Home Cure for Varicose Veins
Chronic venous insufficiency produces skin changes in the lower leg (varicose eczema, lipodermatosclerosis. ulceration) due to sustained venous hypertension which in turn is due to reflux (90 ) and or obstruction (10 ) in the superficial and or deep veins. DVT is a common cause of chronic venous insufficiency, which, in turn, is the commonest cause of leg ulceration,
Patients with decreased cardiac output secondary to heart failure may become mentally confused and disoriented. Such symptoms also may be due to hypoxia, to drugs that are invariably prescribed for such patients, and to renal or hepatic failure.2 A completed stroke may be caused by a lacunar infarct, cerebral hemorrhage, cerebral arterial thrombosis, or a cerebral embolus (see Chap. 89). A transient cerebral ischemic attack is commonly due to an embolus. The embolus may originate in an atheromatous ulcer in the carotid artery system or the aortic arch be related to infective endocarditis, a recent MI, atrial fibrillation, or clots on a prosthetic valve or originate in the leg veins and pass through a patent foramen ovale to the brain (see Chap. 89).
3D CE MR portography can demonstrate the in-trahepatic and extrahepatic portal venous system as well as hepatic veins. Its advantages over DSA include its large field of view, its short imaging time, and its noninvasive nature and low risk of complications, which permit repeated studies. Clinical applications of 3D CE MR portographyin-clude portal hypertension (portosystemic shunt, portal veinobstruction, hepatic vein obstruction), hepatic encephalopathy, ascending portal thrombophlebitis, hepatocellular carcinoma and pancre-atobiliary tumors, gastrointestinal hemorrhage, and differentiation of splanchnic arterial disease from portal venous disease 1, 15 . In patients with portal hypertension, 3D MR portography can be used to evaluate portosystemic shunt, hepatopetal collateral pathways, and obstruction of the portal or hepatic veins. Inplanning treatment for hepatic encephalopathy, it is important to identify the causative portosystemic shunt. In suspected cases of ascending portal...
Chronic liver injury can lead to a sequence of changes that terminates with fatal bleeding from esophageal blood vessels. In most forms of chronic liver injury, stellate cells are transformed into collagen-secreting myofi-broblasts. These cells deposit collagen into the sinusoids, interfering with the exchange of compounds between the blood and hepatocytes and increasing resistance to portal venous flow. The resistance appears to be further increased when stellate cells contract. The increased resistance results in increased hepatic portal pressure and decreased liver blood flow. This disorder is seen in approximately 80 of patients with cirrhosis. In a compensatory effort, new channels are formed or dormant venous tributaries are expanded, resulting in the formation of varicose (unnaturally swollen) veins in the abdomen. Although varicose veins develop in many areas, portal
The KT and PW syndromes consist of vascular malformations involving the lower limbs primarily, with the following dominant features cutaneous capillary malformation, varicose veins, and limb hypertrophy. The KT syndrome comprises primarily venous anomalies, while the PW syndrome has more arteriovenous shunts.23 Spinal cord involvement with pial arteriovenous fistulas or malformations can be present.
Other types of obstruction include intussusception (Fig. 12-8), slipping of a part of the intestine into a part below it volvulus, twisting of the intestine (see Fig. 12-8) and ileus, intestinal obstruction often caused by lack of peristalsis. Hemorrhoids are varicose veins in the rectum associated with pain, bleeding, and, in some cases, prolapse of the rectum.
Explain How Valves In Veins Breathing And Skeletal Muscle Contractions Help Venous Blood Return To The Heart
The accumulation of blood in the veins of the legs over a long period of time, as may occur in people with occupations that require standing still all day, can cause the veins to stretch to the point where the venous valves are no longer efficient. This can also result from the compression of abdominal veins by a fetus during pregnancy. Venous congestion and stretching produced in this way can result in varicose veins. Venous congestion in the lower limbs is reduced during walking, when movements of the foot activate the soleus muscle pump. This effect can be produced in bedridden people by extending and flexing the ankle joints.
Hypovolemia and hemoconcentration need immediate corrections. When necessary, intravenous crystalloid infusion or plasma expanders are given to maintain central venous pressure. Replacement may require central venous pressure monitoring. Diuretics should not be given with, as the fluids in the abdominal and thoracic cavity are not responsive to diuretics and the further intravascular depletion can cause hypotension, shock, and thrombosis. Administration of low-dose heparin to prevent thromboembolism needs to be balanced against the risk of ovarian bleeding, possible need for paracentesis, and the possibility of heparian-induced thrombocytopenia. Most of our hospitalized patients are commenced on heparin 5000 U x 2 day subcutaneously on admission and reviewed after 24 hr. Heparin should be continued until discharge from the hospital if the patient has risk factors or past history of thrombosis, family history of thromboembolism, smoking, obesity, or varicose veins. Heparin should also...
The severity of the symptoms may bear little relationship to the gravity of the underlying pathology. For example life-threatening, deep venous thrombosis (DVT) may be asymptomatic. There are four cardinal symptoms of lower limb venous disease. 1. Pain. Patients with uncomplicated varicose veins may complain of an aching discomfort in Ihe leg, itching and a feeling of swelling. Symptoms arc typically aggravated by prolonged standing and are often worse towards the end of the day. 2. Swelling may be associated with varicose veins, deep venous reflux and deep venous thrombosis. 3. Discoloration. Chronic venous insufficiency is associated with deposition of haemosiderin in the skin leading to lipoderrnatosclerosis (LDS). This may vary from deep blue black to purple or even bright red. It typically affects the medial aspect of the lower third of the leg but may be laterally placed if superficial reflux predominates in the short saphenous veins.
A breakdown in the valves of the veins in combination with a chronic dilatation of these vessels results in varicose veins. These appear twisted and swollen under the skin, most commonly in the legs. Contributing factors include heredity, obesity, prolonged standing, and pregnancy, which increases pressure in the pelvic veins. This condition can impede blood flow and lead to edema, thrombosis, hemorrhage, or ulceration. Treatment includes the wearing of elastic stockings and, in some cases, surgical removal of the varicosities, after which collateral circulation is established. A varicose vein in the rectum or anal canal is referred to as a hemorrhoid.
Organs responsible for development of iron-deficiency anaemia are the uterus (increased menstrual blood loss, pregnancy), the oesophagus (varicose veins in patients with liver cirrhosis), the stomach and bulbus duodeni (hiatus hernia, aspirin and detrimental effects of other non-steroidal antiinflammatory drugs, peptic ulcer, carcinoma, partial gastrectomy), the small intestine (hookworm, coeliac disease, diverticulosis, morbus Crohn, angiodysplasia), the colon and rectum (carcinoma, diverticulosis, angiodysplasia, varices, colitis) and, rarely, the kidney and lung. Increased demands for iron, not met by adequate iron intake, occur in premature infants, during any period associated with increased growth, and during pregnancy. Poor diet is also a cause of iron deficiency in some socioeconomic groups in developed countries. Female blood donors in particular may develop iron deficiency. Self-inflicted blood loss is a diagnosis that should be considered if no cause can be found for severe...
Following the development of gradient echo techniques, TOF MR venography quickly evolved as a clinically reliable method for detecting DVT of the pelvic and lower extremity veins (Fig. 6) 16-18 . Although TOF venography can detect venous thrombosis in the femoral and trifurcation veins 19 , lengthy acquisition times have limited its use mainly to the pelvis. Due to in-plane flow saturation preventing reliable depiction of perforating veins which run in the horizontal plane, and the technique's lack of sensitivity to slow or retrograde flow, TOF MR venography has not been employed for assessing varicose veins or post-thrombotic changes. Contrast-enhanced 3D MR venography overcomes the limitations inherent to TOF venog-raphy. Specifically, direct MR venography with unilateral or bilateral injection of diluted paramagnetic contrast agent allows the display of all vessels, regardless of the underlying flow characteristics and the orientation of the vessel (Fig. 7, 8). Thus in-plane...
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