VARICOSITIES:
Varicosities are abnormally dilated and full of twist & turn veins. The veins of lower extremities are involved in varicosities is called varicose veins. The veins of other parts of the body which are affect the lower oesophageal, the anal region result -: oesophageal varices & haemorrhoids, spermatic cord varicocele.
VARICOSE VEINS:
Varicose veins are permanently dilated and tortuous superficial veins of the lower extremities, especially the long saphenous vein and its tributaries. About 10-12% of the general population develops varicose veins of lower legs, with the peak incidence in 4th and 5th decades of life.
Adult females are affected more commonly than the males, especially during pregnancy.
This is attributed to venous stasis in the lower legs because of compression on the iliac veins by pregnant uterus.
PATHOGENESIS (causes):-
A number of etiologic and pathogenetic factors are involved in causing varicose veins.
These are as follows:-
i) Familial weakness of vein walls and valves is the most common cause.
ii) Increased intraluminal pressure due to prolonged upright posture e.g. in nurses, policemen, surgeons etc.
iii) Compression of iliac veins e.g. during pregnancy, intravascular thrombosis, growing tumour etc.
iv) Hormonal effects on smooth muscle.
v) Obesity, & Chronic constipation.
Varicosities of Other Sites:-
Venous dilations in two other sites merit special attention.
• Esophageal varices-:
Liver cirrhosis (and less frequently, portal vein obstruction or hepatic vein thrombosis) causes portal venous hypertension. This, in turn, leads to the opening of porto-systemic shunts and increased blood flow into veins at the:-
(1) gastroesophageal junction (forming esophageal varices);
(2) rectum (forming hemorrhoids);
(3) periumbilical veins of the abdominal wall (forming a caput medusae).
Esophageal varices are most important since they are prone to ruptures that can lead to massive (even fatal) upper gastrointestinal hemorrhage.
• Hemorrhoids-:
Hemorrhoids are varicose dilations of the venous plexus at the anorectal junction that result from prolonged pelvic vascular congestion associated with pregnancy or straining to defecate. Hemorrhoids are a source of bleeding and are prone to thrombosis and painful ulceration.
Clinical Features.
Varicose dilation renders the venous valves incompetent and leads to lower-extremity stasis, congestion, edema, pain, and,thrombosis.
The most disabling sequelae include persistent edema in the extremity and secondary ischemic skin changes, including stasis dermatitis and ulcerations.
The latter can become chronic varicose ulcers as a consequence of poor wound healing and superimposed infections Of note, embolism from these superficial veins is very rare, in contrast with the relatively frequent emboli that arise from thrombosed deep veins.
MORPHOLOGIC FEATURES.
The affected veins, especially of the lower extremities, are dilated, tortuous, elongated and nodular. Intraluminal thrombosis and valvular deformities are often found.
Histologically -:
there is variable fibromuscular thickening of the wall of the veins due to alternate dilatation and hypertrophy. Degeneration of the medial elastic tissue may occur which may be followed by calcific foci. Mural thrombosis is commonly present which may get organised and hyalinised leading to irregular intimal thickening.
EFFECTS.
Varicose veins of the legs result in venous stasis which is followed by congestion, oedema, thrombosis, stasis, dermatitis, cellulitis and ulceration.
Secondary infection results in chronic varicose ulcers.
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