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Surgery.(General 2).Vascular > Venous.4.CVI and CVU > Flashcards

Venous.4.CVI and CVU Flashcards

1
Q

Venous return of the L.L depends on

A

a good veno-muscular pump.

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2
Q

The veno-muscutar pump is composed of

A

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

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3
Q

Benefits of A competent veno-muscular pump

A

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

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4
Q

The ambulatory venous pressure

A
  • It’s the ankle venous pressure
    during walking
  • it should be < 25 mmHg.
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5
Q

DEFINITION OF CVI

A

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

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6
Q

ETIOLOGY of CVI

A

1ry CVI

2ry CVI “Post-phlebitic syndrome” :

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7
Q

Etiology of 1ry CVI

A

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

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8
Q

Pathogenesis of 1ry CVI

A

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

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9
Q

PATNOGENESIS of 2ry CVI

A

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.

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10
Q

CLINICAL PICTURE of CVI

A

Early & mild cases :

Late & severe cases:

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11
Q

Early & mild cases of CVI

A
  1. 2ry V.V.
  2. L.L edema :
  3. Postural discomfort & dull aching pain of the limb :
  4. Night muscular cramps.
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12
Q

L.L edema of Early & mild cases of CVI

A

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

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13
Q

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

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

* Relieved by leg elevation.

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14
Q

Late & severe cases of CVI

A
  1. Pigmentation, dermatitis, itching & eczema.
  2. Lipodermatosclerosis.
  3. Venous ulcer.
  4. Venous claudication :
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15
Q

Lipodermatosclerosis in Late & severe cases of CVI

A

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.

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16
Q

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

A

due to Lipodermatosclerosis:

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

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17
Q

Venous claudication in Late & severe cases of CVI

A

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

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18
Q

aim of INVESTIGATIONS of CVI

A
  1. Identify existence, site and degree of venous reflux

2. confirm patency of deep system

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19
Q

INVESTIGATIONS of CVI

A

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

b. Venous duplex is the gold standard investigation.

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20
Q

a bed side test for competency of SFJ.

A

Doppler

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21
Q

alternative names for Venous ulcer

A

Post-Phelbetic ulcer

Chronic venous ulceration “CVU”

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22
Q

PATHOGENESIS & THEORIES of venous ulcer

A

I- The fibrin cuff hypothesis

II- The WBC trapping hypothesis

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23
Q

The fibrin cuff hypothesis in the PATHOGENESIS of venous ulcer

A
  • 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.
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24
Q

according to the fibrin cuff hypothesis, Incompetent ankle perforators cause

A

reflux of blood from deep to superficial veins

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25
Q

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

A

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

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26
Q

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

A

medial side has 3 direct ankle perforators

lateral side has one direct ankle perforator

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27
Q

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

A

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

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28
Q

Pathogenesis of dermititis and pigmentation around the venous ulcer

A

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

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29
Q

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

A

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)

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30
Q

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

A

minor trauma

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31
Q

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

A

because of congestion & infection, so it turns chronic

Excess fibrosis makes its base and edge hard and such ulcer resists healing (indolent )

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32
Q

The WBC trapping hypothesis in the PATHOGENESIS of venous ulcer

A
  • 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.
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33
Q

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

A

leucocytes trapping & sequestration in the microcirculation of the leg.

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34
Q

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

A

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

35
Q

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

A

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

36
Q

Points to be disussed in CHARACTERS OF THE VENOUS ULCER

A 
number 
site 
size
shape
Edge
floor
Base
margin
37
Q

number of the venous ulcer

A

Single or multiple.

38
Q

site of the venous ulcer

A

At medial malleolus (ulcer-bearing area).

39
Q

size of the venous ulcer

A

Variable size

40
Q

shape of the venous ulcer

A

Circular, oval or irregular shape.

41
Q

Edge of the venous ulcer

A
  • Punched out edge.

* In healing ulcer, the edge becomes sloping.

42
Q

floor of the venous ulcer

A
  • Contains unhealthy granulation tissue.

* Purulent discharge may occur

43
Q

base of the venous ulcer

A
  • Tender.
  • Soft if recent or hard if chronic.
  • May become fixed to tibia leading to underlying periosteitis
44
Q

Margin of the venous ulcer

A
  • Shows varicosities, edema and brown pigmentation.
45
Q

in healing venous ulcer, the edge becomes

A

sloping

46
Q

soft base of the venous ulcer indicates

A

recent venous ulcer

47
Q

hard base of the venous ulcer indicates

A

chronic venous ulcer

48
Q

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

A

underlying periosteitis

49
Q

Limb examination in a case with chronic venous ulcer

A

reveals

  • All manifestations of post-phlebetic
    syndrome
  • Tender inguinal nodes.
50
Q

COMPTICATIONS OF THE VENOUS ULEER

A
  1. Infection
  2. Malignancy (Marjolin’s ulcer),
  3. Periosteitis :
  4. Bleeding occurs if a vein is eroded.
  5. Talipes equinus :
51
Q

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

A

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

52
Q

Periosteitis in venous ulcer is suspected if:

A

ulcer is fixed to tibia which is thick & tender

53
Q

Treatment of Periosteitis in venous ulcer

A

Saucerization.

54
Q

Meaning of Saucerization

A

Excavation of tissues to form a shallow shelving depression

usually performed to facilitate drainage of infected areas of bone

55
Q

Meaning of Talipes equinus

A

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

56
Q

complications of Talipes equinus

A

After some years, tendo-Achilles shortens

57
Q

Indications of investigations of venous ulcer

A

For suspected complications ( not routine )

58
Q

INVESTIGATIONS of venous ulcer

A
  1. Biopsy for suspected malignancy.

2. X-ray for suspected periosteitis

59
Q

TREATMENT OF CVI and THE VENOUS ULCER :

A

(A) Conservative:

(B) Surgical :

60
Q

Conservative TREATMENT OF CVI and THE VENOUS ULCER :

A
  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.
61
Q

Indications of Surgical TREATMENT OF CVI and THE VENOUS ULCER :

A

a. Failed conservative treatment.

b. Large or complicated ulcers.

62
Q

Modalities of Surgical TREATMENT OF CVI and THE VENOUS ULCER :

A
  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”
63
Q

Subfascial ligation of ankle perforators “Cockett & Dodd” operation.

A

This operation is not done nowadays.

It is associated with a poor healing scar & a high recurrence rate.

64
Q

Subfascial endoscopic perforator surgery “SEPS”

A

Endoscopic subfascial ligation of ankle perforators

65
Q

CEAP classification of CVI AND V.V

A

C: Class.

E: Etiology.

A: Anatomy.

P: Pathophsiology

66
Q

Class of CEAP classification of CVI AND V.V

A

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

67
Q

C1 in CEAP classification of CVI AND V.V

A

Telengiectasia or reticular veins

68
Q

C2 in CEAP classification of CVI AND V.V

A

Large sized V.V.

69
Q

C3 in CEAP classification of CVI AND V.V

A

Edema

70
Q

C4 in CEAP classification of CVI AND V.V

A

Skin changes as eczema, pigmentation & dermatitis

71
Q

C5 in CEAP classification of CVI AND V.V

A

Healed ulcer

72
Q

C6 in CEAP classification of CVI AND V.V

A

Active or unhealed ulcer

73
Q

Etiology of CEAP classification of CVI AND V.V

A

E1: Primary

E2: Secondary

74
Q

E1 in CEAP classification of CVI AND V.V

A

Primary

75
Q

E2 in CEAP classification of CVI AND V.V

A

Secondary

76
Q

Anatomy of CEAP classification of CVI AND V.V

A

A1: Deep

A2: Superficial

A3: Perforators

A4: Long & short systems

77
Q

A1 in CEAP classification of CVI AND V.V

A

Deep

78
Q

A2 in CEAP classification of CVI AND V.V

A

Superficial

79
Q

A3 in CEAP classification of CVI AND V.V

A

Perforators

80
Q

A4 in CEAP classification of CVI AND V.V

A

Long & short systems

81
Q

Pathophsiology of CEAP classification of CVI AND V.V

A

P1: Reflux

P2: Obstruction

82
Q

P1 in CEAP classification of CVI AND V.V

A

Reflux

83
Q

P2 in CEAP classification of CVI AND V.V

A

Obstruction

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

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