Values and Interpretation

Editor: Preeti Rout Updated: 1/11/2024 2:23:02 AM

Summary / Explanation

Platelets, or thrombocytes, are disc-shaped, anuclear cellular fragments that measure 3 to 4 μm in diameter. Platelets are formed in the bone marrow from megakaryocytes; most platelets exist in the bloodstream, with a smaller percentage in the liver and spleen. The primary role of platelets is maintaining vascular integrity through aggregation and initiation of the coagulation cascade. Platelets may be quantified with a platelet count, ordered singly or as part of a standard complete blood count (CBC). Platelet quantity and function are negatively affected by a myriad of disease processes. The normal range of platelet counts will vary slightly among laboratories but typically falls between 150,000 and 450,000 platelets per μL of blood. Platelet counts outside the normal range may indicate an underlying disease process.

Etiologies of Thrombocytopenia

Thrombocytopenia is typically defined as a platelet count of less than 150,000/μL. The differential diagnosis of thrombocytopenia is broad but may be classified as disorders of platelet production, destruction, sequestration, or increased consumption.[1] Examples of these disorders include but are not limited to:

  • Disorders of platelet production include disease processes that affect thrombopoiesis in the bone marrow, such as leukemia, lymphoma, or specific myelodysplastic syndromes. Platelet production may also be suppressed by pharmaceuticals such as chemotherapeutics or antibiotics and by some illicit drugs. Many common viral infections, including hepatitis C and HIV, may suppress thrombopoiesis and result in thrombocytopenia.[2]
  • Disorders of platelet destruction include several autoimmune diseases, including but not limited to immune-mediated thrombocytopenia, immune thrombocytopenic purpura, and heparin-induced thrombocytopenia.
  • Disorders of increased platelet sequestration include any disease process that may result in splenomegaly. While severe hepatomegaly can theoretically result in thrombocytopenia, this is rare.
  • Increased consumption of platelets is seen in disseminated intravascular coagulopathy and other thrombotic disorders.

Mild thrombocytopenia may be clinically silent. However, thrombocytopenia may manifest clinically as easy bruising, prolonged or heavy bleeding, or petechiae. Correctly identifying and addressing the etiology of thrombocytopenia is crucial for effective treatment.[3]

Etiologies of Thrombocytosis

Thrombocytosis is typically defined as a platelet count greater than 450,000/μL. The differential diagnosis of thrombocytosis is also broad but may be classified as primary or secondary.[4] Primary thrombocytosis is a bone marrow disorder, most commonly polycythemia vera or essential thrombocytosis. Secondary causes of thrombocytosis include but are not limited to:

  • Reactive thrombocytosis is seen in chronic inflammatory states such as rheumatoid arthritis and other autoimmune diseases, acute and chronic infections, iron deficiency anemia, various hematologic malignancies, including lymphoma and leukemia, and solid organ malignancies such as bronchogenic carcinoma and adenocarcinoma of the colon or ovary.
  • Splenectomy may also result in a relative thrombocytosis due to decreased sequestration.

Mild thrombocytosis is typically clinically silent. Severe thrombocytosis, with platelet counts over 1 million/μL, can result in inappropriate and excessive intravascular thrombosis with resulting tissue and organ infarction.[5]

Platelet Morphology

Platelets affected by various disease processes may exhibit atypical morphology and altered aggregation.[6]

  • Giant platelets are seen in disorders such as Bernard-Soulier syndrome and May-Hegglin anomaly; bleeding time may or may not be prolonged. Gray platelet syndrome is a rare inherited disorder characterized by macrothrombocytopenia and decreased α-granules in platelets and megakaryocytes; decreased granules result in pale-appearing platelets. Electron microscopy of granular platelets in gray platelet syndrome will reveal vacuolization; vacuolization is also seen in Chediak-Higashi syndrome.
  • Platelet satellitosis or satellitism is a rare disorder characterized by pseudothrombocytopenia secondary to abnormal adhesion of platelets to circulating leukocytes, especially neutrophils.

Accurately identifying atypical platelet morphologies within the pertinent clinical context is a valuable diagnostic tool and facilitates timely and appropriate management.

Conclusion

Atypical platelet counts frequently indicate underlying pathology and may be the earliest or only manifestation of a disease process. Accurately interpreting platelet counts within the correlating clinical context facilitates timely diagnosis and initiation of appropriate treatment strategies, improving outcomes for patients with many platelet disorders.

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

References


[1]

. Thrombocytopenia. American family physician. 2022 Sep:106(3):Online     [PubMed PMID: 36126010]


[2]

Kam T, Alexander M. Drug-induced immune thrombocytopenia. Journal of pharmacy practice. 2014 Oct:27(5):430-9. doi: 10.1177/0897190014546099. Epub 2014 Aug 17     [PubMed PMID: 25134884]


[3]

Swain F, Bird R. How I approach new onset thrombocytopenia. Platelets. 2020:31(3):285-290. doi: 10.1080/09537104.2019.1637835. Epub 2019 Jul 3     [PubMed PMID: 31269407]


[4]

Schafer AI. Thrombocytosis. JAMA. 2015 Sep 15:314(11):1171-2. doi: 10.1001/jama.2015.8515. Epub     [PubMed PMID: 26372588]


[5]

Parnes A, Ravi A. Polycythemia and Thrombocytosis. Primary care. 2016 Dec:43(4):589-605. doi: 10.1016/j.pop.2016.07.011. Epub     [PubMed PMID: 27866579]


[6]

Thon JN, Italiano JE. Platelets: production, morphology and ultrastructure. Handbook of experimental pharmacology. 2012:(210):3-22. doi: 10.1007/978-3-642-29423-5_1. Epub     [PubMed PMID: 22918725]

Level 3 (low-level) evidence