There are fewer patients that I appreciate more than the ones that come in with a list of their home medications. A quick scan through the list is helpful, as it provides insight into the severity of the patient’s medical problems. One class of medications that we are all often on the lookout for are the colloquially-termed “blood thinners.” The inferred risks of bleeding and clots become apparent and often influence patient management.

To better appreciate these classes of medications, we must take a step back and ask ourselves: what are blood thinners? How do they work? Why do they matter? What does it imply for the patient and their management in the ED setting? By answering these questions, I hope to help you better appreciate these medications when encountered in the clinical setting.

What are blood thinners?

When there’s a traumatic injury to the body, hemostasis is the body’s way of minimizing blood loss. Hemostasis is a two-step process: (1) platelet aggregation which results in an initial platelet plug and (2) the coagulation cascade that creates a fibrin mesh to stabilize the clot. Blood clots (thrombi and emboli) can also form pathologically and cause multiple problems (such as acute coronary syndrome, ischemic stroke, and pulmonary embolism). When we want to reduce the rate of clot formation, blood thinners (more formally known as antithrombotics) are used. Antithrombotics are agents that block the clot formation during either of the two aforementioned steps of the hemostasis process.

 

How do blood thinners work?

There are two main classes of antithrombotics – antiplatelets and anticoagulants. Antiplatelets are medications that inhibit the formation of the initial platelet plug, and anticoagulants are medications that block a step in the coagulation cascade. Multiple biochemical processes are required to create the initial platelet plug (figure 1), and hence multiple classes of antiplatelet drugs exist to inhibit platelet aggregation (table 1).  

Figure 1

(from: Kumar, et al, 2009)

 

Class/MOA Examples Misc Information
COX Inhibitors aspirin
ADP receptor inhibitors clopidogrel, ticagrelor
GP IIb/IIa antagonists abciximab, eptifibatide IV form only
Misc dipyridamole, cilostazol Dipyridamole is used primarily for peripheral vascular disease

Table 1

 

In a similar fashion, the coagulation cascade (figure 2) comprises multiple steps that may be inhibited to help reduce thrombus formation. The various anticoagulants, including the newer class of direct oral anticoagulants (DOACs) are listed (table 2).  

 

Figure 2 

(from: Ilesanmi, 2010)

 

Class/MOA Examples Misc
Factor Xa inhibitor unfractionated heparin (UFH), low molecular weight heparin (LMWH, i.e. enoxaparin), fondaparinux LMWH and fondaparinux are subQ, renally dosed; risk of HIT with UFH/LMWH
Vitamin K antagonist warfarin Contraindicated in pregnancy
DOAC – Direct Thrombin Inhibitor dabigatran, bivalirudin, argatroban Contraindicated in renal insufficiency, pregnancy, prosthetic valves, only dabigatran is oral
DOAC – Factor Xa inhibitor rivaroxaban, apixaban Contraindicated in renal insufficiency, pregnancy, prosthetic valves

Table 2

 

Why are these medications so important?

Generally, these antithrombotics help reduce the incidence of disease states caused by thombi and emboli, including processes such as ACS, TIA, stroke, DVT, and PE.3 The precipitants of these clots can be understood through Virchow’s triad of hemostasis, endothelial injury, and hypercoagulability. Antithrombotics help reduce the rate of clots which may be due to hemostasis (i.e. atrial fibrillation, immobilization), endothelial injury (i.e. after PCI), or hypercoagulability (i.e. antiphospholipid syndrome).

 

The DOACs are an important class of anticoagulants that are becoming more prevalent as well.  They were created as an easier alternative to LMWH and warfarin for patients requiring chronic anticoagulation.4 Although they offer several benefits, including quick onset and decreased blood test monitoring, these medications are more difficult to reverse when patients are bleeding.

 

What does this mean for us in the ED?

Antithrombotics have a significant role in management of patients in the ED. For example, in patients with active bleeding or the potential to bleed, e.g. GI bleed or trauma, the presence of antithrombotics in the patient will influence care. Although obtaining labs such as CBC and coags can be helpful, the effect of many of the medications such as the newer DOACs, aren’t adequately reflected on routine labs.5 Obtaining a patient’s antithrombotic regimen can help direct you in choosing the proper reversal agent.3,6

In addition, different antithrombotics at different doses are frequently started in the ED for diseases ranging from myocardial infarction to pulmonary embolism. A familiarity with them can mean life-saving results. Lastly, be on the lookout for these antithrombotics on a patient’s medication list. The medication and the dosage can help clarify a patient’s medical history when not readily available to help create a more accurate clinical picture. The information may also offer insight into severity of their underlying medical condition, which may help you to risk stratify and deliver better care.

 

Resources

  1.       Kumar V, Abbas AK, Aster JC. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Saunders Elsevier; 2009.
  2.      Ilesanmi OO. Pathological basis of symptoms and crises in sickle cell disorder: implications for counseling and psychotherapy. Hematology Reports 2010;2(1):2.
  3.      Hanlon D. An Evidence-Based Approach To Managing The Anticoagulated Patient in The Emergency Department. Emergency Medicine Practice 2011;13(1):1–20.
  4.       Raja A, Geyer B. Emergency Department Management Of Patients On Novel Oral Anticoagulant Agents. Emergency Medicine Practice 2013;15(10):1–20.
  5.       Jennings LK, Kotha J. The Utility of Platelet and Coagulation Testing of Antithrombotics: Fusing Science with Patient Care. Drug Development Research 2013;74(8):587–93.
  6.       Tawil I, Seder D, Duprey J. Emergency Management Of Coagulopathy In Acute Intracranial Hemorrhage. EM Critical Care 2012;2(2):4–5.
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