PERIPHERAL VASCULAR DISEASE

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PERIPHERAL VASCULAR DISEASE

ANATOMY

GENERAL FEATURE OF BLOOD VESSELS

Blood vessels outside of the heart can be placed in two classes:

SYSTEMIC VESSELS

Transport blood through all parts of the body from the left ventricle and back to the right atrium.

Blood flowing through the systemic circulation supplies oxygen and nutrients to all tissues of the body and carries away carbon dioxide and waste.

PULMONARY VESSELS

Transport blood from the right ventricle through the lungs and back to the left atrium.

Blood flowing through the pulmonary circulation takes up oxygen through the lungs and release carbon dioxide.

LAYERS OF BLOOD VESSEL WALL

TUNICA INTIMA

Consists of endothelium composed of simple squamous epithelial cells and small amount of connective tissue.

TUNICA MEDIA

Consists of smooth muscle cells arranged circularly around the blood vessel.

It also contains variable amounts of elastic and collagen fibers, depending on the size and type of vessel.

TUNICA ADVENTITIA

Composed of connective tissue, which varies from dense connective tissue adjacent to the tunica media to loose connective tissue toward the outer portion of blood vessel wall.

ARTERIES

Are blood vessels that carry blood away from the heart. Blood is pumped from the ventricles of the heart into large elastic arteries, which branch repeatedly to form progressively smaller arteries. As they become smaller, the arteries undergo a gradual transition from having walls containing more elastic tissue than smooth muscle to having walls with more smooth muscle than elastic tissue. Although the arteries form a continuum from the largest to the smallest branch they are normally classified as:

Elastic Arteries (Aorta and large arteries)

Are the largest diameter arteries and have the thickest wall.

Stretched when the ventricles of heart pump blood into them. The elastic tissue allows them to distend during systole to accommodate the stroke volume with only a moderate increase in pressure.

The elastic recoil prevents blood pressure from falling rapidly and maintains blood flow while the ventricles are relaxed.

Function as WINKESSEL VESSELS.

Muscular Arteries

Included medium-sized and small-diameter arteries.

Medium-sized arteries are frequently called distributing arteries because the smooth muscle tissue enables these vessels to control blood flow to different regions of the body by either constricting or dilating. It supplied blood to small-diameter arteries.

Small-diameter arteries have about the same structure as the medium-sized arteries except for its diameter.

Arterioles

Transport blood from the small arteries to capillaries and are smallest arteries in which the three tunics can be identified.

When the smooth muscles of the small arteries and arterioles are activated, they allow the vessels to constrict their lumen, causing an increase in the pressure centrally and decrease the pressure peripherally.

These vessels function as RESISTANCE VESSEL.

CAPILLARIES

Capillaries have thinner walls, blood flow through them more slowly, and there are far more of them than any other blood vessel type.

The capillary wall consists of endothelium and is surrounded by delicate layer of loose connective tissue. Capillaries are 0.5 to 1mm long, and they branch without a change in their diameter.

Function as EXCHANGE VESSELS.

Capillaries branch off from the metaterioles. Metaterioles branch off from the arterioles at right angles. They serve as through-channels to the venules or high resistance tubes between arterioles and veins. Blood flow from arterioles into capillaries, which branch to form networks. Red blood cells flow through most capillaries in single file and are frequently folded as they pass through the smaller diameter capillaries. Blood flow through the capillaries is regulated by smooth muscle cells called PRECAPILLARY SPHINCTERS located at the origin of the branches. These sphincters serve as the main control over capillary flow, and such function is SPHINCTER VESSELS. As blood flows through the capillaries, blood gives up oxygen and nutrients to the tissue spaces and takes up carbon dioxide and other byproducts of metabolism.

VEINS

The walls of the vein and venules are very thin, with only small amounts of elastin and limited smooth muscle. They contain about four times more blood than the arterial system because of their great distensibility.

They function as CAPACITANCE VESSELS.

Venules

Are tubes with a diameter larger than capillaries and are composed of endothelium resting on a delicate connective tissue membrane.

The structure of venules, except for their diameter, is very similar to capillaries.

Small Veins

Are slightly larger in diameter than venules, and their walls contain a continuous layer of smooth muscle cells.

Medium-Sized Veins

Collect blood from small vein and deliver it to large veins.

Veins having diameter greater than 2 mm contain valves. The valves allow blood to flow toward the heart but not in the opposite direction. There are many valves in the medium-sized veins. There are more valves in veins of the legs than in veins of the arms. This prevents the flow of blood toward the feet in response to the pull of gravity.

Large Veins

Contains the largest blood volume in the circulation.

ARTERIOVENOUS ANASTOMOSES

Short channels that connect arterioles to venules, bypassing the capillaries.

Predominant in the palms, fingers, and ear lobes.

Abundantly innervated by vasoconstrictor nerve fibers.

Function as SHUNT VESSELS.PHYSIOLOGY

BLOOD PRESSURE

Refers to the force the blood exerts against a vessel wall.

Because liquid flows only from a higher to a lower pressure, the pressure is highest in the arteries, lower in the capillaries, and lowest in the veins.

SYSTOLIC PRESSURE

The highest pressure exerted by the blood against the arterial walls during cardiac contraction.

DIASTOLIC PRESSURE

The lowest pressure exerted by the blood against the arterial wall during cardiac relaxation.

PULSE PRESSURE

Difference between systolic pressure and diastolic pressure.

REGULATORY MECHANISMS

LOCAL CONTROL OF BLOOD VESSELS

Local control of blood flow is achieved by periodic contraction and relaxation of the precapillary sphincter. Because of t he contraction and relaxation of the precapillary sphincters, blood flow through the capillaries is cyclic. The precapillary sphincters are controlled by the metabolic needs of the tissues. Blood flow increase when oxygen levels decrease, or to a lesser degree, when glucose, amino acids, fatty acids, and other nutrients decrease. Blood flow also increase when byproducts of metabolism build up in tissue spaces. An increase in carbon dioxide or decrease in pH causes the precapillary sphincters to relax.

NERVOUS CONTROL OF BLOOD VESSELS

AFFERENT RECEPTORS

BARORECEPTORS (Pressoreceptors)

Stimulated by stretch of the vessel wall from alteration in pressure.

CAROTID SINUSES

Baroreceptors that are located at the carotid arteries.

Monitor the blood pressure to the brain.

AORTIC SINUSES

Baroreceptors that are located at the aortic arch.

Responsible for monitoring the blood pressure throughout the body.

If there will be an increase in blood pressure, the baroreceptors will send an input to the vasomotor center which will results to inhibition of the vasoconstrictor center of the medulla and excitation of the vagal center. This results in decrease heart rate, decrease force of cardiac contraction, vasodilation, and subsequent decrease in blood pressure. When there is a drop in blood pressure the opposite mechanism will happen.

CHEMORECEPTORS

Stimulated by reduction of arterial oxygen concentrations, increase in carbon dioxide tension, and increased hydrogen ions concentration.

CAROTID BODIES

Chemoreceptors located at the carotid arteries.

AORTIC BODIES

Chemoreceptors located at the aortic arch.

Impulses from these receptors travel to the brain (cardioregulatory and vasomotor center) via afferent pathways in the vagus and glossopharyngeal nerves. Efferent impulse from these centers, in response to alterations in blood pressure, will alter the heart rate, strength of cardiac contractions, and size of blood vessel.

VASOMOTOR CENTER

Is located bilaterally in the lower pons and upper medulla. It transmits impulses through sympathetic nerves to all vessels of the body. The vasomotor center is tonically active, producing a slow, continual firing in all vasoconstrictor nerve fibers. It is this slow, continual firing that maintains a partial state of contraction of blood vessels and provides a normal VASOMOTOR TONE. The vasomotor center assist in providing a stable arterial pressure required to maintain blood flow to body tissue and organs. This occurs because of its close connection to the cardiac controlling center in the medulla. Additionally, the vasomotor and cardiac controlling centers require input from afferent receptors.

HORMONAL CONTROL OF BLOOD VESSELS

ADRENAL MEDULLARY MECHANISM

Epinephrine released from the adrenal medulla as a result of sympathetic stimulation increase heart rate, stroke volume, and vasoconstriction.

RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM

Renin is released by the kidneys in response to lower blood pressure. Renin promotes the production of angiotensin which, when activated, causes vasoconstriction and increase in aldosterone secretion. Aldosterone reduces urine output.

VASOPRESSIN MECHANISM

Antidiuretic hormone (vasopressin) released from the posterior pituitary causes vasoconstriction and reduces urine output.

ATRIAL NATRIURETIC MECHANISM

Atrial natriuretic factor is released from the heart when atrial blood pressure increases. It stimulates an increase in urine production, causing a decrease in blood volume and blood pressure.

FACTORS THAT INFLUENCE BLOOD PRESSURE

Blood volume

Elasticity of blood vessels

Cardiac output

Age

Exercise

Valsalva maneuver

Blood viscosity

Positioned between the layers of endothelial cells and perivascular nerves are the smooth muscle cells responsible for the control of arterial and venous tone and distribution of blood flow throughout the body. The connections between the arteries and veins can be divided into the resistance vessels (arterioles), exchange vessels (capillaries), and capacitance vessels (venules). The regulatory mechanism in the above components involves humoral and nervous mechanisms, with complex interactions between smooth muscle cells, perivascular nerves, and endothelium and the local metabolic products. The smooth muscle cells form circular layers around the vessels and are innervated by perivascular nerve fibers. Transmitters released by these fibers activate receptors on the vascular smooth muscle cell membrane with resultant vasoconstriction or vasodilation. The major neurologic control of blood vessel tone is accomplished by sympathetic nerves and norepinephrine is the principal neurotransmitter that causes vasoconstriction via alpha adrenoreceptors, along with receptor-operated calcium channels. The amount of neurotransmitter release depends on the degree of stimulation of the sympathetic fibers and the presence of local metabolic and circulating vasoactive substances as well as autoregulation.

Newer research has shown the role of endothelial cells in the regulation of blood flow. Endothelial cells respond to various stimuli regulating the tone of the in the smooth muscle cells. These stimuli include substances such as endothelium-derived relaxing factor, prostacyclin, endothelium-derived contracting factor, and angiotensin II, which effect platelet aggregation, platelet adhesion, and smooth muscle proliferation.

In order to develop strategies for prevention and treatment of vascular diseases, it is imperative to understand how vascular smooth muscle cells contract and relax in response to physical and chemical stimulation, the role that endothelium plays in this complex process, and the pathophysiology of the disease processes that disturb the fine balance in this regulation.

PATHOPHYSIOLOGY

Congenital or acquired defects in endothelial cell function could lead to imbalance to imbalance between relaxing and contracting factors, which is one of the major factors leading to pathophysiologic changes in the function of blood vessel walls. Endothelial dysfunction has been demonstrated in the several diseases of the peripheral blood vessels, including hypertension, diabetes, atherosclerosis, hyperlipidemia, and vasospasm.

Changes in the morphology and histology of the vascular system may range from thickening of capillary basement membrane, a decrease in the density of the microvessels, endothelial cell degeneration, and increased platelet adhesion and aggregation in diabetes mellitus, to endothelial injury, endothelial fat accumulation with fatty streak formation, and smooth muscle proliferation in atherosclerosis.

ETIOLOGY

There are many causes of arterial occlusive disease, the most common of which is atherosclerosis obliterans (ASO). Other disease processes include thromboangitis obliterans (Buergers disease), vasospastic disorders (Raynauds phenomenon, livedo reticularis, and acrocyanosis), thrombosis, embolism, dissection, vasculitis and fibromuscular dysplasia.

ATHEROSCLEROSIS

Atherosclerosis in its advanced form is a systemic disorder involving the coronary, cerebral, pulmonary, renal, and peripheral vessels. The earliest manifestation of atherosclerosis appears to be the intimal streak, although the eventual progression of streaks to fibrous or complicated plaques remains uncertain. The plaques tend to develop at branch points, bifurcations, zones of rapid tapering, and areas where arteries follow a tortuous course. Arherosclerosis typically involves multiple level of the arterial tree; however, it tends to be a segmental disease in which intervening arterial segments can be remarkably free of involvement or minimally involved. Associated conditions can affect the location of disease. In diabetics, atherosclerosis occurs with equal frequency in both femoral and tibial arteries, whereas in nondiabetics the most common sites of severe disease are the abdominal aorta and iliac and femoral arteries. Potentially reversible factors that increase the risk of atherosclerosis include smoking, hyperlipidemia, hypertension, diabetes, and obesity. Most people younger than 65 years who have atherosclerosis have one or more identifiable risk factors. The presence of multiple risk factors further increases the risk of atherosclerosis. Cigarette smoking is by far the most common risk factor, competing with juvenile diabetes mellitus and certain rare congenital hyperlipidemias as the most serious. Smoking acts synergistically with other risk factors such as hypertension, or hypercholesterolemia to enhance progression of atherosclerotic lesions. The calculated risk of developing claudication is 15 times higher in male smokers than in nonsmokers, 7 times higher in female smokers than in nonsmokers, and directly related to the number of cigarette smoked.

Atherosclerosis of the arteries in the lower limbs is one of the strongest indicators of atherosclerosis in other vessels in the body, such as the coronary and cerebral blood vessels. In the lower extremities it involves mostly the large and medium sized arteries. Lesions tend to develop at major arterial bifurcations and sites of acute vessel angulation. The disease does not affect all arteries to the same extent but shows a predilection for coronary arteries, carotid bifurcation, aortoiliac and lower extremity vessels. The lower extremity site most commonly affected is the arterial segment between the superficial femoral and popliteal arteries in Hunters canal. In nondiabetics, aortoiliac disease is the second most likely location, whereas in diabetics, popliteal and tibial disease are more likely to follow femoral disease.

RISK FACTORS

A number of factors predispose to the development or acceleration of atherosclerosis:

1. Clinical and experimental studies have established that elevated plas-

Ma concentration of lipoproteins, particularly low-density lipoproteins,

Increase the risk and rate of progression of atherosclerosis. Cholesterol is a major constituent of advanced lesions. In patients with significant atherosclerosis, the mean plasma cholesterol was found to be more than 50 mg/dl higher than in controls.

2. Smoking is described as the single most powerful risk factor for peripheral vascular disease. Relative risk of smoking in the development of leg arterial disease ranges from 1.4 to more than 10 times depending on age, sex, definition of a smoker, and methods of evaluation of arterial disease. Three quarters of cases of intermittent claudication could eventually be attributed to smoking.

3. Hypertension exacerbates atherosclerosis with each incremental increase in pressure, directly increasing the risk of coronary artery disease. Systolic blood pressure appears to be a better predictor of arterial disease than diastolic blood pressure. Hypertension was found in 25 % of patient with symptomatic disease of the aortoiliac and femoral popliteal arteries, but was found in only 9 % of age-matched controls. The mechanism appears to be related to endothelial injury from hypertensive pressure or hemodynamic shearing.

4. Diabetes mellitus is associated with the earlier onset of atherosclerosis and a more rapid disease progression. The obstructive disease of the large arteries in diabetes, usually designated as macroangiopathy, is commonly held as indistinguishable from atherosclerosis in nondiabetes. In diabetes, distal vessels are more involved than are aortoiliac vessels; proposed mechanisms include disturbance of normal platelet, endothelial, and smooth muscle cell function, secondary to hyperglycemia, causing vasoconstriction and smooth muscle proliferation.

5. Other risk factors for generalized atherosclerosis include obesity, hyperuricemia, sedentary life-style, and a positive family history.

COMMON PERIPHERAL VASCULAR DISEASES

ARTERIAL DISEASES

CHRONIC ARTERIAL DISEASE

1. THOMBOANGITIS OBLITERANS

A disease involving thrombosis and inflammation of small peripheral arteries and veins. The process tends to begin in the smaller peripheral arteries of the extremities. Lesions are usually located distal to the knee or elbow. Most theories implicate some component of cigarette smoking that predisposes the arterial wall to inflammation, possibly through the formation of immune complexes.

It initially occurs in the small arteries of the feet and hands and progresses proximally and results in vasoconstriction, decreased arterial circulation to the extremities, ischemia, and eventual necrosis and ulceration of soft tissues.

The inflammatory reaction and resulting signs and symptoms can be controlled if the patient stops smoking.

This is predominantly seen in young, male patient who smoke, involves an inflammatory reaction of the arteries to nicotine.

The pathology responsible for the clinical symptoms of decreased temperature and eventual tissue necrosis, is an inflammatory process in the veins and arteries that appears to be directly related to tobacco use. Nicotine is also a very potent vasoconstrictor and is responsible for the more immediate decrease in skin temperature seen in smokers.

2. ARTERIOSCLEROSIS OBLITERANS

Other names:

Chronic arteriosclerotic vascular disease

Atherosclerotic occlusive disease

Progressive arterial occlusive disease

The circulation progressively deteriorates because of narrowing, fibrosis, and occlusion of the large and medium arteries, usually in the lower extremities.

It is the most common of all arterial disease affecting the lower extremities.

It is a manifestation of the generalized disease, ATHEROSCLEROSIS.

The disease is most often seen in elderly patients and is common associated with DIABETES MELLITUS.

Since it is a slowly developing, degenerative process, its manifestations occur insidiously. The disease begins with monocytes adherence to the endothelial wall following some form of physical damage such as trauma, hypertension, or a biochemical process. A fatty streak begins to develop and subsequently results in the production of an atheromatous plaque in the intima of the artery. As the plaque increases in size the lumen is narrowed and linear flow of blood is impaired.

CLINICAL PRESENTATION:

Intermittent claudication(earliest presenting symptom)

As the disease progresses, the arterial flow may become impaired to the point that pain is present even at rest.

Diminished/absent pedal pulse

Positive sign for rubor dependency

Trophic changes(more pronounced disease)

Ulceration

3. DIABETIC ANGIOPATHY

Diabetes mellitus is a major risk factor in peripheral vascular disease. Diabetes presents with both metabolic and vascular components, which are likely strongly interrelated.

Metabolically, there is an inappropriate elevation in the blood glucose level, which is associated with a disturbed lipid and protein metabolism.

The vascular dysfunction involves an accelerated version of atherosclerotic process.

The alteration in the coetaneous sensation becomes a major problem, as patients tend to develop neurotrophic ulcers due to an inability to perceive pressure on the body parts, particularly the feet.

4. TAKAYASUSS DISEASE

Pulseless disease

Primary Aortic Arteritis

An idiopathic inflammatory condition of the aorta and its branches that results to absence in the arterial pulse.

Affects the tunica intima and tunica adventitia of the artery

Common in young adults

5. MONCKEBERGS MEDIAL SCLEROSIS

A condition characterized by isolated rings of calcification in the tunica media with normal tunica intima.

Common in the elderly and affects large arteries in the lower extremities

ACUTE ARTERIAL DISEASES

1. RAYNAUDS PHENOMENON

Is a vascular spasm of unknown etiology.

Raynaud described the attack of digital ischemia in women those results from cold exposure and emotional stress. Specific hypotheses for the etiology include abnormal sympathetic activity, abnormal digital vessels or an immunologic process.

Most frequently involves the hands but can also affect the feet. With exposure to cold or emotional stress, spasm of the small arteries and arterioles of the fingers results in ischemia (pallor or cyanosis), pain, and subsequent vasodilation with hyperemia. It can be idiopathic or occur as a manifestation of a potentially serious underlying systemic disease.

It is caused by an abnormality of the sympathetic nervous system and is usually seen in young adults.

Symptoms are slowly relieved by warm.

DIAGNOSIS

Vasospasm precipitated by cold and emotional stress

Symptoms for more than 2 years

Bilateral involvement

Minimal or absent gangrene of fingertips

Absence of other diseases associated with vasospastic attack

CLINICAL FEATURES

Classic triad:

Digital pallor with numbness

Cyanosis

Reactive hyperemia and rubor of skin

Sensitivity to cold

Blanching and cyanosis of the fingertips and nailbeds

Severe pain, sensory loss(tingling or numbness), decrease function in the hand

Gangrene(rare)

Atrophic changes:

Atrophy of the skin

Wasting of tissues in the finger pads

Irregular nail growth

TREATMENT

Treatment is directed primarily at symptom relief.

For majority of patient with Raynauds, maintaining local and general body warmth is adequate. Avoidance of cold, nicotine, and exacerbating drugs is essential.

Biofeedback benefits some individuals by teaching them to warm their hands or dilate the blood vessels.

Additional measures include relaxation training and stress management if stress is the inciting factor.

2. ACUTE ARTERIAL OCCLUSION

It is usually caused by thrombus formation, embolism, or trauma to an artery.

The most common location of an arterial embolus is at the femoral popliteal bifurcation.

An occlusion will result in absent or diminished pulses and complete or partial interruption of circulation to an extremity.

The severity of the problem is dependent upon the location and size of the occlusion and the availability of collateral circulation. If little or no collateral circulation is available, an acute arterial occlusion will cause tissue ischemia and possibly gangrene of the distal limb.

ARTERIAL EMBOLISM

Most frequently encountered form of acute arterial disease.

Emboli can arise from any numerous sites and be composed of various substances. Probably, one of the most frequently occurring types results from the dislodging of a preexisting thrombus in the heart. The thrombus then migrates to a peripheral arterial vessel.

ARTERIAL THROMBUS

Usually occur in the area of a previously existing atherosclerotic lesion.

When the arterial lumen narrows in the presence of an atherosclerotic lesion, the blood flow becomes turbulent. This swirling motion of blood slows its passage through the area and permits platelets to collect. The platelets aggregate, together with significant amounts of fibrin, leads to the development of the thrombus.

VASOSPASTIC DISEASE

Characterized by changes in skin color and temperature. The arterial spasm that occurs appears to be localized to the small arteries and arterioles.

3. CRITICAL LEG ISCHEMIA

Critical leg ischemia is initially defined by Rutherford included patients with ischemic ulcers or rest pain whose ankle systolic pressure was below 40-60 mmHg.

Chronic critical leg ischemia in both diabetic and nondiabetic patients is defined by either of the following two criteria:

Persistent recurring ischemic rest pain requiring regular adequate analgesia for at least 2 weeks, with an ankle systolic pressure no more than 50 mmHg, and or a toe systolic pressure no more than 30 mmHg.

Ulceration or gangrene of the foot or toes, with an ankle systolic pressure no more than 50 mmHg or toe systolic pressure of no more than 30 mmHg.

MANAGEMENT

Management depends on the severity of the arterial disease and ability of the patient to tolerate certain treatment options.

Candidates for medical management

Patient with mild to moderate disease and only symptoms of claudication Patients with recent onset of disease who do not have fully developed collaterals

Patients who have failed vascular reconstruction or are high surgical risk

EDUCATION

The patient must be educated about the disease to improve understanding and compliance with treatment and alleviate the fear of amputation.

RISK REDUCTION

Smoking is the major contributing factor, in terms operative risk and promotion of disease progression. Patient must stop smoking.

Hypertension must be controlled.

Reduction in calories and possibly cholesterol intake to control body weight

TREATMENT OF ASSOCIATED DISEASE

Attention on the associated disease that exacerbates atherosclerosis.

Congestive heart failure should be treated to maximize heart function and reduced peripheral edema

Diabetes must be controlled because of the association of arterial disease progression and neuropathy

FOOT CARE

Attention on the lower extremity especially the foot

Overall the tissue oxygen demand should be decreased by avoiding trauma, inflammation, and heat.

Meticulous foot care is essential

EDEMA CONTROL

Edema can decrease arterial perfusion

Elevating the head of the bed 6 to 8 inches allow pain-free sleep with minimal edema formation.

Vascular stockings are not too tight and constricting also help resolve edema.

MEDICAL MANAGEMENT

The goal of treatment is restoration of function and relief of pain, along with the treatment of any treatable associated disease. The long term goal is to prevent progression and promote regression.

Analgesics (Acetamenophen)

For reduction of pain

Antiplatelet agents (aspirin)

Reduces platelet aggregation and are effective in low doses

Ticlopidine

Increase cutaneous temperature and transcutaneous partial pressure of oxygen.

Hemorrheologic agents

Affect RBC flexibility and have been associated with significant increase in walking distances in a double blinded study of patient with intermittent claudication

Protanoids

Treatment option for patient who are not candidate for reopening procedure

Heparin

Best manage acute thrombosis or acute arterial embolus followed by arteriography to define the lesion.

SURGICAL MANAGEMENT

It is indicated in:

Intractable ischemic pain

Severe ischemia with nonhealing ulcer or gangrene

Increase disability

The following surgical options may be exercised:

Reopening procedures

Angioplasty is indicated for focal stenosis or short segmental occlusion with relative disease-free adjacent vessels.

Advantages of this procedure include:

Short inpatient stay

Low incidence of morbidity

Fairly successful long-term results

Limb Salvage Procedures

Bypass surgery, which uses prosthetic materials.

Indicated for diffuse arterial disease

Amputation

Primary Amputation

Indicated in patients with failed bypass surgery or spreading infection or toxemia.

Delayed Elective Amputation

Performed in the later stage of the disease to achieve a more pain-free functional status after a careful review of risk-to-benefit and cost-to-benefit ratios.

PHYSICAL REHABILITATION

EXERCISE

This is important at all stages of the disease.

Mechanisms of beneficial effect of exercise:

Improve peripheral utilization of oxygen

Increase patency of collateral circulation

Improve oxidative and glycolytic capacity

Exercise therapy is contraindicated in the presence of an ischemic ulcer or rest pain. A baseline treadmill exercise test should be performed in the absence of contraindications. Training may consist of walking, jogging, bicycling, or swimming; the upright exercise posture is preferable to the horizontal because it improves lower extremity perfusion.

Walking programs should be individualized considering the precautions and contraindications in each case. Standard prescription includes a gradual increase in duration from 30 to 60 minutes three to five times a week at 2 miles per hour, as tolerated, with the provision of rest when claudication develops.

In program of group therapy three times per week with each session including walking, jogging, leg stretching, and leg relaxation, the patients doubled their walking distance after 3 months.

Low-level pain-free endurance training is also effective in increasing walking distance, exercise time, and energy expenditure.

PROPER SHOE WEAR

Proper shoe wear should prescribe as needed. New shoe should be broken in slowly and carefully.

ORTHOTICS

Although infrequently used, an ankle-foot orthosis may decrease improvement and increase in walking distances. Occasionally a patient who refuses amputation for ischemic ulcers may ambulate safely with patellar tendon-bearing orthosis.

CLINICAL SIGNS AND SYMPTOMS OF ARTERIAL DISEASE

CHANGES IN THE SKIN

Pallor- a chalky, white color, blanching of the skin

Shiny and waxy appearance of the skin

Decreased hair growth distal to the insufficiency

Decreased skin temperature

Dryness of the skin

Ulceration(weight bearing areas)

Gangrene

SENSORY DISTURBANCES

Decreased tolerance to hot or cold temperature

Paresthesia

Tingling and eventual numbness in the distal portion of the extremities

PAIN

Intermittent Claudication (exercises pain)

Occur when there is insufficient blood supply and ischemia in an exercising muscle.

Cramping occurs in musculature distal to the occluded vessel.

Most common site is the calf muscle because of the occlusion of the femoral artery.

Pain slowly diminishes at rest

Exercise tolerance progressively decreases, and ischemic pain occurs more readily as the disease progresses.

Pain at Rest

A burning, tingling pain in the extremities occurs as a result of severe ischemia.

It frequently occurs at night because the heart rate and blood volume flow to the extremities decreases with rest.

Partial or complete relief of pain may be achieved if the leg is placed in a dependent position.

Elevation of the limb will cause an increase in pain.

PARALYSIS

Loss of motor function

Atrophy of muscles

CLINICAL EVALUATION OF ARTERIAL DISORDERS

HISTORY AND CLINICAL FINDINGS

ACUTE ARTERIAL OCCLUSION

The clinical presentation in acute arterial occlusion includes:

Sudden onset of toe, foot, and leg pain

Absence of pulse

Skin discoloration

Six Ps

Pulselessness

Pain

Polar (cold)

Pallor

Paresthesia

Paralysis

The most common cause of acute arterial embolism is cardiac (atrial fibrillation, recent myocardial infarction, cardiomyopathy, native or prosthetic heart valve replacement, and rarely, atrial myxoma)

CHRONIC ARTERIAL OCCLUSION

The most common symptom is intermittent claudication.

The site of claudication is of rough value for indicating the level of occlusion. Patients with occlusion at or above the ankle can present with claudication in the arch of the foot. Calf claudication suggests occlusion at or above the calf. Patients with isolated aortoiliac disease generally present with buttock pain or sexual dysfunction.

As the disease process advances, resting blood flow rates are affected, and ischemia at rest and impaired skin metabolism result.

Clinical findings of ischemia can include:

Trophic changes

Dependent rubor

Paresthesia

Cutaneous ulceration

PALPATION OF PULSES

Basis of any integrity of the arterial system in distal portion of the extremities

Pulselessness is a sign of severe arterial insufficiency

SKIN TEMPERATURE

Temperature of the skin can be grossly assessed by palpation. A limb with diminished arterial blood flow will be cool to the touch.

SKIN INTEGRITY ANG PIGMENTATION

Diminished or absent arterial blood flow to an extremity causes trophic changes in the skin periphery.

The patients skin is dry and color is diminished.

Hair loss and a shiny appearance to the skin also occur.

Skin ulceration may also be present.

VASCULAR TESTING

Testing may be needed for the following reasons:

To establish a diagnosis

To determine the severity of the disease

To confirm failure or success of treatment

To document the disease process

NONINVASIVE STUDIES

TEST FOR RUBOR

Changes in skin color that occurs with elevation and dependency of the limb as the result of altered blood flow.

Procedure:

The legs are elevated for several minutes above the level of the heart while the patient is lying supine.

Pallor of the skin will occur in the feet within 1 minute or less if arterial circulation is poor.

The time necessary for blanching to develop is noted.

The legs are then placed in a dependent position, and the color of the feet is noted.

Normally, a pinkish flush appears in the feet after several seconds.

In occlusive arterial disease, a bright reddening or rubor of the distal legs and feet occurs.

The rubor may take as long as 30 seconds to appear.

Reactive Hyperemia

Evaluated by temporary restricting the blood flow to the distal portion of the lower extremity with blood pressure cuff.

This restriction causes an accumulation of CO2 and lactic acid in the distal extremity. These metabolites are vasodilators and affect the vascular bed of the blood flow (deprived area)

When the cuff is released and blood flow resumes to the extremity, a normal hyperemia(flushing) of the extremity should occur within 10 seconds.

In arteriosclerotic vascular disease it may take as long as 1 to 2 minutes for a flush to appear.

CLAUDICATION TIME

The amount of time a patient can exercise before experiencing cramping and pain in the distal musculature.

A common test is to have the patient walk at a slow predetermined speed on a level treadmill(1 to 2 mph). The time that the patient is able to walk before the onset of pain or before pain prohibits further walking is noted.

This measurement should be taken to determine a BASELINE for exercise tolerance before initiating a program to improve exercise tolerance.

SEGMENTAL PRESSURE

Arterial pressure is recorded from different segments of the lower extremity arterial tree and referenced against brachial pressure to create a pressure index.

VENOUS FILLING TIME

This test measures the time necessary for the superficial veins to refill after emptying. The test is only of use in persons with normal venous system since any valvular problems could permit retrograde venous flow and not give a good picture of filling via the normal arterial pathway.

The patient is placed supine for this test also, and the legs are elevated and milked of venous blood. After this has been accomplished, the patient hangs the legs over the edge of the table. The time necessary for the veins to refill is noted. A time greater than 10 to 15 seconds indicates arterial insufficiency.

PLETHYSMOGRAPHY

Used to measure mean blood flow by recording the rate of increase in limb volume after sudden interruption of venous outflow.

To perform a plethysmographic flow measurement, the limb is placed in a neutral, relaxed position and the venous occlusion cuff is rapidly inflated. Blood that flows into the limb becomes trapped, and the limb expands. The rate at which expansion occurs is measured by the plethysmograph, from which arterial inflow can be estimated.

DUPLEX ULTRASONOGRAPHY

Combines a pulsed Doppler with real-time-B mode scanning.

Duplex scanning combines exact anatomical localization of disease with physiological blood flow studies to define the hemodynamic significance of the lesion.

DOPPLER ULTRASONOGRAPHY

A non-invasive assessment that uses the Doppler principle to determine the relative velocity of blood flow in the major arteries and veins.

A sound head, covered with coupling gel, is placed on the skin directly over the artery to be evaluated. An ultrasonic beam is directed transcutaneously to the artery. Blood cells moving in the path of the beam cause a shift in the frequency of the reflected sound. The frequency of the reflected sound emitted varies with the velocity of blood flow. This information is transmitted visually, onto an oscilloscope or printed tape or audibly, via a loudspeaker or stethoscope.

TRANSCUTANEOUS OXYGEN TENSION

Is an objective indicator of ischemia of the skin in a patient with peripheral occlusive arterial disease.

INVASIVE STUDY

ARTERIOGRAPHY

This is an invasive procedure and is usually the last test to be performed.

A radiopaque dye is injected in an artery. A series of x-ray examinations are taken to detect any restriction of movement of the dye, indicating a complete or partial occlusion of blood flow. It gives the most accurate picture of the location and extent of arterial obstruction.

TREATMENT OF ARTERIAL DISORDERS

ACUTE ARTERIAL OCCLUSION

THROMBOSIS

Acute thrombosis is generally best managed with an initial course of HEPARIN therapy followed by arteriography to define the lesion and the status of the inflow and outflow vessels.

Early intervention can prevent neuromuscular injury, enhance limb salvage, and avoid myonecrosis, myogobinuria, and associated renal failure.

EMBOLIC ISCHEMIA

HEPARIN should be given as soon as the diagnosis of acute arterial embolus is suspected.

Large doses of heparin are required to inhibit coagulation and to prevent clot propagation in patients in whom thrombus is already present.

DISSECTION

It depends on the location:

ASCENDING AORTA (Stanford type A)

Management includes control of arterial systolic blood pressure and emergency surgical repair to correct or prevent cardiac tamponade, acute aortic insufficiency, or coronary artery occlusion.

DESCENDING THORACIC/ABDOMINAL AORTA (Stanford type B)

Medical management of pain and arterial blood pressure is usually the treatment of choice

Postoperative care by the physical therapist centers on preventing pressure, monitoring pulse, and temperature, and enhancing venous return. The patient should be checked to assure there is no binding clothing to impede blood flow. A turning schedule should be instituted making sure that the surgical site is always visible.

CHRONIC ARTERIAL OCCLUSION

General Management:

1. Goals:

Develop effective therapy that prevents progression of the disease process.

Promotes regression of existing lesions.

Improve circulation

Instruct the patient in home management

2. Patient and family education

3. Protection from trauma

4. Orthoses

5. Exercise

6. Risk factor modifications

7. Behavioral modifications

9. Diet

10. Behavioral modifications

11. Diet

VENOUS DISEASES

ETIOLOGY AND PATHOGENESIS

Thumb frequently arises from clot formation in the cusp of venous valves, with thrombi then propagating out of the cusp into the major venous channels.

Another site of thrombus development is at the entrance of a tributary vein. The thrombus can go on to occlude a major venous channel by prograde or retrograde propagation.

RISK FACTORS

Virchows Triad:

1. Changes in blood flow

2. Alteration in the vessel wall

3. Variation in the coagulability of blood

Prior history of deep vein thrombosis

Immobilization

Postoperative state

Age(older than 40 years)

Cardiac disease

Limb trauma

Post-thrombotic state or coagulation abnormalities

Hormonal therapy

Pregnancy and postpartum state

Obesity

Neoplasm

CHRONIC VENOUS DISORDERS

1. CHRONIC VENOUS INSUFFICIENCY

Previously termed as VENOUS STASIS

Is usually the result of congenital or acquired valvular incompetence and, less frequently, obstruction of the veins.

PATHOPHYSIOLOGY

The basic underlying pathophysiologic mechanism is increased pressure in the deep venous system. This venous hypertension is caused either by blocking of outflow or backflow.

Usually manifested by:

Dilated veins(most common initial sign and is most apparent along the dependent portion of the limb)

Leg pain(limb heaviness or aches)

Chronic edema

Cutaneous changes

It can be the result of:

Venous occlusion

Valvular defect

Problems in the calf muscle pumping mechanism

CHARACTERISTICS

Dependent edema

Associated with standing and sitting for prolonged period of time

Usually worse at the end of the day

Edema decreases if the leg is elevated while the patient lies supine

Aching or tiredness in the leg

Increase pigmentation and stasis of the limb

Skin ulceration and secondary infection, which can lead to cellulitis

Chronic venous insufficiency results in:

Chronic edema

Scarring

Obliteration of cutaneous lymphatics

Decreased skin integrity

Hemosiderin deposition(resultant brownish discoloration)

Dermatitis

Ulceration

CHRONIC VENOUS INSUFFICIENCY

STAGESYMPTOMSPHYSICAL FINDINGS

IPain

Heaviness

Mild swelling

Superficial varicosities

Edema along perimalleolar are

IIHeaviness

Pigmentation, pruritis

Moderate to severe swelling

Moderate varicosities

Pigmentation

Dermatitis

Moderate to severe edema

IIIUlceration

Severe swelling

Calf pain with or without venous claudicationMultiple varicusitis

Marked skin pigmentation

Ulceration

Severe edema

MANAGEMENT

It is important to have patient education.

Conservative Therapy for Chronic Venous Insufficiency

STAGE I

Custom-fitted elastic compression stockings

Ace wrap or variant

Circ-aid

Intermittent external pneumatic compression

Skin care

STAGE II

Custom-fitted elastic compression stockings

Skin care with water-based lotion

Topical steroids for dermatitis

Surgical consultation

STAGE III

Ulcer care

Wet to dry saline dressings

Douderm

Unna boot

Four-layer high compression bandage

Custom fitted elastic compression stockings

2. VARICOSE VEINS

TYPES OF VARICOSE VEIN

Hereditary Varicosities

Often have family history and are predominantly female

Connective tissue laxity is believed to be the underlying mechanism, and terminal valve incompetence of the greater and lesser saphenous veins is the major abnormality.

Acquired varicosities (secondary)

Associated with chronic abnormalities of the deep venous system and are the result of ambulatory venous hypertension.

Result from proximal obstruction to venous return, as seen with pregnancy of a pelvic mass.

The increase in pressure placed on the venous system leads to valve failure and the tortuous appearance noted in the more superficial veins.

ACUTE VENOUS DISORDERS

1. ACUTE THROMBOPHLEBITIS

An acute inflammatory condition with occlusion of a superficial or deep vein by a thrombus.

Superficial venous thrombosis

If blood clot is lodged in one of the superficial veins, the condition usually resolves without long-term complications.

MANAGEMENT

Elevation

Appropriate compressive stockings (30-40 mmHg)

Aspirin/NSAIDs

Deep Venous Thrombosis

Thrombophlebitis of one of the deeper veins can result in a pulmonary embolism and is life threatening.

The pathogenesis of DVT is related to the VIRCHOWS TRIAD.

STASIS or altered blood flow in the lower limb deep veins results from immobility, paralysis or surgery. The stasis contributes to venous thrombosis by preventing the activated coagulation factors being diluted by non-activated blood, preventing clearance and mixing with naturally occuring inhibitors.

INJURY TO VESSEL WALL has been suggested to be the strongest risk factor for venous thrombosis. The damage endothelium leads to platelet adhesion, aggregation, and platelet release, with activation of components of both intrinsic and extrinsic pathways of coagulation.

HYPERCOAGULABILITY

Results in imbalance between thrombosis and hemorrhage.

MANAGEMENT

Standard therapy for acute DVT consist of:

Anticoagulation

Bed rest

Elevation

Support of the extremity

Patients with calf vein thrombosis are confined to bed for 72 hours, followed by gradual mobilization.

Patients with proximal venous thrombosis require 4 to 7 days of bed rest t with gradual mobilization when pain and swelling has subsided

All patients wear gradient elastic stockings when they are mobilized.

Phlebothrombosis

Used to describe the occlusion of a vein by a blood clot.

RISKS FACTORS ASSOCIATED WITH THROMBOPHLEBITIS

1. Immobility and bed rest over a prolonged period

2. Obesity

3. Age of the patient

4. Orthopedic injuries

5. Postoperative patients

6. Congestive heart failure

7. Malignancy

8. Use of oral contraceptives

9. Pregnancy

EVALUATION OF VENOUS DISORDERS

PHLEBOGRAPHY

An invasive procedure similar to angiography

Using an X-ray study and radiopaque dye injected into the venous system.

The procedure is used to detect a venous thrombosis.

GIRTH MEASUREMENT

The girth of the involved extremity may be compared with the girth of the uninvolved extremity.

One accepted method is to take circumferential measurements every 10 cm along the entire length of the extremity.

PERCUSSION TEST

A test used for varicose vein.

Procedure:

Ask the patient to stand until the varicosities in the leg fill with blood.

Palpate a portion of the saphenous vein below the knee and then sharply percuss the vein above the knee.

If a thrust of blood is felt with the palpating finger below the knee, the valves are incompetent.

HOMAN SIGN

With patient supine, forcefully dorsiflex the foot and squeeze the posterior calf muscles.

Many patients, but not all, with thrombophlebitis will experience significant pain in the calf muscles.

APPLICATION OF BLOOD PRESSURE CUFF

Inflate the cuff until the patient experience pain in the calf.

Patient with acute thrombophlebitis usually cannot tolerate pressures above 40 mmHg.

IMPEDANCE PLETHYSMOGRAPHY

Assesses volume changes at rest produced by a proximal, pneumatic, veno-occlusive cuff.

EXERCISE VENOUS PLETHYSMOGRAPHY

Lower limb venous function is tested by performing a plethysmographic evaluation of limb volume before, during, and after exercise.

DUPLEX SCANNING

Used to diagnose deep or superficial venous thrombosis, assess venous incompetence, and map the superficial veins before surgical harvest for bypass operation.

ARTERIOVENOUS FISTULAS AND MALFORMATION

Vascular malformations are classified as either:

1. CONGENITAL ARTERIOVENOUS MALFORMATION

Related to the stage of embryonic maturity at the time of development arrest.

2. ACQUIRED ARTERIOVENOUS MALFORMATION

Results from surgical construction of angioaccess for dialysis, penetrating injury, infection neoplasm and aneurysmal erosion.

CLINICAL FINDINGS:

Pulsating hematoma

Palpable thrill

Bruits

Ischemia pain paresthesia

Muscular weakness

Swelling

Discoloration

Dermatitis

Ulceration

TREATMENT

Early recognition and management of an acquired arteriovenous fistula are preferred.

Elastic support is beneficial

Appropriate footwear

Maintain mobility of the joint and soft tissue

Preserve normal gait pattern

LYMPHATIC SYSTEM

ANATOMY

The three components of the lymphatic system:

Lymphatic Capillaries and peripheral plexuses

Are the most peripheral structures in the system and anastomose to form what are termed as peripheral plexuses.

These plexuses, consisting solely of a layer of endothelial cells, lie in direct contact with the tissues and give rise to short channels that lead to collecting ducts.

Collecting ducts

The main difference in the ducts are the number of muscular layers present. The range in complexity from those with single muscular layer, to those with two, and finally three layers of muscles.

These vessels are more plentiful than veins and tend to accompany the veins as they course through the body. Their thin walls make them susceptible to trauma.

Any injury significant enough to affect venous return most likely inflicts damage to the lymphatics. The ramifications for edema becomes apparent.

Lymph nodes

Consist of small accumulation of lymphocytes housed in an encapsulated network of connective tissue.

FUNCTIONS:

Filtering and phagocytosis system

Nodes work to rid the body of unwanted substances that have been deposited into their dense network.

Production of lymphocytes

The lymphatic and venous systems work in harmony to absorb the arterial capillary filtrate. It is estimated that approximately 10 percent of this filtrate, and almost all protein molecules, are handled via the lymphatic system.

LYMPHATIC DISORDERS

LYMPHEDEMA

Manifested by an excessive accumulation of tissue fluid due to disruption of the lymph channels.

It is caused by a disturbance of the water and protein balance across the capillary membrane. It is characterized by overaccumulation of fluid in the interstitial tissues and fibrotic changes in the soft tissue. These changes start in the subcutaneous fatty tissue and generally extend superficially to involve the skin and deep to involve the fascial sheets of the muscle.

The overall incidence is uncertain. A female:male ration of 10:1 has been described. The peak incidence of onset is in the first decade after menarche.

PATHOPHYSIOLOGY

The lymphatic system is specifically designed to remove plasma proteins that filter into tissue spaces. Obstruction or removal of lymphatic vessels causes retention of proteins in tissue spaces. The increase protein concentration draws greater amounts of water into the interstitial space, leading to lymphedema.

There are three structural defects in lymphedema from or cause overaccumulation of protein-enriched interstitial fluid.

1. Obstruction of superficial and deep lymphatic with fibrosis of regional lymph node

2. Increase in subcutaneous fatty tissue with fibrosis of interlobar septa

3. Thickening of deep fascia

CLASSIFICATIONS

CONGENITAL LYMPHEDEMA

Have a faulty lymphatic system due to a complete failure of lymph vessel to develop (AGENESIS) or poorly developed vessels (APLASIA)

a. MILROYS DISEASE (HEREDITARY FORM)

Transmitted as autosomal dominant trait.

The clinical characteristics are predominantly an enlargement of an extremity at birth with firm, nonpitting edema.

The childs development and activities are not impaired.

b. LYMPHEDEMA PRAECOX

This group is composed primarily of females in the second and third decades of life.

It presents spontaneously without an apparent etiology.

The edema is initially soft and pitting but becomes firm and nonpitting over time.

There is no pain or ulceration, but recurrent infection can occur

c. LYMPHEDEMA TARDA

Patient who develop lymphedema after the age of 35 years.

This occur without obvious etiology

The edema is nonpitting and firm

Pain and ulceration do not occur, but recurrent infections are common

SECONDARY LYMPHEDEMA

Due to another pathology or disease process (infectious, malignant, traumatic, iatrogenic)

SIGNS AND SYPMTOMS

1. Edema

Painless swelling of the distal extremity most often seen over the dorsum of the hand or foot.

PITTING EDEMA

Indicates short-duration swelling

BRAWNY EDEMA (hard edema)

Associated with long-term venous insufficiency

There are four causes of edema:

1. Increased capillary permeability

2. Decreased osmotic pressure of plasma proteins

3. Increased pressure in venules and capillaries

4. Obstruction to lymphatic flow

2. Increase weight or heaviness of the extremity

3. Sensory disturbances (paresthesia) of the hand or foot

4. Stiffness of the fingers or toes

5. Tautness of skin

6. Susceptibility to skin breakdown

7. Decreased resistance to infection, causing frequent episode of cellulitis

EVALUATION OF LYMPHATIC DISORDERS

1. Girth measurements of the extremity

2. Volumetric measurements

The involved extremity is immersed in the tank of water

The amount of water displaced as the extremity is lowered into the water is measured

3. Palpation of the dependent limb to different pitting edema from brawny edema with subcutaneous fibrosis.

MANAGEMENT

The general aim of treatment:

1. Mobilization of fluid

2. Reduction of girth

3. Prevention of complications

Etiology should be determined before starting the treatment.

The majority of patients in the clinical setting have lymphedema secondary to obstruction of the lymphatic system from trauma, infection, radiation, or surgery. If the patient is at risk for developing lymphedema, PREVENTION is the best goal.

To increase lymphatic drainage, the HYDROSTATIC pressure of the tissues must be increased. This is accomplished by external compression of the skin.

Lymphatic and venous return can also be increased by elevation of the limb.

Lymphedema caused by lymphatic disorders, such as lymphagitis and cellulitis, does not diminish as readily with elevation as does edema secondary to venous disorders.

CONSERVATIVE TREATMENT

Intermittent compression

80-120 mmHg as tolerated is applied preferably twice a day for 40 to 45 minutes each time and should be used with the extremity elevated.

Manual Massage

Pressure garment

Isometric exercises

Skin and nail care

Range of motion exercises

Weight reduction

Generalized conditioning program

Patient education

GUIDELINES FOR LYMPHEDEMA CARE

Define etiology

History and physical examination

Laboratory

Treatment in hospital

Pneumatic compression

Gradient elastic compression stocking

Education of patient and family

Antibiotics

Diuretics

Discharge

Extremity compression prescribed for 2 to 4 hours/day

Use of gradient elastic stocking

Skin care

Observation for signs and symptoms of infection

Note:

Please include to study REHABILITATION OF DIABETIC FOOT PROBLEMS of Rehabilitation Medicine by Joel A. De Lisa. This is included in the PRELIM EXAMINATION.

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