pathophysiology of varicose veins

GOOD MORNING

PROF.S.P.GAYATHRE.M.S

ASSISTANT PROFESSORS: Dr.G.KARTHIKEYAN,M.S Dr.R.SYED RAJ,M.S

S4 UNIT

PATHOPHYSIOLOGY OF

VENOUS DISEASES

1.What are the two major veins of hand?

2.Have you ever seen varicose veins of hands?

Ulnar and radial vein

3.Do you know why?

GRAVITY

To overcome the effect of GRAVITY LOWER LIMB has some special mechanism

PRESSURE GRADIENT

HIGH PRESSURE

LOW PRESSURE

PERIPHERAL PUMP Calf , Thigh & Foot pump UNIDIRECTIONAL

NONREFLUXINGVALVES

NEGATIVEINTRATHORACIC PRESSURE

VIS-A-TERGOVENA COMITANTES

SYMPATHETIC ACTIVITY

FACTORS RESPONSIBLE FOR NORMAL

VENOUS RETURN

MOTOR PIPE TANKSOLEUS MUSCLE VEINS HEART

1.MUSCLE PUMP

STRUCTURE

DURING MUSCLE RELAXATION, PRESSURE WITHIN CALF COMPARTMENT FALLS

BLOOD FROM SUPERFICIAL VEINS ENTER DEEP VEINS

SUPERFICIAL VENOUS pressure cont. To fall TILL THRESHOLD IS REACHED

THRESHOLD IS APPROX. 30mmHg

VENOUS INFLOW NOW KEEPS PACE WITH EJECTION FROM DEEP VEINS

Patency of veinsCompetent valves

RELAXATION PHASE

RELAXATION CONTRACTION

DURING MUSCLE CONTRACTION, PRESSURE WITHIN CALF COMPARTMENT RISES TO 200-

300mmHg

BLOOD FROM DEEP VEINS ENTER IVC

VALVES OF PERFORATOR VEINS CLOSED

TO PREVENT REFLUX

CONTRACTION PHASE

AMBULATORY VENOUS HYPERTENSION

REFLUX OBSTRUCTIVE

2. NON REFLUXING VALVES

3.NEGATIVE INTRATHORACICPRESSURE

4.VIS-A-TERGO

12mmHg 32 mmHg

5.VENAE COMITANTES

PATHOGENESIS

Changes in Vein

Wall

Smooth Muscle Proliferation

Increased MMP

Collagen deposition

Decreased elastin content

Changes in vein wall

over stretching of veins

increase in size of veins but valve leaflets don’t expand

Secondary valvular Incompetence Backflow( reflux)

Pooling and further dilation of veins

Varicosity – Dilated Tortuous Veins

COMPETENT VALVE

INCOMPETENT VALVE

PRIMARY: Congenital weakness in vessel wall

Congenital absence of valves

Congenital Valvular incompetence

Familial (FOX C2 gene)

Lysosomal enzyme activity(Haardt)

Chronic inflammatory process(Class II MHC & Macrophages)

ETIOLOGY

SECONDARY :

OBSTRUCTION TO FLOW:

DESTRUCTION OF VALVES:

1.Pregnancy 2.Pelvic tumor: Ovarian ca Fibroid uterus3.Ascites4.Retroperitoneal fibrosis5.Iliac vein thrombosis

1.Deep vein thrombosis

HIGH PRESSURE FLOW:1.AV fistula

KLIPPEL TRENAUNAY SYNDROME

Gender

Age Ethnicity

Body mass index&height

Family history Pregnancy

occupation and lifestyle factor;

smokers, constipation occupations which involve

prolonged standing.

Traffic police Bus conductors Sports man Nurses Surgeons hair stylists Factory workers

OTHER RISK FACTORS

• C = CLINICAL CLASSIFICATION

• E = ETIOLOGICAL CLASSIFICATION

• A = ANATOMICAL CLASSIFICATION

• P =PATHO-PHYSIOLOGICAL

CEAP CLASSIFICATION

TELANGECTASIA :<1 mm

Spider veins, thread veins, hyphen webs

RETICULAR VEINS:Dilated, subdermal veins

1-3mm in diameter

CLASS 1

VARICOSE VEINS:Varicose veins are defined as dilated, usually tortuous, subcutaneous veins 3 mm in diameter measured in the upright position with demonstrable reflux.

CLASS 2

CLASS 3

DEPENDENT PITTING EDEMA:Result of increase in volume of fluid

Elevation/compression bandaging

CLASS 4A

PIGMENTATION:Brownish Discolouration

Hemosiderin depositionECZEMA :Erythematous dermatitis

Progress to blistering, weeping or scaling eruption of the skin

CLASS 4B

LIPODERMATOSCLEROSIS:Localised chronic inflammation and fibrosis of skin and subcutaneous tissueSevere stage of chronic venous diseaseATROPHIE BLANCHE:Localized white atrophic skin - dilated capillaries and hyperpigmentation

site

CLASS 5

HEALED ULCER:

CLASS 6

ACTIVE ULCER:epidermal defect

gaiter area

IDENTIFIED

IDENTIFIED

SAPHENA VARIX:Large groin varicosity

Painless lump

standing

recumbent

Cough impulse

CORONA PHLEBECTASIA:Fan shaped patterns of small intradermal veins

Site

Malleolar or Ankle Flares