Heparin-induced thrombocytopenia natural history, complications and prognosis: Difference between revisions
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===Disseminated Intravascular Coagulation (DIC)=== | ===Disseminated Intravascular Coagulation (DIC)=== | ||
Disseminated intravascular coagulation is a pathologic condition causes by widespread activation of the coagulation cascade with simultaneous consumption of clotting factors. It is characterized by hypercoagulation and hyperfibrinolysis.<ref name="pmid25315802">{{cite journal| author=Tattersall TL, Thangasamy IA, Reynolds J| title=Bilateral adrenal haemorrhage associated with heparin-induced thrombocytopaenia during treatment of Fournier gangrene. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=25315802 | doi=10.1136/bcr-2014-206070 | pmc=4202074 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25315802 }} </ref> It can manifest clinically as bleeding, thrombosis, or both. Laboratory findings in DIC include elevation of the partial thromboplastin time (PTT), prothrombin time (PT), and bleeding time, as well as thrombocytopenia.<ref name="pmid25315802">{{cite journal| author=Tattersall TL, Thangasamy IA, Reynolds J| title=Bilateral adrenal haemorrhage associated with heparin-induced thrombocytopaenia during treatment of Fournier gangrene. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=25315802 | doi=10.1136/bcr-2014-206070 | pmc=4202074 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25315802 }} </ref> | Disseminated intravascular coagulation is a pathologic condition causes by widespread activation of the coagulation cascade with simultaneous consumption of clotting factors. It is characterized by hypercoagulation and hyperfibrinolysis.<ref name="pmid25315802">{{cite journal| author=Tattersall TL, Thangasamy IA, Reynolds J| title=Bilateral adrenal haemorrhage associated with heparin-induced thrombocytopaenia during treatment of Fournier gangrene. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=25315802 | doi=10.1136/bcr-2014-206070 | pmc=4202074 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25315802 }} </ref> It can manifest clinically as bleeding, thrombosis, or both. Laboratory findings in DIC include elevation of the partial thromboplastin time (PTT), prothrombin time (PT), and bleeding time, as well as thrombocytopenia.<ref name="pmid25315802">{{cite journal| author=Tattersall TL, Thangasamy IA, Reynolds J| title=Bilateral adrenal haemorrhage associated with heparin-induced thrombocytopaenia during treatment of Fournier gangrene. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=25315802 | doi=10.1136/bcr-2014-206070 | pmc=4202074 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25315802 }} </ref> Treatment aims at addressing the underlying hemostatic or coagulopathic state: if a patient is bleeding, blood products should be administered. If a person has ongoing clotting, anticoagulation should be administered. | ||
==Prognosis== | ==Prognosis== | ||
Revision as of 20:00, 9 July 2017
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Heparin-induced thrombocytopenia |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Shyam Patel [2]
Overview
Natural History
Complications
Complications of HIT are most thrombotic in nature. These can be quite devastating, which high morbidity and mortality. Venous thrombosis includes deep vein thrombosis (DVT) and pulmonary embolism (PE). Arterial thrombosis includes stroke and acute limb ischemia.
Venous Thrombosis
- Deep vein thrombosis
- Pulmonary embolism[1]
- Post-phlebitis syndrome: This can occur after DVT and results in inflammation of the leg and its veins due to chronic occlusion.
- Cerebral venous sinus thrombosis
Arterial Thrombosis
- Acute limb ischemia[1]: This can sometimes require limb amputation to prevent further tissue damage and sepsis from the thrombotic arm or leg.
- Stroke[1]: This is due to acute occlusion of vessel in the cerebral arterial system. It can result in permanent neurologic deficits if not treated promptly.
- Myocardial infarction: This is characterized by myocyte death due to ischemic injury from coronary artery occlusion. It is also known more commonly as a heart attack.
- Skin necrosis[1]: This can occur after warfarin is given to a patient with HIT. Warfarin-induced skin necrosis appears to be more common in the context of HIT treatment compared to use of warfarin in the absence of associated HIT.[2] Tissue necrosis an predispose a patient to sepsis and can require amputation or surgical debridement of the affected body part.
Hemorrhagic Complications
- Adrenal hemorrhage[3]: This is a rare but potentially fatal complication of HIT. Hemorrhage occurs due to a combination of initial adrenal venous thrombosis (leading to obstruction of outflow), thrombocytopenia, and impaired normal coagulation. The risk is approximately 1.6% in persons with HIT. It is most commonly associated with a post-operative state (i.e. after an orthopedic surgery) and usually occurs bilaterally (90% of cases).[3] This complication can result in Waterhouse-Friderichsen syndrome, which is characterized by cardiovascular dysfunction resulting in a sepsis-like state.[3] Disseminated intravascular coagulation (DIC) can result if the pathophysiological state continues. Treatment can be challenging since anticoagulation is contraindication in hemorrhage, but ongoing thrombosis can occur if HIT is not treated. The decision about initiating anticoagulation must weight the risks and benefits.
Disseminated Intravascular Coagulation (DIC)
Disseminated intravascular coagulation is a pathologic condition causes by widespread activation of the coagulation cascade with simultaneous consumption of clotting factors. It is characterized by hypercoagulation and hyperfibrinolysis.[3] It can manifest clinically as bleeding, thrombosis, or both. Laboratory findings in DIC include elevation of the partial thromboplastin time (PTT), prothrombin time (PT), and bleeding time, as well as thrombocytopenia.[3] Treatment aims at addressing the underlying hemostatic or coagulopathic state: if a patient is bleeding, blood products should be administered. If a person has ongoing clotting, anticoagulation should be administered.
Prognosis
Reference
- ↑ 1.0 1.1 1.2 1.3 Linkins LA, Dans AL, Moores LK, Bona R, Davidson BL, Schulman S; et al. (2012). "Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e495S–e530S. doi:10.1378/chest.11-2303. PMC 3278058. PMID 22315270.
- ↑ Fawaz B, Candelario NM, Rochet N, Tran C, Brau C (2016). "Warfarin-induced skin necrosis following heparin-induced thrombocytopenia". Proc (Bayl Univ Med Cent). 29 (1): 60–1. PMC 4677858. PMID 26722173.
- ↑ 3.0 3.1 3.2 3.3 3.4 Tattersall TL, Thangasamy IA, Reynolds J (2014). "Bilateral adrenal haemorrhage associated with heparin-induced thrombocytopaenia during treatment of Fournier gangrene". BMJ Case Rep. 2014. doi:10.1136/bcr-2014-206070. PMC 4202074. PMID 25315802.