Heparin-induced thrombocytopenia: Difference between revisions

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==Background==
==Background==
*Despite low plt count pt is actually hypercoagulable; bleeding is unusual
*Pathologic activation / consumption of platelets due to antibodies against heparin-platelet complex
*Pathophysiology
*Can be caused by [[unfractionated heparin]] or [[LMWH]] (10 times more common in unfranctionated)
**Pathologic activation / consumption of platelets due to Ab against heparin-plt complex
*Occurs in 0.5-5% of patients treated with heparin<ref name="Lovecchio"> Lovecchio F. Heparin-induced thrombocytopenia. Clin Toxicol (Phila). 2014 Jul;52(6):579-83</ref>
**Activated platelets then cause blood clot formation
*Thrombosis occurs in 35-75% of patients ; 20-30% die within 1 month<ref name="Lovecchio"></ref>
***Platelet count falls b/c plts are bound in clots
*HYPER-coagulable, ''despite'' low platelet count
**Can be caused by unfrationated or LMWH (10x common in the former)
**activated platelets bound in clot, thus low platelet count
***Occurs in 0.5-5% of pts tx'd w/ heparin
**bleeding is unusual
*Thrombosis occurs in 35-75% of pts; 20-30% die w/in 1 month
 
===Type 1 HIT===
*Onset within 48h of initiating heparin
*Drop in platelet count due to platelet activation by heparin
*Platelet count usually normalizes in a few days with continued heparin treatment<ref name="guidelines hit">Warkentin T. et al. Heparin-induced thrombocytopenia: recognition, treatment, and prevention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126(3 Suppl):311S-337S</ref>
===Type 2 HIT===
*Immune-mediated process
*Onset typically 5-10 days after exposure to heparin
*Complicated by thrombosis<ref name="guidelines hit"></ref>


==Clinical Features==
==Clinical Features==
*Typical
*The 4 Ts
**Symptoms begin 5-10d after initiation of heparin
**[[Thrombocytopenia|'''T'''hrombocytopenia]]
***>50% decrease in plt count (median nadir is ~60K; rarely <20K)
**'''T'''iming (5-14d)
***DVT or PE
**[[thromboembolism|'''T'''hrombosis]]
***Cerebral vein or adrenal vein thrombosis
**No o'''T'''her cause
***Limb arterial occlusion
 
***CVA
===Immediate Symptoms===
***MI
*Flushing
***Skin necrosis
*[[Tachycardia]]
*Rapid onset
*[[Hypotension]]
**Symptoms begin within hours of initiation of heparin
*[[Dyspnea]]
***Due to preexisting circulating antibody from sensitization several weeks earlier
 
***Sudden drop in plt count
===Delayed Symptoms===
***Thrombosis
*>50% decrease in platelet count (median nadir is ~60K; rarely <20K)
***Flushing
*[[DVT]] or [[PE]]
***Tachycardia
*Cerebral vein or adrenal vein thrombosis
***Hypotension
*[[Acute arterial ischemia|Limb arterial occlusion]]
***Dyspnea
*[[CVA]]
*Delayed onset
*[[MI]]
**Symptoms begin several days after heparin stopped
*Skin necrosis
**Severe thromboses
 
==Differential Diagnosis==
{{Thrombocytopenia}}
 
{{Hemolytic anemia DDX}}
 
==Pre-test Probability Scoring<ref>Janz TG, Hamilton GC: Disorders of Hemostasis, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 120: p 1578-1589.</ref>==
*Thrombocytopenia
**2 points: platelets > 50% fall AND nadir > 20k
**1 points: patient 30-50% fall OR nadir 10-19k
*Timing
**2 points: clear onset 5-10 days OR platelet fall < 1 day with prior heparin exposure within 30 days
**1 point: likely onset 5-10 days OR fall < 1 day with prior heparin exposure 30-100 days
*Thrombosis
**2 points: new thrombosis or skin necrosis at injection sites
**1 point: suspected thrombosis or progressive/recurrent thrombosis
*Likelihood of other causes
**2 points: none apparent
**1 point: possible
*Scoring
**≤ 3, low probability (≤5%)
**4-5, intermediate prob (~15%)
**≥ 6, high prob (~65%)
 
==Evaluation==
*Serotonin release assay (SRA) = gold standard
*Anti-PF4 plus SRA has combined sensitivity of 99% <ref>
Warkentin TE, et al. Chest. 2008;133(6 Suppl):340S-380S.</ref>
*Positivity determined by optical density (OD) reported with assay (same concept as a titer)
**OD <1 = <5% chance of HIT
**OD 1.4 = 50% chance of HIT
**OD >2 = 90% chance of HIT
 
==Management==
*Discontinue all [[heparin]] products
*Do '''not''' give [[platelets]] (may precipitate thrombosis)
*Start anticoagulation with no heparin based compound such as a direct thrombin inhibitor: [lepirudin (unless renal failure), [[argatroban]] (unless hepatobiliary disease), [[bivalirudin]]] or direct Xa inhibitor ([[fondaparinux]], danaparoid)
*''Avoid [[warfarin]] until platelets >100K-150K''


==Treatment==
==Disposition==
#Discontinue all heparin products
*Admit (with hematology consult)
#Do not give platelts (may precipitate thrombosis)
#Start anticoagulation
##Consider lepirudin, argatroban, danaparoid, fondaparinux, bivalirudin
##Avoid warfarin


==Dispostion==
==See Also==
*Admit
*[[Unfractionated heparin]]
*[[Low molecular weight heparin]]
*[[Coagulopathy (main)]]
*[[Hirudins]]


==Source==
==References==
Tintinalli
<references/>


[[Category:Heme/Onc]]
[[Category:Heme/Onc]]

Revision as of 16:54, 3 April 2020

Background

  • Pathologic activation / consumption of platelets due to antibodies against heparin-platelet complex
  • Can be caused by unfractionated heparin or LMWH (10 times more common in unfranctionated)
  • Occurs in 0.5-5% of patients treated with heparin[1]
  • Thrombosis occurs in 35-75% of patients ; 20-30% die within 1 month[1]
  • HYPER-coagulable, despite low platelet count
    • activated platelets bound in clot, thus low platelet count
    • bleeding is unusual

Type 1 HIT

  • Onset within 48h of initiating heparin
  • Drop in platelet count due to platelet activation by heparin
  • Platelet count usually normalizes in a few days with continued heparin treatment[2]

Type 2 HIT

  • Immune-mediated process
  • Onset typically 5-10 days after exposure to heparin
  • Complicated by thrombosis[2]

Clinical Features

Immediate Symptoms

Delayed Symptoms

Differential Diagnosis

Thrombocytopenia

Decreased production

Increased platelet destruction or use

Drug Induced

Comparison by Etiology

ITP TTP HUS HIT DIC
↓ PLT Yes Yes Yes Yes Yes
↑PT/INR No No No +/- Yes
MAHA No Yes Yes No Yes
↓ Fibrinogen No No No No Yes
Ok to give PLT Yes No No No Yes

Microangiopathic Hemolytic Anemia (MAHA)

Pre-test Probability Scoring[3]

  • Thrombocytopenia
    • 2 points: platelets > 50% fall AND nadir > 20k
    • 1 points: patient 30-50% fall OR nadir 10-19k
  • Timing
    • 2 points: clear onset 5-10 days OR platelet fall < 1 day with prior heparin exposure within 30 days
    • 1 point: likely onset 5-10 days OR fall < 1 day with prior heparin exposure 30-100 days
  • Thrombosis
    • 2 points: new thrombosis or skin necrosis at injection sites
    • 1 point: suspected thrombosis or progressive/recurrent thrombosis
  • Likelihood of other causes
    • 2 points: none apparent
    • 1 point: possible
  • Scoring
    • ≤ 3, low probability (≤5%)
    • 4-5, intermediate prob (~15%)
    • ≥ 6, high prob (~65%)

Evaluation

  • Serotonin release assay (SRA) = gold standard
  • Anti-PF4 plus SRA has combined sensitivity of 99% [4]
  • Positivity determined by optical density (OD) reported with assay (same concept as a titer)
    • OD <1 = <5% chance of HIT
    • OD 1.4 = 50% chance of HIT
    • OD >2 = 90% chance of HIT

Management

  • Discontinue all heparin products
  • Do not give platelets (may precipitate thrombosis)
  • Start anticoagulation with no heparin based compound such as a direct thrombin inhibitor: [lepirudin (unless renal failure), argatroban (unless hepatobiliary disease), bivalirudin] or direct Xa inhibitor (fondaparinux, danaparoid)
  • Avoid warfarin until platelets >100K-150K

Disposition

  • Admit (with hematology consult)

See Also

References

  1. ↑ 1.0 1.1 Lovecchio F. Heparin-induced thrombocytopenia. Clin Toxicol (Phila). 2014 Jul;52(6):579-83
  2. ↑ 2.0 2.1 Warkentin T. et al. Heparin-induced thrombocytopenia: recognition, treatment, and prevention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126(3 Suppl):311S-337S
  3. ↑ Janz TG, Hamilton GC: Disorders of Hemostasis, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 120: p 1578-1589.
  4. ↑ Warkentin TE, et al. Chest. 2008;133(6 Suppl):340S-380S.
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