Classification ICD-10: D69 (https://icd.who.int/browse10/2019/en#/D69) · ICD-9-CM: 287(http://www.icd9data.com/getICD9Code.ashx?icd9=287) ·MeSH: D011693 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D011693) ·DiseasesDB:25619 (http://www.diseasesdatabase.com/ddb25619.htm)ExternalresourcesMedlinePlus:003232 (https://www.nlm.nih.gov/medlineplus/ency/article/003232.htm)OCLC 960844656 (https://www.worldcat.org/oclc/960844656).5. Muirhead, Trevor T.; Eide, Melody J. (2011). \"Toxic Effects of Levamisole in a Cocaine User\".New England Journal of Medicine. The New England Journal of Medicine. 364 (24): e52.doi 10.1056/NEJMicm1008722 (https://doi.org/10.1056%2FNEJMicm1008722):.PMID 21675882 (https://pubmed.ncbi.nlm.nih.gov/21675882).6. Anderson JE, DeGoff W, McNamara M (1999). \"Autoerythrocyte sensitization (psychogenicpurpura): a case report and review of the literature\". Pediatric Emergency Care. 15 (1): 47–48. doi 10.1097/00006565-199902000-00014 (https://doi.org/10.1097%2F00006565-199902:000-00014) PMID 10069314 (https://pubmed.ncbi.nlm.nih.gov/10069314). .7. Lotti T, Benci M, Sarti MG, Teofoli P, Senesi C, Bonan P, et al. (1993). \"Psychogenic purpurawith abnormally increased tPA dependent cutaneous fibrinolytic activity\". InternationalJournal of Dermatology. 32 (7): 521–23. doi 10.1111/j.1365-4362.1993.tb02840.x (https://doi.:org/10.1111%2Fj.1365-4362.1993.tb02840.x) PMID 8340191 (https://pubmed.ncbi.nlm.nih.g. ov/8340191) S2CID 38433734 (https://api.semanticscholar.org/CorpusID:38433734). .Evaluating the Child with Purpura (http://www.aafp.org/afp/20010801/419.html) from American Academy of FamilyPhysiciansRetrieved from \"https://en.wikipedia.org/w/index.php?title=Purpura&oldid=1016385273\"This page was last edited on 6 April 2021, at 22:00 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.External linksD
ThrombocytopeniaOthernamesThrombocytopaenia,thrombopeniaA photomicrograph of the blood showingthrombocytopeniaSpecialtyHematologyCausesBone marrow not making enough,body destroying platelets, spleenholding too many platelets[1]DiagnosticmethodComplete blood count[1]TreatmentNone, immunosuppressants,platelet transfusion, surgicalremoval of the spleen[1]ThrombocytopeniaThrombocytopenia is a condition characterizedby abnormally low levels of platelets, also knownas thrombocytes, in the blood.[2] It is the mostcommon coagulation disorder among intensivecare patients and is seen in 20% of medicalpatients and a third of surgical patients.[3]A normal human platelet count ranges from150,000 to 450,000 platelets per microliter ofblood.[4] Values outside this range do notnecessarily indicate disease. One commondefinition of thrombocytopenia requiringemergency treatment is a platelet count below50,000 per microliter.[5] Thrombocytopenia canbe contrasted with the conditions associated withan abnormally high level of platelets in the blood:thrombocythemia (when the cause is unknown),and thrombocytosis (when the cause isknown).[6][7]Signs and symptomsCausesDecreased productionIncreased destructionMedication-inducedOther causesDiagnosisTreatmentPlatelet transfusionsThrombotic thrombocytopenic purpuraImmune thrombocytopenic purpuraHeparin-induced thrombocytopeniaCongenital amegakaryocyticthrombocytopeniaHuman induced pluripotent stem cell-derived plateletsNeonatal thrombocytopeniaReferencesExternal linksContents
Petechia on the lower leg fromthrombocytopeniaRight upper limb with purpuracaused by thrombocytopenia inperson with septic shockThrombocytopenia usually has no symptoms and is pickedup on a routine complete blood count. Some individuals withthrombocytopenia may experience external bleeding such asnosebleeds, or bleeding gums. Some women may haveheavier or longer periods or breakthrough bleeding.Bruising, particularly purpura in the forearms and petechiaein the feet, legs, and mucous membranes, may be caused byspontaneous bleeding under the skin.[8][9]Eliciting a full medical history is vital to ensure the lowplatelet count is not secondary to another disorder. Ensuringthat the other blood cell types, such as red blood cells andwhite blood cells are not also suppressed, is alsoimportant.[8] Painless, round, and pinpoint (1 to 3 mm indiameter) petechiae usually appear and fade, and sometimesgroup to form ecchymoses. Larger than petechiae,ecchymoses are purple, blue, or yellow-green areas of skinthat vary in size and shape. They can occur anywhere on thebody.[8]A person with this disease may also complain of malaise,fatigue, and general weakness (with or withoutaccompanying blood loss). Acquired thrombocytopenia maybe associated with the use of certain drugs. Inspectiontypically reveals evidence of bleeding (petechiae orecchymoses), along with slow, continuous bleeding from anyinjuries or wounds. Adults may have large, blood-filled bullae in the mouth.[10] If the person'splatelet count is between 30,000 and 50,000/mm , bruising with minor trauma may be3expected; if it is between 15,000 and 30,000/mm , spontaneous bruising will be seen (mostly on3the arms and legs).[11]Thrombocytopenia can be inherited or acquired.[12]Abnormally low platelet production may be caused by:[13]Dehydration, Vitamin B or folic acid deficiency12Leukemia, myelodysplastic syndrome, or aplastic anemiaDecreased production of thrombopoietin by the liver in liver failureSepsis, systemic viral or bacterial infectionLeptospirosisHereditary syndromes[14]ACTN1-related thrombocytopeniaAmegakaryocytic thrombocytopenia with radio-ulnar synostosisANKRD26 related thrombocytopeniaSigns and symptomsCausesDecreased production
TTPAutosomal dominant thrombocytopeniaBernard–Soulier syndrome (associated with giant platelet disorder)Congenital amegakaryocytic thrombocytopeniaCongenital amegakaryocytic thrombocytopenia and radioulnar synostosisCYCS-related thrombocytopeniaEpstein syndrome (associated with giant platelet disorder)ETV6 related thrombocytopeniaFanconi anemiaFilaminopathies AFYB related thrombocytopeniaGlanzmann's thrombastheniaGNE myopathy with congenital thrombocytopeniaGray platelet syndrome (associated with giant platelet disorder)Harris platelet syndrome (associated with giant platelet disorder)Macrothrombocytopenia and hearing lossMay–Hegglin anomaly (associated with giant platelet disorder)MYH9-related disease]] (associated with giant platelet disorder)PRKACG-related thrombocytopeniaParis-Trousseau thrombocytopenia/Jacobsen syndromeSebastian syndromeSLFN14-related thrombocytopeniaStormorken syndromeTRPM7-related thrombocytopeniaThrombocytopenia absent radius syndromeTropomyosin 4-related thrombocytopeniaTUBB1-related thrombocytopeniaUpshaw–Schulman syndromeWiskott–Aldrich syndromeX-linked thrombocytopeniaX-linked thrombocytopenia with thalassemiaAbnormally high rates of platelet destruction may be due toimmune or nonimmune conditions, including:[15]Immune thrombocytopenic purpuraThrombotic thrombocytopenic purpuraHemolytic–uremic syndromeDisseminated intravascular coagulationParoxysmal nocturnal hemoglobinuriaAntiphospholipid syndromeSystemic lupus erythematosusPost-transfusion purpuraNeonatal alloimmune thrombocytopeniaHypersplenismDengue feverIncreased destruction
Gaucher's diseaseZika virusThese medications can induce thrombocytopenia through direct myelosuppression:[16]Valproic acidMethotrexateCarboplatinInterferonIsotretinoinPanobinostatH blockers and proton-pump inhibitors2Lab error, possibly due to the anticoagulant EDTA in CBC specimen tubes; a citrated plateletcount is a useful follow-up study[17]Snakebite[18]Niacin toxicity[19]Lyme disease[20]Thrombocytapheresis (also called plateletpheresis)Niemann–Pick disease[21][22]Laboratory tests for thrombocytopenia might include full blood count, liver enzymes, kidneyfunction, vitamin B levels, folic acid levels, erythrocyte sedimentation rate, and peripheral12blood smear. If the cause for the low platelet count remains unclear, a bone marrow biopsy isusually recommended to differentiate cases of decreased platelet production from cases ofperipheral platelet destruction.[23]Thrombocytopenia in hospitalized alcoholics may be caused by spleen enlargement, folatedeficiency, and most frequently, the direct toxic effect of alcohol on production, survival time,and function of platelets.[24] Platelet count begins to rise after 2 to 5 days' abstinence fromalcohol. The condition is generally benign, and clinically significant hemorrhage is rare.In severe thrombocytopenia, a bone marrow study can determine the number, size, and maturityof the megakaryocytes. This information may identify ineffective platelet production as the causeof thrombocytopenia and rule out a malignant disease process at the same time.[25]Treatment is guided by the severity and specific cause of the disease. Treatment focuses oneliminating the underlying problem, whether that means discontinuing drugs suspected to causeit or treating underlying sepsis. Diagnosis and treatment of serious thrombocytopenia is usuallyMedication-inducedOther causesDiagnosisTreatment
Oral petechiae/purpura - Immunethrombocytopenic purpuradirected by a hematologist. Corticosteroids may be used to increase platelet production. Lithiumcarbonate or folate may also be used to stimulate platelet production in the bone marrow.[26]Platelet transfusions may be suggested for people who have a low platelet count due tothrombocytopenia.[27]Treatment of thrombotic thrombocytopenic purpura (TTP) is a medical emergency, since theassociated hemolytic anemia and platelet activation can lead to kidney failure and changes in thelevel of consciousness. Treatment of TTP was revolutionized in the 1980s with the application ofplasmapheresis. According to the Furlan-Tsai hypothesis,[28] this treatment works by removingantibodies against the von Willebrand factor-cleaving protease ADAMTS-13. The plasmapheresisprocedure also adds active ADAMTS-13 protease proteins to the patient, restoring a normal levelof von Willebrand factor multimers. Patients with persistent antibodies against ADAMTS-13 donot always manifest TTP, and these antibodies alone are not sufficient to explain howplasmapheresis treats TTP.[29]Many cases of immune thrombocytopenic purpura (ITP) alsoknown as idiopathic thrombocytopenic purpura, can be leftuntreated, and spontaneous remission (especially inchildren) is not uncommon. However, counts under 50,000are usually monitored with regular blood tests, and thosewith counts under 10,000 are usually treated, as the risk ofserious spontaneous bleeding is high with such low plateletcounts. Any patient experiencing severe bleeding symptomsis also usually treated. The threshold for treating ITP hasdecreased since the 1990s; hematologists recognize thatpatients rarely spontaneously bleed with platelet countsgreater than 10,000, although exceptions to this observation have been documented.[30][31]Thrombopoetin analogues have been tested extensively for the treatment of ITP. These agentshad previously shown promise, but had been found to stimulate antibodies against endogenousthrombopoietin or lead to thrombosis. Romiplostim (trade name Nplate, formerly AMG 531) wasfound to be safe and effective for the treatment of ITP in refractory patients, especially those whorelapsed following splenectomy.[32]Discontinuation of heparin is critical in a case of heparin-induced thrombocytopenia (HIT).Beyond that, however, clinicians generally treat to avoid thrombosis.[33] Treatment may includea direct thrombin inhibitor, such as lepirudin or argatroban. Other blood thinners sometimesused in this setting include bivalirudin and fondaparinux. Platelet transfusions are not routinelyused to treat HIT because thrombosis, not bleeding, is the primary problem.[34] Warfarin is notrecommended until platelets have normalized.[34]Platelet transfusionsThrombotic thrombocytopenic purpuraImmune thrombocytopenic purpuraHeparin-induced thrombocytopenia
Bone marrow/stem cell transplants are the only known cures for this genetic disease. Frequentplatelet transfusions are required to keep the patient from bleeding to death before thetransplant can be performed, although this is not always the case.[35]Human induced pluripotent stem cell-derived platelets is a technology currently beingresearched by the private sector, in association with the Biomedical Advanced Research andDevelopment Authority and the U.S. Department of Health and Human Services, that wouldcreate platelets outside the human body.[36]Thrombocytopenia affects a few newborns, and its prevalence in neonatal intensive care units ishigh. Normally, it is mild and resolves without consequences. Most cases affect preterm birthinfants and result from placental insufficiency and/or fetal hypoxia. Other causes, such asalloimmunity, genetics, autoimmunity, and infection, are less frequent.[37]Thrombocytopenia that starts after the first 72 hours since birth is often the result of underlyingsepsis or necrotizing enterocolitis.[37] In the case of infection, PCR tests may be useful for rapidpathogen identification and detection of antibiotic resistance genes. Possible pathogens includeviruses (e.g. cytomegalovirus,[37] rubella virus,[37] HIV[37]), bacteria (e.g. Staphylococcusspp.,[38]Enterococcus spp.,[38]Streptococcus agalactiae,[37]Listeria monocytogenes,[37]Escherichia coli,[37][38]Haemophilus influenzae,[37]Klebsiella pneumoniae,[38]Pseudomonasaeruginosa,[38][39]Yersinia enterocolitica[39]), fungi (e.g. Candida spp.[38]), and Toxoplasmagondii.[37] The severity of thrombocytopenia may be correlated with pathogen type; someresearch indicates that the most severe cases are related to fungal or Gram-negative bacterialinfection.[38] The pathogen may be transmitted during[40] or before birth, by breastfeeding,[41][42][43] or during transfusion.[44] Interleukin-11 is being investigated as a drug formanaging thrombocytopenia, especially in cases of sepsis or necrotizing enterocolitis (NEC).[37]1. \"Thrombocytopenia\" (https://www.nhlbi.nih.gov/health-topics/thrombocytopenia). NationalHeart, Lung, and Blood Institute. Retrieved 4 January 2018.2. Deutschman, Clifford S.; Neligan, Patrick J. (2010). Evidence-based Practice of Critical Care(https://books.google.com/books?id=4j2pMp-KbKgC&pg=PA645). Elsevier Health Sciences.ISBN 978-1416054764. Retrieved 2015-04-30.3. Marini, John J; Dries, David J (2019). Critical care medicine: the essentials and more.Philadelphia: Wolters Kluwer. ISBN 978-1-4963-0291-5 OCLC 1060947164 (https://www.wor. ldcat.org/oclc/1060947164).4. \"Platelet count: MedlinePlus Medical Encyclopedia\" (https://www.nlm.nih.gov/medlineplus/ency/article/003647.htm). www.nlm.nih.gov. Retrieved 2015-05-01.5. \"What Is Thrombocytopenia? - NHLBI, NIH\" (http://www.nhlbi.nih.gov/health/health-topics/topics/thcp). www.nhlbi.nih.gov. Retrieved 2015-05-01.6. Schafer AI (March 2004). \"Thrombocytosis\". N. Engl. J. Med. 350 (12): 1211–9.doi 10.1056/NEJMra035363 (https://doi.org/10.1056%2FNEJMra035363) PMID 15028825:. (https://pubmed.ncbi.nlm.nih.gov/15028825).Congenital amegakaryocytic thrombocytopeniaHuman induced pluripotent stem cell-derived plateletsNeonatal thrombocytopeniaReferences
7. \"Thrombocythemia and Thrombocytosis | NHLBI, NIH\" (https://www.nhlbi.nih.gov/health-topics/thrombocythemia-and-thrombocytosis). www.nhlbi.nih.gov. Retrieved 5 August 2020.8. Bhatia, M.P.S. \"B.E. Project on Platlet Count Using Image Processing Techniques\" (http://cs.nyu.edu/~sg4187/Platelet.pdf) (PDF). BTP_Report. Retrieved 30 November 2014.9. Houghton, Andrew R.; Gray, David (2010). Chamberlain's Symptoms and Signs in ClinicalMedicine 13th Edition, An Introduction to Medical Diagnosis (https://books.google.com/books?id=IXynWiryyjoC&q=thrombocytopenia+symptoms+signs&pg=PA294). CRC Press.ISBN 9780340974254. Retrieved 2015-05-01.10. Interpreting Signs and Symptoms (https://books.google.com/books?id=PcARTQwHLpIC&pg=PA293). Lippincott Williams & Wilkins. 2007. p. 293. ISBN 9781582556680.11. Rosdahl, Caroline Bunker; Kowalski, Mary T. (2008). Textbook of Basic Nursing (https://books.google.com/books?id=odY9mXicPlYC&q=thrombocytopenia++signs+fatigue&pg=PA1256).Lippincott Williams & Wilkins. ISBN 9780781765213. Retrieved 2015-05-01.12. \"What Causes Thrombocytopenia?\" (http://www.nhlbi.nih.gov/health/health-topics/topics/thcp/causes). National Heart, Lung, and Blood Institute. Retrieved 4 December 2014.13. Fiebach, Nicholas H.; Barker, Lee Randol; Burton, John Russell; Zieve, Philip D. (2007).Principles of Ambulatory Medicine (https://books.google.com/books?id=UGVylX6g4i8C&q=thrombocytopenia+decreased+production&pg=PA841). Lippincott Williams & Wilkins.ISBN 9780781762274. Retrieved 2015-04-30.14. Almazni I, Stapley R, Morgan NV (2019) Inherited Thrombocytopenia: Update on genes andgenetic variants which may be associated With bleeding. Front Cardiovasc Med15. Rodak, Bernadette F.; Fritsma, George A.; Keohane, Elaine (2013). Hematology: ClinicalPrinciples and Applications (https://books.google.com/books?id=-tHsAwAAQBAJ&q=thrombocytopenia+decreased+production&pg=PA695). Elsevier Health Sciences.ISBN 9780323292696. Retrieved 2015-04-30.16. Gresele, Paolo; Fuster, Valentin; Lopez, Jose A.; Page, Clive P.; Vermylen, Jos (2007).Platelets in Hematologic and Cardiovascular Disorders: A Clinical Handbook (https://books.google.com/books?id=kB4C84kCDZEC&q=thrombocytopenia+medication+induced&pg=PA168). Cambridge University Press. ISBN 9781139468763. Retrieved 2015-04-30.17. Tan, GC; Stalling, M; Dennis, G; Nunez, M; Kahwash, SB (2016). \"Pseudothrombocytopeniadue to Platelet Clumping: A Case Report and Brief Review of the Literature\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164902). Case Reports in Hematology. 2016: 1–4.doi 10.1155/2016/3036476 (https://doi.org/10.1155%2F2016%2F3036476) PMC 5164902 (h:. ttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164902) PMID 28044112 (https://pubmed.nc. bi.nlm.nih.gov/28044112).18. Waldmann, Carl; Soni, Neil; Rhodes, Andrew (2008). Oxford Desk Reference: Critical Care(https://books.google.com/books?id=eLqMpXfAlEcC&q=thrombocytopenia++snake+bites&pg=PA388). Oxford University Press. ISBN 9780199229581. Retrieved 2015-05-01.19. Dart, Richard C. (2004). Medical Toxicology (https://books.google.com/books?id=BfdighlyGiwC&q=thrombocytopenia+niacin+toxicity&pg=PA644). Lippincott Williams & Wilkins.ISBN 9780781728454. Retrieved 2015-05-01.20. Greer, John P.; Arber, Daniel A.; Glader, Bertil; List, Alan F.; Means, Robert T.; Paraskevas,Frixos; Rodgers, George M. (2013). Wintrobe's Clinical Hematology (https://books.google.com/books?id=NYCeAgAAQBAJ&q=thrombocytopenia+lyme+disease&pg=PA1103). LippincottWilliams & Wilkins. ISBN 9781469846224. Retrieved 2015-05-01.21. \"Niemann-Pick disease\" (https://ghr.nlm.nih.gov/condition/niemann-pick-disease#inheritance). Genetics Home Reference.22. https://www.mayoclinic.org/diseases-conditions/niemann-pick/symptoms-causes/syc-2035588723. \"How Is Thrombocytopenia Diagnosed? - NHLBI, NIH\" (http://www.nhlbi.nih.gov/health/health-topics/topics/thcp/diagnosis). www.nhlbi.nih.gov. Retrieved 2015-05-19.
24. Lieber, Charles S. (2012). Medical and Nutritional Complications of Alcoholism: Mechanismsand Management (https://books.google.com/books?id=KkL0BwAAQBAJ&q=alcoholics+thrombocytopenia&pg=PA264). Springer Science & Business Media. ISBN 9781461533207.25. Hillyer, Christopher D.; Abrams, Charles S.; Shaz, Beth H.; Roshal, Mikhail; Zimring, JamesC.; Abshire, Thomas C. (2009). Transfusion Medicine and Hemostasis: Clinical andLaboratory Aspects (https://books.google.com/books?id=cGBaz0hp_fcC&q=thrombocytopenia+++diagnosis&pg=PA489). Elsevier. ISBN 9780080922300. Retrieved 2015-05-01.26. Lawrence, Peter F.; Bell, Richard M.; Dayton, Merril T. (2012-10-31). Essentials of GeneralSurgery (https://books.google.com/books?id=LNapiMBi_csC&q=Thrombotic+thrombocytopenic+purpura+treatment+corticosteroids&pg=PA439). Lippincott Williams & Wilkins.ISBN 9780781784955.27. Estcourt, Lise J; Malouf, Reem; Hopewell, Sally; Doree, Carolyn; Van Veen, Joost (2018-04-30). Cochrane Haematological Malignancies Group (ed.). \"Use of platelet transfusions priorto lumbar punctures or epidural anaesthesia for the prevention of complications in peoplewith thrombocytopenia\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5957267). CochraneDatabase of Systematic Reviews. : CD011980. 4doi 10.1002/14651858.CD011980.pub3 (htt:ps://doi.org/10.1002%2F14651858.CD011980.pub3) PMC 5957267 (https://www.ncbi.nlm.ni. h.gov/pmc/articles/PMC5957267) PMID 29709077 (https://pubmed.ncbi.nlm.nih.gov/297090. 77).28. Chapman, Kent; Seldon, Michael; Richards, Ross (2012). \"Thrombotic microangiopathies,thrombotic thrombocytopenic purpura, and ADAMTS-13\" (http://www.thieme-connect.com).Seminars in Thrombosis and Hemostasis. 38 (1): 47–54. doi 10.1055/s-0031-1300951 (http:s://doi.org/10.1055%2Fs-0031-1300951) PMID 22314603 (https://pubmed.ncbi.nlm.nih.gov/. 22314603).29. \"How Is Thrombotic Thrombocytopenic Purpura Treated? - NHLBI, NIH\" (https://www.nhlbi.nih.gov/health/health-topics/topics/ttp/treatment). www.nhlbi.nih.gov. Retrieved 2015-05-20.30. Thrombocytopenic Purpura: New Insights for the Healthcare Professional: 2013 Edition:ScholarlyPaper (https://books.google.com/books?id=x-RMkItgNWQC&pg=PA7).ScholarlyEditions. 2013-07-22. ISBN 9781481662420.31. \"Idiopathic thrombocytopenic purpura (ITP): MedlinePlus Medical Encyclopedia\" (https://www.nlm.nih.gov/medlineplus/ency/article/000535.htm). www.nlm.nih.gov. Retrieved2015-05-20.32. \"Nplate (romiplostim) for subcutaneous injection\" (https://www.fda.gov/safety/medwatch/safetyinformation/ucm182233.htm). www.fda.gov. Retrieved 2015-05-02.33. Warkentin, Theodore E.; Greinacher, Andreas (2007-07-23). Heparin-InducedThrombocytopenia (https://books.google.com/books?id=79OEYE4RnRQC&pg=PA1e). CRCPress. ISBN 9781439826423.34. Ahmed, I; Majeed, A; Powell, R (2007). \"Heparin induced thrombocytopenia: diagnosis andmanagement update\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600013).Postgraduate Medical Journal. 83 (983): 575–582. doi 10.1136/pgmj.2007.059188 (https://do:i.org/10.1136%2Fpgmj.2007.059188) ISSN 0032-5473 (https://www.worldcat.org/issn/0032-. 5473) PMC 2600013 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600013). .PMID 17823223 (https://pubmed.ncbi.nlm.nih.gov/17823223).35. Smit-Sibinga, C. Th (2010-05-10). Neonatology and Blood Transfusion (https://books.google.com/books?id=wBjr7pkmNSIC&pg=PA48). Springer Science & Business Media.ISBN 9780387236001.36. Clark, Douglas (2019-10-02). \"New technology may aid emergency preparedness\" (https://homelandprepnews.com/stories/37483-new-technology-may-aid-emergency-preparedness/).Homeland Preparedness News. Retrieved 2019-10-23.
Classification ICD-10: D69.6 (https://icd.who.int/browse10/2019/en#/D637. Roberts, I; Murray, N. A. (2003). \"Neonatal thrombocytopenia: causes and management\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1721612). Archives of Disease in Childhood:Fetal and Neonatal Edition. 88 (5): F359–64. doi 10.1136/fn.88.5.F359 (https://doi.org/10.113:6%2Ffn.88.5.F359) ISSN 1468-2052 (https://www.worldcat.org/issn/1468-2052). .PMC 1721612 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1721612) PMID 12937037 (ht. tps://pubmed.ncbi.nlm.nih.gov/12937037).38. Guida, JD; Kunig, AM; Leef, KH; McKenzie, SE; Paul, DA (2003). \"Platelet count and sepsisin very low birth-weight neonates: is there an organism-specific response?\". Pediatrics. 111(6 Pt 1): 1411–15. doi 10.1542/peds.111.6.1411:(https://doi.org/10.1542%2Fpeds.111.6.1411) PMID 12777561 (https://pubmed.ncbi.nlm.nih.. gov/12777561).39. Pacifico, L; Chiesa, C; Mirabella, S; Panero, A; Midulla, M (1987). \"Early-onsetPseudomonas aeruginosa sepsis and Yersinia enterocolitica neonatal infection: a uniquecombination in a preterm infant\". European Journal of Pediatrics. 146 (2): 192–93.doi 10.1007/BF02343233 (https://doi.org/10.1007%2FBF02343233) PMID 3569360 (https://:. pubmed.ncbi.nlm.nih.gov/3569360) S2CID 20198866 (https://api.semanticscholar.org/Corpu. sID:20198866).40. Rempen, A; Martius, J; Hartmann, AA; Wecker, I (1987). \"Transmission rate of Ureaplasmaurealyticum, Mycoplasma spp., Gardnerella vaginalis, B-streptococci, Candida spp. andChlamydia trachomatis from the mother to the newborn\". Archives of Gynecology andObstetrics. 241 (3): 165–70. doi 10.1007/BF00931313 (https://doi.org/10.1007%2FBF009313:13) PMID 3324978 (https://pubmed.ncbi.nlm.nih.gov/3324978) S2CID 11251976 (https://ap. . i.semanticscholar.org/CorpusID:11251976).41. Olver, WJ; Bond, DW; Boswell, TC; Watkin, SL (2000). \"Neonatal group B streptococcaldisease associated with infected breast milk\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1721104). Archives of Disease in Childhood: Fetal and Neonatal Edition. 83 (1): F48–49.doi 10.1136/fn.83.1.F48 (https://doi.org/10.1136%2Ffn.83.1.F48) PMC 1721104 (https://ww:. w.ncbi.nlm.nih.gov/pmc/articles/PMC1721104) PMID 10873172 (https://pubmed.ncbi.nlm.ni. h.gov/10873172).42. Kotiw, M; Zhang, GW; Daggard, G; Reiss-Levy, E; Tapsall, JW; Numa, A (2003). \"Late-onsetand recurrent neonatal Group B streptococcal disease associated with breast-milktransmission\". Pediatric and Developmental Pathology. (3): 251–56. 6doi 10.1007/s10024-:001-0276-y (https://doi.org/10.1007%2Fs10024-001-0276-y) PMID 12687430 (https://pubme. d.ncbi.nlm.nih.gov/12687430) S2CID 20696142 (https://api.semanticscholar.org/CorpusID:2. 0696142).43. Gastelum, DT; Dassey, D; Mascola, L; Yasuda, LM (2005). \"Transmission of community-associated methicillin-resistant Staphylococcus aureus from breast milk in the neonatalintensive care unit\". The Pediatric Infectious Disease Journal. 24 (12): 1122–24.doi 10.1097/01.inf.0000189983.71585.30 (https://doi.org/10.1097%2F01.inf.0000189983.715:85.30) PMID 16371885 (https://pubmed.ncbi.nlm.nih.gov/16371885). .44. Jagielski, Marek; Rastawicki, Waldemar; Kałużewski, Stanisław; Gierczyński, Rafał (2007).\"Jersinioza – niedoceniana choroba zakaźna\" (https://web.archive.org/web/20111003164323/http://www.pzh.gov.pl/oldpage/przeglad_epimed/56-1/561_07.pdf) [Yersiniosis –unappreciated infectious diseases] (PDF). Przegl Epidemiol (in Polish). 56 (1): 57–64.PMID 12150068 (https://pubmed.ncbi.nlm.nih.gov/12150068). Archived from the original (http://www.pzh.gov.pl/oldpage/przeglad_epimed/56-1/561_07.pdf) (PDF) on 2011-10-03.Retrieved 2011-04-10.External linksD
9.6) · ICD-9-CM:287.5 (http://www.icd9data.com/getICD9Code.ashx?icd9=287.5) · MeSH:D013921 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D013921)ExternalresourcesPatient UK:Thrombocytopenia(https://patient.info/doctor/thrombocytopenia)Retrieved from \"https://en.wikipedia.org/w/index.php?title=Thrombocytopenia&oldid=1037759984\"This page was last edited on 8 August 2021, at 15:06 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.
ThrombosisCyanosis of the lower right extremity, resultingfrom acute arterial thrombosis of the right leg(on the left side of the image)SpecialtyVascular surgery, internalmedicine, pulmonologySymptomsDependent on locationThrombosisThrombosis (from Ancient Greek θρόμβωσιςthrómbōsis \"clotting”) is the formation of a bloodclot inside a blood vessel, obstructing the flow ofblood through the circulatory system. When ablood vessel (a vein or an artery) is injured, thebody uses platelets (thrombocytes) and fibrin toform a blood clot to prevent blood loss. Even whena blood vessel is not injured, blood clots may formin the body under certain conditions. A clot, or apiece of the clot, that breaks free and begins totravel around the body is known as anembolus.[1][2]Thrombosis may occur in veins (venousthrombosis) or in arteries (arterial thrombosis).Venous thrombosis leads to congestion of theaffected part of the body, while arterial thrombosis(and rarely severe venous thrombosis) affects theblood supply and leads to damage of the tissuesupplied by that artery (ischemia and necrosis). Apiece of either an arterial or a venous thrombuscan break off as an embolus which can travelthrough the circulation and lodge somewhere elseas an embolism. This type of embolism is knownas a thromboembolism. Complications can arise when a venous thromboembolism (commonlycalled a VTE) lodges in the lung as a pulmonary embolism. An arterial embolus may travelfurther down the affected blood vessel where it can lodge as an embolism.Signs and symptomsVenous thrombosisArterial thrombosisLimb ischemiaCausesMechanismPathogenesisPathophysiologyPreventionTreatmentAnticoagulationThrombolysisSurgeryEndovascular treatmentContents
Antiplatelet agentsTargeting ischemia/reperfusion injuryNeonatal thrombosisSee alsoReferencesBibliographyExternal linksThrombosis is generally defined by the type of blood vessel affected (arterial or venousthrombosis) and the precise location of the blood vessel or the organ supplied by it.Deep vein thrombosis (DVT) is the formation of a blood clot within a deep vein. It mostcommonly affects leg veins, such as the femoral vein. Three factors are important in theformation of a blood clot within a deep vein—these are the rate of blood flow, the thickness of theblood and qualities of the vessel wall. Classical signs of DVT include swelling, pain and redness ofthe affected area.Paget-Schroetter disease or upper extremity DVT (UEDVT) is the obstruction of an arm vein(such as the axillary vein or subclavian vein) by a thrombus. The condition usually comes to lightafter vigorous exercise and usually presents in younger, otherwise healthy people. Men areaffected more than women.[3]Budd-Chiari syndrome is the blockage of a hepatic vein or of the hepatic part of the inferior venacava. This form of thrombosis presents with abdominal pain, ascites and enlarged liver.Treatment varies between therapy and surgical intervention by the use of shunts.[4]Portal vein thrombosis affects the hepatic portal vein, which can lead to portal hypertension andreduction of the blood supply to the liver.[5] It usually happens in the setting of another diseasesuch as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.[6]Renal vein thrombosis is the obstruction of the renal vein by a thrombus. This tends to lead toreduced drainage from the kidney.\"Renal vein thrombosis: MedlinePlus Medical Encyclopedia\"(https://medlineplus.gov/ency/article/000513.htm). medlineplus.gov. Retrieved 27 May 2019.Signs and symptomsVenous thrombosisDeep vein thrombosisPaget-Schroetter diseaseBudd-Chiari syndromePortal vein thrombosisRenal vein thrombosis
</ref>Cerebral venous sinus thrombosis (CVST) is a rare form of stroke which results from theblockage of the dural venous sinuses by a thrombus. Symptoms may include headache, abnormalvision, any of the symptoms of stroke such as weakness of the face and limbs on one side of thebody and seizures. The diagnosis is usually made with a CT or MRI scan. The majority of personsaffected make a full recovery. The mortality rate is 4.3%.[7]Jugular vein thrombosis is a condition that may occur due to infection, intravenous drug use ormalignancy. Jugular vein thrombosis can have a varying list of complications, including:systemic sepsis, pulmonary embolism, and papilledema. Though characterized by a sharp pain atthe site of the vein, it can prove difficult to diagnose, because it can occur at random.[8]Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, wherethere is thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread ofinfection and endothelial damage from the danger triangle of the face. The facial veins in thisarea anastomose with the superior and inferior ophthalmic veins of the orbit, which draindirectly posteriorly into the cavernous sinus through the superior orbital fissure. Staphyloccoalor Streptococcal infections of the face, for example nasal or upper lip pustules may thus spreaddirectly into the cavernous sinus, causing stroke-like symptoms of double vision, squint, as wellas spread of infection to cause meningitis.\"Guidelines Cavernous sinus thrombosis\" (https://www.sun.ac.za/english/faculty/healthsciences/surgical-sciences/Documents/Specialist%20Guidelines/Cavernous%20sinus%20thrombosis.pdf) (PDF).</ref>Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterialthrombosis follows rupture of atheroma (a fat-rich deposit in the blood vessel wall), and istherefore referred to as atherothrombosis. Arterial embolism occurs when clots then migratedownstream and can affect any organ.[9]Alternatively, arterial occlusion occurs as a consequence of embolism of blood clots originatingfrom the heart (\"cardiogenic\" emboli). The most common cause is atrial fibrillation, whichcauses a blood stasis within the atria with easy thrombus formation, but blood clots can developinside the heart for other reasons too.A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to thebrain. This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (ableed). In thrombotic stroke, a thrombus (blood clot) usually forms around atheroscleroticplaques. Since blockage of the artery is gradual, the onset of symptomatic thrombotic strokes isslower. Thrombotic stroke can be divided into two categories—large vessel disease and smallvessel disease. The former affects vessels such as the internal carotids, vertebral and the circle ofWillis. The latter can affect smaller vessels such as the branches of the circle of Willis.Cerebral venous sinus thrombosisJugular vein thrombosisCavernous sinus thrombosisArterial thrombosisStroke
Acute thrombus in the right MCA M1branchMyocardial infarction (MI) or heart attack, is caused byischemia, (restriction in the blood supply), often due to theobstruction of a coronary artery by a thrombus. Thisrestriction gives an insufficient supply of oxygen to the heartmuscle which then results in tissue death (infarction). Alesion is then formed which is the infarct. MI can quicklybecome fatal if emergency medical treatment is not receivedpromptly. If diagnosed within 12 hours of the initial episode(attack) then thrombolytic therapy is initiated.An arterial thrombus or embolus can also form in the limbs,which can lead to acute limb ischemia.[10]Hepatic artery thrombosis usually occurs as a devastating complication after livertransplantation.[11]Thrombosis prevention is initiated with assessing the risk for its development. Some people havea higher risk of developing thrombosis and its possible development into thromboembolism.[12]Some of these risk factors are related to inflammation. \"Virchow's triad\" has been suggested todescribe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wallinjury, and altered blood coagulation.[13][14] Some risk factors predispose for venous thrombosiswhile others increase the risk of arterial thrombosis. Newborn babies in the neonatal period arealso at risk of a thromboembolism.[15]Myocardial infarctionLimb ischemiaOther sitesCauses
Risk factors for thrombosisFactorNotesReferencesPrevious episodes of thrombosis[13]Vasoconstriction[16]Slow or turbulent blood flowslow flow is modifiable with exercise[16]Stroke[17]Heart failure[17]Sedentary life stylemodifiable[16]Plaster casttransient[17]Dehydrationmodifiable[16]Acute respiratory failure[17]Dysrhythmias[16]Shock[16]Obesitymodifiable[12][17][18][19][20]Pregnancy and the post-partum period[12][19][20]Varicose veins[17][19]Surgery[12][19]Trauma[12][17][19]Estrogen-based oral contraceptivediscontinuation reduces risk[12][16][19]Hormone replacement therapydiscontinuation reduces risk[12]Ovarian hyper-stimulation therapy to treat infertility[12]Compression of a vein or artery by abnormality, tumor,hematoma[12]Long surgeries[18]Pacing wires[19][21]Local vein damage, incompetent valves[16][19][20]Central venous catheters[19]Dialysis catheters[19]Repetitive motion injury[19]Immobilitymodifiable risk[17][19]Spinal cord injury[19]Age[12][16][17][19]Cancers[19]Sepsis[19]Polycythemia[19]Protein C and/or S deficiencycongenital; associated with Warfarinnecrosis[19]Antiphospholipid antibody syndromealtered coagulation[19]
FactorNotesReferencesFactor V Leiden defectaltered coagulation[19]Prothrombin G20210A defectaltered coagulation[19]Hyperhomocysteinemiaaltered coagulation[19]Elevated factors II, VIII, IX, XIaltered coagulation[19]Antithrombin III deficiencyaltered coagulation[19]Falls and hip fracturerelated to immobility[22]Selective estrogen-receptor modulators[12]Erythropoiesis-stimulating agents[12]Acute medical illness[12]Inflammatory bowel disease[12]Nephrotic syndrome[12]Myeloproliferative disorders[12]Paroxysmal nocturnal hemoglobinnuria[12]Thrombophilias[12]Post-menopausal hormone replacement therapydiscontinuation reduces risk[12]Right heart failure[20]Venous inflammation/phlebitiswhen a thrombus forms, it isthrombophlebitis[16]Ambient air pollutionthought to be related to inflammation[23][24][25]The main causes of thrombosis are given in Virchow's triad which lists thrombophilia,endothelial cell injury, and disturbed blood flow. Generally speaking the risk for thrombosisincreases over the life course of individuals, depending on life style factors like smoking, diet,and physical activity, the presence of other diseases like cancer or autoimmune disease, whilealso platelet properties change in aging individuals which is an important consideration as well.[26]Hypercoagulability or thrombophilia, is caused by, for example, genetic deficiencies orautoimmune disorders. Recent studies indicate that white blood cells play a pivotal role in deepvein thrombosis, mediating numerous pro-thrombotic actions.[27]MechanismPathogenesisHypercoagulabilityEndothelial cell injury
Cancer-associated thrombosis canresult from: (1) stasis, i.e., directpressure on blood vessels by thetumor mass, poor performancestatus, and bed rest followingsurgical procedures; (2) iatrogenic,due to treatment with antineoplasticmedications; and (3) secretion ofheparanase from malignant tumorsthat results in degradation ofendogenous heparin. Source:Potential Mechanisms of Cancer-Related Hypercoagulability. NasserNJ, Fox J, Agbarya A. Cancers(Basel). 2020 Feb 29;12(3):566.https://doi.org/10.3390/cancers120305Any inflammatory process, such as trauma, surgery or infection, can cause damage to theendothelial lining of the vessel's wall. The main mechanism is exposure of tissue factor to theblood coagulation system.[28] Inflammatory and other stimuli (such as hypercholesterolemia)can lead to changes in gene expression in endothelium producing to a pro-thrombotic state.[29]When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is akey modulator of thrombin activity.[30] The end result is a sustained activation of thrombin andreduced production of protein C and tissue factor inhibitor, which furthers the pro-thromboticstate.[29]Endothelial injury is almost invariably involved in the formation of thrombi in arteries, as highrates of blood flow normally hinder clot formation. In addition, arterial and cardiac clots arenormally rich in platelets–which are required for clot formation in areas under high stress due toblood flow.[29]Causes of disturbed blood flow include stagnation of bloodflow past the point of injury, or venous stasis which mayoccur in heart failure,[28] or after long periods of sedentarybehaviour, such as sitting on a long airplane flight. Also,atrial fibrillation, causes stagnant blood in the left atrium(LA), or left atrial appendage (LAA), and can lead to athromboembolism.[28] Cancers or malignancies such asleukemia may cause increased risk of thrombosis by possibleactivation of the coagulation system by cancer cells orsecretion of procoagulant substances (paraneoplasticsyndrome), by external compression on a blood vessel whena solid tumor is present, or (more rarely) extension into thevasculature (for example, renal cell cancers extending intothe renal veins).[28] Also, treatments for cancer (radiation,chemotherapy) often cause additional hypercoagulability.[28]There are scores that correlate different aspects of patientdata (comorbidities, vital signs, and others) to risk ofthrombosis, such as the POMPE-C, which stratifies risk ofmortality due to pulmonary embolism in patients withcancer, who typically have higher rates of thrombosis.[32]Also, there are several predictive scores for thromboembolicevents, such as Padua,[33] Khorana,[34][35] and ThroLyscore.[36]Fibrinolysis is the physiological breakdown of blood clots by enzymes such as plasmin.Organisation: following the thrombotic event, residual vascular thrombus will be re-organisedhistologically with several possible outcomes. For an occlusive thrombus (defined as thrombosiswithin a small vessel that leads to complete occlusion), wound healing will reorganise theocclusive thrombus into collagenous scar tissue, where the scar tissue will either permanentlyobstruct the vessel, or contract down with myofibroblastic activity to unblock the lumen. For aDisturbed blood flowPathophysiologyNatural history
mural thrombus (defined as a thrombus in a large vessel that restricts the blood flow but doesnot occlude completely), histological reorganisation of the thrombus does not occur via theclassic wound healing mechanism. Instead, the platelet-derived growth factor degranulated bythe clotted platelets will attract a layer of smooth muscle cells to cover the clot, and this layer ofmural smooth muscle will be vascularised by the blood inside the vessel lumen rather than by thevasa vasorum.Ischemia/infarction: if an arterial thrombus cannot be lysed by the body and it does notembolise, and if the thrombus is large enough to impair or occlude blood flow in the involvedartery, then local ischemia or infarction will result. A venous thrombus may or may not beischemic, since veins distribute deoxygenated blood that is less vital for cellular metabolism.Nevertheless, non-ischemic venous thrombosis may still be problematic, due to the swellingcaused by blockage to venous drainage. In deep vein thrombosis this manifests as pain, redness,and swelling; in retinal vein occlusion this may result in macular oedema and visual acuityimpairment, which if severe enough can lead to blindness.A thrombus may become detached and enter circulation as an embolus, finally lodging in andcompletely obstructing a blood vessel, which unless treated very quickly will lead to tissuenecrosis (an infarction) in the area past the occlusion. Venous thrombosis can lead to pulmonaryembolism when the migrated embolus becomes lodged in the lung. In people with a \"shunt\" (aconnection between the pulmonary and systemic circulation), either in the heart or in the lung, avenous clot can also end up in the arteries and cause arterial embolism.Arterial embolism can lead to obstruction of blood flow through the blood vessel that isobstructed by it, and a lack of oxygen and nutrients (ischemia) of the downstream tissue. Thetissue can become irreversibly damaged, a process known as necrosis. This can affect any organ;for instance, arterial embolism of the brain is one of the causes of stroke.The use of heparin following surgery is common if there are no issues with bleeding. Generally, arisk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding.[37] Inpeople admitted to hospital, thrombosis is a major cause for complications and occasionallydeath. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 thatthe annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired.[38] Hence thromboprophylaxis (prevention of thrombosis) is increasingly emphasized.In patients admitted for surgery, graded compression stockings are widely used, and in severeillness, prolonged immobility and in all orthopedic surgery, professional guidelines recommendlow molecular weight heparin (LMWH) administration, mechanical calf compression or (if allelse is contraindicated and the patient has recently suffered deep vein thrombosis) the insertionof a vena cava filter.[39][40] In patients with medical rather than surgical illness, LMWH too isknown to prevent thrombosis,[40][41] and in the United Kingdom the Chief Medical Officer hasissued guidance to the effect that preventative measures should be used in medical patients, inanticipation of formal guidelines.[38]The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on theperson, and the risk of complications from treatment.EmbolizationPreventionTreatment
Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reducethromboembolic occurrence. Where a more effective response is required, heparin can be given(by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding isincreased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany,about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing(according to one 2012 study).[42] Other medications such as direct thrombin inhibitors anddirect Xa inhibitors are increasingly being used instead of warfarin.Thrombolysis is the pharmacological destruction of blood clots by administering thrombolyticdrugs including recombinant tissue plasminogen activator, which enhances the normaldestruction of blood clots by the body's enzymes. This carries an increased risk of bleeding so isgenerally only used for specific situations (such as severe stroke or a massive pulmonaryembolism).[43]Arterial thrombosis may require surgery if it causes acute limb ischemia.Mechanical clot retrieval and catheter-guided thrombolysis are used in certain situations.[44]Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugssuch as aspirin may reduce the risk of recurrence or progression.[45]With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes celldeath in reperfused tissue[46] and contributes significantly to post-reperfusion mortality andmorbidity.[47][48] For example, in a feline model of intestinal ischemia, four hours of ischemiaresulted in less injury than three hours of ischemia followed by one hour of reperfusion.[46] InST-elevation myocardial infarction (STEMI), IRI contributes up to 50% of final infarct sizedespite timely primary percutaneous coronary intervention. This is a key reason for thecontinued high mortality and morbidity in these conditions, despite endovascular reperfusiontreatments and continuous efforts to improve timeliness and access to these treatments. Hence,protective therapies are required to attenuate IRI alongside reperfusion in acute ischemicconditions to improve clinical outcomes.[49] Therapeutic strategies that have potential toimprove clinical outcomes in reperfused STEMI patients include remote ischemic conditioning(RIC), exenatide, and metoprolol. These have emerged amongst a multitude of cardioprotectiveinterventions investigated with largely neutral clinical data.[50] Of these, RIC has the most robustclinical evidence, especially in the context of STEMI, but also emerging for other indications suchas acute ischemic stroke and aneurysmal subarachnoid hemorrhage.[49]AnticoagulationThrombolysisSurgeryEndovascular treatmentAntiplatelet agentsTargeting ischemia/reperfusion injury
Treatment options for full-term and preterm babies who develop thromboembolism includeexpectant management (with careful observation), nitroglycerin ointment, pharmacologicaltherapy (thrombolytics and/or anticoagulants), and surgery.[15] The evidence supporting thesetreatment approaches is weak. For anticoagulant treatment, t is not clear if unfractionatedand/or low molecular weight heparin treatment is effective at decreasing mortality and seriousadverse events in this population.[15] There is also insufficient evidence to understand the risk ofadverse effects associated with these treatment approaches in term or preterm infants.[15]Blood clotting testsDisseminated intravascular coagulationHepatic artery thrombosisThrombotic microangiopathy1. Furie B, Furie BC (2008). \"Mechanisms of thrombus formation\". New England Journal ofMedicine. 359 (9): 938–949. doi 10.1056/NEJMra0801082 (https://doi.org/10.1056%2FNEJM:ra0801082) PMID 18753650 (https://pubmed.ncbi.nlm.nih.gov/18753650). .2. Handin RI (2005). \"Chapter 53: bleeding and thrombosis\". In Kasper DL, Braunwald E, FauciAS, et al. (eds.). Harrison's Principles of Internal Medicine (16th ed.). New York, NY:McGraw-Hill. ISBN 978-0-07-139140-5.3. Hughes, E. S. R. (1949-02-01). \"Venous obstruction in the upper extremity; Paget-Schroetter's syndrome; a review of 320 cases\". Surgery, Gynecology & Obstetrics. 88 (2):89–127. ISSN 0039-6087 (https://www.worldcat.org/issn/0039-6087) PMID 18108679 (http. s://pubmed.ncbi.nlm.nih.gov/18108679).4. \"shunt\" (https://www.cancer.gov/publications/dictionaries/cancer-terms/def/shunt). NationalCancer Institute. Retrieved 5 July 2021.5. Webster, GJ; Burroughs AK, Riordan SM (January 2005). \"Review article: portal veinthrombosis – new insights into aetiology and management\" (https://archive.today/20121210090509/http://www3.interscience.wiley.com/cgi-bin/fulltext/118696389/HTMLSTART).Alimentary Pharmacology & Therapeutics. 21 (1): 1–9. CiteSeerX 10.1.1.536.2660 (https://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.536.2660) doi 10.1111/j.1365-. :2036.2004.02301.x (https://doi.org/10.1111%2Fj.1365-2036.2004.02301.x) PMID 15644039. (https://pubmed.ncbi.nlm.nih.gov/15644039) S2CID 5673778 (https://api.semanticscholar.or. g/CorpusID:5673778). Archived from the original (http://www3.interscience.wiley.com/cgi-bin/fulltext/118696389/HTMLSTART) on 2012-12-10.6. DeLeve LD, Valla DC, Garcia-Tsao G (2009). \"Vascular disorders of the liver\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6697263). Hepatology. 49 (5): 1729–64.doi 10.1002/hep.22772 (https://doi.org/10.1002%2Fhep.22772) PMC 6697263 (https://www.:. ncbi.nlm.nih.gov/pmc/articles/PMC6697263) PMID 19399912 (https://pubmed.ncbi.nlm.nih.g. ov/19399912).7. Canhão, P; Ferro JM, Lindgren AG; et al. (August 2005). \"Causes and predictors of death incerebral venous thrombosis\" (https://doi.org/10.1161%2F01.STR.0000173152.84438.1c).Stroke. 36 (8): 1720–1725. doi 10.1161/01.STR.0000173152.84438.1c (https://doi.org/10.116:1%2F01.STR.0000173152.84438.1c) PMID 16002765 (https://pubmed.ncbi.nlm.nih.gov/160. 02765).8. eMedicine Article on Internal Jugular Vein Thrombosis by Dale K. Mueller (http://www.emedicine.com/med/topic2762c.htm)Neonatal thrombosisSee alsoReferences
9. MDGuidelines > Arterial Embolism And Thrombosis (http://www.mdguidelines.com/arterial-embolism-and-thrombosis) From The Medical Disability Advisor by Presley Reed, MD.Retrieved on April 30, 201010. Creager, Mark A.; Kaufman, John A.; Conte, Michael S. (7 June 2012). \"Acute LimbIschemia\". New England Journal of Medicine. 366 (23): 2198–2206.doi 10.1056/NEJMcp1006054 (https://doi.org/10.1056%2FNEJMcp1006054):.PMID 22670905 (https://pubmed.ncbi.nlm.nih.gov/22670905).(subscription required)11. Bekker, J.; Ploem, S.; de Jong, K. P. (April 2009). \"Early Hepatic Artery Thrombosis afterLiver Transplantation: A Systematic Review of the Incidence, Outcome and Risk Factors\" (https://doi.org/10.1111%2Fj.1600-6143.2008.02541.x). American Journal of Transplantation. 9(4): 746–757. doi 10.1111/j.1600-6143.2008.02541.x (https://doi.org/10.1111%2Fj.1600-6143.:2008.02541.x) PMID 19298450 (https://pubmed.ncbi.nlm.nih.gov/19298450). .12. Hoffman, p. 960.13. Moliterno, p. 306.14. Brunner, p. 874.15. Romantsik, Olga; Bruschettini, Matteo; Zappettini, Simona; Ramenghi, Luca Antonio; Calevo,Maria Grazia (2016-11-07). \"Heparin for the treatment of thrombosis in neonates\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6464761). The Cochrane Database of SystematicReviews. 11: CD012185. doi 10.1002/14651858.CD012185.pub2 (https://doi.org/10.1002%2:F14651858.CD012185.pub2) ISSN 1469-493X (https://www.worldcat.org/issn/1469-493X). .PMC 6464761 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6464761) PMID 27820879 (ht. tps://pubmed.ncbi.nlm.nih.gov/27820879).16. Copstead, p. 320.17. Moliterno, p. 307.18. Abele.19. Brunner, p. 875.20. Copstead, p. 329.21. \"Pacing wire\" (http://medical-dictionary.thefreedictionary.com/pacing+wire). The FreeDictionary. Retrieved 2016-12-18.22. Brunner, p. 876.23. Ho, Andrew F. W.; Zheng, Huili; De Silva, Deidre A.; Wah, Win; Earnest, Arul; Pang, Yee H.;Xie, Zhenjia; Pek, Pin P.; Liu, Nan (November 2018). \"The Relationship Between Ambient AirPollution and Acute Ischemic Stroke: A Time-Stratified Case-Crossover Study in a City-StateWith Seasonal Exposure to the Southeast Asian Haze Problem\". Annals of EmergencyMedicine. 72 (5): 591–601. doi 10.1016/j.annemergmed.2018.06.037 (https://doi.org/10.101:6%2Fj.annemergmed.2018.06.037) ISSN 1097-6760 (https://www.worldcat.org/issn/1097-67. 60) PMID 30172448 (https://pubmed.ncbi.nlm.nih.gov/30172448) S2CID 52144033 (https://. . api.semanticscholar.org/CorpusID:52144033).24. Ho, Andrew Fu Wah; Zheng, Huili; Earnest, Arul; Cheong, Kang Hao; Pek, Pin Pin; Seok,Jeon Young; Liu, Nan; Kwan, Yu Heng; Tan, Jack Wei Chieh (2019-03-19). \"Time Stratified‐Case Crossover Study of the Association of Outdoor Ambient Air Pollution With the Risk ofAcute Myocardial Infarction in the Context of Seasonal Exposure to the Southeast AsianHaze Problem\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6475051). Journal of theAmerican Heart Association. (6): e011272. 8doi 10.1161/JAHA.118.011272 (https://doi.org/1:0.1161%2FJAHA.118.011272) ISSN 2047-9980 (https://www.worldcat.org/issn/2047-9980). .PMC 6475051 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6475051) PMID 31112443 (ht. tps://pubmed.ncbi.nlm.nih.gov/31112443).
25. Ho, Andrew Fu Wah; Wah, Win; Earnest, Arul; Ng, Yih Yng; Xie, Zhenjia; Shahidah, Nur;Yap, Susan; Pek, Pin Pin; Liu, Nan (2018-11-15). \"Health impacts of the Southeast Asianhaze problem - A time-stratified case crossover study of the relationship between ambient airpollution and sudden cardiac deaths in Singapore\". International Journal of Cardiology. 271:352–358. doi 10.1016/j.ijcard.2018.04.070 (https://doi.org/10.1016%2Fj.ijcard.2018.04.070):.ISSN 1874-1754 (https://www.worldcat.org/issn/1874-1754) PMID 30223374 (https://pubme. d.ncbi.nlm.nih.gov/30223374).26. Faria, Alessandra V.S.; Andrade, Sheila S; Peppelenbosch, Maikel P.; Ferreira-Halder,Carmen V.; Fuhler, Gwenny M. (December 2020). \"Platelets in aging and cancer-\"double-edged sword\" \" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC458881). Cancer andMetastasis Reviews. 39 (4): 1205–1221. doi 10.1007/s10555-020-09926-2 (https://doi.org/1:0.1007%2Fs10555-020-09926-2) PMC 458881 (https://www.ncbi.nlm.nih.gov/pmc/articles/P. MC458881) PMID 32869161 (https://pubmed.ncbi.nlm.nih.gov/32869161). .27. Swystun, L. L.; Liaw, P. C. (27 June 2016). \"The role of leukocytes in thrombosis\" (https://doi.org/10.1182%2Fblood-2016-05-718114). Blood. 128 (6): 753–762. doi 10.1182/blood-2016-:05-718114 (https://doi.org/10.1182%2Fblood-2016-05-718114) PMID 27354721 (https://pub. med.ncbi.nlm.nih.gov/27354721).28. labtestsonline > Hypercoagulable Disorders (http://www.labtestsonline.org/understanding/conditions/hypercoagulable_disorders-3.html) Archived (https://web.archive.org/web/20070618165003/http://www.labtestsonline.org/understanding/conditions/hypercoagulable_disorders-3.html) 2007-06-18 at the Wayback Machine This article was last reviewed on May 23, 2007 andwas last modified on March 6, 2010.29. Kumar, Vinay (2015). Robbins and Cotran Pathologic Basis of Disease. Philadelphia, PA,USA: Elsevier. pp. 122–130. ISBN 978-1-4557-2613-4.30. Ito, Takashi; Kakihana, Yasuyuki; Maruyama, Ikuro (2016-01-01). \"Thrombomodulin as anintravascular safeguard against inflammatory and thrombotic diseases\". Expert Opinion onTherapeutic Targets. 20 (2): 151–158. doi 10.1517/14728222.2016.1086750 (https://doi.org/1:0.1517%2F14728222.2016.1086750) ISSN 1744-7631 (https://www.worldcat.org/issn/1744-. 7631) PMID 26558419 (https://pubmed.ncbi.nlm.nih.gov/26558419) S2CID 207486815 (http. . s://api.semanticscholar.org/CorpusID:207486815).31. Nasser, Nicola J.; Fox, Jana; Agbarya, Abed (March 2020). \"Potential Mechanisms ofCancer-Related Hypercoagulability\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139427). Cancers. 12 (3): 566. doi 10.3390/cancers12030566 (https://doi.org/10.3390%2Fcancers:12030566) PMC 7139427 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139427). .PMID 32121387 (https://pubmed.ncbi.nlm.nih.gov/32121387).32. van der Hulle, T; den Exter, PL; Kooiman, J; van der Hoeven, JJ; Huisman, MV; Klok, FA(2014). \"Meta-analysis of the efficacy and safety of new oral anticoagulants in patients withcancer-associated acute venous thromboembolism\". J Thromb Haemost. 12 (7): 1116–20.doi 10.1111/jth.12605 (https://doi.org/10.1111%2Fjth.12605) PMID 24819040 (https://pubme:. d.ncbi.nlm.nih.gov/24819040) S2CID 19395326 (https://api.semanticscholar.org/CorpusID:1. 9395326).33. BARBAR, S.; NOVENTA, F.; ROSSETTO, V.; FERRARI, A.; BRANDOLIN, B.; PERLATI, M.;DE BON, E.; TORMENE, D.; PAGNAN, A.; PRANDONI, P. (November 2010). \"A riskassessment model for the identification of hospitalized medical patients at risk for venousthromboembolism: the Padua Prediction Score\" (https://doi.org/10.1111%2Fj.1538-7836.2010.04044.x). Journal of Thrombosis and Haemostasis. (11): 2450–2457. 8doi 10.1111/j.1538-:7836.2010.04044.x (https://doi.org/10.1111%2Fj.1538-7836.2010.04044.x) ISSN 1538-7933. (https://www.worldcat.org/issn/1538-7933) PMID 20738765 (https://pubmed.ncbi.nlm.nih.go. v/20738765).34. Khorana, Alok A.; Francis, Charles W.; Culakova, Eva; Fisher, Richard I.; Kuderer, Nicole M.;Lyman, Gary H. (2006-01-20). \"Thromboembolism in Hospitalized Neutropenic CancerPatients\". Journal of Clinical Oncology. 24 (3): 484–490. doi 10.1200/jco.2005.03.8877 (http:s://doi.org/10.1200%2Fjco.2005.03.8877) ISSN 0732-183X (https://www.worldcat.org/issn/0. 732-183X) PMID 16421425 (https://pubmed.ncbi.nlm.nih.gov/16421425). .
35. Khorana, Alok A.; Kuderer, Nicole M.; Culakova, Eva; Lyman, Gary H.; Francis, Charles W.(2008-05-15). \"Development and validation of a predictive model for chemotherapy-associated thrombosis\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2384124). Blood. 111(10): 4902–4907. doi 10.1182/blood-2007-10-116327 (https://doi.org/10.1182%2Fblood-2007:-10-116327) ISSN 0006-4971 (https://www.worldcat.org/issn/0006-4971) PMC 2384124 (htt. . ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2384124) PMID 18216292 (https://pubmed.ncb. i.nlm.nih.gov/18216292).36. Antic, Darko; Milic, Natasa; Nikolovski, Srdjan; Todorovic, Milena; Bila, Jelena; Djurdjevic,Predrag; Andjelic, Bosko; Djurasinovic, Vladislava; Sretenovic, Aleksandra; Vukovic, Vojin;Jelicic, Jelena (2016-07-22). \"Development and validation of multivariable predictive modelfor thromboembolic events in lymphoma patients\". American Journal of Hematology. 91 (10):1014–1019. doi 10.1002/ajh.24466 (https://doi.org/10.1002%2Fajh.24466) ISSN 0361-8609:. (https://www.worldcat.org/issn/0361-8609) PMID 27380861 (https://pubmed.ncbi.nlm.nih.go. v/27380861) S2CID 1724916 (https://api.semanticscholar.org/CorpusID:1724916). .37. National Institute for Health and Clinical Excellence. Clinical guideline 92: Venousthromboembolism: reducing the risk for patients in hospital (https://www.nice.org.uk/guidance/CG92). London, January 2010.38. Hunt BJ (March 2008). \"Awareness and politics of venous thromboembolism in the Unitedkingdom\" (https://doi.org/10.1161%2FATVBAHA.108.162586). Arterioscler. Thromb. Vasc.Biol. 28 (3): 398–9. doi 10.1161/ATVBAHA.108.162586 (https://doi.org/10.1161%2FATVBAH:A.108.162586) PMID 18296598 (https://pubmed.ncbi.nlm.nih.gov/18296598). .39. National Institute for Health and Clinical Excellence. Clinical guideline 46: Venousthromboembolism (surgical) (https://www.nice.org.uk/guidance/CG46). London, April 2007.40. Geerts WH, Pineo GF, Heit JA, et al. (September 2004). \"Prevention of venousthromboembolism: the Seventh ACCP Conference on Antithrombotic and ThrombolyticTherapy\" (https://archive.today/20041011003734/http://www.chestjournal.org/cgi/content/full/126/3_suppl/338S). Chest. 126 (3 Suppl): 338S–400S. doi 10.1378/chest.126.3_suppl.338S:(https://doi.org/10.1378%2Fchest.126.3_suppl.338S) PMID 15383478 (https://pubmed.ncbi.. nlm.nih.gov/15383478). Archived from the original (http://www.chestjournal.org/cgi/content/full/126/3_suppl/338S) on 2004-10-11.41. Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA (February 2007). \"Meta-analysis:anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalizedmedical patients\". Ann. Intern. Med. 146 (4): 278–88. CiteSeerX 10.1.1.694.4563 (https://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.694.4563) doi 10.7326/0003-4819-146-4-. :200702200-00007 (https://doi.org/10.7326%2F0003-4819-146-4-200702200-00007).PMID 17310052 (https://pubmed.ncbi.nlm.nih.gov/17310052) S2CID 27605124 (https://api.s. emanticscholar.org/CorpusID:27605124).42. Heneghan C, Ward A, Perera R (2012). \"Self-monitoring of oral anticoagulation: systematicreview and meta-analysis of individual patient data\" (http://discovery.ucl.ac.uk/1468252/1/Gardiner_28.%20Heneghan%20Lancet%202011.pdf) (PDF). The Lancet. 379 (9813): 322–334.doi 10.1016/S0140-6736(11)61294-4 (https://doi.org/10.1016%2FS0140-6736%2811%29612:94-4) PMID 22137798 (https://pubmed.ncbi.nlm.nih.gov/22137798). .43. Tran HA, Gibbs H, Merriman E, Curnow JL, Young L, Bennett A, Tan C, Chunilal SD, WardCM, Baker R, Nandurkar H (March 2019). \"New guidelines from the Thrombosis andHaemostasis Society of Australia and New Zealand for the diagnosis and management ofvenous thromboembolism\". The Medical Journal of Australia. 210 (5): 227–235.doi 10.5694/mja2.50004 (https://doi.org/10.5694%2Fmja2.50004) PMID 30739331 (https://p:. ubmed.ncbi.nlm.nih.gov/30739331) S2CID 73433650 (https://api.semanticscholar.org/Corpu. sID:73433650).
44. Berkhemer, Olvert A.; Fransen, Puck S.S.; Beumer, Debbie; van den Berg, Lucie A.;Lingsma, Hester F.; Yoo, Albert J.; Schonewille, Wouter J.; Vos, Jan Albert; Nederkoorn, PaulJ.; Wermer, Marieke J.H.; van Walderveen, Marianne A.A.; Staals, Julie; Hofmeijer,Jeannette; van Oostayen, Jacques A.; Lycklama à Nijeholt, Geert J.; Boiten, Jelis; Brouwer,Patrick A.; Emmer, Bart J.; de Bruijn, Sebastiaan F.; van Dijk, Lukas C.; Kappelle, L. Jaap;Lo, Rob H.; van Dijk, Ewoud J.; de Vries, Joost; de Kort, Paul L.M.; van Rooij, Willem Jan J.;van den Berg, Jan S.P.; van Hasselt, Boudewijn A.A.M.; Aerden, Leo A.M.; Dallinga, René J.;Visser, Marieke C.; Bot, Joseph C.J.; Vroomen, Patrick C.; Eshghi, Omid; Schreuder, TobienH.C.M.L.; Heijboer, Roel J.J.; Keizer, Koos; Tielbeek, Alexander V.; den Hertog, Heleen M.;Gerrits, Dick G.; van den Berg-Vos, Renske M.; Karas, Giorgos B.; Steyerberg, Ewout W.;Flach, H. Zwenneke; Marquering, Henk A.; Sprengers, Marieke E.S.; Jenniskens, SjoerdF.M.; Beenen, Ludo F.M.; van den Berg, René; Koudstaal, Peter J.; van Zwam, Wim H.;Roos, Yvo B.W.E.M.; van der Lugt, Aad; van Oostenbrugge, Robert J.; Majoie, CharlesB.L.M.; Dippel, Diederik W.J.; et al. (1 January 2015). \"A Randomized Trial of IntraarterialTreatment for Acute Ischemic Stroke\". New England Journal of Medicine. 372 (1): 11–20.doi 10.1056/NEJMoa1411587 (https://doi.org/10.1056%2FNEJMoa1411587):.hdl 2066/153000 (https://hdl.handle.net/2066%2F153000) PMID 25517348 (https://pubmed.:. ncbi.nlm.nih.gov/25517348).45. \"Aspirin Monograph for Professionals\" (https://www.drugs.com/monograph/aspirin.html).Drugs.com. Retrieved 2020-06-09.46. Grace, P. A. (May 1994). \"Ischaemia-reperfusion injury\". The British Journal of Surgery. 81(5): 637–647. doi 10.1002/bjs.1800810504 (https://doi.org/10.1002%2Fbjs.1800810504):.ISSN 0007-1323 (https://www.worldcat.org/issn/0007-1323) PMID 8044536 (https://pubmed.. ncbi.nlm.nih.gov/8044536) S2CID 34608929 (https://api.semanticscholar.org/CorpusID:3460. 8929).47. Yellon, Derek M.; Hausenloy, Derek J. (2007-09-13). \"Myocardial Reperfusion Injury\". NewEngland Journal of Medicine. 357 (11): 1121–1135. doi 10.1056/nejmra071667 (https://doi.or:g/10.1056%2Fnejmra071667) ISSN 0028-4793 (https://www.worldcat.org/issn/0028-4793). .PMID 17855673 (https://pubmed.ncbi.nlm.nih.gov/17855673).48. Bai, Jilin; Lyden, Patrick D. (2015-01-19). \"Revisiting Cerebral Postischemic ReperfusionInjury: New Insights in Understanding Reperfusion Failure, Hemorrhage, and Edema\".International Journal of Stroke. 10 (2): 143–152. doi 10.1111/ijs.12434 (https://doi.org/10.111:1%2Fijs.12434) ISSN 1747-4930 (https://www.worldcat.org/issn/1747-4930). .PMID 25598025 (https://pubmed.ncbi.nlm.nih.gov/25598025) S2CID 25953179 (https://api.s. emanticscholar.org/CorpusID:25953179).49. Ho, Andrew Fu Wah; Jun, Chong; Ong, Marcus Eng Hock; Hausenloy, Derek J. (April 2019).\"Remote Ischemic Conditioning in Emergency Medicine—Clinical Frontiers and ResearchOpportunities\" (https://discovery.ucl.ac.uk/id/eprint/10093574/1/Hausenloy_Manuscript%2023%20Mar%202019%20accepted%20version.pdf) (PDF). SHOCK (3): 269–276.doi 10.1097/SHK.0000000000001362 (https://doi.org/10.1097%2FSHK.0000000000001362):.ISSN 1073-2322 (https://www.worldcat.org/issn/1073-2322) PMID 32045394 (https://pubme. d.ncbi.nlm.nih.gov/32045394) S2CID 149537443 (https://api.semanticscholar.org/CorpusID:. 149537443).50. Hausenloy, Derek J.; Botker, Hans Erik; Engstrom, Thomas; Erlinge, David; Heusch, Gerd;Ibanez, Borja; Kloner, Robert A.; Ovize, Michel; Yellon, Derek M. (2016-04-26). \"Targetingreperfusion injury in patients with ST-segment elevation myocardial infarction: trials andtribulations\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381598). European HeartJournal. 38 (13): 935–941. doi 10.1093/eurheartj/ehw145 (https://doi.org/10.1093%2Feurhea:rtj%2Fehw145) ISSN 0195-668X (https://www.worldcat.org/issn/0195-668X) PMC 5381598. . (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381598) PMID 27118196 (https://pubmed.n. cbi.nlm.nih.gov/27118196).Bibliography
Classification ICD-10: I80 (https://icd.who.int/browse10/2019/en#/I80)-I82 (https://icd.who.int/browse10/2019/en#/I82) · ICD-9-CM:437.6 (http://www.icd9data.com/getICD9Code.ashx?icd9=437.6), 453 (http://www.icd9data.com/getICD9Code.ashx?icd9=453), 671.5 (http://www.icd9data.com/getICD9Code.ashx?icd9=671.5),671.9 (http://www.icd9data.com/getICD9Code.ashx?icd9=671.9) · MeSH:D013927 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D013927)Brunner, Lillian (2010). Brunner & Suddarth's textbook of medical-surgical nursing.Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9780781785907.Copstead, Lee (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 9781455726509.Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical.ISBN 9780071716727.Moliterno, David (2013). Therapeutic advances in thrombosis. Chichester, West Sussex:Wiley-Blackwell. ISBN 9781405196253.Abele, H (2014). Atlas of gynecologic surgery. Stuttgart: Thieme. ISBN 9783136507049;Access provided by the University of Pittsburgh Media related to Thrombosis at Wikimedia CommonsThrombosis (https://curlie.org/Health/Conditions_and_Diseases/Cardiovascular_Disorders/Vascular_Disorders/Thrombosis/) at CurlieRetrieved from \"https://en.wikipedia.org/w/index.php?title=Thrombosis&oldid=1037760114\"This page was last edited on 8 August 2021, at 15:08 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By usingthis site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.External linksD
VasculitisOther namesVasculitides[1]Petechia and purpura on the lower limb due tomedication-induced vasculitis.Pronunciation/væskjʊˈlaɪtɪs/SpecialtyRheumatologySymptomsWeight loss, fever, myalgia,purpuraComplicationsGangrene, MyocardialinfarctionVasculitisVasculitis is a group of disorders that destroy bloodvessels by inflammation.[2] Both arteries and veinsare affected. Lymphangitis (inflammation oflymphatic vessels) is sometimes considered a type ofvasculitis.[3] Vasculitis is primarily caused byleukocyte migration and resultant damage. Althoughboth occur in vasculitis, inflammation of veins(phlebitis) or arteries (arteritis) on their own areseparate entities.Signs and symptomsCauseClassificationDiagnosisTreatmentReferencesExternal linksPossible signs and symptoms include:[4]General symptoms: Fever, unintentional weightlossSkin: Palpable purpura, livedo reticularisMuscles and joints: Muscle pain or inflammation,joint pain or joint swellingNervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acutevisual lossHeart and arteries: Heart attack, high blood pressure, gangreneRespiratory tract: Nose bleeds, bloody cough, lung infiltratesGI tract: Abdominal pain, bloody stool, perforations (hole in the GI tract)Kidneys: Inflammation of the kidney's filtration units (glomeruli)Vasculitis can be classified by the cause, the location, the type of vessel or the size of vessel.ContentsSigns and symptomsCauseClassification
Underlying cause. For example, the cause of syphilitic aortitis is infectious (aortitis simply refersto inflammation of the aorta, which is an artery.) However, the causes of many forms of vasculitisare poorly understood. There is usually an immune component, but the trigger is often notidentified. In these cases, the antibody found is sometimes used in classification, as in ANCA-associated vasculitides. Clinical studies with immunosuppressive drugs targeting specificcytokines and cells can also be used to understand the heterogeneous immunopathogenicmechanisms of vasculitis and support a mechanistic immunological classification.[5]Location of the affected vessels. For example, ICD-10 classifies \"vasculitis limited to skin\" withskin conditions (under \"L\"), and \"necrotizing vasculopathies\" (corresponding to systemicvasculitis) with musculoskeletal system and connective tissue conditions (under \"M\").Arteritis/phlebitis on their own are classified with circulatory conditions (under \"I\").Type or size of the blood vessels that they predominantly affect. Apart from the[6]arteritis/phlebitis distinction mentioned above, vasculitis is often classified by the caliber of thevessel affected. However, there can be some variation in the size of the vessels affected.A small number have been shown to have a genetic basis. These include adenosine deaminase 2deficiency and haploinsufficiency of A20.According to the size of the vessel affected, vasculitis can be classified into:[7][8]Large vessel: Takayasu's arteritis, Temporal arteritisMedium vessel: Buerger's disease, Kawasaki disease, Polyarteritis nodosaSmall vessel: Behçet's syndrome, Eosinophilic granulomatosis with polyangiitis, Cutaneousvasculitis, granulomatosis with polyangiitis, Henoch–Schönlein purpura, and microscopicpolyangiitis. Condition of some disorders have vasculitis as their main feature. The major typesare given in the table below:Comparison of major types of vasculitisVasculitisAffected organsHistopathologyCutaneous small-vesselvasculitisSkin, kidneysNeutrophils, fibrinoidnecrosisGranulomatosis withpolyangiitisNose, lungs, kidneysNeutrophils, giant cellsEosinophilic granulomatosiswith polyangiitisLungs, kidneys, heart, skinHistiocytes, eosinophilsBehçet's diseaseCommonly sinuses, brain, eyes and skin; can affectother organs such as lungs, kidneys, jointsLymphocytes,macrophages,neutrophilsKawasaki diseaseSkin, heart, mouth, eyesLymphocytes,endothelial necrosisBuerger's diseaseLeg arteries and veins (gangrene)Neutrophils,granulomas\"Limited\" granulomatosis withpolyangiitis vasculitisCommonly sinuses, brain, and skin; can affect otherorgans such as lungs, kidneys, joints;Takayasu's arteritis, polyarteritis nodosa and giant cell arteritis mainly involve arteries and are thussometimes classed specifically under arteritis.Furthermore, there are many conditions that have vasculitis as an accompanying or atypical feature,including:Rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, anddermatomyositisCancer, such as lymphomas
Micrograph showing a vasculitis(Eosinophilic granulomatosis withpolyangiitis). H&E stain.Severe vasculitis of the majorvessels, displayed on FDG-PET/CTInfections, such as hepatitis CExposure to chemicals and drugs, such as amphetamines, cocaine, and anthrax vaccines whichcontain the Anthrax Protective Antigen as the primary ingredient.In pediatric patients varicella inflammation may be followed by vasculitis of intracranial vessels.This condition is called post varicella angiopathy and this may be responsible for arterial ischaemicstrokes in children.[9]Several of these vasculitides are associated with antineutrophil cytoplasmic antibodies.[10] Theseare:Granulomatosis with polyangiitisEosinophilic granulomatosis with polyangiitisMicroscopic polyangiitisLaboratory tests of blood or body fluids are performed forpatients with active vasculitis. Their results will generallyshow signs of inflammation in the body, such as increasederythrocyte sedimentation rate (ESR), elevated C-reactiveprotein (CRP), anemia, increased white blood cell count andeosinophilia. Other possible findings are elevatedantineutrophil cytoplasmic antibody (ANCA) levels andhematuria.Other organ functional tests may be abnormal. Specificabnormalities depend on the degree of various organsinvolvement. A Brain SPECT can show decreased bloodflow to the brain and brain damage.The definite diagnosis of vasculitis is established after abiopsy of involved organ or tissue, such as skin, sinuses,lung, nerve, brain, and kidney. The biopsy elucidates thepattern of blood vessel inflammation.Some types of vasculitis display leukocytoclasis,which is vascular damage caused by nuclear debrisfrom infiltrating neutrophils.[11] It typically presents aspalpable purpura.[11] Conditions with leucocytoclasismainly include hypersensitivity vasculitis (also calledleukocytoclastic vasculitis) and cutaneous small-vesselvasculitis (also called cutaneous leukocytoclasticangiitis).An alternative to biopsy can be an angiogram (x-ray test ofthe blood vessels). It can demonstrate characteristicpatterns of inflammation in affected blood vessels.18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT)has become a widely used imaging tool in patients with suspected Large VesselVasculitis, due to the enhanced glucose metabolism of inflamed vessel walls.[12] The combinedevaluation of the intensity and the extension of FDG vessel uptake at diagnosis can predict theclinical course of the disease, separating patients with favourable or complicated progress.[13]Acute onset of vasculitis-like symptoms in small children or babies may instead be the life-threatening purpura fulminans, usually associated with severe infection.Diagnosis
Laboratory Investigation of Vasculitic Syndromes[14]DiseaseSerologic testAntigenAssociated laboratory featuresSystemic lupuserythematosusANA includingantibodies todsDNA and ENA[including SM, Ro(SSA), La (SSB),and RNP]Nuclear antigensLeukopenia, thrombocytopenia, Coombs' test,complement activation: low serum concentrations ofC3 and C4, positive immunofluorescence usingCrithidia luciliae as substrate, antiphospholipidantibodies (i.e. anticardiolipin, lupus anticoagulant,false-positive VDRL)Goodpasture'sdiseaseAnti-glomerularbasementmembraneantibodyEpitope onnoncollagendomain of typeIV collagenSmall vesselvasculitisMicroscopicpolyangiitisPerinuclearantineutrophilcytoplasmicantibodyMyeloperoxidaseElevated CRPGranulomatosiswith polyangiiitisCytoplasmicantineutrophilcytoplasmicantibodyProteinase 3(PR3)Elevated CRPEosinophilicgranulomatosiswith polyangiitisperinuclearantineutrophilcytoplasmicantibody in somecasesMyeloperoxidaseElevated CRP and eosinophiliaIgA vasculitis(Henoch-Schönleinpurpura)NoneCryoglobulinemiaCryoglobulins, rheumatoid factor, complementcomponents, hepatitis CMedium vesselvasculitisClassicalpolyarteritisnodosaNoneElevated CRP and eosinophiliaKawasaki'sDiseaseNoneElevated CRP and ESRIn this table: ANA = Antinuclear antibodies, CRP = C-reactive protein, ESR = ErythrocyteSedimentation Rate, dsDNA = double-stranded DNA, ENA = extractable nuclear antigens, RNP =ribonucleoproteins; VDRL = Venereal Disease Research LaboratoryTreatments are generally directed toward stopping the inflammation and suppressing the immunesystem. Typically, corticosteroids such as prednisone are used. Additionally, other immunesuppression medications, such as cyclophosphamide and others, are considered. In case of aninfection, antimicrobial agents including cephalexin may be prescribed. Affected organs (such as theheart or lungs) may require specific medical treatment intended to improve their function duringthe active phase of the disease.TreatmentReferences
1. \"Vasculitis - Definition from the Merriam-Webster Online Dictionary\" (http://www.merriam-webster.com/dictionary/Vasculitis) Archived (https://web.archive.org/web/20160701173404/http://www.. merriam-webster.com/dictionary/vasculitis) from the original on 1 July 2016. Retrieved 8 January2009.2. \"Glossary of dermatopathological terms. DermNet NZ\" (http://dermnetnz.org/pathology/pathology-glossary.html) Archived (https://web.archive.org/web/20081220232449/http://dermnetnz.org/p. athology/pathology-glossary.html) from the original on 20 December 2008. Retrieved 8 January2009.3. \"Vasculitis (https://web.archive.org/web/20090628224336/http://www.mercksource.com/pp/us/cns/cns_hl_dorlands_split.jsp?pg=/ppdocs/us/common/dorlands/dorland/eight/000114505.htm)\" atDorland's Medical Dictionary4. \"The Johns Hopkins Vasculitis Center - Symptoms of Vasculitis\" (https://web.archive.org/web/20090227141353/http://vasculitis.med.jhu.edu/whatis/symptoms.html). Archived from the original(http://vasculitis.med.jhu.edu/whatis/symptoms.html) on 27 February 2009. Retrieved 7 May2009.5. Torp, Christopher Kirkegaard; Brüner, Mads; Keller, Kresten Krarup; Brouwer, Elisabeth; Hauge,Ellen-Margrethe; McGonagle, Dennis; Kragstrup, Tue Wenzel (2021). \"Vasculitis therapy refinesvasculitis mechanistic classification\" (https://doi.org/10.1016%2Fj.autrev.2021.102829).Autoimmunity Reviews. 20 (6): 102829. doi 10.1016/j.autrev.2021.102829 (https://doi.org/10.101:6%2Fj.autrev.2021.102829) PMID 33872767 (https://pubmed.ncbi.nlm.nih.gov/33872767). .6. Jennette JC, Falk RJ, Andrassy K, et al. (1994). \"Nomenclature of systemic vasculitides.Proposal of an international consensus conference\" (https://doi.org/10.1002%2Fart.1780370206). Arthritis Rheum. 37 (2): 187–92. doi 10.1002/art.1780370206 (https://doi.org/10.1002%2Fart.:1780370206) PMID 8129773 (https://pubmed.ncbi.nlm.nih.gov/8129773). .7. \"Overview of Vasculitis\" (http://www.merckmanuals.com/professional/musculoskeletal_and_connective_tissue_disorders/vasculitis/overview_of_vasculitis.html) Archived (https://web.archive.or. g/web/20150403172946/http://www.merckmanuals.com/professional/musculoskeletal_and_connective_tissue_disorders/vasculitis/overview_of_vasculitis.html) from the original on 3 April 2015.Retrieved 5 October 2016.8. Gündüz, Özgür (18 October 2011). \"Histopathological Evaluation of Behçet's Disease andIdentification of New Skin Lesions\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199096).Pathology Research International. 2012: 209316. doi 10.1155/2012/209316 (https://doi.org/10.11:55%2F2012%2F209316) ISSN 2090-8091 (https://www.worldcat.org/issn/2090-8091). .PMC 3199096 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199096) PMID 22028988 (http. s://pubmed.ncbi.nlm.nih.gov/22028988).9. Nita R Sutay, Md Ashfaque Tinmaswala, Shilpa Hegde . \"International Journal of MedicalResearch and Health Sciences | 404 Page\" (http://ijmrhs.com/post-varicella-angiopathy-a-case-report) Archived (https://web.archive.org/web/20151117161119/http://ijmrhs.com/post-varicella-a. ngiopathy-a-case-report/) from the original on 17 November 2015. Retrieved 19 August 2015.10. Millet A, Pederzoli-Ribeil M, Guillevin L, Witko-Sarsat V, Mouthon L (2013) Antineutrophilcytoplasmic antibody-associated vasculitides: is it time to split up the group? Ann Rheum Dis11. A Brooke W Eastham, Ruth Ann Vleugels and Jeffrey P Callen (12 July 2021). \"LeukocytoclasticVasculitis\" (https://emedicine.medscape.com/article/333891-overview). Medscape. Updated: Oct25, 201812. Maffioli L, Mazzone A (2014). \"Giant-Cell Arteritis and Polymyalgia Rheumatica\" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277693). NEJM. 371 (17): 1652–1653.doi 10.1056/NEJMc1409206 (https://doi.org/10.1056%2FNEJMc1409206) PMC 4277693 (http:. s://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277693) PMID 25337761 (https://pubmed.ncbi.nlm.. nih.gov/25337761).13. Dellavedova L, Carletto M, Faggioli P, Sciascera A, Del Sole A, Mazzone A, Maffioli LS (2015).\"The prognostic value of baseline 18F-FDG PET/CT in steroid-naïve large-vessel vasculitis:introduction of volume-based parameters\". European Journal of Nuclear Medicine and MolecularImaging. 55 (2): 340–8. doi 10.1007/s00259-015-3148-9 (https://doi.org/10.1007%2Fs00259-01:5-3148-9) PMID 26250689 (https://pubmed.ncbi.nlm.nih.gov/26250689) S2CID 21446786 (http. . s://api.semanticscholar.org/CorpusID:21446786).
Classification ICD-10: I77.6 (https://icd.who.int/browse10/2019/en#/I77.6), I80 (https://icd.who.int/browse10/2019/en#/I80), L95 (https://icd.who.int/browse10/2019/en#/L95), M30 (https://icd.who.int/browse10/2019/en#/M30)-M31(https://icd.who.int/browse10/2019/en#/M31) · ICD-9-CM:446 (http://www.icd9data.com/getICD9Code.ashx?icd9=446), 447.6 (http://www.icd9data.com/getICD9Code.ashx?icd9=447.6) · MeSH:D014657 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D014657) ·DiseasesDB:13750 (http://www.diseasesdatabase.com/ddb13750.htm)ExternalresourcesPatient UK:Vasculitis (https://patient.info/doctor/vasculitis)Retrieved from \"https://en.wikipedia.org/w/index.php?title=Vasculitis&oldid=1042903796\"This page was last edited on 7 September 2021, at 10:17 (UTC).Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using thissite, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the WikimediaFoundation, Inc., a non-profit organization.14. Burtis CA, Ashwood ER, Bruns DE (2012). Tietz Textbook of Clinical Chemistry and MolecularDiagnostics, 5th edition. Elsevier Saunders. p. 1568. ISBN 978-1-4160-6164-9.External linksD
Search
Read the Text Version
- 1
- 2
- 3
- 4
- 5
- 6
- 7
- 8
- 9
- 10
- 11
- 12
- 13
- 14
- 15
- 16
- 17
- 18
- 19
- 20
- 21
- 22
- 23
- 24
- 25
- 26
- 27
- 28
- 29
- 30
- 31
- 32
- 33
- 34
- 35
- 36
- 37
- 38
- 39
- 40
- 41
- 42
- 43
- 44
- 45
- 46
- 47
- 48
- 49
- 50
- 51
- 52
- 53
- 54
- 55
- 56
- 57
- 58
- 59
- 60
- 61
- 62
- 63
- 64
- 65
- 66
- 67
- 68
- 69
- 70
- 71
- 72
- 73
- 74
- 75
- 76
- 77
- 78
- 79
- 80
- 81
- 82
- 83
- 84
- 85
- 86
- 87
- 88
- 89
- 90
- 91
- 92
- 93
- 94
- 95
- 96
- 97
- 98
- 99
- 100
- 101
- 102
- 103
- 104
- 105
- 106
- 107
- 108
- 109
- 110
- 111
- 112
- 113
- 114
- 115
- 116
- 117
- 118
- 119
- 120
- 121
- 122
- 123
- 124
- 125
- 126
- 127
- 128
- 129
- 130
- 131
- 132
- 133
- 134
- 135
- 136
- 137
- 138
- 139
- 140
- 141
- 142
- 143
- 144
- 145
- 146
- 147
- 148
- 149
- 150
- 151
- 152
- 153
- 154
- 155
- 156
- 157
- 158
- 159
- 160
- 161
- 162
- 163
- 164
- 165
- 166
- 167
- 168
- 169
- 170
- 171
- 172
- 173
- 174
- 175
- 176
- 177
- 178
- 179
- 180
- 181
- 182
- 183
- 184
- 185
- 186
- 187
- 188
- 189
- 190
- 191
- 192
- 193
- 194
- 195
- 196
- 197
- 198
- 199
- 200
- 201
- 202
- 203
- 204
- 205
- 206
- 207
- 208
- 209
- 210
- 211
- 212
- 213
- 214
- 215
- 216
- 217
- 218
- 219
- 220
- 221
- 222
- 223
- 224
- 225
- 226
- 227
- 228
- 229
- 230
- 231
- 232
