4 December 2025 by Shahriar Lahouti.

CONTENTS

• Preface
• Hemostasis Balance
• Bleeding Patients
  • Step 1:Identify the agent
    • 📊Table: Anticoagulant agents
  • Step 2: Managing Major bleeding-The Reversal Road Map
    • 📊Table: Reversal agents
• Patient with Thrombosis
  • When to start anticoagulation in the ED: Initiation & Disposition
  • Optimal timing for initiation
    • 📊Table: Risk assessment tools
    • 📊Table: Bleeding risk assessment tools
  • Patient disposition pathway
  • Beyond the first dose: Patient education & coordination & follow-up
    • 📊Table: Monitoring anticoagulants
  • Specific population
    • Elderly patient & fall risk
    • Renal impairment
    • Hepatic impairment & liver disease
    • Cancer-associated thrombosis
    • Concomitant antiplatelet therapy 
      • 📊Table: Antiplatlet agents
    • Pregnancy and postpartum period
    • Integration with fibrinolytic therapy
      • 📊Table: Fibrinolytic agents
    • Peri-procedural management (Bridging) 
    • Management of bleeding complications
      • 📊Table: Bleeding Severity
    • Summary & implementory guide 
• Appendix
• References

Preface

The emergency department is ground zero for the complications and critical decisions surrounding anticoagulant therapy. From the patient with a life-threatening bleed on an unfamiliar direct oral anticoagulant (DOAC) to the newly diagnosed pulmonary embolism who may be safe for discharge, these drugs demand swift, confident management. This guide cuts through the complexity to provide the emergency physician with a pragmatic, actionable framework. We will focus on the core tasks: rapidly identifying the agent, managing major hemorrhage with specific reversal strategies, safely initiating therapy when indicated, and making sound disposition decisions. By anchoring our approach in physiology and clinical evidence, this article aims to transform anticoagulant management from a source of anxiety into a structured, executable component of your emergency practice.

Hemostatic Balance

A Primer for the Emergency Physician

Before we can safely disrupt the clotting system, we must understand the elegant, balanced physiology we are targeting. Normal hemostasis is a self-limiting, localized cascade designed to seal vascular injury without causing systemic thrombosis or excessive bleeding. It operates as a dynamic equilibrium, constantly tipped toward clot formation at sites of injury and toward clot inhibition elsewhere. For the emergency physician, visualizing this balance is key to predicting the effects, and complications of our interventions.

◾️From Physiology to Pathology: Arterial vs. Venous Clots

• This hemostatic system can be dysregulated to form pathologic thrombi, and the type of thrombus dictates the type of drug we use.
  • Arterial Thrombi (“White Clots”)
    • Form under high shear stress at sites of ruptured atherosclerotic plaque.
    • They are platelet-rich, with thin fibrin strands.
    • ✅ Both antiplatelets and anticoagulants can be effective for prevention and treatment.
  • Venous Thrombi (“Red Clots”)
    • Form in low-flow/stasis conditions (e.g., deep veins).
    • They are fibrin- and red cell-rich, with a large, loose structure.
    • ✅ Anticoagulants are the cornerstone of prevention and treatment; antiplatelets are ineffective.
• This fundamental difference explains why a patient with atrial fibrillation (a stasis risk) needs an anticoagulant, while a patient with a coronary stent (a platelet-driven risk) needs an antiplatelet. When both risks coexist, we combine therapies, accepting a higher bleeding risk.

◾️The Four Phases of Hemostasis:

1. Vasoconstriction
   • Immediate neural and local mediator response to limit blood flow.
2. Primary Hemostasis (The “Platelet Plug”)
   • Platelets adhere to exposed subendothelial collagen (via von Willebrand Factor), activate, change shape, and aggregate to form a fragile mechanical plug.
   • ✅ This is the target of antiplatelet agents (e.g., aspirin, clopidogrel).
3. Secondary Hemostasis (The “Fibrin Clot”):
   • The coagulation cascade, a series of amplified enzymatic reactions culminating in the conversion of prothrombin (Factor II) to thrombin (IIa).
   • Thrombin then converts soluble fibrinogen (I) to insoluble fibrin (Ia), which forms a stabilizing mesh around the platelet plug.
   • ✅ This is the target of all anticoagulants (e.g., heparin, warfarin, DOACs).
4. Fibrinolysis (The “Clean-Up”)
   • Once healing begins, the fibrin clot is broken down by plasmin.
   • ✅ This pathway is hijacked by thrombolytic agents (e.g., alteplase/tPA).

◾️Why This Matters in the ED:

• A patient’s bleeding or thrombotic risk is determined by which part of this system is affected by disease or medication.
  • A patient on clopidogrel has a deficient platelet plug; one on rivaroxaban has impaired fibrin formation; and a patient receiving tPA has uncontrolled fibrinolysis.
  • Catastrophic hemorrhage, such as an intracranial bleed after thrombolysis in a fully anticoagulated patient, occurs when we disrupt multiple pillars of hemostasis simultaneously.
• The following visual summarizes this critical balance, highlighting the specific targets of the pharmacologic agents you will manage.

With this framework in mind, we can now move from physiology to pharmacology, beginning with the first critical step in any encounter: identifying what the patient is taking.

Bleeding Patients

Step 1: Identify the Agent 

The first critical task when managing a bleeding patient or initiating therapy is to answer one question: “What specific drug is the patient taking?” This is more challenging than ever, with multiple direct oral anticoagulants (DOACs), traditional warfarin, and various injectables. Guessing is not an option.

The Rapid ED Drug Identification Framework

Use this systematic approach to cut through the confusion.

1. Ask Directly & Specifically: Don’t just ask, “Are you on blood thinners?” Patients may not consider aspirin or clopidogrel as “blood thinners.” Ask:
   • “Are you on medication to prevent strokes or for an irregular heartbeat (like atrial fibrillation)?”
   • “Are you on medication for clots in the legs or lungs (DVT or PE)?”
   • “Are you on warfarin (Coumadin®), Eliquis®, Xarelto®, Pradaxa®, or Lovenox® shots?”
2. Check Available Records: Pull medication lists from the EHR, previous discharge summaries, or pharmacy records. Look for generic names.
3. Use a Bedside Clue (For Bleeding Patients): If the patient is on an unknown anticoagulant and bleeding, two rapid tests can provide hints while you await specific assays:
   • PT/INR: If markedly elevated (>2.0) → Think Warfarin. (May be mildly elevated with some Factor Xa DOACs).
   • aPTT: If prolonged → Could indicate unfractionated heparin, argatroban, or (less reliably) dabigatran.

⚠️ Critical Caution: These are clues only, not diagnostic. A normal INR does not rule out a therapeutic level of a DOAC. When in doubt, treat empirically for major bleeding and consult pharmacy/hematology.

📊Anticoagulant agents: To streamline identification, use the following reference table. 

• ⚙️Mechanism of action of anticoagulant: Anticoagulants prevent clotting through different targets *. 

1. 1. Direct Oral Anticoagulants (DOACs): Directly bind to the clotting factor.
      • Direct thrombin inhibitor: Dabigatran
      • Direct Factor Xa inhibitors: Apixaban, Rivaroxaban, Edoxaban
   2. Indirect Anticoagulants (require antithrombin):
      • Inhibit IIa & Xa (via antithrombin): Unfractionated Heparin (UFH)
      • Primarily inhibit Xa (via antithrombin): Low Molecular Weight Heparins (Enoxaparin, Dalteparin)
      • Selectively inhibit Xa only (via antithrombin): Fondaparinux
   3. Vitamin K Antagonists (VKAs): Inhibit the synthesis of clotting factors.
      • Warfarin, Acenocoumarol
   4. Direct Thrombin Inhibitors (DTIs – Parenteral): Directly bind to thrombin.
      • Bivalirudin, Argatroban

⚠️The Special Case of Heparin-Induced Thrombocytopenia (HIT)

• If a patient on heparin (UFH or LMWH) has a >50% drop in platelet count (typically days 5-10), think of HIT, a pro-thrombotic emergency.
• Use the 4T’s Score immediately 👉 MDCalc
• Do not wait for lab confirmation to stop heparin if clinical probability is intermediate or high *.

With the agent identified, you are now prepared to make the pivotal decisions: managing the bleeding patient or safely initiating therapy. We will tackle the most urgent scenario first.

Step 2: Managing Major Bleeding

The Reversal Roadmap

When faced with major bleeding in an anticoagulated patient, your management follows two parallel tracks: universal supportive care and drug-specific reversal. Panic is not a plan; a systematic approach is.

◾️The Universal ED Response (For Any Anticoagulant)

• Initiate these actions immediately, concurrently with identifying the agent:
  1. ABCs & Resuscitation: Secure airway, obtain large-bore IV access, begin balanced resuscitation.
  2. Call for Help: Activate massive transfusion protocol if indicated. Notify blood bank, pharmacy, and relevant specialists (hematology, interventional radiology, surgery).
  3. Blood Products: Empirically transfuse as needed:
     • Packed Red Blood Cells (PRBCs) for anemia/shock.
     • Fresh Frozen Plasma (FFP) or 4-Factor Prothrombin Complex Concentrate (PCC) for general coagulation factor support.
     • Platelets if thrombocytopenic or on antiplatelets.
     • Tranexamic Acid (TXA) 1g IV for hyperfibrinolysis (consider in all major traumatic bleeds).
  4. Local Control: Apply direct pressure. Consider topical hemostatic agents. Consult GI, IR, or surgery for procedural control as needed.

◾️Drug-Specific Reversal: From General to Specific

• Once the agent is identified, escalate to targeted therapy. The goal is to restore hemostasis, not necessarily to normalize a lab value.
  1. For Warfarin (VKA) Over-anticoagulation & Bleeding
     • Life-Threatening Bleed (ICH, hemodynamic instability):
       1. 4-Factor PCC (e.g., Kcentra®) — Dose based on INR and weight. This is first-line for rapid factor repletion (works in minutes).
       2. IV Vitamin K (5-10 mg) — Co-administer with PCC. It takes 6-24 hours to work but prevents rebound anticoagulation.
          • Do NOT use FFP as first-line if PCC is available (slower, volume overload risk).
     • Non-Major Bleed or High INR (>4.5) without bleed:
       • Hold warfarin.
       • Oral or low-dose IV Vitamin K.
       • Re-assess and reload warfarin carefully once INR is therapeutic.
  2. For Direct Oral Anticoagulants (DOACs)
     • First, Determine Timing: When was the last dose? If within 2-3 hours, consider activated charcoal if the airway is protected.
     • Life-Threatening Bleed:
       • For Dabigatran (Direct Thrombin Inhibitor):
         • Idarucizumab (Praxbind®) 5g IV x 2. This is the specific, fast-acting antidote. Repeat if re-bleeding occurs.
       • For Apixaban/Rivaroxaban/Edoxaban (Factor Xa Inhibitors):
         • Andexanet Alfa (Andexxa®) — Weight-based bolus + infusion. This is the specific antidote.
         • If Andexanet is unavailable: Use 4-Factor PCC (50 U/kg) as a second-line hemostatic agent (not a true reversal). Do not use FFP.
     • Non-Major Bleed:
       • Supportive care. Hold next 1-2 doses. Most DOACs have short half-lives (8-15 hours in normal renal function). Time is an antidote.
  3. For Heparins & Fondaparinux:
     • Unfractionated Heparin (UFH):
       • Protamine Sulfate: 1 mg IV per 100 units of UFH given in the previous 2-3 hours. Maximum 50 mg. Infuse slowly (risk of hypotension, anaphylaxis).
     • Low Molecular Weight Heparin (e.g., Enoxaparin):
       • Protamine Sulfate (Partial Reversal): 1 mg IV per 1 mg of enoxaparin if last dose within 8 hours. It reverses anti-IIa activity (~60%) but only partially reverses anti-Xa activity.
     • Fondaparinux:
       • No specific antidote. Consider recombinant Factor VIIa (rFVIIa) or PCC in catastrophic bleeding, but evidence is weak. Consult hematology.
  4. Critical Interaction Alert: Concurrent Antiplatelet Therapy
     • If the patient is also on aspirin, clopidogrel, etc., bleeding is more severe. Consider platelet transfusion for life-threatening bleeding, especially with recent (<24-48h) intake of irreversible agents like clopidogrel.

💡 The Reversal Decision Guide

• 📊The following table summarizes this critical pathway for rapid reference.
• The most important question is: “Is this bleed immediately life-threatening (ICH, compartment syndrome, hemodynamic instability)?”
  • If YES, move to specific reversal immediately.
  • If NO, time and supportive care may suffice.

📍Bottom Line for the EP: Your first moves are universal resuscitation + rapid drug ID. Your next move is targeted reversal based on that ID. With this roadmap, you can approach even the most intimidating bleeding scenario with a clear, life-saving plan.

Patients with thrombosis

When to Start Anticoagulants in the ED

Initiation & Disposition

The decision to initiate anticoagulation in the ED hinges on balancing two imperatives: the urgent need to reduce stroke risk and the imperative to avoid preventable harm. Our data, demonstrating a low rate of major bleeding with ED initiation, support a proactive approach for appropriate patients. The following framework guides timing, patient selection, and disposition

Optimal Timing for Initiation

Initiation should be considered immediately upon confirmation of an indication (e.g., diagnosis of new non-valvular atrial fibrillation, acute VTE) and completion of a rapid, structured dual-risk assessment. This assessment must occur before the first dose and is the cornerstone of safe prescribing. The decision to anticoagulate is based on the net clinical benefit, where the estimated thromboembolic risk significantly outweighs the projected bleeding risk.

The Dual-Risk Assessment includes:

1. Thromboembolic Risk Stratification: Calculate a validated risk score specific to the indication to quantify the risk of stroke, systemic embolism, or VTE recurrence if untreated *.
2. Bleeding Risk Stratification: Calculate a validated bleeding risk score to identify modifiable risk factors and quantify the baseline hazard of therapy.
3. Review of Organ Function & Comorbidities: Point-of-care renal function (serum creatinine/eGFR), hepatic function, complete blood count, and a focused history for high-risk lesions, recent trauma/surgery, and fall risk.
4. Review of Concomitant Medications: Screen for drug-drug interactions (e.g., antiplatelets, NSAIDs, strong P-gp/CYP inducers or inhibitors).

There is no benefit to delaying therapy for stable patients once this assessment is complete. Delays increase the period of unprotected thromboembolic risk without mitigating bleeding risk.

📊The following tables provide a reference for the key validated risk-assessment tools.

🩸More on assessing risk of bleeding

Assessing bleeding risk is a critical prerequisite to anticoagulation initiation. Multiple validated scoring systems exist, each with distinct components, predictive strengths, and clinical contexts.

📊The following table compares the most widely used bleeding risk assessment tools to guide clinician selection and interpretation at the point of care.

Patient Disposition Pathways

Disposition is determined by clinical stability, bleeding risk, and system/social factors.

1. Safe Discharge Home with DOAC Prescription

• Candidate Profile
  • Clinically stable patient with a clear indication, low-to-moderate bleeding risk (e.g., HAS-BLED ≤3), normal renal function, no active high-risk features, demonstrated understanding of therapy, and a reliable plan for follow-up and medication access.
• ED Actions
  • Provide the first dose in the ED under observation if feasible.
  • Issue a complete prescription with clear instructions. The use of “starter packs” or a direct-dispense model from the ED pharmacy is highly encouraged to ensure immediate access.
  • Deliver structured, verbal, and written education on the drug name, dose, timing, indications, signs of bleeding and thrombosis, and drug interactions.
  • Arrange and communicate a specific follow-up plan (e.g., with primary care, cardiology, or an anticoagulation clinic) within 3-7 days.

2. Management in an Emergency Department Observation Unit (EDOU)

• Candidate Profile: Patients who are not immediate discharge candidates but do not require inpatient resources. This includes those with:
  • Moderate or unclear bleeding risk needing short-term monitoring after the first dose.
  • Social or logistical barriers (e.g., unable to fill a prescription until morning).
  • Need for further diagnostic clarification (e.g., echocardiogram) that can be obtained within 24 hours.
  • Complex medication reconciliation or requirement for multidisciplinary planning (e.g., social work, pharmacy consultation).
• ED/EDOU Actions: Allows for the first 1-2 doses to be administered under monitoring, completion of ancillary tests, reinforcement of education, and confirmation of follow-up plans, facilitating safe discharge within 24 hours.

3. Inpatient Hospital Admission

• ⚠️Indications: Admission is warranted for patients with:
  • Absolute contraindications to immediate anticoagulation (e.g., active major bleeding, recent intracranial hemorrhage, severe uncontrolled hypertension).
  • High bleeding risk requiring procedural intervention before anticoagulation (e.g., need for urgent surgery, endoscopic evaluation of a GI bleed).
  • Clinical instability related to the arrhythmia or comorbidities (e.g., heart failure exacerbation, acute coronary syndrome).
  • Life-threatening complications of thrombosis (e.g., hemodynamically significant PE, stroke).
  • Severe renal/hepatic impairment requiring complex dosing or alternative management.

🚫 Absolute Contraindications to ED Initiation

• A clear “stop” rule is essential. Do not initiate in the ED if the patient has:
  • Active, clinically significant bleeding (meeting criteria for major bleeding).
  • Known or suspected intracranial pathology at high risk for bleeding (recent stroke, aneurysm, AVM, primary or metastatic brain cancer).
  • Recent major trauma, surgery (within 48-72 hours), or spinal puncture.
  • Severe, uncontrolled hypertension (e.g., systolic BP >200 mmHg).
  • Documented hypersensitivity to the chosen agent.
  • Pregnancy (for most DOACs).

📍Conclusion: For the majority of stable ED patients with a clear indication for anticoagulation, initiation in the ED is safe, effective, and aligns with the goal of timely stroke prevention. A structured approach using risk stratification to guide disposition—favoring discharge with robust support—can improve patient outcomes and optimize healthcare resource utilization. The subsequent section will detail the essential components of patient education and follow-up coordination required to ensure the safety of this approach beyond the ED doors.

Beyond the First Dose

Patient Education, Coordination, and Follow-up

Initiating anticoagulation in the emergency department is not a singular event but the first step in a longitudinal care process. The safety and efficacy demonstrated in clinical trials and cohort studies, including our own, are predicated on structured support systems. Successful ED initiation, therefore, depends on three pillars that extend beyond the first dose: comprehensive education, seamless care coordination, and guaranteed short-term follow-up.

1. Structured Patient Education

• Education must be initiated in the ED, delivered in a clear, concise, and multimodal fashion to address health literacy barriers.
  • Core Content (“The Four W’s”):
    • WHY: Explain the specific reason for anticoagulation (e.g., “This medication is a blood thinner to prevent strokes caused by your irregular heart rhythm”).
    • WHAT & WHEN: State the drug’s brand and generic name, exact dose, and precise timing (e.g., “You will take rivaroxaban, 20 mg, one pill once daily with your evening meal”). Emphasize adherence.
    • WARNINGS:
      • Bleeding Signs: Instruct patients to seek immediate care for head injury, uncontrollable bleeding, red/black stools, coughing/vomiting blood, severe headache, or weakness.
      • Thrombosis Signs: Reinforce symptoms of stroke (FAST: Face, Arm, Speech, Time) or PE (sudden shortness of breath, chest pain).
    • INTERACTIONS & PRECAUTIONS: Review avoidance of NSAIDs (e.g., ibuprofen), caution with alcohol, and the need to inform all other healthcare providers (including dentists) about their anticoagulant use.
  • Delivery Method: Combine verbal teaching (teach-back method), written materials (take-home instructions in plain language), and, if available, video resources or links to reputable websites (e.g., the American Heart Association).

2. Care Coordination and Systems Support

• The ED must act as a bridge, not a cliff. This requires intentional system design.
  • Medication Access: The single greatest point of failure is the patient leaving without medication. Systems must ensure the first dose is administered in the ED and that a full supply is immediately accessible. This can be achieved via:
    • ED pharmacy dispensation of a “starter pack” (3-7 day supply).
    • A verified e-prescription sent to a 24-hour pharmacy with a confirmed patient pickup plan.
    • Use of manufacturer patient-assistance programs or sample kits where appropriate and compliant.
  • 📊Monitoring Requirements for Anticoagulant Agents
    • The following table would compare Warfarin, DOACs, LMWH, etc., on parameters like:
      • Routine monitoring test [INR, aPTT, Anti-Xa, CrCl].
      • Monitoring frequency [daily, monthly, every 3-6 months].
      • Key parameters to track [renal function, liver function, CBC, signs of bleeding].
      • Special notes. 
    • 🔬Anticoagulants that require routine monitoring of specific laboratory parameters:
      • 🔎Routine monitoring is mandatory only for IV UFH (aPTT) and Warfarin (INR).
      • ✅DOACs and prophylactic LMWH are designed for fixed dosing without monitoring.
      • ⚠️Special situations (renal failure, pregnancy, extremes of size) shift LMWH and sometimes DOACs into the “monitor with Anti-Xa or drug level” category.
    • 💡This “monitor vs. no monitor” distinction is a key practical advantage of DOACs over warfarin in outpatient care.

• • Information Transmission
    • A direct handoff is ideal. The ED must communicate the initiation to the patient’s Primary Care Provider (PCP) and/or managing cardiologist/hematologist via a structured mechanism (e.g., direct phone call, secure message in the electronic health record, or faxed summary) on the day of discharge.
    • This communication should include the indication, agent/dose, renal function, bleeding risk assessment, and the planned follow-up date.
  • Anticoagulation Management Service (AMS) Referral
    • Where available, an immediate referral to a dedicated AMS or pharmacist-led clinic provides expert longitudinal management and is a best practice.

3. Mandatory Short-Term Follow-Up

• A specific, scheduled follow-up appointment within 3 to 7 days is non-negotiable for ED-initiated patients. This appointment serves multiple critical functions:
  • Reinforcement: Re-educate and assess understanding.
  • Safety Check: Review for early signs of bleeding or adverse effects, re-check renal function if indicated, and assess adherence.
  • Therapy Adjustment: Confirm appropriate long-term agent and dose based on more comprehensive outpatient evaluation.
  • Continuity: Formally transfer care from the episodic ED setting to the longitudinal outpatient provider.
• The Follow-Up “Safety Net”: Patients must be given explicit, written instructions on what to do if they cannot secure or attend their follow-up appointment (e.g., “Call this clinic number or return to the ED for guidance”). This closes the loop and prevents patients from falling out of care.

📍Conclusion: The ED as an Initiator within a System of Care

• The emergency department is uniquely positioned to identify patients who would benefit from immediate anticoagulation and to begin therapy safely. However, this practice is only sustainable and safe when embedded within a larger system designed to support it. By standardizing education, guaranteeing medication access, proactively coordinating with outpatient providers, and mandating early follow-up, the ED transforms from a point of episodic care into a powerful initiator of essential, long-term preventive therapy. This integrated approach maximizes the benefit of timely stroke prevention while systematically mitigating the inherent risks of anticoagulation.

Special Populations and Complex Scenarios

While the general pathway for ED anticoagulation initiation provides a robust framework, specific patient subgroups present unique challenges that require tailored decision-making. A “one-size-fits-all” approach risks either under-treatment or harm. This section addresses key considerations for special populations and complex clinical scenarios frequently encountered in the ED.

Elderly Patient and Fall Risk

Advanced age is a component of both stroke (CHA₂DS₂-VASc) and bleeding (HAS-BLED) risk scores, creating a perceived therapeutic dilemma. However, evidence strongly supports anticoagulation in the elderly with AF, as their higher baseline stroke risk means the net clinical benefit remains favorable.

• Key Principle
  • A history of falls alone is not an absolute contraindication to anticoagulation. The risk of traumatic intracranial hemorrhage (ICH) must be weighed against the significant daily risk of cardioembolic stroke.
• ED Assessment & Mitigation
  • Quantify the Risk
    • Distinguish between a single, accidental fall and recurrent, mechanical falls, indicating syncope, gait instability, or neurodegenerative disease.
  • Focus on Modifiable Factors
    • Screen for orthostatic hypotension, review medications contributing to fall risk (e.g., sedatives, antihypertensives), and initiate referrals for gait assessment and home safety evaluations.
  • Agent Consideration
    • While all anticoagulants carry bleeding risk, some data suggest apixaban may have a lower risk of ICH compared to warfarin, which may be a consideration in this population. Dose adjustment for age, weight, and renal function is paramount.
• Disposition
  • For a patient with recurrent, unexplained falls, initiation may be safely deferred for 24-48 hours in an ED Observation Unit or inpatient setting to allow for urgent outpatient geriatric or cardiology evaluation to address the root cause, while stroke risk is briefly managed with bridging strategies if deemed high risk.

Renal Impairment

Renal function dictates DOAC eligibility, dosing, and safety.

• ED Action Algorithm:
  • Obtain a Serum Creatinine & Estimate GFR (eGFR) on all patients before initiation.
  • eGFR >30 mL/min
    • All DOACs are generally permissible with appropriate dose adjustments (refer to specific agent guidelines).
    • Apixaban or rivaroxaban may be preferred in moderate impairment (CrCl 30-50 mL/min) due to their studied dosing schemes.
  • eGFR 15-30 mL/min (Severe Impairment)
    • Apixaban is the only DOAC with specific dosing guidance and outcome data in this range. Use with caution and at a reduced dose.
    • Warfarin remains an alternative, but requires bridging and complex outpatient management.
  • eGFR <15 mL/min or on Dialysis
    • DOACs are contraindicated.
    • Initiation of anticoagulation for AF in this population is highly complex and requires shared decision-making with nephrology.
    • ED initiation is generally not appropriate; consultation and admission for coordinated planning are advised.

💡Pearl

• Clinical Decision Guide for Renal Disease
  • ⚠️Most Renal-Dependent: Dabigatran > Enoxaparin > Edoxaban > Fondaparinux
  • ✅Safest in Renal Failure: UFH, Argatroban, Warfarin (no dose adjustment, but other risks).
  • ☑️Preferred DOAC for Moderate Renal Impairment: Apixaban (least renal clearance).
  • 🧐Intermediate & Requiring Caution: Bivalirudin (requires dose reduction in severe renal failure, CrCl <30 mL/min).

Hepatic Impairment and Liver Disease

The liver synthesizes both clotting factors and proteins involved in anticoagulant metabolism, creating a dual risk of thrombosis and bleeding. Assessment is more nuanced than renal function.

• Risk Stratification: Use the Child-Pugh classification (based on bilirubin, albumin, INR, ascites, encephalopathy) for cirrhotic patients.
  • Child-Pugh A (Mild)
    • DOACs (particularly apixaban or rivaroxaban) may be considered with caution and often at reduced dose, though data are limited.
    • Consultation with hepatology or hematology is strongly advised before ED initiation.
  • Child-Pugh B (Moderate)
    • DOACs are generally not recommended. The bleeding risk is significantly elevated, and metabolism is unpredictable.
    • For acute VTE or high-risk AF, admission for consultation and consideration of low-dose LMWH (e.g., enoxaparin 0.5 mg/kg twice daily) is typically required.
  • Child-Pugh C (Severe)
    • Anticoagulation is contraindicated in most circumstances due to profound coagulopathy and high bleeding risk.
    • ED initiation must not occur. These patients require urgent hepatology consultation, and management of portal hypertension/thrombosis is highly specialized.
• Non-Cirrhotic Liver Disease
  • For patients with acute hepatitis or significant cholestasis, DOACs are also poorly studied. A conservative approach with LMWH and specialist consultation is prudent.

🏥ED Action: For any patient with known or suspected significant liver disease (evidenced by elevated INR not on warfarin, hypoalbuminemia, jaundice, or ascites), ED initiation of a DOAC is strongly discouraged.

• 🏨The pathway should involve consultation and, typically, inpatient admission for multidisciplinary evaluation.

💡Bottom Line

• ✅In significant liver disease (Child-Pugh B/C or coagulopathy), Unfractionated Heparin (UFH) is the safest and most controllable option.
• ⚠️All DOACs and warfarin carry high, often prohibitive risk.
• 👉The prescribing rule: Liver failure → Think Heparin (UFH/LMWH with monitoring).

Cancer-Associated Thrombosis (CAT)

Patients with active cancer have a 5-7 times higher risk of VTE and often require anticoagulation. The ED is a common point of diagnosis.

• First-Line Therapy
  • Low-Molecular-Weight Heparin (LMWH), such as enoxaparin, has been the long-standing standard for CAT due to superior efficacy over warfarin.
• DOACs in CAT
  • Select DOACs (edoxaban, rivaroxaban, apixaban) are now approved for CAT. However, they require careful patient selection due to increased bleeding risk, particularly in patients with:
    • Gastrointestinal (especially upper GI) cancers.
    • Genitourinary cancers are at risk of mucosal bleeding.
    • Thrombocytopenia (platelets <50,000/μL).
• 🏥ED Approach
  • For stable CAT patients without high bleeding risk features or severe thrombocytopenia, ED initiation of a DOAC (following renal/hepatic dosing) is reasonable and aligns with modern guidelines.
  • For patients with GI malignancies, severe thrombocytopenia, or other high-risk features, consultation with oncology or hematology and consideration of LMWH (which can be taught for self-injection) is prudent. Admission may be required for complex cases.

Concomitant Antiplatelet Therapy

Initiating anticoagulation in a patient on antiplatelet therapy is one of the most common and high-risk decisions in the ED. The combination multiplies bleeding risk, requiring a clear, indication-driven strategy. The guiding principle is that every additional antithrombotic agent must have a distinct and compelling indication.

◾️Risk Stratification and General Rule

• The bleeding risk escalates with each agent:
  • Anticoagulant alone: Baseline risk.
  • Anticoagulant + single antiplatelet (SAPT): ~1.5x increased major bleeding risk.
  • Anticoagulant + dual antiplatelet therapy (DAPT): ~2-3x increased major bleeding risk (“triple therapy”).

🏥The default ED action for a stable patient starting anticoagulation for stroke prevention (AF) or VTE treatment is to discontinue non-essential antiplatelets.

• The anticoagulant provides superior efficacy for its indication.

📊Reference: Antiplatelet Agent Profiles

• To make informed decisions, clinicians must understand the pharmacology of the antiplatelet agents their patients are taking. The following table summarizes key characteristics.

◾️ED Decision Framework by Scenario: Using the pharmacological principles above, apply the following framework:

• Scenario 1: New Anticoagulation for AF or VTE in a Patient on Chronic Antiplatelets
  • Patient on Aspirin for Primary Prevention (no history of CAD, stroke, PAD):
    • Action: Discontinue aspirin. Start anticoagulant alone.
    • Rationale: The bleeding risk of combined therapy outweighs the minimal benefit of aspirin.
  • Patient on SAPT or DAPT for Stable CAD / Secondary Prevention (>12 months from ACS/stent):
    • Action: Discontinue antiplatelet(s). Start anticoagulant alone for the new indication (AF/VTE).
    • Rationale: For stable vascular disease, the ischemic risk of stopping antiplatelets is low, while the bleeding risk of combination is high. The decision for long-term combination therapy should be deferred to cardiology.
  • Patient on DAPT for Recent Coronary Stent or ACS (Timeline is Critical):
    • < 1 month from stent/ACS: Extremely High Thrombotic Risk. Do not disrupt DAPT. Starting an anticoagulant forces “triple therapy.” This requires immediate cardiology consultation and inpatient admission.
    • 1-6 months from stent/ACS: High Thrombotic Risk. Urgent cardiology consultation is mandatory. A common strategy is to continue DAPT and delay anticoagulation unless stroke risk is exceptional. If anticoagulation is essential, admit.
    • 6-12 months from stent/ACS: Consider de-escalating to anticoagulant + single antiplatelet (usually clopidogrel). Consult cardiology. ED discharge is rarely safe.
    • >12 months from stent/ACS: DAPT is often no longer required. Transition to anticoagulant alone or anticoagulant + single antiplatelet based on outpatient cardiology assessment.
• Scenario 2: Patient on Chronic Anticoagulation Needing Antiplatelet for New ACS/Stent
  • This is typically an inpatient decision. The ED role is to recognize the conflict, start standard ACS care (which includes loading with antiplatelet(s) per the table above), and admit for coordinated management. Do not hold therapeutic anticoagulation for cardiac catheterization without cardiology consultation.

🏥Key ED Actions and Documentation

1. Accurate Medication History
   • Explicitly ask about over-the-counter aspirin, NSAIDs, and herbal supplements.
2. Indication & Timeline Clarification
   • Determine the reason and start date for every antiplatelet agent.
3. Clear Communication
   • Document the specific plan in discharge instructions (e.g., “STOP aspirin; CONTINUE clopidogrel”).
4. Consultation Rule
   • When timelines are unclear or within 12 months of a coronary event/stent, obtain cardiology consultation before discharge.

📍Conclusion: Managing anticoagulant-antiplatelet combinations requires respecting two opposing risks: thrombosis and bleeding. By using the coronary timeline as the primary guide, leveraging knowledge of antiplatelet pharmacology, and erring on the side of consultation for recent interventions, the ED provider can navigate this complexity safely. The safest approach in ambiguous outpatient scenarios is often to initiate the anticoagulant alone and facilitate rapid specialist follow-up.

Pregnancy and Postpartum Period

Pregnancy is a hypercoagulable state, but management is dictated by fetal safety and the need to avoid teratogenicity.

• First-Line Agent
  • ✅LMWH (e.g., enoxaparin) is the anticoagulant of choice throughout pregnancy and the immediate postpartum period. It does not cross the placenta and is safe for the fetus.
• DOACs and Warfarin
  • 🚫DOACs: Contraindicated in pregnancy.
    • They cross the placenta, and animal studies show fetal harm. They should also be avoided in women who are breastfeeding due to secretion into milk.
  • 🚫Warfarin: Teratogenic in the first trimester and associated with fetal bleeding/central nervous system abnormalities later in pregnancy.
    • It is typically avoided except in very select patients with mechanical heart valves.

🏥ED Approach:

1. Confirm Pregnancy
   • Perform a urine or serum β-hCG in any woman of childbearing potential before anticoagulant initiation.
2. If Anticoagulation is Indicated
   • For acute VTE or very high-risk AF (e.g., mechanical valve), initiate therapeutic LMWH in the ED. This requires patient education on self-injection or arrangement for home health nursing.
3. Coordinate Care
   • This is a high-risk scenario requiring immediate consultation with obstetrics (maternal-fetal medicine) and hematology.
   • Disposition is almost always to inpatient admission for definitive treatment planning, monitoring, and coordination of long-term prenatal care.
4. Postpartum
   • For women within 6 weeks of delivery, LMWH remains first-line.
   • Warfarin or DOACs can be considered after delivery and once the risk of postpartum hemorrhage has diminished, but this decision is made in the outpatient setting by the obstetric and hematology team.

Integration with Fibrinolytic Therapy:

Peri-Lytic Anticoagulation Management

The intersection of fibrinolytic therapy (for life-threatening thrombosis) and therapeutic anticoagulation presents one of the highest-risk pharmacologic management challenges in the ED. Decisions are bidirectional: holding anticoagulation to allow safe fibrinolysis, and restarting or initiating it afterward. Managing this transition is critical to balance thrombotic recurrence against catastrophic bleeding.

◾️Holding Anticoagulation for Fibrinolytic Administration

When a patient on therapeutic anticoagulation presents with a life- or limb-threatening thrombosis (e.g., massive PE, STEMI, acute limb ischemia) requiring immediate fibrinolysis, a deliberate pause in anticoagulation is mandatory.

• Core Principle
  • The combined hemostatic insult of full-dose anticoagulation plus systemic fibrinolysis carries an unacceptably high risk of major bleeding, particularly intracranial hemorrhage. Anticoagulation must be temporarily withheld.
• Action by Anticoagulant Class:
  • Direct Oral Anticoagulants (DOACs)
    • Hold for at least 24-48 hours prior to planned fibrinolysis, if the clinical situation permits a delay.
    • Use the agent’s half-life and patient’s renal function to guide timing (e.g., longer holds for dabigatran in renal impairment).
    • For emergent lysis, proceed but anticipate increased bleeding risk; check specific reversal agent availability (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors).
  • Vitamin K Antagonists (Warfarin)
    • Hold and reverse if INR is >1.7. For emergent lysis with an elevated INR, administer Vitamin K (5-10 mg IV) and 4-factor Prothrombin Complex Concentrate (PCC) to rapidly correct coagulation factors.
  • Parenteral Agents
    • Discontinue any heparin infusion immediately.
    • For subcutaneous Low-Molecular-Weight Heparin (LMWH), consider the time since the last dose (half-life ~4-6 hours).
    • Protamine sulfate can be given for partial reversal if the last dose was within 8 hours.
• Bridging During the Hold
  • If the thrombotic risk during the brief hold is deemed extreme (e.g., mechanical mitral valve, known left atrial appendage thrombus), bridge with a short-acting, titratable intravenous unfractionated heparin (UFH) infusion.
    • This infusion can be stopped 60 minutes prior to lytic administration, allowing for rapid offset.
• Post-Lytic Anticoagulation Resume
  • Follow the guidelines in following below section . The timing and agent for resumption depend on the original indication for anticoagulation and the success of the fibrinolysis.

📊Reference: Fibrinolytic Agent Profiles

• The pharmacological properties of the fibrinolytic agent used directly impact the timing and safety of subsequent anticoagulation.

◾️Initiating Anticoagulation After Fibrinolytic Therapy

The administration of a fibrinolytic agent creates a profound, time-limited systemic lytic state. Initiating or resuming therapeutic anticoagulation requires strict adherence to evidence-based timelines to avoid hemorrhagic complications.

• The “Fibrinolytic Milieu”
  • Characterized by depletion of fibrinogen and clotting factors, and generation of anticoagulant fibrin degradation products.
  • Bleeding risk is highest in the first 24 hours.
• Recommended Waiting Periods Before Starting/Therapeutic Anticoagulation:
  • 📍General Rule
    • Wait at least 24 hours post-fibrinolytic administration. Always confirm clinical stability and the absence of bleeding complications.
  • 🫀Post-Fibrinolysis for STEMI
    • If no concomitant anticoagulant was given, wait 24-48 hours. If therapeutic UFH/LMWH was part of the protocol, continue it and transition to oral agents only after the 24-hour mark.
  • 🧠Post-Thrombolysis for Acute Ischemic Stroke
    • Absolute minimum 24-hour wait.
    • A follow-up non-contrast head CT must be obtained at 24 hours to exclude hemorrhagic transformation before any anticoagulant is considered. For large infarcts, many neurologists prefer to wait 48-72 hours.
  • 🫁Post-Fibrinolysis for Massive PE
    • A therapeutic UFH infusion is typically started concurrently with or immediately after the lytic infusion (avoid boluses).
    • Transition to oral anticoagulation can occur once the infusion has been therapeutic for at least 24 hours and the patient is hemodynamically stable.
• Agent Choice and Dosing Post-Lysis:
  • Immediate Post-Lytic Period (24-72 hours)
    • A parenteral agent with a short half-life and reversibility (UFH) is preferred, as it allows rapid discontinuation if bleeding occurs.
  • DOAC Initiation
    • If starting a DOAC after the waiting period, consider a standard or reduced dose (e.g., apixaban 2.5 mg BID) for the first week, especially if fibrinogen levels are not fully recovered.
• Monitoring: Before initiation, check fibrinogen level, CBC, and creatinine. Avoid initiating anticoagulation if fibrinogen remains severely depressed (<100-150 mg/dL).

🏥ED-Specific Scenarios and Consultation

1. Patient Presents Post-Lysis from Transfer
   • Obtain exact time, agent, and dose of fibrinolytic. Do not restart home anticoagulation until the safe waiting period has elapsed.
2. New Indication Arises Shortly After Lysis (e.g., new AF detected)
   • Adhere to the 24-hour minimum wait. For extremely high-risk indications, consult hematology/cardiology for potential bridging with a low-dose, monitored UFH infusion.
3. Bleeding Complication
   • This is a hematologic emergency. Manage per the “Management of Bleeding Complications” section, with immediate cryoprecipitate (for fibrinogen replacement), tranexamic acid, and specialist consultation.

📍Conclusion: The peri-lytic period demands respect for the potent pharmacologic effects of both fibrinolytics and anticoagulants. A structured approach—holding anticoagulation safely before lysis, understanding the properties of the lytic used, and respecting mandatory waiting periods afterward—is essential to navigate between the Scylla of thrombosis and the Charybdis of hemorrhage.

Peri-Procedural Management

“Bridging”

A patient on anticoagulation who requires an urgent procedure (e.g., incision and drainage, pacemaker) presents a common ED challenge.

• Key Question: Does the procedure require interruption of anticoagulation?
• Low Bleeding Risk Procedures (e.g., most dental work, cataract surgery, minor dermatologic procedures)
  • Typically, DOACs do not need to be interrupted. Instruct the patient to take their dose after the procedure.
• High Bleeding Risk Procedures
  • Interruption is required. The need for “bridging” with a short-acting parenteral agent (therapeutic LMWH) depends on the patient’s thromboembolic risk.
    1. High Thromboembolic Risk (e.g., mechanical mitral valve, recent stroke/TIA, CHA₂DS₂-VASc >6, recent VTE <3 months)
       • Bridging is usually recommended.
       • This often necessitates inpatient admission for coordinated peri-procedural management.
    2. Low-Moderate Thromboembolic Risk
       • Bridging is often not beneficial and increases bleeding risk.
       • A simple instruction to hold the DOAC for 24-48 hours pre-procedure (depending on renal function) is sufficient.
       • The ED role is to provide clear written instructions and ensure follow-up with the proceduralist or PCP.

🏥ED Action: For patients requiring bridging, the ED role is to consult the relevant service (e.g., cardiology, hematology, surgery) and facilitate admission for planned management.

• Do not initiate complex bridging regimens in isolation.

Management of Bleeding Complications

◾️Despite rigorous patient selection and precautionary measures, bleeding complications will occur. It is essential to distinguish between definitions used for outcome measurement and categories used for immediate clinical triage and management, as this dictates the urgency, resources, and aggressiveness of the intervention.

• For study outcomes and quality metrics, ‘Major Bleeding’ is defined by specific criteria (e.g., ISTH: bleeding accompanied by a fall in hemoglobin of ≥2 g/dL or transfusion of ≥2 units of packed red blood cells, or bleeding in a critical site).
• For bedside clinical decision-making in the ED, bleeding severity exists on a spectrum. The most critical distinction is between major bleeding that is controlled and major bleeding that is life-threatening or potentially life-threatening. The management of these two states differs fundamentally in urgency, resource utilization, and therapeutic intervention.

📊The following table provides a rapid clinical triage guide to categorize bleeding severity and initiate the appropriate management pathway.

The table above provides the framework for triage. 👩‍⚕️The following clinical vignettes illustrate the critical distinction in practice:

• ⚠️🩸Example of Major (Non-Life-Threatening) Bleeding
  • A 70-year-old man on rivaroxaban for atrial fibrillation presents with melena. He is hemodynamically stable (BP 130/85, HR 88). His hemoglobin is 9.5 g/dL, down from 12.5 g/dL two weeks prior. He receives 2 units of packed red blood cells with a good response.
    • This meets ISTH criteria for Major Bleeding (Hb drop ≥2 g/dL and transfusion ≥2 units). Management involves admission, holding the anticoagulant, and performing an elective endoscopy the next day.
• ☠️🩸Example of Life-Threatening (Critical) Bleeding
  • The same patient presents with massive hematemesis, is pale and diaphoretic with a BP of 78/40 and HR of 130. His hemoglobin is 7.0 g/dL. He requires immediate intubation, vasopressor initiation, and activation of the massive transfusion protocol.
    • This is Life-Threatening Bleeding, a subset of Major Bleeding. Management must immediately escalate to include administration of a reversal agent (e.g., andexanet alfa or PCC) alongside resuscitation and urgent endoscopic or interventional radiology intervention.

☠️🩸Detailed Management Protocol for Life-Threatening Bleeding

◾️Once life-threatening bleeding is identified, management follows a strict, sequential protocol:

1. ABCs & Immediate Resuscitation
   • Secure the airway and ensure adequate oxygenation/ventilation.
   • Obtain large-bore intravenous access (x2) and initiate aggressive fluid resuscitation with crystalloids.
   • Transfuse blood products immediately per massive transfusion protocol: Packed Red Blood Cells (PRBCs), Fresh Frozen Plasma (FFP), and platelets.
2. Hold the Anticoagulant
   • Immediately discontinue all anticoagulant and antiplatelet medications.
3. Administer Specific Reversal Agent (if available and indicated):
   • Dabigatran
     • Idarucizumab (Praxbind®) 5g IV. (Dose: 2.5g/50ml IV x 2 consecutive infusions).
   • Apixaban, Rivaroxaban, Edoxaban:
     • Andexanet alfa (Andexxa®) for life-threatening bleeding.
       • Low-dose regimen (400 mg IV bolus, then 4 mg/min for 120 min) for last dose >7 hours ago or unknown;
       • High-dose regimen (800 mg IV bolus, then 8 mg/min for 120 min) for last dose ≤7 hours ago or if taking >10 mg/day rivaroxaban or >5 mg/day apixaban.
     • Second-line/If Andexanet Unavailable: 4-Factor Prothrombin Complex Concentrate (PCC) (25-50 units/kg, max 3000-5000 units).
   • Warfarin
     • Vitamin K (10 mg slow IV) + 4-Factor PCC (25-50 units/kg) or FFP if PCC unavailable.
   • Unfractionated Heparin (UFH)
     • Protamine sulfate (1 mg per 100 units of UFH, max 50 mg).
   • Low-Molecular-Weight Heparin (LMWH)
     • Protamine sulfate (1 mg per 1 mg of enoxaparin given in last 8 hours; 1 mg per 100 anti-Xa units of dalteparin/tinzaparin).
4. Consult Immediately: Simultaneously activate consultations with Hematology, Critical Care, and the relevant surgical or interventional radiology service (e.g., Neurosurgery for ICH, GI for uncontrolled GI bleed).
5. Identify and Treat the Source: Perform urgent imaging (e.g., CT head for ICH, CT angiography for GI bleed) to localize the source. Pursue definitive interventions (angiographic embolization, endoscopic hemostasis, surgical evacuation) as rapidly as possible.
6. Supportive Measures & Monitoring:
   • Correct coagulopathy: Re-check fibrinogen; administer cryoprecipitate if fibrinogen <150 mg/dL.
   • Consider tranexamic acid (1g IV load over 10 min, then 1g IV over 8 hours) for ongoing bleeding, especially in traumatic or surgical contexts.
   • Admit to an intensive care unit for continuous hemodynamic monitoring and serial laboratory assessments (CBC, coagulation panels, electrolytes).

📍Conclusion: A structured approach to bleeding complications, beginning with rapid severity categorization and escalating to protocol-driven reversal, resuscitation, and source control is essential to mitigate morbidity and mortality. This framework ensures that the high-risk decision to initiate anticoagulation in the ED is backed by a clear, actionable plan for managing its most serious potential adverse effect.

Summary and Implementation Guide

The emergency department is uniquely positioned to identify patients who will benefit from immediate anticoagulation and to act as the catalyst for long-term preventive therapy. By adopting the structured, evidence-based approach outlined in this guide, one that emphasizes systematic risk assessment informed by patient-specific factors (renal, hepatic, age) and pharmacologic complexities (antiplatelets, fibrinolytics), and that is supported by intentional care coordination, ED providers can safely expand this practice.

This protocol does not propose that the ED manage long-term anticoagulation. Rather, it positions the ED to responsibly initiate therapy within a system of care, ensuring the right patient gets the right drug at the right time, with a safety net firmly in place. This transforms a high-risk decision into a standardized, safe, and effective process that improves outcomes for patients at risk of stroke and thromboembolism.

Safe ED anticoagulation initiation is not merely a prescribing decision; it is the deliberate activation of a preventive care pathway.

Core Principles for ED Anticoagulation Initiation

1. Timely Intervention ⏳
   • Initiate anticoagulation immediately upon confirmation of a clear indication (e.g., new AF with CHA₂DS₂-VASc ≥2, acute VTE) and completion of a mandatory safety screen. Delaying therapy in stable patients increases stroke risk without mitigating bleeding risk.
2. Dual Risk Assessment is Non-Negotiable ⚖️
   • Document both thromboembolic risk (e.g., CHA₂DS₂-VASc for AF) and bleeding risk (e.g.,HAS-BLED,ORBIT ) before the first dose.
   • This dual assessment guides agent choice, dose, and disposition.
3. Organ Function is a Primary Decision Driver
   • Renal and hepatic function are not afterthoughts.
   • Use point-of-care testing and validated calculators (Cockcroft-Gault, Child-Pugh) to determine drug eligibility and dosing, as detailed in the accompanying tables.
4. The ED Visit is the First Link in a Chain 🖇️
   • Successful initiation requires a closed-loop system encompassing patient education, guaranteed medication access, direct provider communication, and scheduled short-term follow-up.
   • The first dose is only the beginning.

The ED Provider’s Pre-Prescription Checklist

📋A Checklist for ED Providers

Before prescribing an anticoagulant in the ED, complete this verification:

• Indication
  • A clear diagnosis requiring therapeutic anticoagulation is confirmed and documented.
• Contraindications Absent
  • Screened for active bleeding, recent ICH, severe uncontrolled HTN, and pregnancy (for DOACs).
• Risk Scores Calculated
  • CHA₂DS₂-VASc: ______; HAS-BLED/ORBIT: ______.
• Organ Function Assessed
  • CrCl = ______ mL/min; LFTs/INR reviewed; no advanced cirrhosis (Child-Pugh B/C).
• Drug Interactions Reviewed
  • Concomitant antiplatelets, NSAIDs, and other interacting medications were addressed per guidelines.
• Disposition Pathway Selected
  • 🏠Discharge Home: Stable, low-to-moderate bleeding risk, all barriers resolved.
  • 🏥ED Observation Unit: Needs short-term monitoring, testing, or barrier resolution.
  • 🏨Inpatient Admission: Unstable, high bleeding risk, or complex comorbidity (e.g., post-fibrinolytic, recent stent).
• Education Delivered & Verified
  • Verbal teach-back completed on drug name, dose, bleeding/thrombosis signs, and follow-up plan. Written materials provided.
• Medication Access Guaranteed
  • First dose given in ED and/or starter pack/dispensed prescription provided (e.g., via ED pharmacy or confirmed 24-hour pharmacy plan).
• Handoff Communicated
  • Primary care provider and/or relevant specialist notified (via call or secure message) with key details: indication, agent/dose, renal function, and follow-up plan.
• Follow-Up Secured
  • A specific appointment with a managing provider (PCP, cardiology, anticoagulation clinic) is arranged for within 3-7 days.
• Safety Net Provided
  • Patient instructed on what to do if unable to attend follow-up or if signs of bleeding occur.

✅Recommendations for Health System Implementation

For EDs and health systems establishing or refining an anticoagulation initiation protocol, the following infrastructure supports are critical:

1. Embedded Clinical Decision Support:
   • Integrate risk calculators, renal/hepatic dosing guides, and the disposition algorithm (Figure above) into the electronic health record (EHR) via standardized order sets and documentation templates.
2. Pharmacy Partnership
   • Develop a reliable process for ED dispensing of starter packs or direct coordination with a 24-hour pharmacy to eliminate the post-discharge prescription gap—a major point of failure.
3. Follow-Up Infrastructure: Establish formal, high-priority referral pathways to Anticoagulation Management Services, Cardiology, or designated primary care clinics that guarantee appointment availability within one week.
4. Multidisciplinary Education
   • Implement targeted training for ED physicians, advanced practice providers, nurses, and pharmacists on the unified protocol, with emphasis on special population management and bleeding complication response.
5. Quality Assurance & Iterative Improvement
   • Track key process measures (e.g., % of patients with calculated bleeding risk score, % with follow-up arranged) and outcome measures (e.g., 30-day major bleeding rates, 30-day stroke/VTE recurrence). Use this data for continuous protocol refinement.

Appendix

References