Understanding of Chronic Venous Disease (CVD) - PowerPoint Presentation

Slide1

Understanding of Chronic Venous Disease (CVD)

M.

Shoaib

D/o

Ilaj

bit

Tadbeer

Slide2

Definition

CVD is a disease of lower limb veins in which venous return is

impaired, by

reflux (backflow), obstruction or calf muscles pump failure.

Slide3

Anatomy of Lower Limb

Slide4

Cont..

External Iliac vein

Femoral Vein

Greater Saphenous Vein

Popliteal Vein Small Saphenous Vein Ant. Tibial vein Post. Tibial vein Fibular vein Dorsal Venous Arch of Foot

Slide5

Vein

Normal vein have a series of bicuspid valves (more on distal site) that open and close to direct blood flow from the surface of legs to the deep veins and back to heart.

The valves also control the pressure in the smaller vein on the leg surface.

If the valves within the vein fail to work properly blood can flow backward (venous reflex) in the vein and pool in the legs, leads to which increase pressure within the vein called as venous hypertension.

Slide6

The

pooled blood can increase pressure in the veins which creates problems like

mild

(leg heaviness, aching, dilated or unsightly veins) or

severe

(swelling, skin color change or skin rashes, recurrent infection and chronic ulcers. People who develops these more or severe symptoms are said to have CVD

.

Slide7

Venous system

1-Deep vein 90% 2-Superfecial vein 10%

3-Perforating vein (Connecter b/w them direct the blood from superficial vein to the deep vein)

Slide8

Cont..

Venous drainage of the legs is the function of two parallel and connected system, the deep and the superficial system, connected by perforators (located in foot, medial & lateral calf and mid and distal thigh).

During calf muscles contraction the venous pressure of the foot and ankle drop dramatically. The pressure developing in the muscles compartments during exercise range from 150 to 200 mm Hg, and when there is failure of perforating veins, these high pressure are transmitted to the superficial system.

Slide9

Cont..

Pump mechanism (contraction) of calf muscles which activate and maintain blood flow by squeezing the vein by 150-200mmhg pressure leads to opening the valve (upper) which push the blood upward and closing of the valve (lower) which prevent backward flow and also decreases the venous pressure

.

The

venous system of the legs must move the blood against the force of gravity in the standing position.

Slide10

Physiology of Venous Valve

The space between two cusps of valves called as

Luminal

space

and the flow is known as

Axial flow

while

the space between wall of vein and cusp of valve called as Mural space and the flow is known as Vortex flow. If the pressure on luminal side is more, the valve is open and if pressure on mural side increases then the valve is closed.

Slide11

Cont..

Valve Cycle:

Opening

phase

:

0.27 sec

Equilibrium phase

:Closing phase:Closed phase: 0.41 sec (Muscle activity (dorsal and plantar flexions

of the foot) causes shortening of the closing phase.)Frequency of Valve Cycle:

Standing posture 20/mntLying Posture 35/

mntLumina Space

Axial Flow

Vortex FlowMural space

Slide12

Cont..

In continuous erect and leg hanging posture lead to increase mural pressure is greater than luminal pressure lead to closure of valve which lead to increasing pressure within the vein result in prominence and dilatation of superficial vein which laid the foundation of CVD

.

Varicosities usually start at points where superficial veins communicate with deep veins, particularly at the

saphenofemoral

and

saphenopopliteal

junctions and in the perforating system, because of valvular incompetence.

Slide13

Physiology of venous system of leg

Venous blood flow from capillaries to the heart.

Flow occurs against gravity by

Muscular compression against the veins.

Negative intra-thoracic pressure.

Calf muscles pump.

Slide14

Perforating vein and Reflux

Maintain one way flow from superficial to deep veins.

Perforator valve failure causes:

Higher venous pressure and GSV/branch dilatation.

Slide15

Cont..

Increasing pressure results in GSV valve failure

.

Additional vein branch become varicose

.

Further GSV incompetence and dilatation.

Slide16

Ambulatory Venous Pressure (AVP)

No

ulceration -AVP <30 mmHg

Ulceration -AVP >90 mmHg

Slide17

Epidemiology

50% population

Ulcer 1% (50% ulcer more than 12 months, 72% recurrent)

Affect quality of life

Slide18

Risk factors

Advancing Age

Family history of venous disease (Heredity)

Gender (F>M), Hormonal influence (increase estrogen level)

Gravitational hydrostatic force and hydrodynamic force due to muscular contraction

Pregnancy

Standing occupation

Slide19

Cont..

Obesity/ increase BMI

Prior injury or surgery of lower extremities

Prior venous thrombosis/ high estrogen state

Sedentary lifestyle

Smoking

Any condition which increase intra-abdominal pressure

Slide20

Causes

Superficial venous reflux

Deep venous reflux, occlusion (primary, secondary)

Perforator venous reflux

Slide21

Clinical feature

Swelling (more in the evening and afternoon in (summer) and subside in lying posture.

Itching (

venostasis

- irritation of local nerve fibers by local pressures or accumulation of metabolic waste with consequent of

Ph

shift)

Skin changes, eczema, pigmentation

Slide22

Cont..

Lipo-dermato-scelerosis

:

proliferation

of dermal capillaries and fibrosis on subcutaneous tissues (i.e. induration+

pigmentation + inflammation

)UlcerationVaricose veinPain

Slide23

Pathogenesis

Distal Venous hypertension

leads to

valvular

incompetence, reflux and venous obstruction.

Fibrin cuff

hypothesis

(Fibrous band formed around the capillaries and veins- prevent O2 & Co2 exchange - Ischemia)White cell trapping hypothesis (WBCs trapped between the fibrous band and capillaries lead to lysis of WBCs – release of Inflammatory cytokines & Mediators)

Slide24

CEAP Classification

Clinical:

C0 – No evidence of venous disease

C1 –

Telangectesia

/ Reticular veins

C2 – Varicaose veinsC3 – Oedema associated with vein diseaseC4a – Pigmentation with eczemaC4b – LipodermatoscelerosisC5 – Healed Venous ulcersC6 – Active Venous ulcers

Slide25

Etiological:

Congenital (EC) – disease present since birth.

Primary (EP) – unknown etiology

Secondary (ES) – post traumatic/ thrombotic

Anatomical:

Superficial (AS), Deep (AD) or Perforators vein (AP)

Pathological:

Reflux (PR), Obstruction (PO) or both (PRO)

Slide26

Source of Reflux in Venous Ulcers Patients

Superficial veins – 79%

Perforator veins – 63%

Deep veins – 50%

Slide27

Complication

Eczema

Ulcer

Bleeding

Thrombophlebitis

Thrombosis (DVT)

Slide28

Prevention

Weight control

Adequate physical exercise

Avoidance of smoking

Avoidance of sedentary life

Control of hypertension

Modification of profession

Slide29

Examination

General tips: (ICEPP)

Introduction – be polite and friendly

Consent to examination

Expose adequately

Position (standing initially)

Pain (ask before examining the patient)

Slide30

Inspection

Look at the leg whilst patient is standing

Examine around the medial malleolus, gaiter area

with (

VVVLAPS)

i.e.

Varicose vein – distribution (LSV, SSV)

Venous ulcer/eczema

Slide31

Cont..

Venous

stars

Lipodermatoscelerosis

Atrophy

Pitting edema

Scars

Slide32

Lipodermatoscelerosis

Scarring of skin and fat.

A slow process that occurs over a number of years and has 2 phases.

Acute:

venous pooling – chronic venous hypertension

RBCs forced into surrounding tissues

Haemoglobin

breaks into haemosiderin

Slide33

Chronic

Chronic

haemosiderin

formation lead to fibrin deposition

Skin becomes thick and shiny

Skin around ankle constrict and the inverted

champagne

bottle shape seen

Slide34

Palpation, Percussion and Auscultation

Temperature

– feel with the back of hand should be warm. If cold arterial disease may co-exist.

Palpate the vein

– feel the course of the vein

Cough impulse

– locate the SFJ, feel the smooth swelling and palpable thrill of saphenous vein. If present cough test is +

ev.

Slide35

Cont..

Tap test

– place the finger at any point of varicose vein. Tap the vein proximally (above the finger). Incompetent valve allow the transmission of a fluid thrill to the finger below

.

Direction test

– empty a short section of the vein (place one finger on the vein and slide another finger firmly upwards). If the valves are incompetent the vein will refill when you release the top finger.

Slide36

Cont..

Auscultation

– over a large group of vein may indicate bruit, rare - indicate an underlying

arterio

-venous malformation.

Slide37

Special test

Trendelenburg

test

– use to asses the competence of SFJ (

Sapheno-femoaral

junction).

Patient lies flat, elevate the leg and gently empty the veins, palpate the SFJ and ask the patient to stand whilst maintaining pressure.

Findings – if the vein do not refill, SFJ is incompetent, if the vein do refill SFJ may or may not be incompetent, presence of distal incompetent perforators.

Slide38

Investigation

Doppler ultrasound

Non invasive

Venous reflux: retrograde flow lasting >0.5 sec

In CVI superficial vein reflux present in 90%,

(70-80

% in

GSV)

Slide39

Management

Prevent

increasing Intra-abdominal

pressure

Reduce Distal Venous Pressure

Slide40

Cont..

Conservative management

Compression stocking

Limb elevation

Medication-

Daflon

(

munzij wa mushil sauda)

Slide41

Cont..

Fasd

(

Venesection

)

Leech Therapy

Open

surgery: ligation, stripping and multiple stab avulsion. Venous bypass surgery for deep vein occlusion. Endovenous surgery: EVLA, RFA, Scelerotherapy, Cryoablation.

Slide42

Conservative Treatment

Avoid

long period of standing

While sitting leg should be above the thigh

Avoid crossing leg

Ideal body weight

Slide43

Cont..

Walking

programme

(calf muscles exercise

)

Compression therapy (elastic

compression

bandages, Compression stocking, Pneumatic compression therapy)

Slide44

Thanks