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Thrombocytopenia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Farbod Zahedi Tajrishi, M.D.

Synonyms and keywords: Congenital amegakaryocytic thrombocytopenia, CAMT

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor-In-Chief: Farbod Zahedi Tajrishi, M.D. [2]

Overview

Thrombocytopenia (or -paenia, or thrombopenia in short) is the presence of relatively few platelets in blood.

Generally speaking, a normal platelet count ranges from 150,000 and 450,000 per mm3. These limits, however, are determined by the 2.5th lower and upper percentile, and a deviation does not necessarily imply any form of disease. The number of platelets in a blood sample also decreases quickly with time and a low platelet count may be caused by a delay between sampling and analysis.

Historical Perspective

Classification

Thrombocytopenia can be divided into several categories based on its extent as well as its underlying etiology.

Based on platelet count:

  • mild: (100,000 – 150,000 per µL),
  • moderate (50,000 to 99,000 per µL),
  • severe (<50,000 per µL).

Note that these amounts may not be the same for every condition and one should interpreted them according to the underlying etiology of thrombocytopenia. For example, in idiopathic thrombocytopenia (ITP), a platelet count of <30,000/µL represents severe thrombocytopenia and for gestational thrombocytopenia, a platelet count between 80,000 and 150,000/microL is considered as mild thrombocytopenia.

Based on etiology:

To see the full list of conditions that could cause thrombocytopenia, please click here.

Pathophysiology

Basically, thrombocytopenia is the result of one of these mechanisms or a combination of some of them:

  1. Reduced production of platelets due to bone marrow dysfunction
  2. Increased destruction of platelets in the body
  3. iatrogenic
  4. entrapment of platelets in spleen

Several conditions, some of which mentioned below, can activate the mechanisms that ultimately lead to thrombocytopenia.

Causes

Differentiating [Disease] from Other Diseases

Epidemiology and Demographics

Among people with normal platelet counts:[1][2]

  • The mean platelet count is 266,000/µL in women and 237,000/µL in men.
  • Younger people and those with African-Americans descent have higher platelet counts than the older ones and caucasians, respectively.
  • The variation of the platelet count in a given individual over a certain time course is insignificant.
  • Platelet counts are slightly higher (by approximately 5000/µL) in the fall/winter compared with spring/summer.
  • Almost 2.5 percent of the normal population have platelet counts lower than 150,000/µL.

Risk Factors

Screening

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

References

  1. ↑ Buckley MF, James JW, Brown DE, Whyte GS, Dean MG, Chesterman CN; et al. (2000). “A novel approach to the assessment of variations in the human platelet count”. Thromb Haemost. 83 (3): 480–4. PMID 10744157.
  2. ↑ Segal JB, Moliterno AR (2006). “Platelet counts differ by sex, ethnicity, and age in the United States”. Ann Epidemiol. 16 (2): 123–30. doi:10.1016/j.annepidem.2005.06.052. PMID 16246584.

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] 

Associate Editor(s)-in-Chief:

Overview

Our search to find the history of discovery of low platelet counts was inconclusive. Instead, we have discussed the discovery of platelets in this section.

Historical Perspective

  • George Gulliver in 1841 drew pictures of platelets[1] using the twin lens (compound) microscope invented in 1830 by Joseph Jackson Lister. [2] This microscope improved resolution sufficiently to make it possible to see platelets for the first time.
  • William Addison in 1842 drew pictures of a platelet-fibrin clot.[3]
  • Lionel Beale in 1864 was the first to publish a drawing showing platelets.[4]
  • Max Schultze in 1865 described what he called “spherules”, which he noted were much smaller than red blood cells, occasionally clumped, and were sometimes found in collections of fibrin material.[5]
  • William Osler observed them and, in published lectures in 1886, called them a third corpuscle and a blood plaque and described them as a colorless protoplasmic disc.[6]
  • James Wright examined blood smears using the stain named for him, and used the term plates in his 1906 publication but changed to platelets in his 1910 publication which has become the universally accepted term.[7][8]

The term thrombocyte (clot cell) came into use in the early 1900s and is sometimes used as a synonym for platelet; but not generally in the scientific literature, except as a root word for other terms related to platelets (e.g. thrombocytopenia meaning low platelets).[9]

References

  1. ↑ Lancet, 1882, ii. 916; Notes of Gulliver’s Researches in Anatomy, Physiology, Pathology, and Botany, 1880; Carpenter’s Physiology, ed. Power, 9th ed., see Index under ‘Gulliver.’
  2. ↑ Godlee, Sir Rickman (1917). Lord Lister. London: Macmillan & Co.
  3. ↑ Robb-Smith AH (1967). “Why the platelets were discovered”. Br J Haematol. 13 (4): 618–37. PMID 6029960.
  4. ↑ Beale LS (1864). “On the Germinal Matter of the Blood, with Remarks upon the Formation of Fibrin”. Transactions of the Microscopical Society & Journal. 12: 47–63. doi:10.1111/j.1365-2818.1864.tb01625.x
  5. ↑ Schultze M (1865). “Ein heizbarer Objecttisch und seine Verwendung bei Untersuchungen des Blutes”. Arch Mikrosk Anat. 1 (1): 1–42. doi:10.1007/BF02961404
  6. ↑ Osler W (1886). “On certain problems in the physiology of the blood corpuscles”. The Medical News. 48: 421–25.
  7. ↑ Wright JH (1906). “The Origin and Nature of the Blood Plates”. The Boston Medical and Surgical Journal. 154 (23): 643–45. doi:10.1056/NEJM190606071542301
  8. ↑ Wright JH (1910). “The histogenesis of blood platelets”. Journal of Morphology. 21 (2): 263–78. doi:10.1002/jmor.1050210204
  9. ↑ Jain NC (1975). “A scanning electron microscopic study of platelets of certain animal species”. Thromb Diath Haemorrh. 33 (3): 501–7. PMID 1154309.

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor-In-Chief: Farbod Zahedi Tajrishi, M.D. [2]

Overview

Thrombocytopenia can be divided into several categories based on its extent as well as its underlying etiology.

Classification

Based on platelet count:[1]

  • Mild: (100,000 – 150,000 per µL)
  • Moderate (50,000 to 99,000 per µL)
  • Severe (<50,000 per µL)

Note that these amounts may not be the same for every condition and one should interpreted them according to the underlying etiology of thrombocytopenia. For example, in idiopathic thrombocytopenia (ITP), a platelet count of <30,000/µL represents severe thrombocytopenia and for gestational thrombocytopenia, a platelet count between 80,000 and 150,000/microL is considered as mild thrombocytopenia. Although one may instinctively assume that severe thrombocytopenia is associated with increased probability of bleeding and the subsequent need for treatment, such an association between platelet count and the risk of bleeding is not always predictable.

Based on etiology:

To see the full list of conditions that could cause thrombocytopenia, please click here.

References

  1. ↑ Williamson DR, Albert M, Heels-Ansdell D, Arnold DM, Lauzier F, Zarychanski R; et al. (2013). “Thrombocytopenia in critically ill patients receiving thromboprophylaxis: frequency, risk factors, and outcomes”. Chest. 144 (4): 1207–1215. doi:10.1378/chest.13-0121. PMID 23788287.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor-In-Chief: Farbod Zahedi Tajrishi, M.D. [2]

Overview

Basically, thrombocytopenia is the result of one of these mechanisms or a combination of some of them: Reduced production of platelets due to bone marrow dysfunction, increased destruction of platelets in the body, iatrogenic, and entrapment of platelets in spleen. Several conditions, some of which mentioned below, can activate the mechanisms that ultimately lead to thrombocytopenia.

Pathophysiology

Physiology

Platelets are produced in hematopoiesis by budding off from megakaryocytes, which are produced by pluripotent hematopoietic stem cells.[1] Each megakaryocyte produces 1000 to 5000 platelets. Platelets circulate for approximately one week, and are then destroyed by the spleen and by Kuppfer cells in the liver.

Pathogenesis

It is thought that thrombocytopenia is the result of either of these four main mechanisms:

Some conditions cause thrombocytopenia through a combination of these mechanisms. For instance, primary ITP is associated with antibody-mediated platelet destruction, but it can also cause suppression of megakaryocytes, which is considered a bone marrow dysfunction.

Main cause Mechanism and further explanations Examples
Bone marrow dysfunction  Bone marrow abnormalities that cause decreased platelet production commonly reduce the production of RBCs and WBCs as well, resulting in pancytopenia. Common presentations include symptoms of thrombocytopenia (eg, bleeding, petechiae) or symptoms associated with anemia and/or leukopenia (eg, shortness of breath, fatigue and recurrent infections).
Platelet destruction/consumption Several mechanisms can accelerate the normal platelet degradation process in the body:

Anti-platelet antibodies seen in both primary ITP and its secondary form (associated with systemic autoimmune disorders such as SLE) play a main role. Antibody-mediated reactions can also cause a reduction in other blood cell lines, resulting in combined cytopenias. Some medications and ingested substances can also cause thrombocytopenia through this mechanism.

Dilution Dilutional thrombocytopenia is an iatrogenic form of thrombocytopenia caused by massive fluid resuscitation or massive blood transfusion. There is a correlation between the decrease in platelet count and the number of RBC units transfused during the course of a day.[2][3]
  • Massive transfusion
  • Massive fluid resuscitation
Redistribution/splenomegaly In individuals with normal splenic function, approximately one-third of the platelet mass is found in the spleen, in equilibrium with the circulating platelet pool. Any condition resulting in splenomegaly and/or splenic congestion due to portal hypertension may lead to a reduced platelet count, while the total platelet mass in the body is intact.[4] Severe thrombocytopenia or bleeding accompanied by splenomegaly is an indication for further diagnostic investigations.
  • Splenomegaly
  • Cirrhosis
  • Alcoholic liver disease

References

  1. ↑ Klein LS, Shih HT, Hackett FK, Zipes DP, Miles WM (1992). “Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease”. Circulation. 85 (5): 1666–74. PMID 1572025.
  2. ↑ Counts RB, Haisch C, Simon TL, Maxwell NG, Heimbach DM, Carrico CJ (1979). “Hemostasis in massively transfused trauma patients”. Ann Surg. 190 (1): 91–9. PMC 1344465. PMID 464685.
  3. ↑ Leslie SD, Toy PT (1991). “Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid”. Am J Clin Pathol. 96 (6): 770–3. PMID 1746495.
  4. ↑ Aster RH (1966). “Pooling of platelets in the spleen: role in the pathogenesis of “hypersplenic” thrombocytopenia”. J Clin Invest. 45 (5): 645–57. doi:10.1172/JCI105380. PMC 292742. PMID 5327481.

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2], Farbod Zahedi Tajrishi, M.D. [2]

Overview

There are two broad mechanisms for the causes of thrombocytopenia: Reduced platelet production and increased platelet destruction. Thrombocytopenia is seen in a variety of infectious and genetic disorders as well as a side effect of a large list of medications.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Disseminated intravascular coagulation, endocarditis, pulmonary embolism
Chemical/Poisoning Strontium-89,zinc
Dental No underlying causes
Dermatologic Cholesterol embolism, Elejalde syndrome, Griscelli syndrome type 1, neuroectodermal melanolysosomal disease, post-transfusion purpura
Drug Side Effect Ado-trastuzumab emtansine, albendazole, alemtuzumab, altretamine, amiodarone, Amoxicillin, amphotericin B, amrinone, amsacrine, anagrelide, anazolene, anti-thymocyte globulin, ardeparin, Asenapine maleate, Aspirin, azathioprine, Azacitidine, Aztreonam, bendamustine, benoxaprofen, Beractant, bevacizumab, Boceprevir, bortezomib, bosutinib, brentuximab vedotin, cabazitaxel, Cabozantinib, capecitabine, captopril, carboplatin, carfilzomib, carmustine, caspofungin, Cefadroxil, Cefepime, Cefotaxime sodium, Ceftazidime, Cefaclor, Certolizumab pegol, Chlorpropamide , chlorambucil, chloramphenicol,clofarabine, Cidofovir, cilazapril, cimetidine, cisplatin, cladribine, Clemastine, clofarabine, Clobazam, Cyclophosphamide, Cytarabine, cytosine arabinoside, dacarbazine, Dactinomycin, dasatinib, daunorubicin, decitabine, deferasirox, desferrioxamine, Desmopressin, Dexchlorpheniramine, Dexrazoxane, Dextran Didanosine, diflunisal, docetaxel, Doxorubicin Hydrochloride, doxycycline, Rifampin drug-induced thrombocytopenia, efalizumab, eflornithine, Eltrombopag, enoxaparin, Epirubicin hydrochloride, eptifibatide, Eribulin, Ethambutol, Ethacrynic Acid, etoposide, everolimus, febuxostat, Felbamate, Filgastrim, flucytosine, fludarabine, fluorouracil, fondaparinux, foscarnet, ganciclovir, gemcitabine, gemtuzumab ozogamicin, glycoprotein IIb/IIIa inhibitors, gold salts, guanidinium, Guanidine, haem arginate, heparin, Hydrocodone bitartrate and acetaminophen, hydroxycarbamide, hydroxychloroquine, Hydroxyurea (patient information), ibitumomab tiuxetan, ibuprofen lysine, ibrutinib, idarubicin, ifosfamide, imatinib mesylate, Indinavir, indomethacin, integrilin, interferon alpha, interferon alfacon-1, Imipenem-Cilastatin,Interferon beta- 1a, Interferon gamma, interleukin 10, interleukin 2, irinotecan hydrochloride, Isoniazid, isotretinoin, ixabepilone, Lapatinib,lenalidomide, Letrozole, linezolid, lomustine, low molecular weight heparins, Loxapine, melphalan, mercaptopurine, Meropenem, methimazole, methotrexate, methyldopa, methyldopate, methylphenidate, micafungin sodium, Milnacipran hydrochloride, minocycline hydrochloride, miltefosine, mithramycin, mitomycin, mitoxantrone, MMR vaccine, montelukast, nabumetone, nelarabine, niacin, nilotinib, nitisinone, Nizatidine, obinutuzumab, Ofatumumab, Omacetaxine, omacetaxine mepesuccinate, Olsalazine, oxaliplatin, Oxaprozin, oxcarbazepine, Oxytetracycline, paclitaxel, Palbociclib, panobinostat, para-amino salicylic acid, pazopanib, Pegademase, Peginterferon Beta-1a,pemetrexed, penicillamine, pentamidine Isethionate, pentostatin, phenylbutazone, phenytoin, Pergolide, Pertuzumab, pixantrone, Plerixafor, pomalidomide, ponatinib, pralatrexate, pramipexole, procarbazine, promethazine, proton pump inhibitors, pyrimethamine, quinidine, quinine, Rabeprazole, Radium chloride, raltitrexed, ranitidine, regorafenib, reoPro, repaglinide, rifampicin, Ritonavir, rituximab, romidepsin, Romiplostim, ruxolitinib, Siltuximab, sirolimus, Sodium aurothiomalate, sorafenib, stiripentol, Streptozocin, Sulfacetamide, Sulfamethoxazole/Trimethoprim (oral), sulfasalazine, sulindac, sulfonamides, sunitinib malate, Spironolactone, Tacrolimus, Tamoxifen, temozolomide, temsirolimus, teniposide, thalidomide, thioguanine, thiotepa, Thiothixene, Tiagabine, ticlopidine, tinzaparin, tirofiban, tocilizumab, topotecan, Tolmetin, Tolazamide, Toremifene, tositumomab iodine-131, trabectedin, Trimethadione, trimethoprim-sulfamethoxazole, tolbutamide, valganciclovir, valproic acid, vancomycin, Vinblastine, Vincristine sulfate liposome vinflunine, vinorelbine, vorinostat, ziv-aflibercept, zonisamide
Ear Nose Throat Alport syndrome, Arias oculootoradial syndrome, Epstein’s syndrome, Fechtner syndrome
Endocrine Immunodysregulation polyendocrinopathy and enteropathy, X-linked
Environmental No underlying causes
Gastroenterologic Dibasic aminoaciduria type 2, liver failure, Niemann-Pick disease type b, portal hypertension, Shwachman-Diamond syndrome
Genetic Aicardi-Goutieres syndrome, Alport syndrome, Chediak-Higashi disease, complement factor H deficiency, Elejalde syndrome, Fanconi anaemia, Fechtner syndrome, Griscelli syndrome type 1, holocarboxylase synthase deficiency, iminodipeptiduria, Jacobsen syndrome, MELAS, neuroectodermal melanolysosomal disease, Niemann-Pick disease type b, Omenn syndrome, Paris-Trousseau thrombocytopenia, Shwachman-Diamond syndrome, TAR syndrome, Thrombocytopenia absent radius syndrome, Von Willebrand disease, platelet type, Wiskott-Aldrich syndrome, X-linked hyperimmunoglobulin M syndrome
Hematologic Acquired pure megakaryocytic aplasia, aplastic anemia, Bernard-Soulier syndrome, congenital amegakaryocytic thrombocytopenia (CAMT), disseminated intravascular coagulation, Epstein’s syndrome, familial histiocytic reticulosis, Gasser syndrome, GATA1-related cytopenia, Glanzmann’s thrombasthenia, grey platelet syndrome, hemolytic uremic syndrome, histiocytosis X, hypersplenism, idiopathic thrombocytopenic purpura, Jacobsen syndrome, Kasabach-Merritt syndrome, May-Hegglin anomaly, Moschcowitz syndrome, myelodysplastic syndrome, myelofibrosis, neonatal alloimmune thrombocytopenia, pancytopenia, Paris-Trousseau thrombocytopenia, paroxysmal nocturnal hemoglobinuria, post-transfusion purpura, pulmonary embolism, radial aplasia-thrombocytopenia syndrome, Sebastian platelet syndrome, Shwachman-Diamond syndrome, thrombotic thrombocytopenic purpura, Von Willebrand disease, platelet type, Werlhof disease, Wiskott-Aldrich syndrome
Iatrogenic Cardiac bypass, chemotherapy, intra-aortic balloon pump placement, massive blood transfusion, radiation therapy
Infectious Disease Congenital syphilis, cytomegalovirus, Dengue fever, ehrlichiosis, Epstein-Barr virus, hantavirus, hepatitis C, HIV, human granulocytic ehrlichiosis, human monocytotropic ehrlichiosis, infections, infectious mononucleosis, lassa fever, leptospirosis, malaria, measles, mumps, mycoplasma pneumonia, Oklahoma tick fever, parvovirus, Q fever, rubella, septicaemia, tick-borne encephalitis, toxic shock syndrome (staphylococcal), varicella, visceral leishmaniasis
Musculoskeletal/Orthopedic Arias oculootoradial syndrome, cholesterol embolism, radial aplasia-thrombocytopenia syndrome, TAR syndrome, thrombocytopenia absent radius syndrome
Neurologic Aicardi-Goutieres syndrome, Jacobsen syndrome
Nutritional/Metabolic Dibasic aminoaciduria type 2, folate deficiency, Gaucher disease, holocarboxylase synthase deficiency, iminodipeptiduria, iron deficiency, isovaleric acidaemia, methylmalonic aciduria type 2, platelet glycoprotein 4 deficiency, platelet glycoprotein Ib deficiency, prolidase deficiency, propionyl-CoA carboxylase deficiency, sea blue histiocytosis, sitosterolemia, vitamin B12 deficiency
Obstetric/Gynecologic Eclampsia, HELLP syndrome, pre-eclampsia
Oncologic Acute lymphoblastic leukemia, acute myeloid leukemia, acute promyelocytic leukemia, chronic lymphocytic leukaemia, chronic myeloid leukaemia, hairy cell leukaemia, hepatosplenic T-cell lymphoma, histiocytosis X, Kasabach-Merritt syndrome, lymphoma, myeloma, Non-Hodgkins lymphoma, paraneoplastic syndrome
Ophthalmologic Arias oculootoradial syndrome
Overdose/Toxicity Alcohol, arsenic trioxide, ethanol
Psychiatric No underlying causes
Pulmonary Acute respiratory distress syndrome, Niemann-Pick disease type b, pulmonary embolism
Renal/Electrolyte Alport syndrome, cholesterol embolism, Dibasic aminoaciduria type 2, Epstein’s syndrome, Fechtner syndrome, hemolytic uremic syndrome
Rheumatology/Immunology/Allergy Anticardiolipin syndrome, antiphospholipid syndrome, autoimmune lymphoproliferative syndrome type 1, autoimmune lymphoproliferative syndrome type 2, complement factor H deficiency, Evans syndrome, immunodysregulation polyendocrinopathy and enteropathy, X-linked, macrophage-activation syndrome, neonatal alloimmune thrombocytopenia, Omenn syndrome, paraneoplastic syndrome, systemic lupus erythematosus, Wiskott-Aldrich syndrome, X-linked hyperimmunoglobulin M syndrome
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Snakebites

Causes in Alphabetical Order

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Stasi R (2012). “How to approach thrombocytopenia”. Hematology Am Soc Hematol Educ Program. 2012: 191–7. doi:10.1182/asheducation-2012.1.191. PMID 23233580.
  2. ↑ 2.0 2.1 2.2 2.3 Greenberg EM, Kaled ES (2013). “Thrombocytopenia”. Crit Care Nurs Clin North Am. 25 (4): 427–34, v. doi:10.1016/j.ccell.2013.08.003. PMID 24267279.
  3. ↑ Farid J, Gul N, Qureshi WU, Idris M (2012). “Clinical presentations in immune thrombocytopenic purpura”. J Ayub Med Coll Abbottabad. 24 (2): 39–40. PMID 24397048.
  4. ↑ Nisha S, Amita D, Uma S, Tripathi AK, Pushplata S (2012). “Prevalence and characterization of thrombocytopenia in pregnancy in Indian women”. Indian J Hematol Blood Transfus. 28 (2): 77–81. doi:10.1007/s12288-011-0107-x. PMC 3332269. PMID 23730013.
  5. ↑ Abdel Karim N, Haider S, Siegrist C, Ahmad N, Zarzour A, Ying J; et al. (2013). “Approach to management of thrombotic thrombocytopenic purpura at university of cincinnati”. Adv Hematol. 2013: 195746. doi:10.1155/2013/195746. PMC 3876823. PMID 24396345.

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Differentiating Thrombocytopenia from other Diseases

Differentiating Thrombocytopenia from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2], Farbod Zahedi Tajrishi, M.D. [2]

Overview

Thrombocytopenia has a broad range of potential causes. While a good history and physical examination can be helpful to diagnose some of these causes such as drug-induced thrombocytopenia, they usually don’t suffice and further evaluation is often needed. There are also some useful points that may guide the physician to an appropriate diagnosis. For example, asymptomatic, isolated thrombocytopenia most probably suggests ITP, while thrombocytopenia in critically ill, hospitalized patients is usually suggestive of iatrogenic causes (eg. dilution), platelet consumption, bone marrow suppression from infection/sepsis, or even drug-induced thrombocytopenia. One should consider however, that a wide variety of other conditions such as autoimmune disorders, nutrient deficiencies, thrombotic microangiopathies could all as well cause thrombocytopenia.

Thrombocytopenia Differential Diagnosis

Differentiating the diseases that can cause thrombocytopenia:

Category Condition Etiology Mechanism Inherited Acquried Clinical manifestations Para−clinical findings Gold standard Associated findings
Demography History Symptoms Signs
Lab Findings
Fever Rash Bleeding BP Splenomegaly Jaundice Other CBC PBS Bone marrow exam PT PTT UA
Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Plt HB WBC
Hematology Bone marrow disorders Myelodysplastic syndromes[1]
  • Unknown
  • Mutation
 + − − ± + Elderly Exposure to + Petechiae, purpura, diffuse erythematous rash + Nl + + ↓ ↓ ↓ Nl Nl Nl Bone marrow examination + clinical manifestation
Aplastic anemia[2] + − − ± ± Biphasic (the young and the elderly) − − + Nl − − ↓ ↓ ↓ ↑ ↑ Nl Bone marrow examination +

laboratory findings

Acute leukemia[3][4] + + − ± ± AML in adults
  • Exposure to chemicals
  • Radiation
  • Pre-existent blood disorders
 ± Petechiae + Nl ± − ↓ ↓ ↓
  • Blast cells
 ↑ ↑ Bone marrow examination
Paroxysmal nocturnal hemoglobinuria (PNH)[5]
  • Mutations
 + + − − + Any age

(usually younger adults)

− − − Nl − − ↓/Nl ↓ ↓/Nl
  • Hypocellular marrow in certain stages of the disease
 Nl Nl Flow cytometry
Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Thrombotic microangiopathy (TMA) Thrombotic thrombocytopenic purpura (TTP)[6]
  • Deficiency of, or antibodies to, the metalloprotease ADAMTS13  
 − + − ± + Any age
  • Neurologic manifestations
  • Fatigue due to anemia
 + Petechiae Not common Nl or ↑ − + ↓ ↓ Nl

or ↑

  • Fragmented RBCs
 NA Nl Nl Laboratory findings
Hemolytic uremic syndrome (HUS)[7] − + − ± + Children
  • Exposure to contaminated water or milk
  • Consuming undercooked ground beef
 + Petechiae − ↓ − + ↓ ↓ Nl

or ↑

  • Fragmented RBCs
 NA Nl Nl Laboratory findings
DIC[8][9]
  • Overstimulation of the coagulation system
 + + − − + Any age + + + ↓ − + ↓ ↓↓ ↑ ↑↑ ↑ Clinical manifestation + laboratory findings
Nutrient deficiencies Folate, vitamin B12, copper deficiencies[10][11]
  • Decreased platelet production
 + − − − + Any age
  • Malnutrition
  • Alcohol use
 − − − Nl − − ↓ ↓ Nl Nl Nl Nl Laboratory findings
Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Congenital platelet disorders[12][13][14] MYH9-related disorders[15] + − − + − Any age, very rare
  • Positive family history
 − + Nl − − ↓ ↓ Nl
  • Döhle body-like inclusions in peripheral blood neutrophils
 NA Nl Nl Nl Genetic study
Bernard-Soulier syndrome[16]
  • Absence of Gp Ib-IX-V  
 + − − + − Children, rare
  • Positive family history
 − − + Nl − − − ↓ Nl Nl Nl Nl Nl Flow cytometry
Gray platelet syndrome[17] + − − + − Rare
  • Positive family history
 − +

Mucocutaneous

Nl + − ↓ Nl Nl Nl Nl Nl Genetic study
Wiskott-Aldrich syndrome[18] + − − + − Rare
  • Positive family history
 − + Nl − − Bloody diarrhea ↓ Nl Nl Nl Nl Nl Genetic study
Thrombocytopenia with absent radius (TAR) syndrome[19] + − − + − Children
  • Positive family history
 − + + Nl − − ↓ Nl Nl or ↑ Nl Nl Nl Evidence of absent radius

+

Laboratory findings

  • Cow’s milk allergy
  • Various other anomalies
Fechtner syndrome[20]
  • Mutation of chromosome 22q11-13
 + − − + − Children
  • Positive family history
 −

petechia

+ Mucocutaneous Nl − −
  • Hearing loss
  • Eye abnormalities
 ↓ Nl Nl or ↑ NA Nl Nl Clinical manifestation + genetic study
Von Willebrand disease[21]
  • VWF deficiency/dysfunction
 + − − + Rarely More common with O blood type
  • Positive family history
 − − + − − − − Nl/ ↓ Nl/↓ Nl NA Nl Nl or ↑ Laboratory findings
  • Lifelong bleeding disorder
Category Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Rheumatologic/autoimmune disorders ITP[22] + + − − + Any age − −

petechia

+ Mucocutaneous Nl − − − ↓↓↓ Nl Nl Nl Nl Nl Nl Diagnosis of exclusion
  • Spontaneous remission  
Systemic lupus erythematosus[23] − + − − + Young women, more prevalent in Africans and Asians + Malar rash, generalized maculopapular rash, discoid rash +

Hemoptysis

Nl or ↑ + + ↓ ↓ ↓ ↑ ↑ Clinical manifestation + serology
Antiphospholipid syndrome[24]
  • Autoantibody-mediated syndrome
 − + − + + Middle aged women, more in African American and Hispanic population − − − Nl − − ↓ Nl ↓ Nl ↑ Clinical manifestation + repeated positive tests of aPL
Felty’s syndrome[25] − + + ± + Rare, young women − − Nl + −
  • Lymphadenopathy
 ↓ Nl ↓ Nl Nl Nl Clinical manifestation
Category Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Infection-induced Bacterial infections Sepsis[26] + + − − + Any + ± Nl to ↓ − ± ↓/↑ Nl ↑↑ NA ↑ ↑ +

Depends on the etiology

Clinical manifestation + culture
  • Associated with ↑ mortality
Helicobacter pylori[27]
  • Immune thrombocytopenia
 − + − − + Any − − − − Nl − − ↓ Nl Nl NA Nl Nl Nl Clinical manifestation + culture
Tick-borne infection[28]
  • Immune thrombocytopenia
 − + − − + Endemic area like China, Japan, and Korea
  • Being bitten by a tick
 + ± Nl to ↓ ± ± ↓ Nl ↓ NA Nl Nl PCR
Viral infections HIV[29]
  • Immune thrombocytopenia
 + + + − + Any
  • High risk behaviors
  • Close contact
 + ± Nl to ↓ ± ± ↓ ↓ ↓ ↑ ↑ Isolation of HIV
Other viruses such as rubella, mumps, varicella, parvovirus, hepatitis C, & Epstein-Barr virus[30]
  • Immune thrombocytopenia
 + − − − + Any
  • High risk behaviors
  • Close contact
 + − Nl ± ± ↓ ↓ ↓ Nl Nl Clinical manifestation + lab tests
Parasitic infections Malaria[31]
  • Unknown
  • Immune thrombocytopenia
 + − − − + Endemic area
  • Being bitten by a mosquito
 + − ± Nl to ↓ ± ± ↓ ↓ ↓ Nl Nl Clinical manifestation + microscopic examination of blood smear
Babesiosis[32]
  • Unknown
  • Immune thrombocytopenia
 + − − − + Rare + − ± Nl to ↓ ± ± ↓ ↓ ↓ Nl Nl Clinical manifestation + microscopic examination of blood smear
Category Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Medication/toxicity Antibiotics/

Antiepileptic[33]

  • Occurrence of drug-dependent, platelet-reactive antibodies
 + + − − + Any
  • Drug ingestion or injection
 − − Nl − − − ↓↓ ↓ Nl NA Nl Nl Nl Clinical manifestation + exclusion of the other causes NA
Heparin-induced thrombocytopenia[34]
  • Anti-heparin/PF4 antibody 
 − + − − + Any
  • Heparin injection
 −
  • Necrotic skin lesions
 − Nl − − − ↓ Nl Nl NA Nl Nl Nl ELISA
Cytotoxic chemotherapy[35] + − − − + Patients with malignancy
  • Drug ingestion or injection
  • Cancer
 − − Nl − − − ↓ ↓ ↓
  • Megakaryocytic hypoplasia or aplasia
 ↑ ↑ Hematuria Clinical manifestation + exclusion of the other causes
Radiation therapy[36] + − − − + Patients with malignancy − + Nl − − − ↓ ↓ ↓
  • Megakaryocytic hypoplasia or aplasia
 ↑ ↑ Hematuria Clinical manifestation + exclusion of the other causes
GI Chronic liver disease[37] + − − − + Any − + ↓ + + − ↓ ↓ Nl NA ↑ ↑ Nl Biopsy
Portal hypertension[38] + − − − + Any − + ↓ + + − ↓ ↓ Nl NA ↑ ↑ Nl Clinical manifestation
Category Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings
Vascular Giant capillary hemangioma (Kasabach-Merritt syndrome)[39][40] − + − + − Infants − Intralesional bleeding Nl − − Visceral hemangiomas ↓↓ ↓↓ Nl Normocytic normochromic erythrocytes and markedly reduced platelets Normal erythropoiesis, myelopoiesis, and megakaryocytic hyperplasia ↑ ↑ Hematuria Biopsy
  • Kaposiform hemangioendothelioma
  • Tufted angioma
Cardiopulmonary bypass[41] − + − − + Elderly − + Nl or ↑ − − − ↓ ↓ Nl Normocytic normochromic erythrocytes and markedly reduced platelets NA ↑ ↑ Hematuria Clinical manifestation
Other Alcohol[42] + − + − + Any − − − Nl + + ↓ ↓ ↓ Cytopenia, macrocytosis Cytopenia, macrocytosis ↑ ↑ Nl Clinical manifestation
Post-transfusion purpura[43][44] − + − − + Women − + ↓ − − − ↓↓↓ ↓ Nl Nl NA Nl Nl Nl Positive circulating alloantibody to a common platelet antigen
  • Severe but rare reaction
Gestational thrombocytopenia[45]
  • Might be physiologic adaptation of pregnancy
 − − − − + Pregnant women
  • Positive history of mild thrombocytopenia
 − − − Nl − − − ↓ Nl Nl Nl NA Nl Nl Nl Diagnosis of exclusion
  • Self-limited condition
HELLP syndrome[46][47]
  • Unknown
 − + − − + Pregnant > 25 years − − + ↑ − + ↓ ↓ Nl Schistocytes NA Nl Nl Proteinuria Lab abnormalities
Idiopathic cyclic thrombocytopenia[48] + + − − + Females with the median age of onset 35 years
  • Misdiagnosed as ITP with uniformly poor responses
 − Minor mucocutaneous bleeding Nl − − − ↓ Nl Nl Reduced platelets and megakaryocytes Megakaryocytic hypoplasia or aplasia Nl Nl Nl Diagnosis of exclusion
Pseudothrombocytopenia[49] − − − − + Rare Collected sample in EDTA anticoagulant − − − Nl − − − ↓ Nl Nl Low platelet count and platelet clumps Low platelet count and platelet clumps Nl Nl Nl Repeat collecting sample in a heparin tube Nl
Category Condition Etiology Decreased platelet production Platelet destruction in blood Platelet destruction in spleen Inherited Acquried Demography History Fever Rash Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT UA Gold standard Associated findings

References

  1. ↑ Natelson, Ethan A.; Pyatt, David (2013). “Acquired Myelodysplasia or Myelodysplastic Syndrome: Clearing the Fog”. Advances in Hematology. 2013: 1–11. doi:10.1155/2013/309637. ISSN 1687-9104.
  2. ↑ Townsley, Danielle M.; Desmond, Ronan; Dunbar, Cynthia E.; Young, Neal S. (2013). “Pathophysiology and management of thrombocytopenia in bone marrow failure: possible clinical applications of TPO receptor agonists in aplastic anemia and myelodysplastic syndromes”. International Journal of Hematology. 98 (1): 48–55. doi:10.1007/s12185-013-1352-6. ISSN 0925-5710.
  3. ↑ Oshima, Yasuo; Yuji, Koichiro; Tanimoto, Tetsuya; Hinomura, Yasushi; Tojo, Arinobu (2013). “Association between Acute Myelogenous Leukemia and Thrombopoietin Receptor Agonists in Patients with Immune Thrombocytopenia”. Internal Medicine. 52 (19): 2193–2201. doi:10.2169/internalmedicine.52.0324. ISSN 0918-2918.
  4. ↑ Oshima Y, Yuji K, Tanimoto T, Hinomura Y, Tojo A (2013). “Association between acute myelogenous leukemia and thrombopoietin receptor agonists in patients with immune thrombocytopenia”. Intern. Med. 52 (19): 2193–201. PMID 24088751.
  5. ↑ Brodsky RA (2014). “Paroxysmal nocturnal hemoglobinuria”. Blood. 124 (18): 2804–11. doi:10.1182/blood-2014-02-522128. PMC 4215311. PMID 25237200.
  6. ↑ Noris M, Mescia F, Remuzzi G (November 2012). “STEC-HUS, atypical HUS and TTP are all diseases of complement activation”. Nat Rev Nephrol. 8 (11): 622–33. doi:10.1038/nrneph.2012.195. PMID 22986360.
  7. ↑ Conway EM (October 2015). “HUS and the case for complement”. Blood. 126 (18): 2085–90. doi:10.1182/blood-2015-03-569277. PMID 26396094.
  8. ↑ Schwameis M, Schörgenhofer C, Assinger A, Steiner MM, Jilma B (April 2015). “VWF excess and ADAMTS13 deficiency: a unifying pathomechanism linking inflammation to thrombosis in DIC, malaria, and TTP”. Thromb. Haemost. 113 (4): 708–18. doi:10.1160/TH14-09-0731. PMC 4745134. PMID 25503977.
  9. ↑ Kitchens CS (2009). “Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC)”. Hematology Am Soc Hematol Educ Program: 240–6. doi:10.1182/asheducation-2009.1.240. PMID 20008204.
  10. ↑ Clarke, V.; Weston-Smith, S. (2010). “Severe folate-deficiency pancytopenia”. Case Reports. 2010 (oct18 2): bcr0320102851–bcr0320102851. doi:10.1136/bcr.03.2010.2851. ISSN 1757-790X.
  11. ↑ Blackmer AB, Bailey E (February 2013). “Management of copper deficiency in cholestatic infants: review of the literature and a case series”. Nutr Clin Pract. 28 (1): 75–86. doi:10.1177/0884533612461531. PMID 23069991.
  12. ↑ Nurden AT, Freson K, Seligsohn U (2012). “Inherited platelet disorders”. Haemophilia. 18 Suppl 4: 154–60. doi:10.1111/j.1365-2516.2012.02856.x. PMID 22726100.
  13. ↑ Balduini, Carlo L.; Savoia, Anna (2012). “Genetics of familial forms of thrombocytopenia”. Human Genetics. 131 (12): 1821–1832. doi:10.1007/s00439-012-1215-x. ISSN 0340-6717.
  14. ↑ D’Andrea G, Chetta M, Margaglione M (2009). “Inherited platelet disorders: thrombocytopenias and thrombocytopathies”. Blood Transfus. 7 (4): 278–92. doi:10.2450/2009.0078-08. PMC 2782805. PMID 20011639.
  15. ↑ Zhang S, Zhou X, Liu S, Bai T, Zhang Y, Wang J, Wang S, Zhang X, Wang B (2014). “MYH9-related disease: description of a large Chinese pedigree and a survey of reported mutations”. Acta Haematol. 132 (2): 193–8. doi:10.1159/000356681. PMID 24643058.
  16. ↑ Berndt MC, Andrews RK (March 2011). “Bernard-Soulier syndrome”. Haematologica. 96 (3): 355–9. doi:10.3324/haematol.2010.039883. PMC 3046265. PMID 21357716.
  17. ↑ Michelson AD (January 2013). “Gray platelet syndrome”. Blood. 121 (2): 250. PMID 23427340.
  18. ↑ Candotti F (January 2018). “Clinical Manifestations and Pathophysiological Mechanisms of the Wiskott-Aldrich Syndrome”. J. Clin. Immunol. 38 (1): 13–27. doi:10.1007/s10875-017-0453-z. PMID 29086100.
  19. ↑ Al-Qattan MM (November 2016). “The Pathogenesis of Radial Ray Deficiency in Thrombocytopenia-Absent Radius (TAR) Syndrome”. J Coll Physicians Surg Pak. 26 (11): 912–916. doi:2476 Check |doi= value (help). PMID 27981927.
  20. ↑ Toren A, Amariglio N, Rozenfeld-Granot G, Simon AJ, Brok-Simoni F, Pras E, Rechavi G (December 1999). “Genetic linkage of autosomal-dominant Alport syndrome with leukocyte inclusions and macrothrombocytopenia (Fechtner syndrome) to chromosome 22q11-13”. Am. J. Hum. Genet. 65 (6): 1711–7. doi:10.1086/302654. PMC 1288382. PMID 10577925.
  21. ↑ Langer F, Obser T, Oyen F, Spath B, Holstein K, Greinacher A, White JG, Budde U, Bokemeyer C, Schneppenheim R (April 2014). “Characterisation of the p.A1461D mutation causing von Willebrand disease type 2B with severe thrombocytopenia, circulating giant platelets, and defective α-granule secretion”. Thromb. Haemost. 111 (4): 777–9. doi:10.1160/TH13-06-0462. PMID 24337418.
  22. ↑ Zufferey, Anne; Kapur, Rick; Semple, John (2017). “Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)”. Journal of Clinical Medicine. 6 (2): 16. doi:10.3390/jcm6020016. ISSN 2077-0383.
  23. ↑ Abu-Hishmeh M, Sattar A, Zarlasht F, Ramadan M, Abdel-Rahman A, Hinson S, Hwang C (October 2016). “Systemic Lupus Erythematosus Presenting as Refractory Thrombotic Thrombocytopenic Purpura: A Diagnostic and Management Challenge. A Case Report and Concise Review of the Literature”. Am J Case Rep. 17: 782–787. PMC 5083062. PMID 27777394.
  24. ↑ Artim-Esen, Bahar; Diz-Küçükkaya, Reyhan; İnanç, Murat (2015). “The Significance and Management of Thrombocytopenia in Antiphospholipid Syndrome”. Current Rheumatology Reports. 17 (3). doi:10.1007/s11926-014-0494-8. ISSN 1523-3774.
  25. ↑ Chavalitdhamrong, Disaya; Molovic-Kokovic, Ana; Iliev, Andrey (2009). “Felty’s Syndrome as an initial presentation of Rheumatoid Arthritis: a case report”. Cases Journal. 2 (1): 206. doi:10.1186/1757-1626-2-206. ISSN 1757-1626.
  26. ↑ Wu, Qin; Ren, Jianan; Wu, Xiuwen; Wang, Gefei; Gu, Guosheng; Liu, Song; Wu, Yin; Hu, Dong; Zhao, Yunzhao; Li, Jieshou (2014). “Recombinant human thrombopoietin improves platelet counts and reduces platelet transfusion possibility among patients with severe sepsis and thrombocytopenia: A prospective study”. Journal of Critical Care. 29 (3): 362–366. doi:10.1016/j.jcrc.2013.11.023. ISSN 0883-9441.
  27. ↑ Kuwana M (January 2014). “Helicobacter pylori-associated immune thrombocytopenia: clinical features and pathogenic mechanisms”. World J. Gastroenterol. 20 (3): 714–23. doi:10.3748/wjg.v20.i3.714. PMC 3921481. PMID 24574745.
  28. ↑ Liu Q, He B, Huang SY, Wei F, Zhu XQ (August 2014). “Severe fever with thrombocytopenia syndrome, an emerging tick-borne zoonosis”. Lancet Infect Dis. 14 (8): 763–772. doi:10.1016/S1473-3099(14)70718-2. PMID 24837566.
  29. ↑ Borges ÁH, Lundgren JD, Mocroft A (July 2015). “Thrombocytopenia and cancer risk during HIV infection”. AIDS. 29 (11): 1425–7. doi:10.1097/QAD.0000000000000744. PMID 26098601.
  30. ↑ Saeed M, Dabbagh O, Al-Muhaizae M, Dhalaan H, Chedrawi A (November 2014). “Acute disseminated encephalomyelitis and thrombocytopenia following Epstein-Barr virus infection”. J Coll Physicians Surg Pak. 24 Suppl 3: S216–8. doi:11.2014/JCPSP.S216S218 Check |doi= value (help). PMID 25518779.
  31. ↑ Rodriguez-Morales AJ, Giselle-Badillo A, Manrique-Castaño S, Yepes MC (2014). “Anemia and thrombocytopenia in Plasmodium vivax malaria is not unusual in patients from endemic and non-endemic settings”. Travel Med Infect Dis. 12 (5): 549–50. doi:10.1016/j.tmaid.2014.07.006. PMID 25131143.
  32. ↑ Nackos E, DeSancho M (March 2014). “Anemia and thrombocytopenia: diagnosis from the blood smear”. Blood. 123 (12): 1783. PMID 24783256.
  33. ↑ Visentin GP, Liu CY (August 2007). “Drug-induced thrombocytopenia”. Hematol. Oncol. Clin. North Am. 21 (4): 685–96, vi. doi:10.1016/j.hoc.2007.06.005. PMC 1993236. PMID 17666285.
  34. ↑ Lovecchio, F. (2014). “Heparin-induced thrombocytopenia”. Clinical Toxicology. 52 (6): 579–583. doi:10.3109/15563650.2014.917181. ISSN 1556-3650.
  35. ↑ Parameswaran, R.; Lunning, M.; Mantha, S.; Devlin, S.; Hamilton, A.; Schwartz, G.; Soff, G. (2014). “Romiplostim for management of chemotherapy-induced thrombocytopenia”. Supportive Care in Cancer. 22 (5): 1217–1222. doi:10.1007/s00520-013-2074-2. ISSN 0941-4355.
  36. ↑ Bercovitz RS, Josephson CD (2012). “Thrombocytopenia and bleeding in pediatric oncology patients”. Hematology Am Soc Hematol Educ Program. 2012: 499–505. doi:10.1182/asheducation-2012.1.499. PMID 23233625.
  37. ↑ Loffredo, Lorenzo; Violi, Francesco (2018). “Thrombopoietin receptor agonists and risk of portal vein thrombosis in patients with liver disease and thrombocytopenia: A meta-analysis”. Digestive and Liver Disease. doi:10.1016/j.dld.2018.06.005. ISSN 1590-8658.
  38. ↑ Jia YP, Lu Q, Gong S, Ma BY, Wen XR, Peng YL, Lin L, Chen HY, Qiu L, Luo Y (September 2007). “Postoperative complications in patients with portal vein thrombosis after liver transplantation: evaluation with Doppler ultrasonography”. World J. Gastroenterol. 13 (34): 4636–40. PMC 4611842. PMID 17729421.
  39. ↑ Lewis D, Vaidya R. Kasabach Merritt Syndrome. [Updated 2018 Jul 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: https://www-ncbi-nlm-nih-gov.ezp-prod1.hul.harvard.edu/books/NBK519053/
  40. ↑ Vinod, Kolar Vishwanath; Johny, Joseph; Vadivelan, Mehalingam; Hamide, Abdoul (2017). “Kasabach-Merritt Syndrome in an adult”. Turkish Journal of Hematology. doi:10.4274/tjh.2017.0429. ISSN 1300-7777.
  41. ↑ Ji, Sung-Mi; Kim, Sung-Hoon; Nam, Jae-Sik; Yun, Hye-Joo; Choi, Jeong-Hyun; Lee, Eun-Ho; Choi, In-Cheol (2015). “Predictive value of rotational thromboelastometry during cardiopulmonary bypass for thrombocytopenia and hypofibrinogenemia after weaning of cardiopulmonary bypass”. Korean Journal of Anesthesiology. 68 (3): 241. doi:10.4097/kjae.2015.68.3.241. ISSN 2005-6419.
  42. ↑ Latvala J, Parkkila S, Niemelä O (April 2004). “Excess alcohol consumption is common in patients with cytopenia: studies in blood and bone marrow cells”. Alcohol. Clin. Exp. Res. 28 (4): 619–24. PMID 15100613.
  43. ↑ McCrae, Keith R.; Herman, Jay H. (1996). “Posttransfusion purpura: Two unusual cases and a literature review”. American Journal of Hematology. 52 (3): 205–211. doi:10.1002/(SICI)1096-8652(199607)52:3<205::AID-AJH13>3.0.CO;2-E. ISSN 0361-8609.
  44. ↑ Pavenski, Katerina; Webert, Kathryn E.; Goldman, Mindy (2008). “Consequences of transfusion of platelet antibody: a case report and literature review”. Transfusion. 48 (9): 1981–1989. doi:10.1111/j.1537-2995.2008.01796.x. ISSN 0041-1132.
  45. ↑ Reese, Jessica A.; Peck, Jennifer D.; Deschamps, David R.; McIntosh, Jennifer J.; Knudtson, Eric J.; Terrell, Deirdra R.; Vesely, Sara K.; George, James N. (2018). “Platelet Counts during Pregnancy”. New England Journal of Medicine. 379 (1): 32–43. doi:10.1056/NEJMoa1802897. ISSN 0028-4793.
  46. ↑ Barnhart, Lynette (2015). “HELLP Syndrome and the Effects on the Neonate”. Neonatal Network. 34 (5): 269–273. doi:10.1891/0730-0832.34.5.269. ISSN 0730-0832.
  47. ↑ Haram, Kjell; Svendsen, Einar; Abildgaard, Ulrich (2009). “The HELLP syndrome: Clinical issues and management. A Review”. BMC Pregnancy and Childbirth. 9 (1). doi:10.1186/1471-2393-9-8. ISSN 1471-2393.
  48. ↑ Go, Ronald S. (2005). “Idiopathic cyclic thrombocytopenia”. Blood Reviews. 19 (1): 53–59. doi:10.1016/j.blre.2004.05.001. ISSN 0268-960X.
  49. ↑ Tan, Geok Chin; Stalling, Melissa; Dennis, Gretchen; Nunez, Maria; Kahwash, Samir B. (2016). “Pseudothrombocytopenia due to Platelet Clumping: A Case Report and Brief Review of the Literature”. Case Reports in Hematology. 2016: 1–4. doi:10.1155/2016/3036476. ISSN 2090-6560.
Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-In-Chief: Farbod Zahedi Tajrishi, M.D. [2]

Overview

High risk patients for thrombocytopenia include: Have certain types of cancer, aplastic anemia, or autoimmune diseases, are exposed to certain toxic chemicals, have a reaction to certain medicines, have certain viruses, and have certain genetic conditions.

Risk Factors

People who are at highest risk for thrombocytopenia are those affected by one of the conditions or factors discussed in the “Causes” section. This includes people who:

  • Have certain types of cancer, aplastic anemia, or autoimmune diseases
  • Are exposed to certain toxic chemicals
  • Have a reaction to certain medicines
  • Have certain viruses
  • Have certain genetic conditions

People at highest risk also include heavy alcohol drinkers and pregnant women.[1]

Non-alcoholic fatty liver disease, especially if with cirrhosis, may be associated with thrombocytopenia[2][3].

References

  1. ↑ [https://www.nhlbi.nih.gov/health-topics/thrombocytopenia “Thrombocytopenia | National Heart, Lung, and Blood Institute (NHLBI)”.]“Thrombocytopenia | National Heart, Lung, and Blood Institute (NHLBI)”. 
  2. ↑ Rivera-Álvarez M, Córdova-Ramírez AC, Elías-De-La-Cruz GD, Murrieta-Álvarez I, León-Peña AA, Cantero-Fortiz Y; et al. (2021). “Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia”. Hematol Transfus Cell Ther. doi:10.1016/j.htct.2021.06.004. PMID 34312112 Check |pmid= value (help).
  3. ↑ Panke CL, Tovo CV, Villela-Nogueira CA, Cravo CM, Ferreira FC, Rezende GFM; et al. (2020). “Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis”. Ann Hepatol. 19 (1): 88–91. doi:10.1016/j.aohep.2019.05.011. PMID 31575467.

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farbod Zahedi Tajrishi, M.D.

Overview

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for thrombocytopenia.

Screening

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for thrombocytopenia.

References

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2], Farbod Zahedi Tajrishi, M.D. [2]

Overview

As thrombocytopenia is not an individual disease and has a wide variety of causes, it can produce different natural histories, complications and prognoses. Based on its underlying cause, it can remain assymptomatic and regress spontaneously, or it could develop to be accompanied by chronic diseases such as SLE and even life-threatening malignancies.

Natural History

Studies on the natural history of thrombocytopenia are limited and the natural history itself depends enormously on the underlying cause of thrombocytopenia. Studies had shown that the following complications/prognosis is probable in patients with asymptomatic mild thrombocytopenia:[1]

  • Return to normal platelet status
  • Developing MDS
  • Developing SLE
  • Remain asymptomatic

After five years of follow-up, the majority of participants (64 percent) either experienced:

  • Spontaneous resolution of thrombocytopenia, or
  • Persistent mild thrombocytopenia without development of an associated condition, suggesting a diagnosis of ITP.

Complications

Depending on the underlying cause, the complications of thrombocytopenia include a variety of conditions from no complications at all or easy bruising to severe life-threatening conditions

Prognosis

Generally, the prognosis of thrombocytopenia depends on its underlying cause. In acute coronary syndrome trials and ST elevation MI trials, thrombocytopenia has been associated with an increase risk of major bleeding, transfusion, recurrent MI, stroke and both in-hosptial and 30 day mortality. [2][3][4][5]

References

  1. ↑ Stasi R, Amadori S, Osborn J, Newland AC, Provan D (2006). “Long-term outcome of otherwise healthy individuals with incidentally discovered borderline thrombocytopenia”. PLoS Med. 3 (3): e24. doi:10.1371/journal.pmed.0030024. PMC 1326262. PMID 16401142.
  2. ↑ Gore JM, Spencer FA, Gurfinkel EP, López-Sendón J, Steg PG, Granger CB, FitzGerald G, Agnelli G (2009). “Thrombocytopenia in patients with an acute coronary syndrome (from the Global Registry of Acute Coronary Events [GRACE])”. The American Journal of Cardiology. 103 (2): 175–80. doi:10.1016/j.amjcard.2008.08.055. PMID 19121432. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)
  3. ↑ Merlini PA, Rossi M, Menozzi A, Buratti S, Brennan DM, Moliterno DJ, Topol EJ, Ardissino D (2004). “Thrombocytopenia caused by abciximab or tirofiban and its association with clinical outcome in patients undergoing coronary stenting”. Circulation. 109 (18): 2203–6. doi:10.1161/01.CIR.0000127867.41621.85. PMID 15117843. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)
  4. ↑ Nikolsky E, Sadeghi HM, Effron MB, Mehran R, Lansky AJ, Na Y, Cox DA, Garcia E, Tcheng JE, Griffin JJ, Stuckey TD, Turco M, Carroll JD, Grines CL, Stone GW (2005). “Impact of in-hospital acquired thrombocytopenia in patients undergoing primary angioplasty for acute myocardial infarction”. The American Journal of Cardiology. 96 (4): 474–81. doi:10.1016/j.amjcard.2005.04.005. PMID 16098296. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)
  5. ↑ Wang TY, Ou FS, Roe MT, Harrington RA, Ohman EM, Gibler WB, Peterson ED (2009). “Incidence and prognostic significance of thrombocytopenia developed during acute coronary syndrome in contemporary clinical practice”. Circulation. 119 (18): 2454–62. doi:10.1161/CIRCULATIONAHA.108.827162. PMID 19398666. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)

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Diagnosis

Diagnosis

Diagnostic Study of Choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-ray | Echocardiography and Ultrasound | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

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