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{{Heparin-induced thrombocytopenia}} | {{Heparin-induced thrombocytopenia}} | ||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com] | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com] | ||
==Overview== | ==Overview== | ||
[[Heparin-induced thrombocytopenia]] is diagnosed when the [[platelet]] count falls by > 50% typically after 5-10 days of [[heparin]] therapy. The development of mild to moderate thrombocytopenia (platelet counts of 50-70,000) in the context of heparin exposure is suggestive of a possible diagnosis of HIT while severe thrombocytopenia and platelet counts less than 20,000 are quite unusual for the syndrome.<ref name="pmid20059332">{{cite journal |author=Arepally GM, Ortel TL |title=Heparin-induced thrombocytopenia |journal=Annu. Rev. Med. |volume=61 |issue= |pages=77–90 |year=2010 |pmid=20059332 |doi=10.1146/annurev.med.042808.171814 |url=}}</ref> Given the nadirs in the platelet count, clinically significant bleeding associated with the thrombocoytopenia is quite rare. On the contrary, heparin induced thrombocytopenia is primarily a [[thrombosis|thrombotic]] disorder, with very high rates of [[thrombosis]], in the [[artery|arteries]] with or without [[vein|venous]] complications. | [[Heparin-induced thrombocytopenia]] is diagnosed when the [[platelet]] count falls by > 50% typically after 5-10 days of [[heparin]] therapy. The development of mild to moderate thrombocytopenia (platelet counts of 50-70,000) in the context of heparin exposure is suggestive of a possible diagnosis of HIT while severe thrombocytopenia and platelet counts less than 20,000 are quite unusual for the syndrome.<ref name="pmid20059332">{{cite journal |author=Arepally GM, Ortel TL |title=Heparin-induced thrombocytopenia |journal=Annu. Rev. Med. |volume=61 |issue= |pages=77–90 |year=2010 |pmid=20059332 |doi=10.1146/annurev.med.042808.171814 |url=}}</ref> Given the nadirs in the platelet count, clinically significant bleeding associated with the thrombocoytopenia is quite rare. On the contrary, heparin induced thrombocytopenia is primarily a [[thrombosis|thrombotic]] disorder, with very high rates of [[thrombosis]], in the [[artery|arteries]] with or without [[vein|venous]] complications. | ||
== | ==Historical Perspective== | ||
==Classification== | |||
There are two types of [[HIT]], type I and type II. Type I HIT patients characteristically have a transient decrease in platelet count (rarely <100,000) without any further symptoms and can recover even if heparin is continued to be administered. It occurs in 10-20% of all patients on heparin and is not due to an immune reaction and antibodies are not found upon investigation. HIT-1 is due to heparin-induced platelet clumping; it is innocuous. Type II is due to an autoimmune reaction with antibodies formed against platelet factor 4 (PF4), neutrophil-activating peptide 2 (NAP-2) and interleukin 8 (IL8) which form complexes with heparin. | |||
==Pathophysiology== | ==Pathophysiology== | ||
It is caused by antibodies to complexes between [[heparin]] and [[platelet factor 4]] (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of [[platelet]] and [[endothelium]]. | It is caused by antibodies to complexes between [[heparin]] and [[platelet factor 4]] (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of [[platelet]] and [[endothelium]]. | ||
==Causes== | ==Causes== | ||
'''Heparin-induced thrombocytopenia''' ([[HIT]]) with or without '''[[thrombosis]]''' (HITT) is [[thrombocytopenia]] (low [[platelet]] counts) due to the administration of [[heparin]]. While it is mainly associated with [[unfractionated heparin]] ([[UFH]]), it can also occur with exposure to [[low-molecular weight heparin]] (LMWH), but at significantly lower rates. | '''Heparin-induced thrombocytopenia''' ([[HIT]]) with or without '''[[thrombosis]]''' (HITT) is [[thrombocytopenia]] (low [[platelet]] counts) due to the administration of [[heparin]]. While it is mainly associated with [[unfractionated heparin]] ([[UFH]]), it can also occur with exposure to [[low-molecular weight heparin]] (LMWH), but at significantly lower rates. | ||
==Differentiating Heparin-induced thrombocytopenia from other Diseases== | |||
==Epidemiology and Demographics== | |||
It has been found to occur with increased frequencies in females, white population and patients over age of 60 years. An episode of [[Heparin-induced thrombocytopenia]] increases risks for other future thrombo-embolic events. | |||
==Risk Factors== | |||
==Screening== | |||
==Natural History, Complications, and Prognosis== | |||
===Natural History=== | |||
===Complications=== | |||
===Prognosis=== | |||
==Diagnosis== | ==Diagnosis== | ||
===History and symptoms=== | ===History and symptoms=== | ||
HIT typically develops 4-14 days after the administration of [[heparin]]. The onset of thrombocytopenia in less than 4-5 days after the initiation of heparin treatment is extremely rare due to the time required for antibody production, and alternative explanations should be sought for the development of thrombocytopenia this early in therapy. The primary exception to this is in the case of recent heparin exposures (<100 days) where the patient may have pre-existing antibodies against the heparin-PF4 complex.<ref name="pmid16928996">{{cite journal |author=Arepally GM, Ortel TL |title=Clinical practice. Heparin-induced thrombocytopenia |journal=N. Engl. J. Med. |volume=355 |issue=8 |pages=809–17 |year=2006 |month=August |pmid=16928996 |doi=10.1056/NEJMcp052967 |url=}}</ref> | HIT typically develops 4-14 days after the administration of [[heparin]]. The onset of thrombocytopenia in less than 4-5 days after the initiation of heparin treatment is extremely rare due to the time required for antibody production, and alternative explanations should be sought for the development of thrombocytopenia this early in therapy. The primary exception to this is in the case of recent heparin exposures (<100 days) where the patient may have pre-existing antibodies against the heparin-PF4 complex.<ref name="pmid16928996">{{cite journal |author=Arepally GM, Ortel TL |title=Clinical practice. Heparin-induced thrombocytopenia |journal=N. Engl. J. Med. |volume=355 |issue=8 |pages=809–17 |year=2006 |month=August |pmid=16928996 |doi=10.1056/NEJMcp052967 |url=}}</ref> | ||
=== | |||
===Physical Examination=== | |||
===Laboratory Findings=== | |||
The four commonest diagnostic tests used for heparin-induced thrombocytopenia (HIT) are Serotonin release assay, heparin-induced platelet aggregation assay, solid phase immunoassay (enzyme-linked immunosorbent assay), and particle gel immunoassay. | The four commonest diagnostic tests used for heparin-induced thrombocytopenia (HIT) are Serotonin release assay, heparin-induced platelet aggregation assay, solid phase immunoassay (enzyme-linked immunosorbent assay), and particle gel immunoassay. | ||
===Imaging Findings=== | |||
===Other Diagnostic Studies=== | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy== | |||
Treatment is by prompt withdrawal of [[heparin]] and replacement with a suitable alternative anticoagulant. [[Lepirudin]], [[fondaparinux]], [[bivalirudin]], [[argatroban]], [[danaparoid]] or other [[direct thrombin inhibitor]]s are used to treat the thrombotic state. Out of these lepirudin and argatroban are available for use in USA. | Treatment is by prompt withdrawal of [[heparin]] and replacement with a suitable alternative anticoagulant. [[Lepirudin]], [[fondaparinux]], [[bivalirudin]], [[argatroban]], [[danaparoid]] or other [[direct thrombin inhibitor]]s are used to treat the thrombotic state. Out of these lepirudin and argatroban are available for use in USA. | ||
==Prevention== | ==Prevention== | ||
Patients with HIT should be treated with [[Bivalirudin]], a direct thrombin inhibitor to support future procedures. | Patients with HIT should be treated with [[Bivalirudin]], a direct thrombin inhibitor to support future procedures. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Hematology]] | [[Category:Hematology]] | ||
Revision as of 19:22, 17 June 2016
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Heparin-induced thrombocytopenia |
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Differentiating Heparin-induced thrombocytopenia from other Diseases |
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Diagnosis |
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Treatment |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Overview
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. The development of mild to moderate thrombocytopenia (platelet counts of 50-70,000) in the context of heparin exposure is suggestive of a possible diagnosis of HIT while severe thrombocytopenia and platelet counts less than 20,000 are quite unusual for the syndrome.[1] Given the nadirs in the platelet count, clinically significant bleeding associated with the thrombocoytopenia is quite rare. On the contrary, heparin induced thrombocytopenia is primarily a thrombotic disorder, with very high rates of thrombosis, in the arteries with or without venous complications.
Historical Perspective
Classification
There are two types of HIT, type I and type II. Type I HIT patients characteristically have a transient decrease in platelet count (rarely <100,000) without any further symptoms and can recover even if heparin is continued to be administered. It occurs in 10-20% of all patients on heparin and is not due to an immune reaction and antibodies are not found upon investigation. HIT-1 is due to heparin-induced platelet clumping; it is innocuous. Type II is due to an autoimmune reaction with antibodies formed against platelet factor 4 (PF4), neutrophil-activating peptide 2 (NAP-2) and interleukin 8 (IL8) which form complexes with heparin.
Pathophysiology
It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of platelet and endothelium.
Causes
Heparin-induced thrombocytopenia (HIT) with or without thrombosis (HITT) is thrombocytopenia (low platelet counts) due to the administration of heparin. While it is mainly associated with unfractionated heparin (UFH), it can also occur with exposure to low-molecular weight heparin (LMWH), but at significantly lower rates.
Differentiating Heparin-induced thrombocytopenia from other Diseases
Epidemiology and Demographics
It has been found to occur with increased frequencies in females, white population and patients over age of 60 years. An episode of Heparin-induced thrombocytopenia increases risks for other future thrombo-embolic events.
Risk Factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
History and symptoms
HIT typically develops 4-14 days after the administration of heparin. The onset of thrombocytopenia in less than 4-5 days after the initiation of heparin treatment is extremely rare due to the time required for antibody production, and alternative explanations should be sought for the development of thrombocytopenia this early in therapy. The primary exception to this is in the case of recent heparin exposures (<100 days) where the patient may have pre-existing antibodies against the heparin-PF4 complex.[2]
Physical Examination
Laboratory Findings
The four commonest diagnostic tests used for heparin-induced thrombocytopenia (HIT) are Serotonin release assay, heparin-induced platelet aggregation assay, solid phase immunoassay (enzyme-linked immunosorbent assay), and particle gel immunoassay.
Imaging Findings
Other Diagnostic Studies
Treatment
=Medical Therapy
Treatment is by prompt withdrawal of heparin and replacement with a suitable alternative anticoagulant. Lepirudin, fondaparinux, bivalirudin, argatroban, danaparoid or other direct thrombin inhibitors are used to treat the thrombotic state. Out of these lepirudin and argatroban are available for use in USA.
Prevention
Patients with HIT should be treated with Bivalirudin, a direct thrombin inhibitor to support future procedures.
References
- ↑ Arepally GM, Ortel TL (2010). "Heparin-induced thrombocytopenia". Annu. Rev. Med. 61: 77–90. doi:10.1146/annurev.med.042808.171814. PMID 20059332.
- ↑ Arepally GM, Ortel TL (2006). "Clinical practice. Heparin-induced thrombocytopenia". N. Engl. J. Med. 355 (8): 809–17. doi:10.1056/NEJMcp052967. PMID 16928996. Unknown parameter
|month=ignored (help)