VENOUS DISEASE

FINAL YEAR

VENOUS DISEASE

A clear understanding of the anatomy of the venous system in the legs is essential to understanding pathophysiology as well as treatment.

Venous drainage of the legs is the function of two parallel and connected systems: the deep and the superficial systems connected by perforators .

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Perforating veins connect the superficial venous system to the deep venous system at various points in the leg—the foot, the medial and lateral calf, the mid- and distal thigh .

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The venules, the smallest veins ranging from 0.1 to 1 mm, contain mostly smooth muscle cells, whereas the larger extremity veins contain relatively few smooth muscle cells. These larger caliber veins have limited contractile capacity.

The venous valves prevent retrograde flow, and it is the failure of the valves that leads to reflux and associated symptoms.

Venous valves are most prevalent in the distal lower extremity, whereas as one proceeds proximally, the number of valves decreases to the point that in the superior and inferior vena cava, no valves are present.

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The return of the blood to the heart from the lower extremity is facilitated by the muscle pump function of the calf—a mechanism whereby the calf muscle, functioning as a bellows during exercise, compresses the gastrocnemius and soleal sinuses and propels the blood toward the heart.

The normally functioning valves in the venous system prevent retrograde flow; it is when one or more of these valves become incompetent that symptoms of venous insufficiency can develop.

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

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The term varicose veins is, in the common parlance, a term that encompasses a spectrum of venous dilation that ranges from minor telangiectasia to severe dilated, tortuous varicose veins.

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Varicose veins refer to any dilated, tortuous, elongated vein of any caliber.

Telangiectasias :are intradermal varicosities that are small and tend to be cosmetically unappealing but not symptomatic in and of themselves.

Reticular veins: are subcutaneous dilated veins that enter the tributaries of the main axial or trunk veins.

Trunk veins: are the named veins, such as the greater or lesser saphenous veins or their tributaries.

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The end result of CVI can range from aching, heaviness, pain, and swelling with prolonged standing or sitting in the case of symptomatic varicose veins,

To severe lipodermatosclerosis with edema and ulceration in the patient with severe CVI

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Defects in the strength and characteristics of the venous wall enter into the pathogenesis of varicose veins.

Furthermore, communicating veins connecting the deep with the superficial compartment may have valve failure.

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Pressure studies show that two sources of venous hypertension exist.

The first is gravitational and is a result of venous blood coursing in a distal direction down linear axial venous segments. This is referred to as hydrostatic pressure and is the weight of the blood column from the right atrium.

The second source of venous hypertension is dynamic. It is the force of muscular contraction, usually contained within the compartments of the leg. If a perforating vein fails, high pressures (ranging from 150 to 200 mm Hg) developed within the muscular compartments during exercise are transmitted directly to the superficial venous system. Here, the sudden pressure transmitted causes dilation and lengthening of the superficial veins. Progressive distal valvular incompetence may occur.

CLASSIFICATIONCEAP Classification

Class 0: No visible or palpable signs of venous disease

Class 1 :Telangiectasia, reticular veins, malleolar flare

Class 2: Varicose veins Class 3: Edema without skin changes Class 4: Skin changes ascribed to venous disease

(e.g., pigmentation, venous eczema, lipodermatosclerosis)

Class 5: Skin changes as defined above with healed ulceration

Class 6: Skin changes as defined above with active ulceration

CLASSIFICATION

Etiologic Classification of Chronic Lower Extremity Venous Disease

Congenital (EC ) Cause of the chronic venous disease present since birth

Primary (EP ) Chronic venous disease of undetermined cause

Secondary (ES ) Chronic venous disease with an associated known cause (post-thrombotic, post-traumatic, other)

ANATOMIC CLASSIFICATION (AS , AD , or AP )

The anatomic site(s) of the venous disease should be described as superficial (AS ), deep (AD ), or perforating (AP ) vein(s). One, two, or three systems may be involved in any combination. For reports requiring greater detail, the involvement of the superficial, deep, and perforating veins may be localized by use of the anatomic segments.

PATHOPHYSIOLOGIC CLASSIFICATION (PR,O )

Clinical signs or symptoms of chronic venous disease result from reflux (PR ), obstruction (PO ), or both (PR,O ).

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Your Sub Points

VENOUS DISEASERisk Factors

A combination of risk factors, rather than any one specific risk factor, is a better predictor of the likelihood of a given patient developing symptomatic varicose veins.

Heredity undoubtedly plays a significant role in the development of varicose veins.

Valvular dysfunction and insufficiency

Female sex, gravitation hydrostatic force, and hydrodynamic forces due to muscular contraction.

Hormonal Influence

VENOUS DISEASERisk Factors

VENOUS DISEASESymptoms

The patient with symptomatic varicose veins relates, most often,

symptoms of aching, heaviness, discomfort, and sometimes pain in the calf of the affected limb.

This is particularly worse at the end of the day, most likely due to prolonged sitting or standing that results in venous distention and associated pain.

The symptoms are typically reduced or absent in the morning owing to the fact that the limb has not been in a dependent position through the night.

In the case of women, the symptoms are often most troubling and exacerbated during the menstrual period, particularly during the first day or two.

Primary varicose veins consist of elongated, tortuous, superficial veins that are protuberant and contain incompetent valves.

VENOUS DISEASESymptoms

Primary varicose veins merge imperceptibly into more severe CVI.

Swelling ,edema is moderate to severe, an increased sensation of heaviness occurs with larger varicosities, and early skin changes of mild pigmentation and subcutaneous induration appear.

When CVI becomes severe, marked swelling and calf pain occur after standing, sitting, or walking.

Multiple dilated veins are seen associated with various clusters and heavy medial and lateral supramalleolar pigmentation.

VENOUS DISEASESymptoms

Many causes of leg pain are possible, and most may coexist. Therefore, defining the precise symptoms of venostasis is necessary. Discomfort usually occurs during warm temperatures and after prolonged standing. The pain is characteristically dull, does not occur during recumbency or early in the morning, and is exacerbated in the afternoon, especially after long standing. The discomforts of aching, heaviness, fatigue, or burning pain are relieved by recumbency, leg elevation, or elastic support.

Cutaneous itching is also a sign of venostasis and is often the hallmark of inadequate external support. It is a manifestation of local congestion and may precede the onset of dermatitis. This, and nearly all the symptoms of stasis disease, can be explained by the irritation of superficial nerve fibers by local pressure or accumulation of metabolic end products with a consequent pH shift.

External hemorrhage may occur as superficial veins press on overlying skin within this protective envelope.

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TREATMENT

Indications for treatment are pain, easy fatigability, heaviness, recurrent superficial thrombophlebitis, external bleeding, and appearance.

Nonoperative Management

The cornerstone of therapy for patients with CVI is external compression.

A triple-layer compression dressing, with a zinc oxide paste gauze wrap in contact with the skin, is utilized most commonly from the base of the toes to the anterior tibial tubercle with snug, graded compression.

In general, snug, graded-pressure triple-layer compression dressings effect more rapid ulcer healing than compression stockings alone.

Venous Ablation: Sclerotherapy

Cutaneous venectasia with vessels smaller than 1 mm in diameter do not lend themselves to surgical treatment. Dilute solutions of sclerosant (e.g., 0.2% sodium tetradecyl) can be injected directly into the vessels of the blemish. Care should be taken to ensure that no single injection dose exceeds 0.1 mL but that multiple injections completely fill all vessels contributing to the blemish.

Venules larger than l mm and smaller than 3 mm in size can also be injected with sclerosant of slightly greater concentration (e.g., 0.5% sodium tetradecyl), but limiting the amount injected to less than 0.5 mL.

If their cause is saphenous or tributary venous incompetence, these conditions can be treated surgically.

Surgery is not indicated for the treatment of venous insufficiency in limbs with deep venous incompetence

Surgical Management

Surgical treatment may be used to remove clusters with varicosities greater than 4 mm in diameter. Ambulatory phlebectomy may be performed using the stab avulsion technique with preservation of the greater and lesser saphenous veins, if they are unaffected by valvular incompetence

Surgical Management

When greater or lesser saphenous incompetence is present, the removal of clusters is preceded by limited removal of the saphenous vein (stripping).

Stripping techniques are best done from above downward to avoid lymphatic and cutaneous nerve damage.

Surgical Management

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VENOUS DISEASESubfascial endoscopic perforator vein surgery

perforating vein division using laparoscopic instrumentation. Initial data suggested that perforator interruption produced rapid ulcer healing and a low rate of recurrence.

Direct Venous Reconstruction ??

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