Venous.4.CVI and CVU Flashcards
Venous return of the L.L depends on
a good veno-muscular pump.
The veno-muscutar pump is composed of
a. Superficial & deep veins with competent valves.
b. Competent perforating veins communicating between them.
c. Powerful limb muscles.
Benefits of A competent veno-muscular pump
push the blood towards the heart & thus lowering ambulatory venous pressure “AVP.
The ambulatory venous pressure
- It’s the ankle venous pressure
during walking - it should be < 25 mmHg.
DEFINITION OF CVI
CVI collectively describes the manifestations of impaired venous drainage due to abnormal function of the venous system
ETIOLOGY of CVI
1ry CVI
2ry CVI “Post-phlebitic syndrome” :
Etiology of 1ry CVI
Related to structural weakness of valves
or
venous wall as in eases of 1ry V.V.
Pathogenesis of 1ry CVI
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
PATNOGENESIS of 2ry CVI
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.
CLINICAL PICTURE of CVI
Early & mild cases :
Late & severe cases:
Early & mild cases of CVI
- 2ry V.V.
- L.L edema :
- Postural discomfort & dull aching pain of the limb :
- Night muscular cramps.
L.L edema of Early & mild cases of CVI
Usually at the end of the day or on prolonged standing.
Postural discomfort & dull aching pain of the limb of Early & mild cases of CVI
- Usually at the end of the day or on prolonged standing.
* Relieved by leg elevation.
Late & severe cases of CVI
- Pigmentation, dermatitis, itching & eczema.
- Lipodermatosclerosis.
- Venous ulcer.
- Venous claudication :
Lipodermatosclerosis in Late & severe cases of CVI
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.
inverted champain-bottle shape of the leg in Late & severe cases of CVI
due to Lipodermatosclerosis:
a) Subcutaneous fat is replaced by tough fibrous tissue
b) Sometimes extensive fibrosis & induration often extends up to the mid calf,
Venous claudication in Late & severe cases of CVI
Patients rvith severe CVI may develop claudication or bursting pain during walking due to very high venous pressure.
aim of INVESTIGATIONS of CVI
- Identify existence, site and degree of venous reflux
2. confirm patency of deep system
INVESTIGATIONS of CVI
a. Doppler : a bed side test for competency of SFJ.
b. Venous duplex is the gold standard investigation.
a bed side test for competency of SFJ.
Doppler
alternative names for Venous ulcer
Post-Phelbetic ulcer
Chronic venous ulceration “CVU”
PATHOGENESIS & THEORIES of venous ulcer
I- The fibrin cuff hypothesis
II- The WBC trapping hypothesis
The fibrin cuff hypothesis in the PATHOGENESIS of venous ulcer
- 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.
according to the fibrin cuff hypothesis, Incompetent ankle perforators cause
reflux of blood from deep to superficial veins
according to the fibrin cuff hypothesis, Maximal venous hypertension occurs at
the ulcer-bearing area (gaiter area) at the medial malleolus & the lower 1/3 of the leg
according to the fibrin cuff hypothesis, the reason why Maximal venous hypertension is more commonly on the medial side than on the lateral aspect
medial side has 3 direct ankle perforators
lateral side has one direct ankle perforator
according to the fibrin cuff hypothesis, Long standing venous stasis & congestion in the gaiter area causes
increased intracapillary pressure, which results in diapedesis of RBCs & fibrinogen in the S.C tissues
Pathogenesis of dermititis and pigmentation around the venous ulcer
The RBCs disintegrate & their contained haemoglobin is converted into haemosiderin, which stains tissues brown & is responsible of the dermatitis & pigmentation.
according to the fibrin cuff hypothesis, pathogenesis of decreased vitality of the skin at the ulcer bearing area
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)
according to the fibrin cuff hypothesis, Ulceration usually occurs at the ulcer-bearing area after
minor trauma
according to the fibrin cuff hypothesis, the reason why venous ulcer fails to heal
because of congestion & infection, so it turns chronic
Excess fibrosis makes its base and edge hard and such ulcer resists healing (indolent )
The WBC trapping hypothesis in the PATHOGENESIS of venous ulcer
- 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.
according to The WBC trapping hypothesis, It has shown that venous hypertension causes
leucocytes trapping & sequestration in the microcirculation of the leg.
according to The WBC trapping hypothesis, The trapped leucocytes become activated & release
proteolytic enzymes & leukotrienes that are normally used in defence against infection.
according to The WBC trapping hypothesis, These proteolytic enrymes & leukotrienes released by the trapped WBC, cause
injury to the capillary endothelium, C.T & skin.
Points to be disussed in CHARACTERS OF THE VENOUS ULCER
number site size shape Edge floor Base margin
number of the venous ulcer
Single or multiple.
site of the venous ulcer
At medial malleolus (ulcer-bearing area).
size of the venous ulcer
Variable size
shape of the venous ulcer
Circular, oval or irregular shape.
Edge of the venous ulcer
- Punched out edge.
* In healing ulcer, the edge becomes sloping.
floor of the venous ulcer
- Contains unhealthy granulation tissue.
* Purulent discharge may occur
base of the venous ulcer
- Tender.
- Soft if recent or hard if chronic.
- May become fixed to tibia leading to underlying periosteitis
Margin of the venous ulcer
- Shows varicosities, edema and brown pigmentation.
in healing venous ulcer, the edge becomes
sloping
soft base of the venous ulcer indicates
recent venous ulcer
hard base of the venous ulcer indicates
chronic venous ulcer
if the base of the venous ulcer become fixed to tibia, this leads to
underlying periosteitis
Limb examination in a case with chronic venous ulcer
reveals
- All manifestations of post-phlebetic
syndrome - Tender inguinal nodes.
COMPTICATIONS OF THE VENOUS ULEER
- Infection
- Malignancy (Marjolin’s ulcer),
- Periosteitis :
- Bleeding occurs if a vein is eroded.
- Talipes equinus :
Malignancy (Marjolin’s ulcer) in venous ulcer is suspected if:
a. Thick raised everted edge.
b. Hard base, fixed to tibia.
c. Hard inguinal nodes
Periosteitis in venous ulcer is suspected if:
ulcer is fixed to tibia which is thick & tender
Treatment of Periosteitis in venous ulcer
Saucerization.
Meaning of Saucerization
Excavation of tissues to form a shallow shelving depression
usually performed to facilitate drainage of infected areas of bone
Meaning of Talipes equinus
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
complications of Talipes equinus
After some years, tendo-Achilles shortens
Indications of investigations of venous ulcer
For suspected complications ( not routine )
INVESTIGATIONS of venous ulcer
- Biopsy for suspected malignancy.
2. X-ray for suspected periosteitis
TREATMENT OF CVI and THE VENOUS ULCER :
(A) Conservative:
(B) Surgical :
Conservative TREATMENT OF CVI and THE VENOUS ULCER :
- avoid prolonged standing & foot elevation at night.
- Below knee elastic stocking or bandaging,
- Regular exercise to improve the muscle pump & overcome mild venous hypertension.
- Daily dressing with saline or EUSOL
. - Systemic antibiotics are indicated in infected ulcers.
- Drugs as pentoxiphylline (Trental) or prostaglandin E1 analogue.
- There is NOTHING called venotonic drugs.
Indications of Surgical TREATMENT OF CVI and THE VENOUS ULCER :
a. Failed conservative treatment.
b. Large or complicated ulcers.
Modalities of Surgical TREATMENT OF CVI and THE VENOUS ULCER :
- Excision of the ulcer & plastic skin coverage by split thickness “Thiersch” graft or by cross leg flap
- Subfascial ligation of ankle perforators “Cockett & Dodd” operation.
- Subfascial endoscopic perforator surgery “SEPS”
Subfascial ligation of ankle perforators “Cockett & Dodd” operation.
This operation is not done nowadays.
It is associated with a poor healing scar & a high recurrence rate.
Subfascial endoscopic perforator surgery “SEPS”
Endoscopic subfascial ligation of ankle perforators
CEAP classification of CVI AND V.V
C: Class.
E: Etiology.
A: Anatomy.
P: Pathophsiology
Class of CEAP classification of CVI AND V.V
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
C1 in CEAP classification of CVI AND V.V
Telengiectasia or reticular veins
C2 in CEAP classification of CVI AND V.V
Large sized V.V.
C3 in CEAP classification of CVI AND V.V
Edema
C4 in CEAP classification of CVI AND V.V
Skin changes as eczema, pigmentation & dermatitis
C5 in CEAP classification of CVI AND V.V
Healed ulcer
C6 in CEAP classification of CVI AND V.V
Active or unhealed ulcer
Etiology of CEAP classification of CVI AND V.V
E1: Primary
E2: Secondary
E1 in CEAP classification of CVI AND V.V
Primary
E2 in CEAP classification of CVI AND V.V
Secondary
Anatomy of CEAP classification of CVI AND V.V
A1: Deep
A2: Superficial
A3: Perforators
A4: Long & short systems
A1 in CEAP classification of CVI AND V.V
Deep
A2 in CEAP classification of CVI AND V.V
Superficial
A3 in CEAP classification of CVI AND V.V
Perforators
A4 in CEAP classification of CVI AND V.V
Long & short systems
Pathophsiology of CEAP classification of CVI AND V.V
P1: Reflux
P2: Obstruction
P1 in CEAP classification of CVI AND V.V
Reflux
P2 in CEAP classification of CVI AND V.V
Obstruction
