2. DeepVenousThrombosis
• Deep vein thrombosis (DVT) is a condition in
which a blood clot (thrombus) forms in one or
more of the deep veins in your body, usually in
your legs.
3. Blood Flow
• Superficial to deep veins
• 100-150ml blood fills in calf (Peripheral Heart)
and deep veins
• Calf contracts, valves in perforators close and
blood goes up the deep veins
• Coming up next: Pathophysiology
4. Pathophysiology
• Is a manifestation of Venous Thromboembolism
• Virchow’s triad:
• Venous Stasis
By anything obstructing or slowing flow of venous blood
• Activation of Coagulation(hypercoagulable state)
Biochemical imbalance between circulating factors
• Vein Damage
Intrinsic or Extrinsic
5. Development ofThrombosis
• Microscopic thrombus formation and dissolution is
continuous process
• Increased stasis (more microthrombi not washed away
by movement), procoagulant factors, endothelial injury,
favors coagulation more than fibrinolysis, thus a
thrombus
• Coagulation is by Intrinsic or Extrinsic pathway
7. Summary of risk factors
• A summary of risk factors is as follows:
• Age 30 year old x 30= 80 year old
• Immobilization longer than 3 days
• Pregnancy and the postpartum period
• Major surgery in previous 4 weeks
• Malignancy (abnormal coagulation, pressure,
chemotherapy)
• Long plane or car trips (> 4 hours) in previous 4
weeks
• Cancer
• Previous DVT
• Anatomical Variations
9. Summary of risk factors
• Thrombocytosis
• PICC Line> CVC
• Inherited disorders of coagulation/fibrinolysis
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Prothrombin 20210A mutation
• Factor V Leiden
• Dysfibrinogenemias and disorders of plasminogen activation
• Intravenous (IV) drug abuse
• Oral contraceptives
• Estrogens
• Heparin-induced thrombocytopenia (HIT)
10. SIGNS AND SX
• Pain
• Limb Edema
• Tenderness
• Warmth or Erythema
• Can be present or absent, unilateral or bilateral,
mild or severe
• Presentation can be of Pulmonary Embolism,
sudden coughing, haemoptysis, sharp chest pain,
rapid breathing or shortness of breath, light
headedness.
12. Physical Examination
• Homan’s sign
Calf pain on dorsiflexion of foot
Positive in less than 33% of DVT patients and
more than 50% in patients without DVT
Warning: it must be noted that it is of
little diagnostic value and is theoretically
dangerous because of the possibility of
dislodgement of loose clot
13. Physical Examination
• Warmth on area of the clot
• Tense leg
• Red or discolored skin
• The most common abnormal hue is reddish
purple from venous engorgement and
obstruction. Can be cyanotic or white.
• Signs and symptoms depending upon the cause.
16. Low pretest probabilty
• Go for a D Dimer test
• D-dimer levels remain elevated in DVT for about
7 days
• Negative value rules out in low pretest
probability
• Negative result in high pretest probability, has
no value, start anti coagulation nonetheless and
go for ultrasound.
17. Intermediate to High Pretest
Probability of DVT
• Ultrasonography is recommended
• Doppler Ultrasound can depict absent or
abnormal flow even if clot isn’t visible in normal
ultrasound.
18. Venography
• Radiography of a vein after injection of a
radiopaque fluid.
• Conclusive diagnosis historically required
invasive and expensive venography, which is still
considered the criterion standard. Since 1990,
the diagnosis has been obtained noninvasively
by means of sonographic examination.
19. CBC and Coagulation Profile
• Can look for
• Polycythemia
• Leucocytosis
• Thrombocytosis
• Low PT, APTT, hypercoaguable state
20. Further Imaging
• CT Scan and MRI if required
• Suspecting iliac vein or inferior vena caval
thrombosis
21. Who to manage inpatient
• Suspected or proven PE
• Significant CV or pulmonary comorbidity
• Ileofemoral DVT
• Contraindication to anticoagulation
• Disorder of Coagulation
• Pregnancy
• Morbid obesity 150kg+
• Renal Failure
• No compliance, far from hospital, resistance to
therapy, no close follow up.
23. Treatment
• The primary objective for the treatment of DVT
are to prevent a PULMONARY EMBOLUS.
• The mainstay of treatment is
ANTICOAGULATION
• Heparin, Vit K antagonists (Warfarin), and
Factor Xa inhibitors(Fondaparinux)
• Anticoagulation resolves immediate symptoms,
intervention is often to reduce 75%long term risk
of PTS
24. Who not to anticoagulate
• Intracranial Bleeding
• Severe Active Bleeding
• Recent brain, spinal cord, eye surgery
• Pregnancy
• Malignant hypertension
• Relative contraindications include Recent Major
surgery, recent CVA, severe Thrombocytopenia
25. Guidelines forAnticoagulation
• Admitted patients are treated with LMWH,
Unfractionated heparin (UFH), Fondaparinux.
• Warfarin 5mg PO is initiated and overlapped for
about 5 days until the INR is >2 for 24 hours.
26. Unfractionated Heparin
• Standard of care in admitted patients with DVT before
LMWH.
• Prevents extension of thrombus and reduce PE risk
• Heparin must be overlapped for 4-5 days with warfarin
till INR>2
• Because of initial transient hypercoaguable state induced
byWarfarin
27. IV heparin Protocol
• Initial bolus of 80U/kg
• Constant maintenance of 18u/kg/hr
• Half life 60-90 min
• 1ml contains 5000u
• Check the aPTT or heparin activity level 6 hrs after bolus
and adjust infusion rate accordingly
• Continue to check the aPTT or heparin every 6 hrs, until
2 successful values therapeutic
• Monitor aPTT, hematocrit, Platelets every 24 hrs (HIT)
• aPTT is 21-35 sec usually, therapeutic is 1.5 times 50+
28. LMW
H
• Clexane (Enoxaparin)
• Increased Bioavailability, prolonged Half Life.
• Treatment of choice in eligible patients.
• 1mg/kg q12 hours leading to therapeutic peak
0.5-1 iu/mL
• Antagonist?
29. Fondaparinux
• Inhibits factor Xa interrupts blood coagulation
• Generally does not increase PT or PTT
• Dose: <50kg: 5 mg SC once daily
• 50-100 kg: 7.5 Sc once daily
• >100kg 10mg SC once daily
• Patients not responding to Heparin
• Prophylaxis of DVT in patient of HIT until patient
can switch to Warfarin 2.5 mg SC daily
• Antagonist?
30. Warfarin
• Warfarin interferes with hepatic synthesis of vitamin K–
dependent coagulation factors.
• Initiate warfarin on day 1 or 2 of LMWH or
unfractionated heparin therapy and overlap until desired
INR, THEN discontinue heparin
• Start 10 mg PO for 2 days in healthy individuals, 2-5 mg
PO/IV qDay for 2 days
• Check INR after 2 days and adjust dose according to
results
• Typical maintenance dose ranges between 2 and 10
mg/day
• Maintain an INR of 2.0-3.0
31. Treatment duration
• Maintain an INR of 2.0-3.0
• Surgery-provoked DVT or PE: Treatment duration of 3 months
• Transient (reversible) risk factor-induced DVT or PE: Treatment
duration of 3 months
• First unprovoked proximal DVT or PE with low or moderate
bleeding risk: Extended treatment consideration with periodic (ie,
annual) risk-benefit analysis
• First unprovoked proximal DVT or PE with high bleeding risk:
Treatment duration of 3 months
32. Treatment duration
• First unprovoked distal DVT regardless of bleeding risk:
Treatment duration of 3 months
• Second unprovoked DVT or PE with low or moderate
bleeding risk: Extended treatment
• Second unprovoked DVT or PE with high bleeding risk:
Treatment duration of 3 months
• DVT/PE and active cancer: Extended treatment, with
periodic risk-benefit analysis (ACCP recommends
LMWH over vitamin K antagonist therapy)
33. Treatment follow up
• Regular check up on INR, around a week
• Warning signs prompting immediate contact
with doctor, stopping warfarin.
• Bleeding from any site in body.
• it is generally considered dangerous to have
an INR above 4.0. An INR above 5.0 may
require a medical dose of vitamin K to bring
the INR down to a lower level.
34. Endovascular Intervention
• Indications for intervention include the relatively rare phlegmasia
or symptomatic inferior vena cava thrombosis that responds poorly
to anticoagulation alone, or symptomatic iliofemoral or
femoropopliteal DVT in patients with a low risk of bleeding.
• The goals of endovascular therapy include reducing the severity and
duration of lower-extremity symptoms, preventing pulmonary
embolism, diminishing the risk of recurrent venous thrombosis, and
preventing postthrombotic syndrome.
35. Endovascular Intervension Procedures
• Percutaneous transcatheter treatment of
patients with deep venous thrombosis (DVT)
consists of thrombus removal with catheter-
directed thrombolysis, mechanical
thrombectomy, angioplasty, and/or stenting of
venous obstructions.
37. InferiorVenaCava Filters
• Inferior vena cava to trap emboli and minimize venous stasis.
Inferior vena cava filter is a mechanical barrier to the flow of
emboli larger than 4 mm.
• Confirmed acute proximal DVT or acute PE in patient with
contraindication for anticoagulation (this remains the most
common indication for inferior vena cava filter placement)
• Recurrent thromboembolism while on anticoagulation
• Active bleeding complications requiring termination of
anticoagulation therapy
38. • Early ambulation on day 2 after initiation of
outpatient anticoagulant therapy in addition to
effective compression is strongly recommended.
• The regular use of graduated elastic compression
stockings reduced the incidence of PTS by 50%
40. PostThrombotic Syndrome
• PTS can affect 23-60% of patients in the two years
following DVT of the leg.
• Signs and symptoms of PTS in the leg may include:
• pain (aching or cramping)
• heaviness
• itching or tingling
• swelling (edema)
• varicose veins
• brownish or reddish skin discoloration
• ulcer
41. Prevention
• prevention of initial and recurrent DVT
• early ambulation
• use of compression stockings
• Electrostimulation devices
• anticoagulant medications.
43. Treatment
• proper leg elevation
• compression therapy with elastic stockings
• wound care for leg ulcers
• angioplasty and vascular stents in proximal thrombosed
veins by an experienced physician can provide
significant relief of swelling and healing of skin ulcers
• Compression bandages are useful to treat edemas