Pathophysiology

and Conservative
Management of
Varicose vein

Moderator: Prof Dr.Kiran Shrestha

Presenter:Dr.Binesh Jha
MS GS 2nd Year
ANATOMY
 VARICOSE VEINS
• Subcutaneous veins in the lower extremities
which are dilated to ≥3 mm in diameter in the
upright position.

• Adult prevalance: 30-50%

 PATHOPHYSIOLOGY
• Veins contain 60% of total blood volume with average
pressure of 5-10mmHg.

• Venous pressure on a foot vein while standing is approx.

100mmHg.

• For return of blood to the heart Pressure gradient is required

between chest and veins of the leg.
– increase in thoracic volume during inspiration decreases
intrathoracic pressure.
– Calf muscle pump with competent valves.
 Venous return
With
dependency
The heart pump Gravity
maintaining a pressure gradient Pooling in dependent limbs may
across the veins reduce cardiac output by 2 L/min
& may cause fainting

Venomotor tone
Under control of sympathetic system This is counter
acted by:
[Upright position -- dependant pooling –
dec. cardiac output -- inc. sympathetic
discharge -- inc. venous tone -- inc. venous
return.]

Calf muscle
contraction With calf muscle
contraction in walking
Blood is pushed upwards
and prevented from retrograde flow by
competent venous valves
• Absence of the pressure gradient or the calf muscle pump
result in Venous Hypertension,which further leads to venous
damage causing a viscious cycle.
Pathology
• 2 sources of Venous hypertension

– Gravitational

– Dynamic
 Gravitational
– Resulting from venous blood coursing in a distal
direction down

– Hydrostatic pressure (weight of blood column

from RA)

– Highest pressure generated evident in ankle and

foot
 Dynamic
– Force of muscle contraction,within compartment
of the leg

– Failure of a perforating vein causes high pressure

(150-200mmHg) transmitted directly to superficial
venous system

– Causing dilatation and lengthening

 Conservative Management
• Weight loss
• Leg elevation
• Compression stockings
• Pharmacological
• Elevation of feet to heart level for 30 minutes
3-4 times per day
– improves cutaneous microcirculation & reduces
edema.

• Daily walking and simple ankle flexion

exercises.
COMPRESSION
• Relies on graduated external pressure.

• British Classification:
– Class I: 14-17mmHg
– Class II: 18-24mmHg
– Class III: 25- 35mmHg

• Significantly improves symptoms but has poor

compliance.
• 20 to 30 mm Hg pressure help with pain and
edema control.

• Patients with venous stasis ulcers are given

30– 40mm Hg stockings

• Applied below knee due to high standing

venous pressure .
Horse chestnut extract(escin) been used in
Europe
• It inhibits platelet aggregation reduces
edema ,capillary permeability & lymphatic
drainage.

• MOA likely related to inhibition of

lipoxygenase, cyclo-oxygenase, and
phosphodiesterase.
• Micronized purified flavonoid fraction
(diosmin)
– reduces symptoms of pain and heaviness and as
an adjunct to compression therapy in ulcer
healing.

• Hydroxyethylrutoside reduces leg volume,

edema, and symptoms of chronic venous
insufficiency .
• Venoactive drugs of natural or synthetic origin
– Flavonoids
– Rutosides
– Aminaphthone
– Calcium dobesilate
– Centella asiatica (gotu kola)
– Naftazone, and chromocarbe.

• These drugs increases venous tone.

Rheologic agents
• Stanozolol, an oral anabolic steroid:
– Stimulates blood fibrinolysis in advanced skin
changes associated with lipodermatosclerosis

• Pentoxifylline:reduces blood viscosity and

inhibits platelet aggregation
THANK YOU