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Surgery.(General 2).Vascular > Venous.3.Venous thrombosis > Flashcards

Venous.3.Venous thrombosis Flashcards

1
Q

Types of Venous thrombosis

A
  1. Superficial venous thrombosis.

2. Deep venous thrombosis :

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2
Q

sites of Deep venous thrombosis.

A
  • Occurring mainly in the calf or iliofemoral veins.

* Less common sites are the inferior vena cava, subclavian, axillary or portal veins.

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3
Q

Etiology of Superficial venous thrombosis.

A
  1. Varicose veins.
  2. Veins cannulated for I.V. infusion.
  3. After injection of irritant drugs, e.g. diazepam.
  4. Migrating thrombophlebitis in association with :
    a. Buerger’s disease.
    b. Visceral malignancy (it may be the earliest sign of malignancy) :Trousseau’s sign.
    c. Polycythaemia.
  5. Idiopathic.
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4
Q

Migrating thrombophlebitis occurs in

A

a. Buerger’s disease.
b. Visceral malignancy (it may be the earliest sign of malignancy) :Trousseau’s sign.
c. Polycythaemia.

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5
Q

Trousseau’s sign

A

Migrating thrombophlebitis in Visceral malignancy (it may be the earliest sign of malignancy)

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6
Q

Clinical picture of Superficial venous thrombosis.

A

l. The vein becomes red, painful and cord like.

2. There may be slight pyrexia.

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7
Q

Complication of Superficial venous thrombosis.

A

l. If infection sets in, rapid upward spread occurs with the danger of extension to the deep veins via the communicating veins
2. The thrombus is adherent to the vein wall as there is inflammation Pulmonary embolism never occurs.

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8
Q

Treatment of majority of cases of Superficial venous thrombosis.

A

l. Compression by elastic stocking.
2. Anti-inflammatory drugs. e.g. aspirin.

These are usually enough for treatment of the majority of cases.

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9
Q

Superficial venous thrombosis Treatment resorted to under special circumstances

A
  1. Antibiotics only if there is evidence of infection.
  2. Anticoagulant therapy ( heparin and warfarin ) is given in severe progressive cases (ascending thrombo-phlebitis ).
  3. Surgerv : Prophylactic sapheno-femoral or sapheno-popliteal disconnection is done if the process of thrombosis is found ascending up towards the junction with the deep system
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10
Q

Etiology of DVT

A

Virchow’s Triad:

  1. Damage to the endothelial lining of the vein wall
  2. Venous stasis

3- Hypercoagulability of blood

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11
Q

in Virchow’s Triad, Damage to the endothelial lining of the vein wall is due to:

A
  • Trauma to the vein wall, €.g. during pelvic operations.

* Inflammatory process near the vein, e.g., pelvic sepsis.

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12
Q

in Virchow’s Triad, Venous stasis is due to:

A
  • Prolonged bed confinement, long trips, or casts.
  • Congestive heart failure.
  • Venous compression by tumours, a pregnant uterus or pillows under the knees.
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13
Q

in Virchow’s Triad, Hypercoagulability of blood is due to:

A
  • Deficiency of antithrombin III, proteins S or C.
  • Polycthaemia.

’ * Postoperative dehydration

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14
Q

proteins S or C.

A

natural anticoagulant inactivates factor 5 and 8

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15
Q

PREDISPOSING FACTORS of DVT

A
  • All the factors mentioned before under Virchow’s triad.
  • Added to those are
  • Obesity.
  • Oral contraceptives intake.
  • Previous DVT.
  • Old age.
  • Malignancy.
  • Major trauma-
  • Major surgery.
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16
Q

PATHOGENESIS of DVT:

A
  1. The process usually starts in the calf venous sinuses or in iliac and femoral veins by adherence of platelets to the endothelial surface forming a grey cluster
  2. Then more platelets adhere. Fibrin and RBCs are deposited as layers in-between the platelets giving a laminated appearance Known as the lines of Zahn.
  3. When the vein is totally occluded propagated thrombus spreads up the vessel as far as the next major tributary.
  4. At this stage the thrombus is loosely attached and it can be easily detached leading to P.E.
  5. Later(After 7 -10 days), the thrombus becomes tightly adherent to the vein wall by fibrin deposition.
  6. It then organizes and contracts thus producing destruction of the valves and luminal narrowing, which are responsible for the eventual development of the post- phlebitic limb syndrome .
  7. Later on the processes of fibrinolysis and phagocytosis start & help in recanalization of the vein but the valves are permanently destroyed.
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17
Q

the reason why When the vein is totally occluded propagated thrombus spreads
up the vessel as far as the next major tributary

A

As the stasis factor is lost

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18
Q

the reason why DVT is more common on the Lt. side

A

because of the anatomical fact that the Rt. common iliac artery crosses over and compresses the Lt. common iliac vein

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19
Q

Clinical picture of DVT

A

A. Silent & asymptomatic

B- The classical picture.

C. Critical types of iliofemoral DVT

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20
Q

Silent & asymptomatic Clinical picture of DVT

A
  • Silent DVT is a frequent occurrence.
  • There are no local symptoms and the patient may present with either P.E or later with the manifestations of CVI.
  • However, it may be suspected by the presence of unexplained rise of temperature or pulse rate
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21
Q

Silent & asymptomatic Clinical picture of DVT may be suspected by

A

the presence of unexplained rise of temperature or pulse rate

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22
Q

The classical picture of DVT

A

Triad of :

  1. Pain
  2. Swelling
  3. Tenderness
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23
Q

Pain in The classical picture of DVT

A

Aching, bursting pain & tightness in the involved calf or thigh, which are aggravated by muscular exercise.

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24
Q

Swelling in The classical picture of DVT

A
  • This is the most reliable physical sign.
  • It is evidenced by Measuring the difference in the circumference between both sides.
  • In calf thrombosis the swelling is limited to the foot and ankle.
  • In femoral thrombosis the swelling involves the calf and lower part of the thigh.
  • While in ilio-femoral thrombosis there is massive swelling affecting the whole lower limb.
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25
Q

site of swelling in calf thrombosis

A

the foot and ankle

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26
Q

site of swelling in femoral thrombosis

A

the calf and lower part of the thigh

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27
Q

site of swelling ilio-femoral thrombosis

A

massive swelling affecting the whole lower limb.

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28
Q

in calf thrombosis the affected vein is

A

Popliteal or soleal venous plexus

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29
Q

Tenderness in the classical picture of DVT

A

Is present on grasping the affected calf or thigh.

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30
Q

Homan’s sign

A

Calf pain on dorsiflexion of the foot.

It is not reliable & may cause showers of P.E on application

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31
Q

Critical types of iliofemoral DVT

A
  1. Phlegmasia alba dolens :

2. Phlegmasia cerulea dolens :

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32
Q

Meaning of Phlegmasia alba dolens

A

Phlegmasia: leg

alba: white
dolens: pale

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33
Q

Meaning of Phlegmasia cerulea dolens

A

Phlegmasia: leg

Cerulae: blue

dolens: pale

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34
Q

Pathogenesis of Phlegmasia alba dolens

A

Massive iliofemoral DVT associated with severe arterial spasm or lymphangitis & so the limb becomes pale, white, and massively swollen with absent peripheral pulses, and may end in venous gangrene

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35
Q

Pathogenesis of Phlegmasia cerulea dolens

A

Very Massive iliofemoral DVT may be associated with severe congestion
and cyanosis and the whole lower limb looks massively swollen and blue and if not properly treated it may lead to venous gangrene.

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36
Q

Complications of DVT

A

A- Early cornplicadons :

  1. Pulmonary embolism.
  2. Venous gangrene ( in phlegmasia cerulea or alba dolens ) .

B- Late cornplications :
* Chronic venous insufficiency or Post-phlebitic syndrome

37
Q

INVESTIGATIONS of DVT

A
  1. Venous Duplex
  2. spiral C.T.( recently)
  3. Radioactive iodine labeled fibrinogen.
38
Q

Venous Duplex of DVT

A

It reveals no venous flow, no vein compressibility and presence of luminal echoes.

39
Q

Radioactive iodine labeled fibrinogen for DVT

A

Used in acute DVT to detect newly formed thrombi ( To detect active or chronic stage)

40
Q

D.D of DVT

A
  • Cellulitis.
  • Contusion of calf muscles
  • Calf haematoma
  • Rupture of plantaris tendon.
  • Ruptured Baker’s cyst
41
Q

Treatment of DVT

A
  1. Prevention of DVT

2. Management of DVT

42
Q

Prevention of DVT

A

Prevention of postoperative DVT is better than cure.

  1. Pre-operative measures:
    * Elastic stocking support especially in the elderly
  2. lntra-operatiue measures:
    * Intra-operative intermittent pneumatic external calf compression
  3. Postoperative measures:
  4. Early ambulation after operations
  5. Active leg exercises while in bed
  6. Adequate postoperative hydration
  7. LMWH is given pre-operative for high risk cases:
  • History of DVT or pulmonary embolism
  • Major surgery, particularly cancer operations.
  • Pelvic surgery
  • Females on contraceptive Pills
  • Elderly patients
  • Obesity
43
Q

The objectives of treatment of DVT

A
  • Prevention of formation of newly thrombi.
  • Prevention of pulmonary embolization.
  • To minimize venous valves damage.
44
Q

Management of DVT

A

1- Red rest and elevation of the lower limb:

2 - Anticoagulant therapy :

3- Thrombolytic therapy

4- Operative treatment :

45
Q

Red rest and elevation of the lower limb in management of DVT

A
  • The patient should be confined to bed with the feet elevated 15-20 degrees above the level of the heart.
  • Elevation reduces edema and pain and increases venous return thus preventing further thrombosis.
  • Thrombi usually take 7-10 days to become adherent to the vein will, the patient should be kept in bed for this period
46
Q

Anticoagulant therapy of DVT :

A

A. Heparin

B. LMWH

C. oral anticoagulant( warfarin)

47
Q

The Classic treatment (in mcq) of DVT is

A

Heparin

48
Q

Alternative name for heparin

A

Unfractionated heparin

49
Q

on talking about heparin as a treatment for DVT we should discuss the following points

A
  1. Mode of action:
  2. Dose
  3. onset of action
  4. Duration of action
  5. Duration of therapy
  6. Methods of administration
  7. follow up
  8. complications
  9. antidote
50
Q

Mode of action of heparin

A
  • Enhances the activity of the naturally occurring antihrombin III.
  • The anti-thrombin Ill-heparin complex neutralizes the effect of thrombin.
  • Neutralizes factors IX, X, and XI.
51
Q

Dose of heparin of heparin

A

50-100 I.U / Kg / 4 hours ( i.e 5000 l.U / 4 hours ).

52
Q

onset of action of heparin

A

Immediately.

53
Q

Duration of action of heparin

A

4 hours

54
Q

Duration of therapy of heparin

A

a. Heparin is given until all signs of active thrombosis subside which is clinically known by disappearance of pain & tenderness.
b. This usually takes 7-10 day

55
Q

Methods of administration of heparin

A

a. Continuous IV infusion. This is the ideal method, but requires hospitalization and a pump which controls the dose.
b. Bolus therapy 5000 IU are administered I.V every 4 hours.

56
Q

follow up of heparin

A

a. Partial thromboplastin tirne (PTT): Test for intrinsic pathway
b. Normal value : 30-40 sec.
c. It should be 2 times normal value.

57
Q

complications of heparin

A

a. Bleeding due to over dosage usually manifests by subcutaneous bruises epistaxis, bleeding gums, hematuria, or gastro-intestinal bleeding.
b. Idiosyncratic thrombocytopenia “HlT”.

58
Q

Antidote of heparin

A

Protamine sulfate, each 1 mg neutralizes 100 I.U of heparin.

59
Q

Meaning of Idiosyncratic

A

Not dose dependent

60
Q

HIT stands for

A

Heparin induced thrombocytopenia

61
Q

Alternative name for LMWH

A

Fractionated heparin

62
Q

on talking about LMWH as a treatment for DVT we should discuss the following points

A
  1. Mode of action:
  2. Dose
  3. onset of action
  4. Duration of action
  5. Duration of therapy
  6. Methods of administration
  7. follow up
  8. complications
63
Q

Mode of action of LMWH

A

Anti factor X.

64
Q

Dose of LMWH

A

1 mg/kg/12hr

65
Q

onset of action of LMWH

A

After 1 hour

66
Q

Duration of action of LMWH

A

12 hours

67
Q

Duration of therapy of LMWH

A

as heparin :

a. given until all signs of active thrombosis subside which is clinically known by disappearance of pain & tenderness.
b. This usually takes 7-10 day

68
Q

Methods of administration of LMWH

A

Subcutaneous injection.

69
Q

follow up of LMWH

A
  • Activated factor X.

* Usually this dose not require tests for adjustment.

70
Q

complications of LMWH

A

Incidence of bleeding with LMW heparin is less than heparin

71
Q

on talking about oral anticoagulant( warfarin) as a treatment for DVT we should discuss the following points

A
  1. Mode of action:
  2. Dose
  3. onset of action
  4. Duration of therapy
  5. Methods of administration
  6. follow up
  7. complications
72
Q

Mode of action of warfarin

A

These drugs block the synthesis of at least 4 vitamin K dependent clotting factors (Prothrombin and factors VII, IX and X).

73
Q

Dose of warfarin

A

5 mg daily dose.

74
Q

onset of action of warfarin

A
  • After 48-72 hours.

* Discontinue heparin after 3 days of overlap treatment

75
Q

Duration of therapy of warfarin

A

For 3-6 months which is the time needed for recanalization & collateralation as evidenced by duplex .

  • In high risk patients, warfarin is given indefinitely
76
Q

Methods of administration of warfarin

A

oral

77
Q

follow up of warfarin

A
  1. Prothrombin time ( PT ) :
    * Normal value : 11-14 sec.
    * It should be 2 times normal value.
    * It should be done every 2 weeks during the course of TTT.
  2. INR :
    * Normal value : 0.8-1.2
    * It should be 2 - 3.
    * INR should be done every 2 weeks during the course of TTT”
78
Q

complications of warfarin

A
  1. Bleeding is the main problem & is treated by lowering the dose & in severe cases 10-20 mg vitamin K IV injection is given.
  2. Interaction may occur between oral anticoagulants and other drugs like aspirin and other NSAIDs, barbiturates or H2 blockers ) thus lead to an increase in this anticoagulant effect.
  3. Teratogenic.
79
Q

in severe cases of bleeding of a case on warfarin we give

A

10-20 mg vitamin K IV injection

80
Q

Thrombolytic therapy in treatment of DVT

A

Fibrinolytic activators dissolve fresh thrombi and produce rapid clearance of the occluded veins and may preserve the competence
and function of venous valves better than anticoagulant therapy

81
Q

Examples of fibrinolytic activators include

A
  • Streptokinase.
  • Urokinase.
  • Tissue plasrninogen activator ( TPA ) which is prepared by recombinant gene technology.
82
Q

Indications of Thrombolytic therapy in treatment of DVT

A

a. Must be given in the first 24 hours.

b. Massive ilio-femoral DVT

83
Q

Absolute Contraindications of Thrombolytic therapy in treatment of DVT

A
  • Active GIT bleeding or recent bleeding within previous 10 days.
  • History of Cerebro-vascular stroke within previous 2 months.
  • Intracranial trauma or neurosurgery operation rvithin previous 3 months
84
Q

Relative Contraindications of Thrombolytic therapy in treatment of DVT

A
  • Cardio-pulmonary resuscitation within previous 10 days.
  • Malor surgery’or trauma within previous 10 days.
  • Uncontrolled hypertension
  • After 24 hours.
  • History of allergic reactions, so it is better to give corticosteroids prior to thrombolytic drugs.
85
Q

Operative treatment of DVT

A

a. Venous thrombectomy :

b. Insertion of vena cava filter “Greenfield fitter”.

86
Q

Venous thrombectomy in Operative treatment of DVT

A

Using Fogarty venous catheter is most likely to be successful if it is performed within the first 24 hours

87
Q

indications of Venous thrombectomy in Operative treatment of DVT

A

Massive iliofemoral thrombosis as

phlegmasia cerulea or alba dolens

88
Q

indications of Insertion of vena cava filter “Greenfield fitter” in Operative treatment of DVT

A

Absolute:

  1. Recurrent showers of P.E inspite of adequate heparinization ( PTT is 100 ).
  2. DVT with contraindication to heparin.

Relative:
3- Recent DVT before major surgery(Like fracture neck of femur)
4. High risk patient (e.g cardiac) with DVT.

Surgery.(General 2).Vascular (16 decks)

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