Coagulopathies

Coagulopathies and Venous Thromboembolic Diseases

Coagulation Mechanisms

The coagulation cascade leads to fibrin formation through enzymatic reactions. Fibrin traps platelets, stopping bleeding.

• Intrinsic      pathway: Activated by factor XII upon contact with collagen in      endothelial injury. Measured by PTT.

• Extrinsic      pathway: Initiated by tissue thromboplastin released after cell      injury. Evaluated by PT.

• Fibrinolytic      system: Plasminogen → plasmin, which degrades fibrin.

  • Tranexamic       acid inhibits fibrinolysis, reducing blood loss in orthopedic surgery       without increasing thrombosis risk.

Hemophilia

A hereditary factor deficiency causing bleeding disorders. Recurrent hemarthroses lead to joint destruction.

• Treatment:     Factor replacement, joint aspiration, splinting, physical therapy.

• Advanced      cases: Radioisotope/arthroscopic synovectomy or total knee      arthroplasty (TKA) may be required.

• Issues:     Inadequate hemostasis, HIV positivity, and central catheter use increase      infection risk.

• Surgery:     Factor levels should be raised to 100% preoperatively; 3–5 days for soft      tissue surgery, 3–4 weeks for major joint surgery. Recombinant factors are      preferred.

• Inhibitors:     Antibodies neutralizing factor VIII/IX may develop; high-dose therapy can      overcome this.

Von Willebrand Disease

A genetic coagulopathy due to vWF deficiency.

• Type      1: Mild, frequent epistaxis, gastrointestinal bleeding, menorrhagia.

• Type      2: Functional defect.

• Type      3: Severe, very rare.

• Diagnosis:     Bleeding time, factor VIII activity, vWF level, and functional assays.

• Treatment:     Desmopressin increases endothelial vWF release; severe cases require      factor VIII + vWF concentrates.

Trauma- and Surgery-Related Coagulopathies

Can develop in major trauma or prolonged surgeries.

• Management:     Fluid replacement, red blood cell transfusion, platelet and fresh frozen      plasma as guided by laboratory monitoring.

Venous Thromboembolic Disease (VTE)

Pathophysiology and Risk Factors

Deep vein thrombosis (DVT) and pulmonary embolism (PE) result from activation of the coagulation cascade and platelet aggregation.

• Virchow’s      triad: Venous stasis, endothelial injury, hypercoagulability.

• Risk:     PE rate up to 7% after hip fracture surgery; TKA has higher DVT risk,      lower PE risk compared to THA; prior VTE increases risk.

Prophylaxis

Mandatory in major orthopedic surgeries (THA, TKA, hip fracture).

• Guidelines:

  • CHEST       2012: Aspirin acceptable, LMWH preferred.

  • AAOS       2011: No specific agent recommended; pharmacologic and/or mechanical       methods can be used; routine ultrasound screening not recommended.

• Strategy:     High bleeding risk → mechanical methods; high VTE risk → pharmacologic +      mechanical combination.

Pharmacologic Methods

Drug Characteristics

Heparin(UFH)

Low efficacy, high bleeding risk, risk of HIT

LMWH

Factor Xa inhibitor, high bioavailability, long half-life;   first dose 12–24 h post-op

Fondaparinux

Synthetic pentasaccharide, Xa inhibitor; reduces DVT risk   but may increase bleeding

Warfarin

Vitamin K antagonist; target INR ~2; delayed onset

Aspirin

Low efficacy alone; reduces PE risk after TKA/THA

DOACs (Rivaroxaban, Apixaban, Dabigatran)

Oral, convenient; bleeding risk and cost are disadvantages

Diagnosis of Thromboembolic Events

• DVT:     Clinical signs nonspecific → lower extremity ultrasound or venography.

• PE:     Dyspnea, tachypnea, tachycardia, fever → CT angiography first choice; V/Q      scan, pulmonary angiography, D-dimer as adjuncts.

Treatment

• Acute:     IV heparin or LMWH first 5 days → warfarin (INR 2–3 for 3–6 months).

• Postoperative:     Dose adjustment important due to bleeding risk.

• IVC      filter: For patients who cannot receive anticoagulation; recommended      short-term use.

• Isolated      calf DVT: Usually not associated with PE; monitored with serial      ultrasound.

Conclusion

Coagulopathies and VTE have high morbidity and mortality in orthopedic practice.

• Critical      for patient safety:

  • Accurate       diagnosis

  • Appropriate       prophylaxis strategies

  • Individualized       treatment planning

References

1. Wu B, Yu W, Li D, Deng X, Pei W. NOACs for VTE prevention in patients with lower limb fracture: a systematic review and meta-analysis. J Orthop Surg Res. 2025;20:40. doi:10.1186/s13018-025-06092-5

2. Jones A, McQueenie R, McCowan C, Sutherland AG, Kwaramba T, Tho LM. Venous Thromboembolism Prophylaxis in Major Lower-Extremity Orthopaedic Procedures: A Narrative Review. J Bone Joint Surg Am. 2023;105(13):1184-1192. doi:10.2106/JBJS.22.00824