Thromboprophylaxis

1. DVT Treatment and
Prophylaxis

2. Definition
DVT is clotting of blood in deep vein of extremity (usually
calf/thigh) or the pelvis.
DVT occurs most commonly in lower extremity or pelvis.
It can also develop in deep veins of upper extremity( 4 to 13% of all
DVT cases).

3. Background:
 It is a common, yet preventable perioperative complication.
 Highest risk in critical care and spinal cord injury patients- 60-80%
 Post- Ortho Procedures: 40-60%
 Post-General Surgery/ Obstetric- 15-40%
 Variable for Urologic Cases

4. Virchow’s triad

5. Etiology

7. Sites :
Ileo-femoral veins (80% )
Popliteal veins
Calf veins(extending proximally
in 30% cases)
Inferior Vena Cava(rarely)
deep veins of upper extremity( 4
to 13% ).

8. Signs and symptoms
DVT may occur in ambulatory patients or as a complication of surgery or major
medical illness.
Among high-risk hospitalized patients, most deep vein thrombi occur in the
small calf veins, are asymptomatic, and may not be detected.
Only 40 percent of patients with venous thrombosis have any clinical signs of
the disorder

9. Clinical features
 Tenderness occurs in 75% confined to the calf muscles or over the
course of the deep veins in the thigh.
 Many patients are asymptomatic.
 Pedal Edema, principally unilateral, is the most specific symptom

10. • Leg pain (50%) & tenderness
• Pain can occur on dorsiflexion of the foot (Homan’s sign)
• Warmthor erythema of skin Can be present
• Moses sign- tenderness elicited by squeezing or pressing firmly on
sole of foot or calf.

13. Diagnosis:
History &clinical features
Physicalexamination(workup)
Probability scoring (well’sscore)
Blood test
D-dimer test
Other blood test
Imaging study
MRI , U/S, venography

16. Management
AIM---
To prevent clot spreading up the vein
To prevent large embolus breaking off producing PE
To reduce risk of future DVT
To reduce mortaliy and morbidity

17. Management
General supportive measures include pain control with analgesics,
which may include short (3- to 5day) courses of an NSAID.
Extended treatment with NSAID’s should be avoided because their
antiplatelet effects may increase the risk of bleeding complications.
elevation of legs (supported by a pillow or other soft surface to
avoid venous compression) is recommended during periods of
inactivity.

18. Mechanical prophylaxis
 Several methods are available:
 Pneumatic compression
 Graduated compression stockings alone or in combination with
pharmacological prophylaxis in high-risk patients

19. Mechanism & effects:
• MECHANISM: The pump provides intermittent cycles of compressed
air which alternately inflate and deflate the chamber garments.
•Effects :
Increases venous return
Decreases venous stasis
Stimulates fibrinolytic activity which causes dissolution of clot and
prevention of thrombus formation

22. Anticoagulants

23. Classification
Anticoagulants and thrombolytics
are commonly used for
prophylaxis and treatment of DVT.
Antiplatelet drugs are more
commonly used in patients with
coronary artery disease, PVD,CVA
& other ischemic conditions to
prevent formation of localized
thrombus

24. Coagulation cascade

25.  Heparin needs to interact with both ATIII and
Thrombin (IIa)
 To enhance its effect on Factor Xa, heparin
needs only to interact with ATIII
 LMWH can only increase the action of ATIII on
Factor Xa and not on thrombin (IIa).
Heparin
ATIII IIa
Heparin
ATIII Xa
LMWH
ATIII Xa
Mechanism of action

26. Pharmacological actions
Anticoagulant:
Powerful anticoagulant both in vivo and vitro
Low concentrations affect intrinstic pathway and high concentrations affect both
pathways.
Antiplatelet:
In higher doses inhibits platelet aggregation and prolongs bleeding time.
Lipaemia clearing:
It clears turbid post-prandial lipaemic plasma by releasing lipoprotein lipase
from vessel wall when injected.

27. Adverse effects
Bleeding in most serious complication due to overdose. haematuria
is the first sign.
Thrombocytopenia (mild and transient)
Alopecia (transient and reversible)
Osteoporosis in long term use.
Hypersensitivity reactions(rare)

28. Contraindications
History of bleeding disorders
Severe hypertension, threatened abortion, piles, G.I. ulcers
Subacute bacterial endocarditis
Ocular, neurosurgery, lumbar puncture
Hepatic and renal diseases.
Aneurysms

29. Dose
 DVT Prophylaxis dose -5,000 USC Q8-12H , aPTT monitoring
not needed
 Therapeutic Dosing I /v Bolus (80U/Kg) + I /v continuous infusion
(18U/Kg/hr), aPTT monitoring is needed in case of prolonged IV
infusion

30. Monitoring
 aPTT - [ normalvalue- 33 to 35 sec] measurement which is kept at
50-80 sec or 1.5-2.5 times the patient’s pretreatment value.
 If not available whole blood clotting time should be measured and
kept at 2 times the normal value.
 After a constant maintenance infusion of 18 U/kg is initiated, the aPTT
is checked 6 hours after the bolus and adjusted accordingly.
 The aPTT is repeated every 6 hours until 2 successive aPTT’s are
therapeutic.
 Thereafter, the aPTT is monitored every 24 hours as well as the
hematocrit and platelet count.

31. Low molecular weight (LMH) Heparin
Heparin is fractionated into LMW forms ( 3000-7000 MW).
Selectively inhibits factor Xa with little effect on factor IIa.( shown
earlier)
Lower incidence of hemorrhagic tendencies and thrombocytopenia
Better bioavailibility (70-90%)
Longer acting (t ½ 4-6 hours)
Laboratory monitoring not needed.
Low risk of osteoporosis in long term.

32. Fondaparinux
 Synthetic pentasaccharide structurally similar to Heparin
 Selective Factor Xa Inhibitor
 Monitoring of factor Xa levels similar to LMWH (renal
dysfunction)
 Dosing -FONDAPARINUX7.5 mg SC daily
 Half- life- 18 to 20 hours.

33. LMWH Treatment dose Prophylactic dose
Dalteparin(Fragmin) 100units/kg sc 12 hourly or
200 units/kg once a day
2500–5000 units once/day
Enoxaparin
(Clexane/Loparin)
1mg/kg sc 12 hourly or
1.5mg/kg once a day
After abdominal surgery: 40 mg
sc once/day
After hip or knee replacement
surgery:
30mg sc 12 hourly
For unstable angina or non-Q
wave MI:
1mg/kg sc 12 hourly
For other patients not
undergoing surgery:
40 mg sc once/day
Tinzaparin 175units/kg sc once/day 3500 units once/day
Dose regimen

34. Protamine Sulfate
Heparin antagonist
Dose: 1mg i.v. per 100 u of heparin.
Commonly used to terminate action of heparin rapidly eg. After
cardiac and vascular surgery.

35. Warfarin:
 Dose- starts from 5 mg PO daily.It is available in various doses of 1mg,
2mg…
 Acts by inhibiting Vitamin Kreductase enzyme, thereby depleting Vitamin
Kdependent clotting factors II, VII, IX and X.
 Good oral absorption but requires 4-5 days to achieve full
anticoagulant effect
 Combine with parenteral till INR reaches at least 2-2.5
 Monitor INR twice weekly for first 2 weeks, then weekly for 2 weeks, then
less frequently
 Reversal of action- Vitamin K, FFP &prothrombin concentrates

37. OTHERUSES
OF WARFARIN:

38. Recommended INR:
 Prophylaxis of DVT- 2- 2.5
 Treatmentof DVT -2– 3
 Recurrent VTE,MI, prosthetic heart valve disease- 3-3.5

40. Neweranticoagulants:
 DABIGATRAN: It is a direct thrombin inhibitor..
 RIVAROXABAN: It inhibits activated factor Xa.
 They have been approved for treatment of venous
thromboembolism[VTE] and pulmonary embolism[PE].

42. Algorithm

43. Alternative therapies

44. IVC Filter:
INDICATIONS OF PLACEMENT:
 Severe haemorrhagic complications due to use of oral
anticoagulants
 Absolute contraindications to use of oral drugs
 Failure of oral anticoagulant therapy such as new or
recurrent venous thrombosis

46. Surgery:
INDICATIONS:
 Anticoagulant therapy is ineffective
 Unsafe
Contraindications
The major surgical procedures for DVT are clot removal and partial
interruption of the inferior vena cava to prevent pulmonary embolism

47. Summary
 If you deal with the risk factor early,DVT can be prevented early
 Early detection &diagnosis can prevent complications
 DVT is 2nd cause of death in pregnancy
 Well’s score& D-dimer and use of U/S can diagnose DVT
 PE& post thrombotic syndrome is the most common
and fatal complication

48. Thank You.