Venous.4.CVI and CVU

Question 1

Venous return of the L.L depends on

Answer 1

a good veno-muscular pump.

Question 2

The veno-muscutar pump is composed of

Answer 2

a. Superficial & deep veins with competent valves.
b. Competent perforating veins communicating between them.
c. Powerful limb muscles.

Question 3

Benefits of A competent veno-muscular pump

Answer 3

push the blood towards the heart & thus lowering ambulatory venous pressure “AVP.

Question 4

The ambulatory venous pressure

Answer 4

• It’s the ankle venous pressure
  during walking
• it should be < 25 mmHg.

Question 5

DEFINITION OF CVI

Answer 5

CVI collectively describes the manifestations of impaired venous drainage due to abnormal function of the venous system

Question 6

ETIOLOGY of CVI

Answer 6

1ry CVI

2ry CVI “Post-phlebitic syndrome” :

Question 7

Etiology of 1ry CVI

Answer 7

Related to structural weakness of valves
or
venous wall as in eases of 1ry V.V.

Question 8

Pathogenesis of 1ry CVI

Answer 8

Venous reflux in cases of 1ry V.V adds extra work on the veno-muscular
pump which should push this blood again to protect the micro-circulation from venous hypertension.

As long as the veno-muscular pump can cope with this extra work )> the patient remains asymptomatic.

Clinical picture of CVI will only start when the pump fails to cope with this extra work

Question 9

PATNOGENESIS of 2ry CVI

Answer 9

Recanalization of the thrombosed deep veins leaves the valves of the deep system & perforating veins incompetent leading to reflux of blood

Occurs 2-5 years after DVT.

Question 10

CLINICAL PICTURE of CVI

Answer 10

Early & mild cases :

Late & severe cases:

Question 11

Early & mild cases of CVI

Answer 11

1. 2ry V.V.
2. L.L edema :
3. Postural discomfort & dull aching pain of the limb :
4. Night muscular cramps.

Question 12

L.L edema of Early & mild cases of CVI

Answer 12

Usually at the end of the day or on prolonged standing.

Question 13

Postural discomfort & dull aching pain of the limb of Early & mild cases of CVI

Answer 13

• Usually at the end of the day or on prolonged standing.

* Relieved by leg elevation.

Question 14

Late & severe cases of CVI

Answer 14

1. Pigmentation, dermatitis, itching & eczema.
2. Lipodermatosclerosis.
3. Venous ulcer.
4. Venous claudication :

Question 15

Lipodermatosclerosis in Late & severe cases of CVI

Answer 15

Subcutaneous fat is replaced by tough fibrous tissue

Sometimes extensive fibrosis & induration often extends up to the mid calf, producing an inverted champain-bottle shape of the leg.

Question 16

inverted champain-bottle shape of the leg in Late & severe cases of CVI

Answer 16

due to Lipodermatosclerosis:

a) Subcutaneous fat is replaced by tough fibrous tissue
b) Sometimes extensive fibrosis & induration often extends up to the mid calf,

Question 17

Venous claudication in Late & severe cases of CVI

Answer 17

Patients rvith severe CVI may develop claudication or bursting pain during walking due to very high venous pressure.

Question 18

aim of INVESTIGATIONS of CVI

Answer 18

1. Identify existence, site and degree of venous reflux

2. confirm patency of deep system

Question 19

INVESTIGATIONS of CVI

Answer 19

a. Doppler : a bed side test for competency of SFJ.

b. Venous duplex is the gold standard investigation.

Question 20

a bed side test for competency of SFJ.

Answer 20

Doppler

Question 21

alternative names for Venous ulcer

Answer 21

Post-Phelbetic ulcer

Chronic venous ulceration “CVU”

Question 22

PATHOGENESIS & THEORIES of venous ulcer

Answer 22

I- The fibrin cuff hypothesis

II- The WBC trapping hypothesis

Question 23

The fibrin cuff hypothesis in the PATHOGENESIS of venous ulcer

Answer 23

• Incompetent ankle perforators cause reflux of blood from deep to superficial veins
• Maximal venous hypertension occurs at the ulcer-bearing area at the medial malleolus & the lower 1/3 of the leg & is more commonly on the medial side (3 direct ankle perforators) than on the lateral aspect (1 direct lateral ankle perforator).
• Long standing venous stasis & congestion in this area causes increased intracapillary pressure, which results in diapedesis of
  RBCs & fibrinogen in the S.C tissues.
• The RBCs disintegrate & their contained haemoglobin is converted into haemosiderin, which stains tissues brown & is responsible of the dermatitis & pigmentation.
• The fibrinogen is converted to fibrin & thus fibrosis results preventing O2 release to the cells leading to anoxia & decrease vitality of the skin at the ulcer-bearing area. (gaiter area)
• Ulceration usually occurs at the ulcer-bearing area after minor trauma
• Usually it fails to heal because of congestion & infection and turns chronic.
• Excess fibrosis makes its base and edge hard and such ulcer resists healing (indolent )
• If it heals, recurrence is common until something is done to correct reflux and venous hypertension at ankle.

Question 24

according to the fibrin cuff hypothesis, Incompetent ankle perforators cause

Answer 24

reflux of blood from deep to superficial veins

Question 25

according to the fibrin cuff hypothesis, Maximal venous hypertension occurs at

Answer 25

the ulcer-bearing area (gaiter area) at the medial malleolus & the lower 1/3 of the leg

Question 26

according to the fibrin cuff hypothesis, the reason why Maximal venous hypertension is more commonly on the medial side than on the lateral aspect

Answer 26

medial side has 3 direct ankle perforators lateral side has one direct ankle perforator

Question 27

according to the fibrin cuff hypothesis, Long standing venous stasis & congestion in the gaiter area causes

Answer 27

increased intracapillary pressure, which results in diapedesis of RBCs & fibrinogen in the S.C tissues

Question 28

Pathogenesis of dermititis and pigmentation around the venous ulcer

Answer 28

The RBCs disintegrate & their contained haemoglobin is converted into haemosiderin, which stains tissues brown & is responsible of the dermatitis & pigmentation.

Question 29

according to the fibrin cuff hypothesis, pathogenesis of decreased vitality of the skin at the ulcer bearing area

Answer 29

The fibrinogen is converted to fibrin & thus fibrosis results preventing O2 release to the cells leading to anoxia & decrease vitality of the skin at the ulcer-bearing area. (gaiter area)

Question 30

according to the fibrin cuff hypothesis, Ulceration usually occurs at the ulcer-bearing area after

Answer 30

minor trauma

Question 31

according to the fibrin cuff hypothesis, the reason why venous ulcer fails to heal

Answer 31

because of congestion & infection, so it turns chronic Excess fibrosis makes its base and edge hard and such ulcer resists healing (indolent )

Question 32

The WBC trapping hypothesis in the PATHOGENESIS of venous ulcer

Answer 32

* It has shown that venous hypertension causes leucocytes trapping & sequestration in the microcirculation of the leg. * The trapped leucocytes become activated & release proteolytic enzymes & leukotrienes that are normally used in defence against infection. * These proteolytic enrymes & leukotrienes cause injury to the capillary endothelium, C.T & skin.

Question 33

according to The WBC trapping hypothesis, It has shown that venous hypertension causes

Answer 33

leucocytes trapping & sequestration in the microcirculation of the leg.

Question 34

according to The WBC trapping hypothesis, The trapped leucocytes become activated & release

Answer 34

proteolytic enzymes & leukotrienes that are normally used in defence against infection.

Question 35

according to The WBC trapping hypothesis, These proteolytic enrymes & leukotrienes released by the trapped WBC, cause

Answer 35

injury to the capillary endothelium, C.T & skin.

Question 36

Points to be disussed in CHARACTERS OF THE VENOUS ULCER

Answer 36

``` number site size shape Edge floor Base margin ```

Question 37

number of the venous ulcer

Answer 37

Single or multiple.

Question 38

site of the venous ulcer

Answer 38

At medial malleolus (ulcer-bearing area).

Question 39

size of the venous ulcer

Answer 39

Variable size

Question 40

shape of the venous ulcer

Answer 40

Circular, oval or irregular shape.

Question 41

Edge of the venous ulcer

Answer 41

* Punched out edge. | * In healing ulcer, the edge becomes sloping.

Question 42

floor of the venous ulcer

Answer 42

* Contains unhealthy granulation tissue. | * Purulent discharge may occur

Question 43

base of the venous ulcer

Answer 43

* Tender. * Soft if recent or hard if chronic. * May become fixed to tibia leading to underlying periosteitis

Question 44

Margin of the venous ulcer

Answer 44

* Shows varicosities, edema and brown pigmentation.

Question 45

in healing venous ulcer, the edge becomes

Answer 45

sloping

Question 46

soft base of the venous ulcer indicates

Answer 46

recent venous ulcer

Question 47

hard base of the venous ulcer indicates

Answer 47

chronic venous ulcer

Question 48

if the base of the venous ulcer become fixed to tibia, this leads to

Answer 48

underlying periosteitis

Question 49

Limb examination in a case with chronic venous ulcer

Answer 49

reveals * All manifestations of post-phlebetic syndrome * Tender inguinal nodes.

Question 50

COMPTICATIONS OF THE VENOUS ULEER

Answer 50

1. Infection 2. Malignancy (Marjolin's ulcer), 3. Periosteitis : 4. Bleeding occurs if a vein is eroded. 5. Talipes equinus :

Question 51

Malignancy (Marjolin's ulcer) in venous ulcer is suspected if:

Answer 51

a. Thick raised everted edge. b. Hard base, fixed to tibia. c. Hard inguinal nodes

Question 52

Periosteitis in venous ulcer is suspected if:

Answer 52

ulcer is fixed to tibia which is thick & tender

Question 53

Treatment of Periosteitis in venous ulcer

Answer 53

Saucerization.

Question 54

Meaning of Saucerization

Answer 54

Excavation of tissues to form a shallow shelving depression usually performed to facilitate drainage of infected areas of bone

Question 55

Meaning of Talipes equinus

Answer 55

A deformity in which the foot is plantar flexed , causing he patient to walk on the toes without touching the heel Walking on toes relieves pain

Question 56

complications of Talipes equinus

Answer 56

After some years, tendo-Achilles shortens

Question 57

Indications of investigations of venous ulcer

Answer 57

For suspected complications ( not routine )

Question 58

INVESTIGATIONS of venous ulcer

Answer 58

1. Biopsy for suspected malignancy. | 2. X-ray for suspected periosteitis

Question 59

TREATMENT OF CVI and THE VENOUS ULCER :

Answer 59

(A) Conservative: (B) Surgical :

Question 60

Conservative TREATMENT OF CVI and THE VENOUS ULCER :

Answer 60

1. avoid prolonged standing & foot elevation at night. 2. Below knee elastic stocking or bandaging, 3. Regular exercise to improve the muscle pump & overcome mild venous hypertension. 4. Daily dressing with saline or EUSOL . 5. Systemic antibiotics are indicated in infected ulcers. 6. Drugs as pentoxiphylline (Trental) or prostaglandin E1 analogue. 7. There is NOTHING called venotonic drugs.

Question 61

Indications of Surgical TREATMENT OF CVI and THE VENOUS ULCER :

Answer 61

a. Failed conservative treatment. | b. Large or complicated ulcers.

Question 62

Modalities of Surgical TREATMENT OF CVI and THE VENOUS ULCER :

Answer 62

1. Excision of the ulcer & plastic skin coverage by split thickness "Thiersch" graft or by cross leg flap 2. Subfascial ligation of ankle perforators "Cockett & Dodd" operation. 3. Subfascial endoscopic perforator surgery "SEPS"

Question 63

Subfascial ligation of ankle perforators "Cockett & Dodd" operation.

Answer 63

This operation is not done nowadays. It is associated with a poor healing scar & a high recurrence rate.

Question 64

Subfascial endoscopic perforator surgery "SEPS"

Answer 64

Endoscopic subfascial ligation of ankle perforators

Question 65

CEAP classification of CVI AND V.V

Answer 65

C: Class. E: Etiology. A: Anatomy. P: Pathophsiology

Question 66

Class of CEAP classification of CVI AND V.V

Answer 66

C1: Telengiectasia or reticular veins C2: Large sized V.V. C3: Edema C4: Skin changes as eczema, pigmentation & dermatitis C5: Healed ulcer C6: Active or unhealed ulcer

Question 67

C1 in CEAP classification of CVI AND V.V

Answer 67

Telengiectasia or reticular veins

Question 68

C2 in CEAP classification of CVI AND V.V

Answer 68

Large sized V.V.

Question 69

C3 in CEAP classification of CVI AND V.V

Answer 69

Edema

Question 70

C4 in CEAP classification of CVI AND V.V

Answer 70

Skin changes as eczema, pigmentation & dermatitis

Question 71

C5 in CEAP classification of CVI AND V.V

Answer 71

Healed ulcer

Question 72

C6 in CEAP classification of CVI AND V.V

Answer 72

Active or unhealed ulcer

Question 73

Etiology of CEAP classification of CVI AND V.V

Answer 73

E1: Primary E2: Secondary

Question 74

E1 in CEAP classification of CVI AND V.V

Answer 74

Primary

Question 75

E2 in CEAP classification of CVI AND V.V

Answer 75

Secondary

Question 76

Anatomy of CEAP classification of CVI AND V.V

Answer 76

A1: Deep A2: Superficial A3: Perforators A4: Long & short systems

Question 77

A1 in CEAP classification of CVI AND V.V

Answer 77

Deep

Question 78

A2 in CEAP classification of CVI AND V.V

Answer 78

Superficial

Question 79

A3 in CEAP classification of CVI AND V.V

Answer 79

Perforators

Question 80

A4 in CEAP classification of CVI AND V.V

Answer 80

Long & short systems

Question 81

Pathophsiology of CEAP classification of CVI AND V.V

Answer 81

P1: Reflux P2: Obstruction

Question 82

P1 in CEAP classification of CVI AND V.V

Answer 82

Reflux

Question 83

P2 in CEAP classification of CVI AND V.V

Answer 83

Obstruction