chapter 18: disorders of blood flow and blood pressure objectives

Distinguish between the pathology and manifestations of aortic aneurysms and dissection of the aorta.

AORTIC ANEURYSMS Aortic aneurysms may involve any part of the aorta: the ascending aorta, aortic arch, descending aorta, thoracoabdominal aorta, or abdominal aorta. Multiple aneurysms may be present. The signs and symptoms of aortic aneurysms depend on the size and location. With both thoracic and abdominal aneurysms, the most dreaded complication is rupture. The likelihood of rupture correlates with increasing aneurysm size. Thoracic aneurysms, which are less common than abdominal aortic aneurysms, may involve one or more aortic segments. Most thoracic aneurysms are due to atherosclerosis. Disorders of connective tissue, such as Marfan syndrome, are rare causes but of important clinical significance. The majority of thoracic aneurysms are asymptomatic. When symptoms occur, they depend largely on the size and position of the aneurysm. Substernal, back, or neck pain may occur. There may be dyspnea, stridor, or a brassy cough caused by pressure on the trachea. Hoarseness may result from pressure on the recurrent laryngeal nerve, and there may be difficulty swallowing because of pressure on the esophagus. The aneurysm also may compress the superior vena cava, causing distention of neck veins and edema of the face and neck. Abdominal aortic aneurysms, which are the most common type of aneurysm, usually develop after age 50 and are associated with severe atherosclerosis. They occur more frequently in men than women, and over half of affected persons are hypertensive. Although abdominal aortic aneurysms usually occur in the context of atherosclerosis, it is thought that other factors such as smoking and a genetic predisposition may play a role. Abdominal aortic aneurysms are most commonly located below the level of the renal artery (>90%) and involve the bifurcation of the aorta and proximal end of the common iliac arteries.1 They can involve any part of the vessel circumference (saccular) or extend to involve the entire circumference (fusiform). Most abdominal aneurysms are asymptomatic. Because an aneurysm is of arterial origin, a pulsating mass may provide the first evidence of the disorder. Typically, aneurysms larger than 4 cm are palpable. The mass may be discovered during a routine physical examination or the affected person may complain of its presence. Calcification, which frequently exists on the wall of the aneurysm, may be detected during abdominal radiologic examination. Pain may be present and varies from mild midabdominal or lumbar discomfort to severe abdominal and back pain. As the aneurysm expands, it may compress the lumbar nerve roots, causing lower back pain that radiates to the posterior aspects of the legs. The aneurysm may extend to and impinge on the renal, iliac, or mesenteric arteries, or to the vertebral arteries that supply the spinal cord. An abdominal aneurysm also may cause erosion of vertebrae. Stasis of blood favors thrombus formation along the wall of the vessel, and peripheral emboli may develop, causing symptomatic arterial insufficiency. [AN ABNORMAL BULGE THAT OCCURS IN THE WALL OF THE AORTA.] DISSECTION OF THE AORTA Aortic dissection (dissecting aneurysm) is an acute, life-threatening condition. It involves hemorrhage into the vessel wall with longitudinal tearing of the vessel wall to form a blood-filled channel. Unlike atherosclerotic aneurysms, aortic dissection often occurs without evidence of previous vessel dilation. The dissection can originate anywhere along the length of the aorta but most often involves the ascending aorta. Aortic dissection is caused by conditions that weaken or cause degenerative changes in the elastic and smooth muscle layers of the aorta. There are two risk factors that predispose to aortic dissection: hypertension and degeneration of the medial layer of the vessel wall. It is most common in 40- to 60-year-old men with an antecedent history of hypertension. Aortic dissection also is associated with connective tissue diseases, such as Marfan syndrome. It also may occur during pregnancy because of changes in the aorta that occur during this time. Other factors that predispose to dissection are congenital defects of the aortic valve (i.e., bicuspid or unicuspid valve structures) and aortic coarctation. Aortic dissections are commonly classified into two types, A and B, as determined by the level of dissection. Type A aneurysms, which involve the proximal aorta (ascending aorta only or both the ascending and the descending aorta), are the most common and potentially serious in terms of complications. Type B aneurysms usually begin distal to the subclavian artery and do not involve the ascending aorta. Dissections usually extend distally from the intimal tear. When the ascending aorta is involved, expansion of the wall of the aorta may impair closure of the aortic valve. There also is the risk of aortic rupture with blood moving into the pericardium and compressing the heart. Although the length of dissection varies, it is possible for the abdominal aorta to be involved with progression into the renal, iliac, or femoral arteries. Partial or complete occlusion of the arteries that arise from the aortic arch or the intercostal or lumbar arteries may lead to stroke, ischemic peripheral neuropathy, or impaired blood flow to the spinal cord. A major symptom of a dissecting aneurysm is the abrupt presence of excruciating pain, described as tearing or ripping. Pain associated with dissection of the ascending aorta frequently is located in the anterior chest, and pain associated with dissection of the descending aorta often is located in the back. In the early stages, blood pressure typically is moderately or markedly elevated. Later, the blood pressure and pulse rate become unobtainable in one or both arms as the dissection disrupts arterial flow to the arms. Syncope, hemiplegia, or paralysis of the lower extremities may occur because of occlusion of blood vessels that supply the brain or spinal cord. Heart failure may develop when the aortic valve is involved. [A TEAR IN THE INNER LAYER OF THE AORTA.]

Describe the etiology and clinical manifestations of chronic venous insufficiency.

Chronic venous disease of the lower extremities is manifested by venous hypertension and a range of signs, the most obvious of which are varicose veins and venous ulcers due to venous insufficiency. Venous hypertension represents a sustained increase in venous blood pressures. ETIOLOGY Chronic venous insufficiency is most commonly caused by reflux through incompetent veins, but can also be caused by venous outflow obstruction and impaired function of the skeletal muscle pumps. Pressure in the veins of the legs is determined by two components: a hydrostatic component related to the weight of a column of blood below the level of the heart, and a hydrodynamic component related to the action of the skeletal muscle pump. Prolonged standing increases venous pressure and causes dilation and stretching of the vessel wall. When a person is in the erect position, the full weight of the venous columns of blood is transmitted to the leg veins. The effects of gravity are compounded in persons who stand for long periods without using their leg muscles to assist in pumping blood back to the heart. CLINICAL MANIFESTATIONS Chronic venous insufficiency is characterized by signs and symptoms associated with impaired venous blood flow. In contrast to the ischemia caused by arterial insufficiency, venous insufficiency leads to tissue congestion, edema, and eventual impairment of tissue nutrition. The edema is exacerbated by long periods of standing. Necrosis of subcutaneous fat deposits occurs, followed by skin atrophy. Brown pigmentation of the skin caused by hemosiderin deposits resulting from the breakdown of red blood cells is common. Secondary lymphatic insufficiency occurs, with progressive sclerosis of the lymph channels in the face of increased demand for clearance of interstitial fluid. In advanced venous insufficiency, impaired tissue nutrition causes stasis dermatitis and the development of stasis or venous ulcers. Stasis dermatitis is characterized by the presence of thin, shiny, bluish brown, irregularly pigmented, desquamative skin that lacks the support of the underlying subcutaneous tissues. Minor injury leads to relatively painless ulcerations that are difficult to heal. The lower part of the leg is particularly prone to development of stasis dermatitis and venous ulcers. Most lesions are located medially over the ankle and lower leg, with the highest frequency just above the medial malleolus. [IMPROPER FUNCTIONING OF THE VEIN VALVES IN THE LEG, CAUSING SWELLING AND SKIN CHANGES.]

Cite the definition of hypertension.

High blood pressure.

Identify lifestyle risk factors associated with hypertension.

Lifestyle factors can contribute to the development of hypertension by interacting with other risk factors. These lifestyle factors include: -high salt intake -excessive calorie intake -obesity -excessive alcohol consumption.

Compare the pathophysiology and manifestations of ischemia associated with peripheral arterial disease, thromboangiitis obliterans, and Raynaud phenomenon.

PERIPHERAL ARTERIAL DISEASE Peripheral artery disease (PAD) refers to the obstruction of large arteries that supply the body's peripheral structures rather than its central structures such as the heart or brain. Often PAD is a term used to refer to atherosclerotic blockages found in the lower extremities. Peripheral artery disease can result from atherosclerosis, inflammatory processes leading to stenosis, embolism, or thrombus formation. It causes either acute or chronic ischemia. The disease is seen most commonly in men in their 60s and 70s. The risk factors for PAD are similar to those for coronary artery disease. Cigarette smoking and diabetes mellitus are the strongest risk factors, with more than 80% of persons with the disorder being current or former smokers. As with atherosclerosis in other locations, the signs and symptoms of vessel occlusion are gradual. The primary symptom of chronic obstructive arterial disease is pain with walking or claudication (from the Latin verb claudicare, "to limp"). Typically, persons with the disorder complain of calf pain because the gastrocnemius muscle has the highest oxygen consumption of any muscle group in the leg during walking. Some persons may complain of a vague aching feeling or numbness, rather than pain. Other activities such as swimming, bicycling, and climbing stairs use other muscle groups and may not incite the same degree of discomfort as walking. Other signs of ischemia include atrophic changes and thinning of the skin and subcutaneous tissues of the lower leg and diminution in the size of the leg muscles. The foot often is cool, and the popliteal and pedal pulses are weak or absent. Limb color blanches with elevation of the leg because of the effects of gravity on perfusion pressure and becomes deep red when the leg is in the dependent position because of an autoregulatory increase in blood flow and a gravitational increase in perfusion pressure. When blood flow is reduced to the extent that it no longer meets the minimal needs of resting muscle and nerves, ischemic pain at rest, ulceration, and gangrene develop. As tissue necrosis develops there typically is severe pain in the region of skin breakdown, which is worse at night with limb elevation and is improved with standing. [A CIRCULATORY CONDITION IN WHICH NARROWED BLOOD VESSELS REDUCE BLOOD FLOW TO THE LIMBS.] THROMBOANGIITIS OBLITERANS Thromboangiitis obliterans, also known as Buerger disease, is a recurring progressive, nonatherosclerotic inflammation and thrombosis of small and medium-sized arteries and veins, usually the plantar and digital vessels in the foot and lower leg. Arteries in the arm and hand also may be affected. Although primarily an arterial disorder, the inflammatory process often extends to involve adjacent veins and nerves. Usually it is a disease of young, heavy cigarette smokers, occurring before the age of 35. The pathogenesis of Buerger disease remains elusive, though cigarette smoking and in some instances tobacco chewing seem to be involved. It has been suggested that the tobacco may trigger an immune response in susceptible persons or it may unmask a clotting defect, either of which could incite an inflammatory reaction of the vessel wall. It is more common in the Mediterranean region, Middle East, and Asia. Pain is the predominant symptom of the disorder. It usually is related to distal arterial ischemia. During the early stages of the disease, there is intermittent claudication in the arch of the foot and the digits. In severe cases, pain is present even when the person is at rest. The impaired circulation increases sensitivity to cold. The peripheral pulses are diminished or absent, and there are changes in the color of the extremity. In moderately advanced cases, the extremity becomes cyanotic when the person assumes a dependent position, and the digits may turn reddish-blue even when in a nondependent position. With lack of blood flow, the skin becomes thin and shiny, hair growth slows, and nail growth is impaired. Chronic ischemia causes thick, malformed nails. If the disease continues to progress, tissues eventually ulcerate and gangrenous changes arise that may necessitate amputation. [A RECURRING PROGRESSIVE INFLAMMATION AND THROMBOSIS (CLOTTING) OF SMALL AND MEDIUM ARTERIES AND VEINS OF THE HANDS AND FEET.] RAYNAID PHENOMENON Raynaud phenomenon is a functional disorder caused by intense vasospasm of the arteries and arterioles in the fingers and, less often, the toes. The disorder is divided into primary and secondary types. Primary Raynaud phenomenon is seen in otherwise healthy young women, and it often is precipitated by exposure to cold or by strong emotions and usually is limited to the fingers. The cause of vasospasm in primary Raynaud phenomenon is unknown or idiopathic. Hyperreactivity of the sympathetic nervous system has been suggested as a contributing cause. Secondary Raynaud phenomenon is associated with previous vessel injury, such as frostbite, occupational trauma associated with the use of heavy vibrating tools, collagen diseases, neurologic disorders, chronic arterial occlusive disorders, and drugs, such as bleomycin. Another occupation-related cause is the exposure to alternating hot and cold temperatures such as that experienced by butchers and food preparers. Raynaud phenomenon often is the first symptom of collagen diseases. It occurs in almost all persons with scleroderma and can precede the diagnosis of scleroderma by many years. The ischemic phase of Raynaud phenomenon is manifested by changes in skin color that progress from pallor to cyanosis, a sensation of cold, and changes in sensory perception, such as numbness and tingling. The color changes usually are first noticed in the tips of the fingers, later moving into one or more of the distal phalanges. After the ischemic episode, there is a period of hyperemia with intense redness, throbbing, and paresthesias. The period of hyperemia is followed by a return to normal color. Primary Raynaud phenomenon attacks typically involve all fingers in a symmetric fashion and are associated with minimal pain, whereas asymmetric finger involvement and intense pain suggest secondary Raynaud phenomenon. In severe progressive cases, trophic skin changes may develop. The nails may become brittle, and the skin over the tips of the affected fingers may thicken. Ulceration and superficial gangrene of the fingers, although infrequent, may occur. [A CONDITION THAT CAUSES BLOOD VESSELS TO NARROW WHEN YOU ARE COLD OR STRESSED = BLOOD CAN'T GET TO SURFACE OF SKIN = AFFECTED AREAS TURN WHITE AND BLUE.]

Differentiate between primary and secondary forms of hypertension.

PRIMARY HYPERTENSION Essential (primary) hypertension is the term applied to hypertension for which no cause can be identified. Although the cause or causes of essential hypertension are largely unknown, both constitutional and lifestyle factors have been implicated, either singly or collectively, as contributing factors. [HYPERTENSION FOR UNKNOWN REASONS.] SECONDARY HYPERTENSION Secondary hypertension, which describes an elevation in blood pressure due to another disease condition, accounts for 5% to 10% of hypertension cases. Unlike essential hypertension, many of the conditions causing secondary hypertension can be corrected or cured by surgery or specific medical treatment. Secondary hypertension tends to be seen in persons younger than 30 and older than 50 years of age. Among the most common causes of secondary hypertension are kidney disease, adrenal cortical disorders, pheochromocytoma, and coarctation of the aorta. Oral contraceptive agents are also implicated as a cause of secondary hypertension. Cocaine, amphetamines, and other illicit drugs can also cause a significant elevations in blood pressure, as can sympathomimetic agents (decongestants, anorectics), erythropoietin, and licorice (including some chewing tobaccos with licorice as an ingredient). Obstructive sleep apnea is an independent risk factor for secondary hypertension. [OTHER DISEASE CONDITION = HYPERTENSION.]

Explain how fluid deficit, medications, aging, and bed rest contribute to the development of orthostatic hypotension.

REDUCED BLOOD VOLUME Orthostatic hypotension often is an early sign of reduced blood volume or fluid deficit. When blood volume is decreased, the vascular compartment is only partially filled; although cardiac output may be adequate when a person is in the recumbent position, it often decreases to the point of causing weakness and fainting when the person assumes the standing position. Common causes of orthostatic hypotension related to hypovolemia are excessive use of diuretics, excessive diaphoresis, loss of gastrointestinal fluids through vomiting and diarrhea, and loss of fluid volume associated with prolonged bed rest. DRUG-INDUCED HYPOTENSION Antihypertensive drugs and psychotropic drugs are a common cause of chronic orthostatic hypotension. In most cases, the orthostatic hypotension is well tolerated. If postural hypotension is severe enough to cause light-headedness or dizziness, it is recommended that the dosage of the drug be reduced or a different drug be used. AGING Weakness and dizziness on standing are common complaints of elderly persons. Orthostatic tolerance is usually well maintained until the age of 70 years, after which there is an increasing tendency toward arterial pressure instability and postural hypotension. Although orthostatic hypotension may be either systolic or diastolic, hypertensoin associated with aging seems more often to be systolic. Several deficiencies in the circulatory response may predispose the elderly to this problem, including diminished ability to produce an adequate increase in the heart rate, ventricular stroke volume, or peripheral vascular resistance; decreased function of the skeletal muscle pumps; and decreased blood volume. Because cerebral blood flow primarily depends on systolic pressure, persons with impaired cerebral circulation may experience symptoms of weakness, ataxia, dizziness, and syncope when their arterial pressure falls even slightly. This may occur in older persons who are immobilized for even brief periods or whose blood volume is decreased owing to inadequate fluid intake or overzealous use of diuretics. Postprandial blood pressure often decreases in elderly persons. The greatest postprandial changes occur after a high-carbohydrate meal. Although the mechanism responsible for these changes is not fully understood, it is thought to result from glucose-mediated impairment of baroreflex sensitivity and increased splanchnic blood flow mediated by insulin and vasoactive gastrointestinal hormones. BED REST Prolonged bed rest promotes a reduction in plasma volume, a decrease in venous tone, failure of peripheral vasoconstriction, and weakness of the skeletal muscles that support the veins and assist in returning blood to the heart. Physical deconditioning follows even short periods of bed rest. After 3 to 4 days, the blood volume is decreased. Loss of vascular and skeletal muscle tone is less predictable but often becomes maximal after approximately 2 weeks of bed rest. Orthostatic intolerance is a recognized problem of space flight—a potential risk after reentry into the earth's gravitational field.

List risk factors and clinical manifestation for atherosclerosis.

RISK FACTORS NONMODIFIABLE -increasing age -male gender -genetic disorders of lipid metabolism -family history of premature coronary artery disease POTENTIALLY MODIFIABLE -cigarette smoking -obesity -hypertension -hyperlipidemia with elevated low-density lipoprotein and low high-density lipoprotein cholesterol -diabetes mellitus ADDITIONAL NONTRADITIONAL -inflammation marked by elevated C-reactive protein levels -hyperhomocysteinemia -increased lipoprotein (a) levels CLINICAL MANIFESTATIONS Atherosclerosis usually doesn't cause signs and symptoms until it severely narrows or totally blocks an artery. Many people don't know they have the disease until they have a medical emergency, such as a heart attack or stroke. Signs and symptoms will depend on the vessels involved and the extent of vessel obstruction. Atherosclerotic lesions produce their effects through narrowing of the vessel and production of ischemia; sudden vessel obstruction due to plaque hemorrhage or rupture; thrombosis and formation of emboli resulting from damage to the vessel endothelium; and aneurysm formation due to weakening of the vessel wall. In larger vessels, such as the aorta, the important complications are those of thrombus formation and weakening of the vessel wall. In medium-sized arteries, such as the coronary and cerebral arteries, ischemia and infarction due to vessel occlusion are more common. Although atherosclerosis can affect any organ or tissue, the arteries supplying the heart, brain, kidneys, lower extremities, and small intestine are most frequently involved.

Cite risk factors associated with venous thrombosis and describe the manifestation of the disorder.

RISK FACTORS VENOUS STASIS -bed rest -immobility -spinal cord injury -acute myocardial infarction -congestive heart failure -shock -venous obstruction HYPERREACTIVITY OF BLOOD COAGULATION -genetic factors -stress and trauma -pregnancy -childbirth -oral contraceptive and hormone replacement use -dehydration -cancer -antiphospholipid syndrome -hyperhomocysteinemia VASCULAR TRAUMA -indwelling venous catheters -surgery -massive trauma or infection -fractured hip orthopedic surgery CLINICAL MANIFESTATIONS Many persons with venous thrombosis are asymptomatic, probably because the vein is not totally occluded or because of collateral circulation. When present, the most common signs and symptoms of venous thrombosis are those related to the inflammatory process: pain, swelling, and deep muscle tenderness. Fever, general malaise, and an elevated white blood cell count and erythrocyte sedimentation rate are accompanying indications of inflammation. There may be tenderness and pain along the vein. Swelling may vary from minimal to maximal. As many as 50% of persons with DVT are asymptomatic. The site of thrombus formation determines the location of the physical findings. The most common site is in the venous sinuses in the soleus muscle and posterior tibial and peroneal veins. Swelling in these cases involves the foot and ankle, although it may be slight or absent. Calf pain and tenderness are common. Femoral vein thrombosis produces pain and tenderness in the distal thigh and popliteal area. Thrombi in ileofemoral veins produce the most profound manifestations, with swelling, pain, and tenderness of the entire extremity. With DVT in the calf veins, active dorsiflexion produces calf pain (i.e., Homans' sign). [A BLOOD CLOT THAT FORMS WITHIN A VEIN.]

Define systolic hypertension and relate the circulatory changes that occur with aging that predispose to the development of systolic hypertension.

SYSTOLIC HYPERTENSION A systolic pressure of 140 mm Hg or greater and a diastolic pressure of less than 90 mm Hg. SYSTOLIC HYPERTENSION IN THE AGING The prevalence of hypertension increases with advancing age to the extent that half of people aged 60 to 69 years and approximately three fourths of people 70 years and older are affected. The age-related rise in systolic blood pressure is primarily responsible for the increase in hypertension that occurs with increasing age. Among the aging processes that contribute to an increase in blood pressure are a stiffening of the large arteries, particularly the aorta; decreased baroreceptor sensitivity; increased peripheral vascular resistance; and decreased renal blood flow. Systolic blood pressure rises almost linearly between 30 and 84 years of age, whereas diastolic pressure rises until 50 years of age and then levels off or decreases. This rise in systolic pressure is thought to be related to increased stiffness of the large arteries. With aging, the elastin fibers in the walls of the arteries are gradually replaced by collagen fibers that render the vessels stiffer and less compliant. Differences in the central and peripheral arteries relate to the fact that the larger vessels contain more elastin, whereas the peripheral resistance vessels have more smooth muscle and less elastin. Because of increased wall stiffness, the aorta and large arteries are less able to buffer the increase in systolic pressure that occurs as blood is ejected from the left heart, and they are less able to store the energy needed to maintain the diastolic pressure. As a result, the systolic pressure increases, the diastolic pressure remains unchanged or actually decreases, and the pulse pressure or difference between the systolic pressure and diastolic pressure widens. Isolated systolic hypertension (systolic pressure ≥140 mm Hg and diastolic pressure <90 mm Hg) is recognized as an important risk factor for cardiovascular morbidity and mortality in older persons. The treatment of hypertension in the elderly has beneficial effects in terms of reducing the incidence of cardiovascular events such as stroke. Studies have shown a reduction in stroke, coronary heart disease, and congestive heart failure in persons who were treated for hypertension compared with those who were not.

Describe the pathogenesis and mechanisms involved in the development of atherosclerosis.

The lesions associated with atherosclerosis are of three different stages or subtypes: fatty streaks, fibrous atheromatous plaques, and complicated lesions. The latter two are responsible for the clinically significant manifestations of the disease. Fatty streaks appear as thin yellow lines running along the major arteries, such as the aorta. The streak consists of smooth muscle cells filled with cholesterol and macrophages (a type of immune system "scavenger" cell that removes harmful substances, such as excess cholesterol particles, from the bloodstream). The first evidence of atherosclerosis, fatty streaks can be found in children 10 to 14 years of age regardless of gender or race. They increase in number until about 20 years of age, and then remain static or regress. The fatty streak alone does not cause any symptoms but, over time, can develop into a more advanced form of atherosclerosis called an atheroma or fibrous plaque. The fibrous atheromatous plaque is the basic lesion of clinical atherosclerosis. It is characterized by the accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, formation of scar tissue, and calcification. The lesions begin as a gray to pearly white, elevated thickening of the vessel intima with a core of extracellular lipid covered by a fibrous cap of connective tissue and smooth muscle. As the lesions increase in size, they encroach on the lumen of the artery and eventually may occlude the vessel or predispose to thrombus formation, causing a reduction of blood flow. Because blood flow is related to the fourth power of the vessel radius, the reduction in blood flow becomes increasingly greater as the disease progresses. Complicated atherosclerotic lesions develop when the fibrous plaque breaks open, producing hemorrhage, ulceration, and scar tissue deposits. Thrombosis is the most important complication of atherosclerosis. It is caused by slowing and turbulence of blood flow in the region of the plaque and ulceration of the plaque. Although the risk factors associated with atherosclerosis have been identified through epidemiologic studies, many unanswered questions remain regarding the mechanisms that contribute to the development of atherosclerotic lesions. [A DISEASE OF THE ARTERIES CHARACTERIZED BY THE DEPOSITION OF PLAQUES OF FATTY MATERIAL ON THEIR INNER WALLS.]

Describe the etiology and clinical manifestations of varicose veins.

Varicose, or dilated, tortuous veins of the lower extremities are common and often lead to secondary problems of venous insufficiency. Varicose veins are described as being primary or secondary. Primary varicose veins originate in the superficial saphenous veins, and secondary varicose veins result from impaired flow in the deep venous channels. Approximately 80% to 90% of venous blood from the lower extremities is transported through the deep channels. The development of secondary varicose veins becomes inevitable when flow in these deep channels is impaired or blocked. The most common cause of secondary varicose veins is deep vein thrombosis. Other causes include congenital or acquired arteriovenous fistulas, congenital venous malformations, and pressure on the abdominal veins caused by pregnancy or a tumor. ETIOLOGY Prolonged standing and increased intra-abdominal pressure are important contributing factors in the development of primary varicose veins. Because there are no valves in the inferior vena cava or common iliac veins, blood in the abdominal veins must be supported by the valves located in the external iliac or femoral veins. When intra-abdominal pressure increases, as it does during pregnancy, or when the valves in these two veins are absent or defective, the stress on the saphenofemoral junction is increased. The high incidence of varicose veins in women who have been pregnant also suggests a hormonal effect on venous smooth muscle contributing to venous dilation and valvular incompetence. Lifting also increases intra-abdominal pressure and decreases flow of blood through the abdominal veins. Occupations that require repeated heavy lifting predispose to development of varicose veins. Prolonged exposure to increased pressure causes the venous valves to become incompetent so they no longer close properly. When this happens, the reflux of blood causes further venous enlargement, pulling the valve leaflet apart and causing more valvular incompetence in sections of adjacent distal veins. Another consideration in the development of varicose veins is the fact that the superficial veins have only subcutaneous fat and superficial fascia for support, whereas the deep venous channels are supported by muscle, bone, and connective tissue. Obesity reduces the support provided by the superficial fascia and tissues, increasing the risk for development of varicose veins. CLINICAL MANIFESTATIONS The signs and symptoms associated with primary varicose veins vary. Most women with superficial varicose veins complain of their unsightly appearance. In many cases, aching in the lower extremities and edema, especially after long periods of standing, may occur. The edema usually subsides at night when the legs are elevated. When the communicating veins are incompetent, symptoms are more common. [GNARLED, ENLARGED VEINS, MOST COMMONLY APPEARING IN THE LEGS AND FEET.]