diseases of veins

8/9/2019 Diseases of Veins

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DISEASES OF THE VEINS

Dr. Pisake Boontham M.D., Ph.D.

Department of surgeryPhramongkutklao hospital


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Lecture Objectives

Anatomy of leg veins

Venous Insufficiency: varicose veins

Deep Vein Thrombosis


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MAJOR VEINS


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Anatomy principles

Superficial venous system

Long saphenous vein

Short saphenous vein Deep venous system

Perforating veins


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Anatomy


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Varicose veins

Varicose veins affect

20 - 25% of adult females

10 - 15% of adult males

75,000 operations are performed annually in

United Kingdom

20% of operations are for recurrent disease

May develop anywhere in body, but most

develop in lower extremities: Long Saphenous


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Factors associated with

varicose veins Inherited

Female > Male: age > 35 years

Pregnancy smooth muscle relaxation

Western lifestyle: Whites > Blacks

Prolonged standing


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Varicose Veins

Causes

Severe damage or trauma to saphenous

vein

Effects of gravity produced by long periodsof standing

Types

Primary: no deep veins involved

Secondary: caused by obstruction of deep

veins (Most Common)


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The long saphenous vein (LSV) and its tributaries most often form varicose

veins The short saphenous vein (SSV) and its tributaries can also become

varicose but less often


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The veins in the leg are divided into two systems; the deep and the superficial veins

The two systems are linked periodically by perforating veins. A superficial vein can

become varicose because a perforating vein is allowing blood to flow the wrong way

(outwards)


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Varicose veins

Consequence of

superficial vein valve

failure (incompetent

valves)

Pooling of blood distal to

incompetent valve (blood

flows backwards, from

deep to superficial veins)

Vein wall distended


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Pathophysiology

Major cause: sustained stretching ofvascular wall die to long-standing increasedintravenous pressure

Valves become incompetent because they

cannot close properly due to stretching Prolonged standing, the force of gravity,

lack of lower limb exercise, & incompetentvenous valves all weaken muscle-pumpingmechanism, & return of venous blood toheart decreases

As client stands for long time, blood poolsand vessel wall continues to stretch, andvalves become increasingly incompetent


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Varicose veins-pathophysiology

Congenital or acquired valvular incompetence ofthe deep and superficial veins along with

weakness of the venous wall

Self-perpetuating cycle of venous reflux leading

to further vein dilatation and valve failure.

Venous hypertension leads to fluid and protein

extravasation into the subcutaneous tissue-

edema

Edema & high venous pressure results in

reduced local capillary flow and reactive hypoxia

leading to further inflammation and tissue

damage.


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Clinical Manifestations

No symptoms

Leg fatigue &/or heaviness

Itching over affected leg (stasis dermatitis)

Feelings of heat in the leg Visibly dilated veins

Telangiectasia veins

Reticular varices

Varicose veins

Severe, aching pain in leg

Thin, discolored skin above ankles

Complications: insufficiency, stasis ulcers,chronic stasis dermatitis, thrombophlebitis


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Signs of venous hypertension

Perimalleolar oedema

Pigmentation

Lipodermatosclerosis Eczema

Ulceration


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Pathogenesis

Result of severe impairment of venous

return causing venous hypertension;

often with deep vein incompetence

Haemosiderin deposition eczema

calf muscle hypertrophy oedema

lipodermatosclerosis

+/- ulceration


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Lipodermatosclerosis


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Assessment: Labs & Diagnostics

No specific labs

Diagnostics

Doppler ultrasound flow tests &angiographic studies or Duplex Doppler

ultrasound

Trendelenburg tests assists w/diagnosis


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Indications for duplex scanning

Suspected short saphenous incompetence

Recurrent varicose veins

Complicated varicose veins (e.g. ulceration,

Lipodermatosclerosis)

History of deep venous thrombosis


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Treatments

Treat varicose veins

Symptom control with compression

therapy

Sclerosant injection for Telangiectasia &

Reticular veins

Surgery to strip veins/disconnect

perforator veins Superficial vein ablation laser/foam


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Conservative Interventions

Conservative measures include

antiembolism stockings and regular

walking & leg elevation

Mild analgesics may relieve pain


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Sclerotherapy

Only suitable for below knee varicose veins

Need to exclude SFJ or SPJ incompetence

Main use is for persistent or recurrent

varicose veins after adequate saphenoussurgery

Complications of sclerotherapy

Extravasation causing pigmentation orulceration

DVT


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Indications for varicose vein surgery

Most surgery is cosmetic or for minor

symptoms

Absolute indications for surgery :

Lipodermatosclerosis leading to venous

ulceration Recurrent superficial thrombophlebitis

Bleeding from ruptured varix


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Treatment of venous ulcer

AFTER EXCLUDING ARTERIAL

DISEASE:

4 layer compression bandaging

Treat varicose veins

Long term compression


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Venous Stripping


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ENDOVENOUS LAZER:an alternative choice for surgery of varicose veins


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Indication

Varicose veins with:

Saphenofemoral junction reflux

Primary insufficiency of GSV

Lasser saphenous vein reflux


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Advantages

Minimally invasive procedure

Ambulatory procedure

Quick method No scaring


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Outcome

Follow up (yr) Treated/

occluded

Continued

occlusion (%)

3 72/72 100


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Procedure


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Reasons for recurrence

Inaccurate clinical assessment Confusion as to whether varicosities are in

LSV or SSV distribution

Can be avoided with use of hand heldDoppler

Inadequate primary surgery 10% cases SFJ not correctly identified

20% cases tributaries mistaken for LSV

Failure to strip LSV

70% of those with SF incompetence treatedwith sclerotherapy alone will developrecurrence

Neovascularisation


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Deep vein thrombosis

Very common especially in hospital patients

Incidence of about 50-150 DVTs per 100,000

population per year

Asymptomatic in 30% (calf veins only)

10% pulmonary embolism when popliteal

vein and above involved


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Deep Vein Thrombosis (DVT)

Most likely to occur in deep

veins of the calf (80%)

25% of thrombi that occur in

calf will extend to the popliteal& femoral veins

PE may be the first sign of DVT


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Risk Factors

Hypercoagulable

state

Age

Obesity

Immobility

Surgery

Pregnancy

OCP

Malignancy

Heart Failure

Infection

Inflammatory bowel

Nephrotic syndrome


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Hypercoagulable state

Factor V Leiden mutation

Prothrombin gene mutation

Protein C or S deficiency Antithrombin III deficiency

Homocysteine

Antiphospholipid syndrome


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DVT Manifestations

When clot is in formative stage, may notice no

symptoms

Usually profound tenderness; affected extremity

may be larger (unilateral edema)

Dull aching esp when walking:Most common

Severe pain, esp when walking

Cyanosis of extremity

Slightly elevated temp

General malaise


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Diagnosis of DVT

History

Examination swelling, tender,

redness, dilated superficial veins, low

grade pyrexia

Duplex US + d-dimer. If still uncertain,

(MRI) venography


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Homans Sign

Was long considered classic

manifestationthis is no longer true

Sign is not specific to DVT & can be elicited

by any condition of the calf

As calf muscles contract, there is risk ofdetaching thrombus from the wall


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DVT


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Prevention of DVT

Mobilise ASAP

Low compression stocking for

inpatients

Prophylactic LMW Heparin


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Conservative Therapy: DVT

Anticoagulants may be prescribed for severe

cases

Strict bed rest until symptoms of tenderness

& edema resolve

Legs elevated, knees slightly flexed, above

heart level to promote venous return &

discourage venous pooling

TEDs or pneumatic compression devices


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IVC filter

Re-embolism despiteanticoagulation

Anticoagulation contraindicated

Extensive thrombus persists


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diseases of veins

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