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Deep Vein Thrombosis
Clinical Pearls
ADE WIJAYA, MD – DECEMBER 2018
Introduction
 Part of VTE
 Most DVT can resolve spontaneously but also can lead to fatal pulmonary embolism
Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008 Mar 6. 358(10):1037-52.
Pathophysiology
Venous
stasis
Vein
damage
Blood
coagulation
Coagulation Pathways
Epidemiology
 80 cases per 100,000 population occur annually
 1 person in 20 develops a DVT in the course of his or her lifetime
 In elderly persons, the incidence is increased four-fold
 M > F (1.2:1)
 Hispanic and Asian  lower risk
Risk Factors
Age
Immobilization longer than 3 days
Pregnancy and the postpartum period
Major surgery in previous 4 weeks
Long plane or car trips (>4 hours) in previous 4
weeks
Cancer
Previous DVT
Stroke
Acute myocardial infarction (AMI)
Congestive heart failure (CHF)
Sepsis
Nephrotic syndrome
Ulcerative colitis
Multiple trauma
CNS/spinal cord injury
Burns
Lower extremity fractures
Systemic lupus erythematosus (SLE) and the
lupus anticoagulant
Risk Factors
Prothrombin 20210A mutation
Factor V Leiden
Dysfibrinogenemias and disorders of
plasminogen activation
Intravenous (IV) drug abuse
Oral contraceptives
Estrogens
Heparin-induced thrombocytopenia (HIT)
Behçet syndrome
Homocystinuria
Polycythemia rubra vera
Thrombocytosis
Inherited disorders of coagulation/fibrinolysis
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Clinical Manifestation
Edema - Most specific symptom
Leg pain - Occurs in 50% of patients but is nonspecific
Tenderness - Occurs in 75% of patients
Warmth or erythema of the skin over the area of thrombosis
Clinical symptoms of PE as the primary manifestation
Physical Examination
Calf pain on dorsiflexion of the foot (Homans sign)
A palpable, indurated, cordlike, tender subcutaneous venous segment
Variable discoloration of the lower extremity
Blanched appearance of the leg because of edema (relatively rare)
WORKUP
Management
(In-patient Indication)
Suspected or proven concomitant PE
Significant cardiovascular or pulmonary
comorbidity
Iliofemoral DVT
Contraindications to anticoagulation
Familial or inherited disorder of coagulation:
antithrombin III (ATIII) deficiency, prothrombin
20210A, protein C or protein S deficiency, or
factor V Leiden
Familial bleeding disorder
Pregnancy
Morbid obesity (>150 kg)
Renal failure (creatinine >2 mg/dL)
Unavailable or unable to arrange close follow-
up care
Unable to follow instructions
Homeless
No contact telephone
Geographic (too far from hospital)
Patient/family resistant to outpatient therapy
Management (Inpatient)
•LMWH :
Prophylaxis: 40 mg SC qDay
Treatment: 1 mg/kg SC q12hr, OR 1.5 mg/kg SC
qDay
•Fondaparinux :
Prophylaxis: 2.5 mg SC once daily
Treatment:
<50 kg: 5 mg SC once daily
50-100 kg: 7.5 mg SC once daily
>100 kg: 10 mg SC once daily
• Unfractioned Heparin (UFH)
Prophylaxis:
5000 units SC q8-12hr, OR
7500 units SC q12hr
Treatment:
80 units/kg IV bolus, THEN continuous infusion of
18 units/kg/hr, OR
5000 units IV bolus, THEN continuous infusion of
1300 units/hr, OR
250 units/kg (alternatively, 17,500 units) SC,
THEN 250 units/kg q12hr
Management (Inpatient)
• Warfarin 5 mg PO daily is initiated and overlapped for about 5 days until the international
normalized ratio (INR) is therapeutic >2 for at least 24 hours.
• For admitted patients treated with UFH, the activated partial thromboplastin time (aPTT) or
heparin activity level must be monitored every 6 hours while the patient is taking intravenous
(IV) heparin until the dose is stabilized in the therapeutic range.
• Heparin or LMWH should be discontinued if the platelet count falls below 75,000. Fondaparinux
is not associated with hepatin-induced thrombocytopenia (HIT)
Management (Outpatient)
• Without cancer: NOAC / Warfarin
-Rivaroxaban: Prophylaxis (10 mg qDay) ; Treatment (15 mg PO q12hr for 21 days with food, THEN
20 mg PO qDay)
- Warfarin: 2 and 10 mg/day
• With cancer: LMWH
Duration of Anticoagulation
For the first episode of deep venous thrombosis (DVT), patients should be treated for 3-6
months. Recurrent episodes should be treated for at least 1 year.
Endovascular Treatment
Indication:
- Phlegmasia or symptomatic inferior vena cava thrombosis that responds poorly to
anticoagulation alone,
- Symptomatic iliofemoral or femoropopliteal DVT in patients with a low risk of bleeding.
Complication
Pulmonary embolism
Paradoxic emboli (rare)
Recurrent DVT
Postthrombotic syndrome (PTS)
Post-Thrombotic Syndrome
Vazquez SR, Freeman A, VanWoerkom RC, Rondina MT. Contemporary issues in the prevention and management of postthrombotic syndrome. Ann Pharmacother. 2009; 43: 1824–1835.
Post-Thrombotic Syndrome
Kahn SR. How I treat postthrombotic syndrome. Blood. 2009; 114: 4624–463
Post-Thrombotic Syndrome
Kahn SR. How I treat postthrombotic syndrome. Blood. 2009; 114: 4624–463
Summary
 DVT is a VTE that can lead to fatal pulmonary embolism
 Clinical suspicion  modified wells score  Ddimer  Doppler ultrasound
 Anticoagulation
 Post-thrombotic syndrome
Deep Vein Thrombosis

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Deep Vein Thrombosis

  • 1. Deep Vein Thrombosis Clinical Pearls ADE WIJAYA, MD – DECEMBER 2018
  • 2. Introduction  Part of VTE  Most DVT can resolve spontaneously but also can lead to fatal pulmonary embolism Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008 Mar 6. 358(10):1037-52.
  • 5. Epidemiology  80 cases per 100,000 population occur annually  1 person in 20 develops a DVT in the course of his or her lifetime  In elderly persons, the incidence is increased four-fold  M > F (1.2:1)  Hispanic and Asian  lower risk
  • 6. Risk Factors Age Immobilization longer than 3 days Pregnancy and the postpartum period Major surgery in previous 4 weeks Long plane or car trips (>4 hours) in previous 4 weeks Cancer Previous DVT Stroke Acute myocardial infarction (AMI) Congestive heart failure (CHF) Sepsis Nephrotic syndrome Ulcerative colitis Multiple trauma CNS/spinal cord injury Burns Lower extremity fractures Systemic lupus erythematosus (SLE) and the lupus anticoagulant
  • 7. Risk Factors Prothrombin 20210A mutation Factor V Leiden Dysfibrinogenemias and disorders of plasminogen activation Intravenous (IV) drug abuse Oral contraceptives Estrogens Heparin-induced thrombocytopenia (HIT) Behçet syndrome Homocystinuria Polycythemia rubra vera Thrombocytosis Inherited disorders of coagulation/fibrinolysis Antithrombin III deficiency Protein C deficiency Protein S deficiency
  • 8. Clinical Manifestation Edema - Most specific symptom Leg pain - Occurs in 50% of patients but is nonspecific Tenderness - Occurs in 75% of patients Warmth or erythema of the skin over the area of thrombosis Clinical symptoms of PE as the primary manifestation
  • 9. Physical Examination Calf pain on dorsiflexion of the foot (Homans sign) A palpable, indurated, cordlike, tender subcutaneous venous segment Variable discoloration of the lower extremity Blanched appearance of the leg because of edema (relatively rare)
  • 11. Management (In-patient Indication) Suspected or proven concomitant PE Significant cardiovascular or pulmonary comorbidity Iliofemoral DVT Contraindications to anticoagulation Familial or inherited disorder of coagulation: antithrombin III (ATIII) deficiency, prothrombin 20210A, protein C or protein S deficiency, or factor V Leiden Familial bleeding disorder Pregnancy Morbid obesity (>150 kg) Renal failure (creatinine >2 mg/dL) Unavailable or unable to arrange close follow- up care Unable to follow instructions Homeless No contact telephone Geographic (too far from hospital) Patient/family resistant to outpatient therapy
  • 12. Management (Inpatient) •LMWH : Prophylaxis: 40 mg SC qDay Treatment: 1 mg/kg SC q12hr, OR 1.5 mg/kg SC qDay •Fondaparinux : Prophylaxis: 2.5 mg SC once daily Treatment: <50 kg: 5 mg SC once daily 50-100 kg: 7.5 mg SC once daily >100 kg: 10 mg SC once daily • Unfractioned Heparin (UFH) Prophylaxis: 5000 units SC q8-12hr, OR 7500 units SC q12hr Treatment: 80 units/kg IV bolus, THEN continuous infusion of 18 units/kg/hr, OR 5000 units IV bolus, THEN continuous infusion of 1300 units/hr, OR 250 units/kg (alternatively, 17,500 units) SC, THEN 250 units/kg q12hr
  • 13. Management (Inpatient) • Warfarin 5 mg PO daily is initiated and overlapped for about 5 days until the international normalized ratio (INR) is therapeutic >2 for at least 24 hours. • For admitted patients treated with UFH, the activated partial thromboplastin time (aPTT) or heparin activity level must be monitored every 6 hours while the patient is taking intravenous (IV) heparin until the dose is stabilized in the therapeutic range. • Heparin or LMWH should be discontinued if the platelet count falls below 75,000. Fondaparinux is not associated with hepatin-induced thrombocytopenia (HIT)
  • 14. Management (Outpatient) • Without cancer: NOAC / Warfarin -Rivaroxaban: Prophylaxis (10 mg qDay) ; Treatment (15 mg PO q12hr for 21 days with food, THEN 20 mg PO qDay) - Warfarin: 2 and 10 mg/day • With cancer: LMWH
  • 15. Duration of Anticoagulation For the first episode of deep venous thrombosis (DVT), patients should be treated for 3-6 months. Recurrent episodes should be treated for at least 1 year.
  • 16. Endovascular Treatment Indication: - Phlegmasia or symptomatic inferior vena cava thrombosis that responds poorly to anticoagulation alone, - Symptomatic iliofemoral or femoropopliteal DVT in patients with a low risk of bleeding.
  • 17. Complication Pulmonary embolism Paradoxic emboli (rare) Recurrent DVT Postthrombotic syndrome (PTS)
  • 18. Post-Thrombotic Syndrome Vazquez SR, Freeman A, VanWoerkom RC, Rondina MT. Contemporary issues in the prevention and management of postthrombotic syndrome. Ann Pharmacother. 2009; 43: 1824–1835.
  • 19. Post-Thrombotic Syndrome Kahn SR. How I treat postthrombotic syndrome. Blood. 2009; 114: 4624–463
  • 20. Post-Thrombotic Syndrome Kahn SR. How I treat postthrombotic syndrome. Blood. 2009; 114: 4624–463
  • 21. Summary  DVT is a VTE that can lead to fatal pulmonary embolism  Clinical suspicion  modified wells score  Ddimer  Doppler ultrasound  Anticoagulation  Post-thrombotic syndrome