1. DEEP VEIN THROMBOSIS

2. DEFINITION : VENOUS THROMBOEMBOLISM Composite term for DVT &PE
The presence of thrombus with in deep veins is termed as deep vein thrombosis
It is a life threatening condition that may lead to sudden death in the short term or long term.
morbidity due to the development of post thrombotic limb and venous ulceration

5. CLASSIFICATION :
PROXIMAL DVT :thrombus formed in veins above the knee joint (femoral, iliac, popliteal)
DISTAL DVT : those formed below the knee joint (calf veins)

6. FACT
Venous thrombosis are difficult to recognize clinically. The documented cases probably represent only tip of the Ice Berg. SILENT KILLER

7. EPIDEMIOLOGY M:F 1.2:1 Age more than 40 years.
VT occur in more than 50% of patient’s having orthopaedic surgical procedures.
10 to 20% of patient with idiopathic DVT have or develop cancer.
1/3rd to 1/4th patient having proximal DVT may develop PE.
About 10% of hospital deaths attributable to PE (from DVT)

8. Calf vein - most common
Ilio femoral - most symtomatic
IVC - most lethal

9. AIR TRAVEL AND DVT
Up to 1 out of 10 air line passengers develop small asymptomatic blood clots.
Due to hypoxia and reduced cabin pressure.
VT occurs in patients regularly without any damaged to the blood vessels.

10. VTE Risk Patient Factors
Age
Previous VTE
Malignancy
Advancing age
Obesity
Prolonged immobility
Trauma
Surgery
Pregnancy/ postpartum
Indwelling central venous catheter
Deficiency of anti-thrombin III
Protein C or S
Contd...

11. Paralysis of lower limbs
Polycythaemia
Medical illness
stroke MI
CHF
pneumonia
COPD
infections
nephrotic syndrome
inflammatory bowel disease
Oral contraceptives
Varicose veins

12. Pregnancy and postpartum period.
Immobilization longer than 3 days
Major surgery in previous 4weeks
Long air or car trips >4hrs in previous 4 weeks

13. PATHO-PHYSIOLOGY VIRCHOW`S TRIAD
Predisposing Factors :
Stasis
Vascular damage
Hyper coagulability
Imbalance between thrombogenesis & thrombolytic agents

14. FATE OF THROMBUS: Propagation Embolization Dissolution
Organization & recanalization
ORGIN
DVT usually originates from veins of calf around the valve cusps or with in soleal plexus
A minority of cases occurs directly in ilio femoral veins

15. In practical terms the development of VT is best understood as activation of coagulation in areas of reduced blood flow.
Majority of calf vein thrombus dissolve completely.
Only 20% progress proximally.
Propagation occurs before embolization.

16. The process of adherence and organization of venous thrombus does not begin until 5 to 10 days after thrombus formation.
This non adherent thrombus may propagate or embolise.
Propagation or organization of venous thrombus  destruction of valves & varying degree of venous outflow obstruction  chronic venous insufficiency.

17. VTE RESULTS IN
Fatal PE
Non-fatal PE
Post-thrombotic syndrome

18. POST-PHLEBETIC SYNDROME
Consequence of recanalization of major venous thrombus
Due to incompetence of valves
Long term morbidity
Causes chronic edema &venous ulcers

19. CLINICAL FEATURES Swelling/edema most specific sign unilateral
Leg pain (50%)
non specific
Redness/erythema
over the thrombus
Tenderness(75%)
calf or along the involved veins
does not correlate size, site, extent
Low grade pyrexia
Signs and symptoms of PE

20. HOMAN`S SIGN
Pain or discomfort in leg on forceful dorsiflexion of foot with knee straight
Present only in 10% of confirmed DVT
Highly non-specific
Present in 50% of cases with out DVT
Misleading sign
No longer used

21. DIFFERENTIAL DIAGNOSIS
In approximately 70% of patients with clinically suspected DVT, alternate diagnoses are ultimately found as follows: Arthritis Cellulitis, lymphangitis Hematoma Lymphedema Muscle or soft tissue injury Neurogenic pain Postphlebitic syndrome Prolonged immobilization or limb paralysis Ruptured Baker cyst Stress fractures or other bony lesions Superficial thrombophlebitis Varicose veins

22. INVESTIGATION D- dimer level :
This cross-linked fibrin degradation product is an indication that thrombosis is occurring , and that the blood clot is being dissolved by plasmin.
D-dimer is measured by latex agglutination or by an enzyme-linked immunosorbent assay (ELISA) test that is considered positive if the level is greater than 500 ng/mL
Other blood tests
Complete blood count (CBC)
Primary coagulation studies (PT ,PTT ,Fibrinogen )
Liver Enzymes
Renal function and electrolytes .

23. Protein S, protein C, anticromin III,, antiphospholipid antibodies and homocysteine levels can be measured.
 investigations for these abnormalities are primarily indicated when DVT is diagnosed in patients younger that 35 years or when venous thrombosis is detected in unusual sites.

24. INVESTIGATION CONTRAST VENOGRAPHY DUPLEX ULTRASONOGRAPHY
IMPEDANCE PLETHYSMOGRAPHY
MRI
CONTRAST C.T.

25. TREATMENT MEDICAL TREATMENT Bed rest
Affected limb is elevated above the level of heart.
Anticoagulant prevent thrombus propagation and allow the endogenous lytic system to operate
Pain relief.

26. UNFRACTIONED HEPARIN
Initial bolus 7500 to IU followed by continuous in infusion to 1000 to IU/hr.
Infusion rate adjusted so that aPTT is approx twice the control value
Every 6 hrs aPTT monitered till therapeutic range is reached
Duration :5 days
Discontinue when platelet count <75,000

27. LOW MOLECULAR WT HEPARIN
Effective and better than conventional heparin.
Different preparations available.
Administered SC in fixed doses once or twice daily.
Duration -7 to 14 days
Anticoagulant effect by inhibiting the activated factor X.
Hemorrhagic complications doesn’t occur

28. WARFARIN To be taken along with heparin for initial 4 to5 days.
Dose adj to maintain prothrombin time at INR 2.0 to3.0
Continued for 3 to6 months for pts with acute idiopathic DVT
For recurrent DVT/PE low intensity warfarin continued indefinitely maintaining INR 1.5 to2.0

29. THROMBOLYTICS Early administration Prompt resolution of symptoms
Accelerate clot lysis
Preserve venous valves
Decrease the potential for developing post- phlebitic syndrome

30. Does not prevent clot propagation or rethrombosis.
Heparin and oral anti coagulant therapy must follow a course of thrombolysis.
Haemorraghic complications reduced by regionally administering with flouroscopic control.
Streptokinase,urokinase.

31. SURGICAL TREATMENT
Indicated when anticoagulant therapy is ineffective, unsafe or contraindicated.
Major surgical procedures : clot removal and partial interruption of IVC to prevent PE.

32. THROMBECTOMY FILTERS FOR DVT
To restore venous patency and valvular function.
Alone it is not indicated because rethrombosis is frequent.
Heparin therapy is a necessary adjunct.
Best reserved for patients with massive vein thrombosis when limb viability is at risk.
FILTERS FOR DVT
First suggested by Trousseau in 1868.
introducing intracaval devices percutaneosly and floating them into position with fluoroscopy is the procedure of choice for filter placement.

33. ACCEPTED INDICATION FOR FILTER PLACEMENT
Severe hemorrhage complications of anticoagulant therapy.
Absolute contra indications to anticoagulation.
Failure of anticoagulation such us new or recurrent VTE or PE.

34. prophylaxis - yes or no?
YES - Overall reduction in DVT and PE is by 40% to 60%

35. PROPHYLAXIS Designed to address stasis & coagulation
Usually combination of therapies
EARLY MOVT & REHABLITATION
MECHANICAL METHODS
lower extremity exercises
graded compression stockings
intermittent pneumatic compression devices

36. PREVENTION OF TRAVELER`S THROMBOSIS
Graduated compression stockings
Exercise
Avoid alcohol &sleeping tablets
HIGH RISK PATIENTS
LMWH ,single dose SC before the flight

37. DVT IN UPPER LIMB PAGET VON SCHROTTER DISEASE
Axillary and sub clavian vein thrombosis
Reduced incidence
Thoracic outlet synd &cervical ribs
Thrombolytic therapy is treatment of choice
Since restoring venous patency more important in upper limb

38. Complications
Early- Progression Pulmonary embolism Paradoxical embolism Acute compartment syndrome venous gangrene
Late Rec DVT, Post phlebitic syndrome