1. بسم الله الرحمن الرحيم

2. By Mohammad Ashraf Balbaa, MD Associate Professor of Surgery
Venous Thrombosis By
Mohammad Ashraf Balbaa, MD
Associate Professor of Surgery

3. Intrinsic pathway XII XIIa Extrinsic pathway XI XIa IX IXa VIIa VII X
HMW kininogen
Prekallikerin
XII
XIIa
HMW kininogen
Extrinsic pathway XI
XIa
TPL IX
IXa
VIIa
VII PL
Ca++
VIIIa
VIII PL
Ca++
TPL X Xa PL
Ca++ Va V
Prothrombin
Thrombin
Fibrinogen
Fibrin
Ca++
XIII
XIIIa

4. Definition:
A venous thrombus is the formation of a semi-solid coagulum within flowing blood in the venous system.

5. Venous Thrombosis Types: Superficial Thrombophlebitis
Deep vein thrombosis

7. SUPERFICIAL THROMBOPHLEBITIS
The term “Superficial Thrombophlebitis” is customarily applied to any kind of thrombotic process in the superficial venous system.
However, it implies existence of an inflammatory component, which is not always present.

8. SUPERFICIAL THROMBOPHLEBITIS
Definition:
Localized inflammation of the vein wall + thrombus formation in the lumen

9. SUPERFICIAL THROMBOPHLEBITIS
Etiology:
Direct trauma.
A direct blow over a superficial vein can result in phlebitis.
Venous intimal damage
Infusion of hypertonic solutions, injurious compounds as antibiotics & chemotherapeutic agents and I.V. drug abuse.
Cannula insertion.
N.B. Traumatic thrombophlebitis can be put to clinical use in the form of sclerotherapy.

10. SUPERFICIAL THROMBOPHLEBITIS

11. SUPERFICIAL THROMBOPHLEBITIS
Clinical Picture:
The vein becomes painful, tender, firm & cord-like.
The overlying skin becomes dusky & edematous.

12. SUPERFICIAL THROMBOPHLEBITIS
Clinical Picture:
Embolization is rare as the thrombus is firmly adherent
Sometimes, it is accompanied with DVT, especially if there is marked edema that can not be explained by simple or superficial phlebitis alone.

13. SUPERFICIAL THROMBOPHLEBITIS

14. SUPERFICIAL THROMBOPHLEBITIS

15. SUPERFICIAL THROMBOPHLEBITIS
Treatment:
Prevention:
The best R/ for traumatic thrombophlebitis is prevention by:
Rotating IV sites every 3 days & changing IV tubing regularly under sterile conditions
Diluting irritant infusions.

16. SUPERFICIAL THROMBOPHLEBITIS
Treatment:
Conservative Measures :
Rest & elevation + elastic bandage.
Warm compresses + non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin.  antibiotics.

17. SUPERFICIAL THROMBOPHLEBITIS
Treatment:
Surgical Measures:
If the thrombus propagates e.g. in the long saphenous vein above the knee  ligation of the sapheno-femoral junction, under local anesthesia.
Excision, in recurrent & symptomatizing phlebitis.

18. Venous Thrombosis Types: Superficial Thrombophlebitis
Deep vein thrombosis

19. Deep Vein Thrombosis Incidence: Prevalence Site Side
Occurs for the first time in about 100 persons per 100,000 each year in the United States. This incidence increases with increasing age.
The recurrence rate with anticoagulation has been noted to be 6% to 7% in the ensuing 6 months.

20. Deep Vein Thrombosis Incidence: Prevalence Site Side Upper limb:
Axillary vein thrombosis.
Lower limb:
venous plexus calf vein thrombosis.
Ilio-femoral thrombosis (phlegmasia alba dolens PAD).
Ilio-frmoral thrombosis + deep pelvic vien thrombosis (phegmasia cerulae dolans PCD).

21. Deep Vein Thrombosis Incidence: Prevalence Site Side
Ilio-femoral thrombosis occurs on the left side > right (3:1) due to:
It is more liable to be compressed by the overlying right common iliac artery against L5
Left iliac vein is longer than the right.

23. Deep Vein Thrombosis Etiology A triad (posited by Virchow in 1856):
Stasis
Intimal damage
Hypercoagulability
1821 -1902

24. Deep Vein Thrombosis Etiology A triad (posited by Virchow in 1856):
STASIS
Intimal damage
Hypercoagulability

25. Virchow Triad STASIS: Stasis in the lower limb is associated with:
Immobilization during anesthesia, after trauma and fractures, post operative recumbency & serious illness.
Diminished cardiac function (heart failure).
Previous DVT: cannot maintain uni-directional venous flow due to valvular incompetence.

26. Deep Vein Thrombosis Etiology A triad (posited by Virchow in 1856):
Stasis
INTIMAL DAMAGE
Hypercoagulability

27. Virchow Triad INTIMAL DAMAGE It caused by: Trauma & fractures.
Infusions.
Infection & toxemia.

28. Deep Vein Thrombosis Etiology A triad (posited by Virchow in 1856):
Stasis
Intimal damage
HYPERCOAGULABILITY

29. Virchow Triad HYPERCOAGULABILITY 1ry or familial causes:
Anti-thrombin III deficiency
Protein S or C deficiency

30. Virchow Triad HYPERCOAGULABILITY 2ry or acquired causes:
Malignancy, dehydration, toxemia and sepsis, polycythemia, D.M., smoking, pregnancy & post partum state.

31. Deep Vein Thrombosis RISK FACTORS Patient factors
Disease or surgical procedure
Age ≥ 60 yr
Obesity
Immobility
Pregnancy
Puerperium
High-dose estrogen therapy
Previous deep vein thrombosis or pulmonary embolism

32. Deep Vein Thrombosis RISK FACTORS Patient factors
Disease or surgical procedure
Trauma or surgery, especially of procedure pelvis, hip and lower limb
Malignancy,
Heart failure
Paralysis of lower limb(s)
Polycythaemia

33. Deep Vein Thrombosis PATHOGENESIS 1ry platelet thrombus
Mural Coralline thrombus
Occluding thrombus
Consecutive clot
Propagated clot
coralline

34. Deep Vein Thrombosis PATHOGENESIS 1ry platelet thrombus
Mural Coralline thrombus
Occluded thrombus
Consecutive clot
Propagated clot

35. Deep Vein Thrombosis
Pathophysiology

36. Pathophysiology Point of Difference Thrombophlebitis Phlebothrombosis
Major cause:
Clinical Presentation:
Size of propagated clot:
Emboli:
Inflammation of the vein wall
Pain + signs of inflammation
Short & fixed
Less liable to embolization.
Stasis & hypercoagulability
Silent  few signs & symptoms
Large & easy detachable
More liable to embolization.

37. Deep Vein Thrombosis
CONSEQUENCES OF THROMBOSIS

38. CONSEQUENCES OF THROMBOSIS
Locally
Distally
Proximally

39. CONSEQUENCES OF THROMBOSIS
LOCALLY
Lysis:
Results from fibrinolytic action of blood
Organization and fibrosis:
→ retraction  post-phlebitic leg (CVI), i.e. recanalization with valve destruction
Infection:
High virulence organisms → septic emboli.

40. CONSEQUENCES OF THROMBOSIS
Distally:
A varying degree of edema after which venous collateral circulation soon opens up  tortuous superficial veins, i.e. 2ry VV.
Phlegmasia alba and cerula.
Post-phlebetic syndrome

41. CONSEQUENCES OF THROMBOSIS
Proximally:
Detachment  pulmonary embolism  pulmonary infarction up to death.

42. Deep Vein Thrombosis
CLINICAL PICTURE

43. CLINICAL PICTURE CLINICAL PRESENTATION
DVT can be completely asymptomatic in about 30-50% of cases.
Passed unnoticed
Detectable PE, which may be sometimes fatal.
Low grade fever which fails to settle after operation.
By the occurrence of local signs of in the limb.

44. CLINICAL PICTURE
Swelling the extent of which depends on the site of the thrombus → (frog-leg position):
Leg is externally rotated
The knee is flexed)

45. CLINICAL PICTURE
Aching pain and heaviness on moving the calf and thigh.
Tenderness on pressure on the instep of the sole of the foot and along the affected veins.

46. CLINICAL PICTURE Increase warmth of the affected limb.
Varicose veins due to distension of the superficial veins (late sign).

47. CLINICAL PICTURE Certain tests: Homan's sign:
Dorsiflexion of the foot → resistance or pain of the calf muscles to forcible dorsiflexion – is not discriminatory and should be abandoned.

48. CLINICAL PICTURE Certain tests: Pratt's sign: Moses's sign:
Compression of the calf against tibia → pain.
Moses's sign:
Compression of the calf from side to side → pain.

49. CLINICAL PICTURE Phlegmasia alba (white) dolens (pain)
(White Leg; Milk Leg)
Phlegmasia cerulae (blue) dolens

50. Phlegmasia Cerulae Dolens

51. Venous gangarene

52. DEEP VEIN THROMBOSIS
COMPLICATIONS

53. COMPLICATIONS 2ry varicose veins: Venous gangrene: Pulmonary embolism:
2ry collaterals develop when the deep system is occluded.
Venous gangrene:
In PCD.
Pulmonary embolism:
When a thrombus becomes dislodged form its attachment to the venous wall & is carried into the pulmonary arteries

54. DEEP VEIN THROMBOSIS
INVESTIGATIONS:

55. INVESTIGATIONS NON INVASIVE INVESTIGATIONS Doppler Ultrasonography
Duplex Imaging
Doppler Color Flow.
Magnetic Resonance Venography (MRV)
Magnetic Resonance Venography (MRV):
It has demonstrated excellent sensitivity in the diagnosis of proximal venous thrombosis. It has the disadvantage of availability, cost, metallic implants, claustrophobia.

56. INVESTIGATIONS NON INVASIVE INVESTIGATIONS Blood Tests
Breakdown products of complexed fibrin (fibrin acted on by factor XIII) generated during physiologic fibrinolysis (D-Dimer).
A negative D-dimer test in patients with suspected DVT has a high negative predictive value. A normal D-dimer reliably excludes DVT.

57. DEEP VEIN THROMBOSIS MANAGEMENT : Prophylaxis of DVT
Treatment of established DVT
Conservative (non-operative) treatment
Operative surgical treatment

58. MANAGEMENT PROPHYLAXIS OF DVT Preoperative measures:
Mechanical prophylaxis:
Elastic compression stockings.
Intermittent pneumatic compression (IPC) devices:

59. MANAGEMENT PROPHYLAXIS OF DVT Preoperative measures:
Pharmacologic prophylaxis:
Low-dose unfractionated heparin:
5000 unites, CS, beginning 2 hours preoperatively
Low-molecular weight heparin (LMWH):
Dose is drug dependent, SC, twice daily, no monitoring or dose adjustment.

61. MANAGEMENT PROPHYLAXIS OF DVT Operative measures:
Reduction of trauma to the calf muscles during surgery; the operating table should be well padded to decrease the pressure on the buttocks, calves and heel.
Elevation and massage of the leg at the end of the operation is a good plan.

62. MANAGEMENT PROPHYLAXIS OF DVT Postoperative measures:
Early ambulation after surgery.
Maintenance of adequate hydration.
Pharmacologic prophylaxis.
Daily examination of the calves & feet for local signs of thrombosis & on suspicion or history, anticoagulants should be considered.

63. DEEP VEIN THROMBOSIS MANAGEMENT : Prophylaxis of DVT
Treatment of established DVT
Conservative (non-operative) treatment
Operative surgical treatment

64. Non-operative Treatment
Bed rest and foot elevation
Anti-coagulants
Thrombolytic (fibrinolytic) & defibrinating agents
Post treatment compression to control leg edema:

65. Anticoagulants 1. Parentral (Heparin) 2. Oral (Dendivan)
Dose and duration
,000 units/6 hours, 7 days, in calf thrombosis and for 14 days in Iliofemoral thrombosis.
Low dose MW: 1 mg/kg/12 hrs.
3 tablets/day reduced to 2 tabs, then one tab for 6 months, started before we stop heparin by 3 days (as it takes 3 days to start its action)

66. Non-operative Treatment
Bed rest and foot elevation
Anti-coagulants
Thrombolytic (fibrinolytic) & defibrinating agents
Post treatment compression to control leg edema:

67. Thrombolytic Treatment
Tissue palsmingen activators : streptokinase & human urokinase.

68. Thrombolytic Treatment
Indications:
Most effective when given to thrombi of 5-7 days duration.
For patients whose clot extends proximally beyond the origin of the deep femoral vein.

69. THANK YOU