Chronic Venous Disorders

Vascular surgery unit

Amr Albayomy
Senior Registrar Vascular Surgery
Venous Disorders
Disorders of the venous system can be divided into thrombotic disease and venous
insufficiency

Thrombotic disease of the veins can lead to venous insufficiency

Venous insufficiency can be mildly symptomatic varicose veins to severe chronic

venous insufficiency (CVI) with ulceration

8/12/22
Chronic venous insufficiency (CVI )
Definition:
CVI is disease of the lower limb veins in which venous return is impaired usually
over years , by reflux , obstruction or calf muscle pump failure

This leads to sustained venous hypertension and ultimately clinical complications

including VV , edema, eczema, lipodermatosclerosis and ulceration

8/12/22
Signs & Symptoms
 Poor cosmesis.
 Itching and dull aching,
burning, pressure pain
 Lower limb edema
 Erythema and skin
color changes
 Lipodermatosclerosis
 Varicose vein
 Venous stasis ulcers

8/12/22
Causes of venous hypertension :
A- Superficial venous reflux
-GSV reflux
-SSV reflux
B- Deep venous reflux and occlusion
-1ry ( idiopathic )
-2ry go DVT or injury
C- Perforating vein reflux
D- Abnormal calf pump
-Neurological
-Musculoskeletal
E- Combination of the above
8/12/22
Etiology
To understand CVI , one must consider the changes that occur on both the larger veins
( macrocirculation ) and the capillary bed ( microcirculation )

8/12/22
Macrocirculation
During exercise in the normal individual effective contraction of calf muscles combined with vein
patency and valvular competence aids venous return and reduces venous pressure in the lower
leg from about 90 mmHg to 30 mmHg

Failure of any of these mechanisms may result in post-ambulatory venous hypertension which
lead to CVI

8/12/22
 The ambulatory venous pressure

 is defined as end-exercise venous pressure at the ankle less than 30mmHg ( normal is 15 -30
mmHg )

 At pressure less 30 mmHg, ulceration is rare, while at pressure 90 mmHg, there is nearly 100%
incidence of ulceration.

8/12/22
Microcirculation :
The pathology in CVI is still not fully understood and the best explained by:
A- White cell trapping hypothesis
B- Fibrin cuff hypothesis
C- A possible explanation lies with matrix metalloproteinases

8/12/22
A- White cell trapping hypothesis :

Increase venous pressure across the capillary bed ,

so white cell plug the capillaries , adherence of white
cells to the endothelium is then stimulated

The trapped white cells release proteolytic enzymes

and O2 free radicals , causing endothelial and tissue
damage

This increase microvascular permeability , which may

explain the presence of Fibrin cuff, and also produces
excessive amount of nitric oxide . This in turn
damages the tissue .

8/12/22
B- Fibrin cuff hypothesis:

A rise in venous pressure causes capillary elongation and widening of the pores between the
endothelial cells , this results in passage of larger molecules out of the intravascular
compartment into the tissue .

Fibrinogen is deposited and polymerises to form fibrin . This may act as a barrier to O2 , resulting
in local tissue ischemia and cell death producing ulceration .

8/12/22
c- A possible explanation lies with matrix metalloproteinases:

These enzyme help remodel the extracellular matrix by protein degeneration, and enhanced MMPs
activity has been demonstrated in lipodermatosclerosis .

An imbalance in matrix turnover then exsits, leading to degradation and ulceration

8/12/22
Clinical features :
1- swelling : due to odema fluid , which is initially pitting , then fibrosis and induration occur .
2- skin changes : varicose eczema common as dry , scaly and itchy skin .
Skin become friable with pigmentation due to deposition of haemosiderin in the tissue , produces a
brown discoloration which together with fibrosis lead to lipodermatosclerosis.

8/12/22
 3-ulceration : it occur predominantly on the lower leg on the medial aspect . these are usually
surrounded by eczema or pigmentation and exude fluid that can cause maceration of the
surrounding skin.

8/12/22
4- varicose veins.

5- pain : patient complain of a general ache and heaviness in the leg of long periods of standing .
this is worse towards the end of the day but improve with elevation .

8/12/22
CEAP classification of severity & etiology of lower
venous disease

 CEAP Classification (1996):

– C = Class ( Clinical ) (0-6)
– E = Etiology (congenital, 1ry, 2ry)
– A = Anatomy (Superficial, Deep, perforators)
– P = Pathology (Reflux, Obstruction, both)

8/12/22
( C ) Class (Clinical)
 (C) Class
 Class 1

 Class 2

 Class 3

 Class 4

 Class 5

 Class 6

8/12/22
(E) Etiology

 Congenital
 Primary
 Secondary

8/12/22
 Congenital
– Valvular aplasia or dysplasia.

8/12/22
 Primary
– Structural abnormality in the wall or valve.
– Valve is redundant & have tendency to evert.

 Secondary
– Post-thrombotic.

8/12/22
(A) Anatomy (P) Pathology

 Superficial  Reflux

 Deep  Obstruction
 Perforators
 Both

8/12/22
INVESTIGATIONS

:Duplex ultrasound

gold standard for assessing

venous competence, allows
measurement of flow through valves
and identification of sources of
venous reflux & provides functional
.as well as anatomical information

8/12/22
 Magnetic Resonance Venography

8/12/22
 Contrast Venography
 Venography:
– Ascending
– Descending

 Used to detect:
– Obstruction
– Incompetence: - Deep
- Superficial
- perforators

8/12/22
Management
 Non-operative
 Leg elevation.
 Exercises.
 Compression stockings.
 Unna boots.
 Pharmacological.

8/12/22
 Operative Management
 Indications:
– Failure if conservative treatment in class 4 or above.
– Cannot tolerate conservative treatment.
– Massive reflux.

 Contraindication:
– Painless swelling without skin changes.

8/12/22
Deep Veins Valve incompetence
Valvoplasty

Or Valve transfer

8/12/22
Deep Vein Obstruction
Bypass graft Venoplasty by
 Synthetic endovascular
techniques
 Saphenous

8/12/22
varicose veins

 Definition:

superficial vein showing elongation , dilatation and , tortuosity (sacculation) and more than 3mm
diameter.
 

8/12/22
Pathophysiology:
VVs are always due to superficial venous reflex which is due to:
1- primary valve failure: primary degenerative changes in the valve annulus and leaflets.
2- secondary valve failure: developmental weakness in the vein wall leads to 2ry widening of the
valve commissars and incompetence.
 
● It's likely that both mechanisms are involved in different Pt's .
 
  

8/12/22
classify VVs
: Primary
.Unknown cause ; often familial & probably a weakness of vein walls

: Secondary
Obstruction to venous outflow :
Pregnancy
Ovarian cyst
Retroperitoneal fibrosis
Pelvic cancer
Valve destruction : DVT
High flow & pressure : AVM

8/12/22
Risk Factors : 1ry VV
A number of these factors are believed to mediate ther effects through increase LLs hydrostatic
pressure directly or through an increase in intra-abdominal pressure with resultant compromise
in blood return to the iliac veins.

 Heredity: the genetics of vvs is not understood

 Age
 Gender
 Occupation (( prolonged standing with strong evidence))

8/12/22
Obesity : A BMI of greater than 30 kg/m2 carries of five fold increase in the prevalence of vvs
mainly in women.

Pregnancy: Although the enlarging uterus is believed to obstruct venous return & contribute to the
formation of vvs , most women report an increase in vvs during their 1st trimester , when the gravid
uterus is not yet large enough to cause mechanical obstruction .The role of estrogen on smooth
muscle relaxation has been well described.
Women with multiple pregnancies also appear to have a higher prevalence of vvs.

Hormones ((oral contraceptive or hormone replacement therapy))

8/12/22
Types of varicose vein :
1) primary trunk VVs :
These are derived from GSF, SSV and \ or their major tributaries .

2)secondary trunk VVs:

Dilated superficial trunk veins may be acting as collateral venous return in the presence of deep
venous disease .

3) reticular varices :
These vein lies just beneath or in the deep layers of the skin and even when normal , may form
visible reticular pattern of dark blue veins .

8/12/22
4) hyphenweb veins :
These dilated intradermal venules ( also called spider veins , telengectasia , phlebectasia and
venous flares ) .

5) vascular malformations :
The commonest venous malformation of the leg is klippel-trenaunay syndrome (KTS ) . KTS is
characterized by port-wine stain ,VVs , and bony and soft tissue hypertrophy . in KTS surgery is
best avoided .
 

8/12/22
Treatment:
 1-Compression therapy
 2-Thermal ablation
RF – LA
 3- sclerotherapy

8/12/22
 4-Surgery:
 Surgical treatment provides symptomatic relief and significant improvement in quality of life in patient with
uncomplicated varicose vein.

 High ligation of great saphenous vein at SFJ with stripping of long saphenous and stab avulsion
 
 Sapheno-pop ligation
 
 Perforator ligation by open surgery or superficial endoscopic perforator surgery (SEPS)

8/12/22
8/12/22
Vein Stripping :

. The surgery involves making one or more incisions

upon the desired area (usually the groin or leg)
followed by insertion of a special wire into the vein.
.The wire is tied to and advanced through the vein to a
desired depth.
.The vein is then pulled out from the body.
.The incisions are stitched up, and pressure dressings
are applied to the incision.

8/12/22
Endovenous laser ablation (EVLA)

 Endovenous laser treatment uses a laser probe to induce thermal damage.

8/12/22
Radio frequency ablation (RFA)

RF pulses are used to heat the vessel wall resulting in closure and fibrosis.

8/12/22
Catheter Directed Foam Sclerotherapy

 - Sclerotherapy: injection of 1% to 3% solution of sodium tetradecyl sulfate, or polidocanol

Used alone for isolated varicosity or to supplement surgical stripping

8/12/22
8/12/22