Generally, hypertension may have no specific symptoms for years until there is damage to different organs. Sometimes the first symptom is a heart attack or stroke. Symptoms of severe hypertension may include headache, dizziness, rapid or irregular heartbeat, fatigue, chest pain, erectile dysfunction (impotence), and shortness of breath.

Making the diagnosis of hypertension is easy if you get regular check ups by your doctor. Untreated high blood pressure is dangerous because the heart has to work much harder to keep blood flowing. It is very important to diagnose hypertension early before the development of heart problems, kidney damage, and stroke.

The initial treatment for mild hypertension is life style modifications. This includes maintaining a low sodium diet, weight loss (if over weight), smoking cessation, limiting alcohol and caffeine consumption and stress management. If life style changes are not effective in controlling hypertension, one or more medications may be needed to control blood pressure and prevent or delay complications. The goals of treatment are to lower blood pressure to a normal level and to reduce your risk of heart disease, kidney disease and stroke.

In summary, hypertension is a manageable disease if diagnosed early in the disease process. Routine check ups and lifestyle modifications is the best prevention. However, if you are diagnosed with hypertension: following your doctor’s advice, taking your medication as prescribed, regular exercise, decreasing alcohol intake, and quitting smoking can help decrease your risk of complications.

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Diagnosis of Deep Vein Thrombosis (DVT) is not always obvious, but if 3 or more risk factors are present along with certain physical findings, its presence is highly likely. Confirmation of the diagnosis is bolstered by Ultrasound/Doppler, MRI, Contrast Venography, etc. Treatment consists of thrombolysis, anticoagulation, bed rest, elevation of the extremity, heat, etc. Prevention is the best approach and consists of basic common sense knowledge such as, not sitting in one position for prolonged periods, wearing support hose, elevating the legs, etc.

Pieces of DVT, called emboli, are trapped in the lung because of the small vessels in that region. If too large an area is blocked off, then oxygen cannot reach the blood stream and the brain is deprived of oxygen. The patient may experience chest pain, shortness of breath, or coughing up of blood and tests will substantiate the diminution of oxygen in the blood. Special lung scans are used to confirm the emboli’s presence. Fibrinolytics, anticoagulants, and even surgery may be necessary, if a large portion of the lung’s vasculature is obstructed. A filter may be placed in the Inferior Vena Cava to prevent further emboli from traveling from DVTs in the legs to the lungs.

Blood has an inherent tendency to clot. This is especially expressed whenever it slows down, encounters rough surfaces, or is in a hypercoagulable state. This is referred to as Virchow’s Triad. These conditions exist in many circumstances, varying from trauma to the venous wall to prolonged sitting to clotting disorders. This is especially likely to occur in the deep veins in the extremities and in the solar plexus vessels and is noteworthy for 2 reasons: Local inflammation and Pulmonary Emboli.

Once a clot (thrombus) forms, it takes from 5 to 10 days to organize and adhere to the lining of the vein wall. Before that, it frequently dissolves, spontaneously, but it some cases, it may propagate proximally, extending into other veins, or a piece (embolus) may break off and travel to the heart and, subsequently, be trapped in the lung (Pulmonary Emboli).

After the Deep Vein clot organizes and adheres to the vein wall, it may slowly undergo recanalization, whereby the center of the clot breaks down and blood can once again traverse this area through the new channel. More frequently, inflammatory changes occur in the venous wall and signs and symptoms develop suggesting inflammation and peripheral obstruction to blood flow develops, such as swelling, warmth, redness and pain. The extent of the DVT will determine the extent of the signs and symptoms. If the thrombus is not dissolved by treatment, often it will disrupt the valves in the deep vein or completely occlude the venous lumen, retarding the blood return through that vein and forcing that blood to return to the heart by the remaining deep veins. This added volume causes the other veins to dilate, often disrupting their valvular integrity, resulting in varicosities, edema, skin breakdown, ulcers and even gangreen.

Risk Factors:

• 1.) Age,
• 2.) Immobilization for 3 or more days,
• 3.) Pregnancy and Post Partum,
• 4.) Major Surgery,
• 5.) Previous DVT,
• 6.) Cancer, which may cause a hypercoagulable state,
• 7.) Congestive Heart Failure, where blood is slowed down in the extremities,
• 8.) Stroke, where the muscle contractions, needed to pump the blood out of the extremities is lost.
• 9.) Acute Heart Attack, necessitating bed rest and diminished blood pulsation,
• 10.) Sepsis,
• 11.) Excessive edema, from fluid retentive illnesses, such as the Nephrotic Syndrome, and diminished Albumin,
• 12.) Ulcerative Colitis,
• 13.) Trauma, which damages the inner lining of the vein,
• 14.) Burns,
• 15.)Fractures,
• 16.)Spinal Cord injury,
• 17.) Polycythemia and Thrombocytosis, which consists of increased red blood cells and platelets, respectively, causing the blood to be to thick and increasing the tendency to clot,
• 18.) Certain drugs such as contraceptives, Estrogen, which induce a hypercoagulable state, and IV drug use, which injures the lining of the vein wall.

Diagnosis: The presence of 3 or more of the above risk factors is very helpful in suggesting the propensity for DVT to develop. Along with this are the signs and symptoms, while not being specific, are very helpful.

Signs &Symptoms: Swelling, Pain, Tenderness, Warmth, unilateral edema, prominent superficial veins, diminished emptying of peripheral veins when the extremity is elevated to and above the heart level. Sometimes a cord is palpable, especially when superficial thrombophlebitis is associated. Fever may be present. Pain in the calf with straight knee and dorsiflexion of foot (Homans Sign) is suggestive, but not specific.

Laboratory Studies: 1.) D-dimer blood test – this is a product of the degeneration of fibrin in the blood. This is a screening test, but is non-specific.
2.) RBC agglutination assay – screening test. (not accurate for Calf Vein Thrombi). (about 50-60 % accurate).
3.) Qualitative ELISA assay – not accurate as a test for Calf Vein Thrombi ( about 79% accurate).

Radiology : 1.) The gold standard for diagnosis of DVT is a venous angiogram, but this is tedious and expensive, and often a test of last resort.
2.) The Duplex Ultrasound study, utilizing Ultrasound and Doppler modalities, measuring the blood flow by compressing the deep vein is 98% specific and sensitive.

3.) Impedence Pletysmography, which measures the blood volume in relationship to venous outflow is used by many Physicians, but is not as sensitive as the Duplex U/S study.

4.) MRI- is an expensive, but very helpful study and is often used in confusing situations.

The most difficult DVT to detect is when the thrombus is either non-occluding, or proximal to the inguinal ligament or in the calf. Sometimes a repeat evaluation and study is necessary when the first test is equivocal.

Treatment: Thromboysis- if instituted early, these drugs, such as may dissolve the clot entirely.
Anticoagulants- started early to prevent the DVT from propagating, proximally, up the vein and to prevent other clots from forming.
Elevation and Support Hose to encourage the blood to flow faster in it’s return to the heart.
Heat to encourage rapid inflammatory resolution and adherence of the clot to the vein wall.

Prevention: This is most important. Sitting or standing for too long stagnates the blood. Crossing the legs, or letting them hang down for long periods slows the blood. Obesity and edema in the lower extremities from other causes places a burden on the deep veins. Failure to elevate the legs after trauma, which distorts the blood flow through damaged veins is causational. Prolonged bed rest without elevation, active and passive exercises of the extremities is a risk. Failure to use Compression Stockings post-operatively or post-partum is risky. Tight elastic top stockings will slow the blood down. Don’t let these things happen!

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Most people know that Shock refers to a fall in blood pressure. Beyond that, they are ignorant of its causes. They do know that if it lasts long enough, that death will ensue. But does the blood pressure have to fall to zero for a person to be in shock? What is the blood pressure level at which shock is felt to be present? And how does the body deal with a fall in blood pressure?

SHOCK occurs when the pressure is too low to propel the blood forward to infuse into the major organs. These organs are the brain and kidney, foremost, and then the liver, heart, and the other organs thereafter. The actual blood pressure level, at which shock occurs, varies from person to person, but when the systolic blood pressure falls below 90 mm. of Mercury, most of the time shock occurs. Of course, irreversible damage may not occur immediately, and depends on the health and the age of the individual, but after some definable time, irreversible damage will set in and ultimately, death will occur.

Since SHOCK ensues when insufficient blood reaches the major organs, it is easy to figure out some of the causes of shock. The first one that comes to mind is when there is insufficient blood to move around, no matter how strong the pump is. This, of course, would occurs in bleeding states, and is called “Hemorrhagic Shock”, a type of “Hypovolemic Shock” (diminished volume).This condition, of course, requires blood or blood products replacement to rectify. Additionally, the cause of the bleeding must be sought for and the bleeding must be stopped. In this type of shock, the body will send out chemicals which will constrict the peripheral arteries, which deliver blood to the skin and subcutaneous muscles, thus, shunting the blood to the deeper more vital organs. Hypovolemic Shock, also occurs in states when the fluid volume, aside from the blood cells, is diminished, as in severe dehydration. In this condition, replenishment of the fluid by a variety of liquids, either intravenously or orally will reverse the shock state.

A second common cause of SHOCK occurs when the pump, which in this case is the heart, is weakened and, despite an adequate amount of blood, the heart is unable to propel the blood to the vital organs. This condition most frequently occurs when the heart muscle is damaged, as with heart attacks (myocardial infarctions). This is a much more difficult condition to treat, than Hypovolemic shock and is referred to as Cardiogenic Shock. Treatment, of course, is to try and keep the blood pressure up sufficiently to propel the blood around, until the heart recovers, as by using an artificial pump, or by the use of medications which will shunt the blood from areas where it is needed less, such as the soft tissues and the skin, to the vital organs instead, where life can be sustained. The body is trying to do its thing, also, but needs help if the heart function is too severely depressed. In cases where there is an irregular heart rhythm, (arrhythmia), the heart function, because of, either the rapid or the irregular pulse, is unable to fill with enough blood during its resting phase to propel sufficient blood forward to the tissues.

Another, not infrequent, cause of SHOCK occurs when some toxin, either infectious or allergic, causes the blood vessels to dilate, which in effect shunts the blood away from the vital organs into vascular beds which supply less essential tissues, thus depriving the vital organs from receiving the blood they need to sustain life. This type of SHOCK is called MALDISTRIBUTION of flow or DISTRIBUTIVE SHOCK. This condition can occur in burns or acute pancreatitis, as other examples. In this group is included those conditions where the blood viscosity is thickened, such that the microcirculation is impeded, resulting in insufficient blood flow. Conditions that thicken the blood and increase viscosity may include Polycythemia vera, multiple myeloma, and macroglobulinemia. Another synonym in “medical jargon” for this condition is Vasomotor Collapse”. This condition is often suspected when there is a drastic drop in the blood pressure accompanied by a slow pulse. In trauma, for example, a reflex, involving the vagus nerve, will initiate a vasovagal reflex, which produces a slow pulse. Neurogenic shock, occurring in an occasional stroke, can manifest a vasodilatation resulting in distributive shock.

Symptoms and Signs: So, even though there are many different causes of shock, the clinical picture is fairly characteristic. There is profound arterial hypotension, restlessness and impaired mentality, diminished urine output, and shortness of breath. The person in shock generally is pale and sweaty with cool skin. Ultimately the person may complain of dizziness, dimming-then loss-of vision and, ultimately, pass out(Syncopy) and become comatose.

Treatment: When Shock is suspected, the first thing to do is to lay the person in a supine position and, if necessary, to facilitate return of venous blood flow to the brain, place the person in a “heads down” position (Trendelenburg position). Concurrently, elevation of the feet will facilitate return of venous blood to the heart, where it can then be propelled to the vital organs, provided the heart pumping action is adequate. It has been estimated, that by merely placing the patient in a supine position with the feet 12 in. or more above the head will supply about 500cc’s of blood for the central circulation. Restlessness, from diminished brain perfusion, may require sedation to help the person rest. Vomiting often occurs when the pressure falls, so that keeping the head turned sideways will minimize any aspiration of gastric secretions and subsequent lung complications. Intravenous fluids are needed to fill the vascular system for greater blood volume and this is the usual first interventional therapy offered. If the shock state continues, then vasopressors or cardio circulatory stimulants are then tried to shunt the blood to the vital organs. Inhalation Oxygen is mandatory, especially in carcinogenic shock, but may be valuable in septic or toxic shock, and shock due to injuries. Hypothermic shock is treated with warming techniques. Antibiotics are necessary in septic shock. Cortisone may be necessary in anaphylactic shock or adrenal insufficiency. Arrhythmic cardiogenic shock will require anti-arrhythmic measures varying from medication to electrical shock.

In many metabolic, toxic, or endocrinological causes of shock, secondary measures alone may not restore circulation. Identification and treatment of the specific underlying etiology is paramount in returning the circulation to a normal status.

SUMMARY: Shock is the condition of insufficient blood flow to the vital organs, caused either by loss of intravascular volume, externally, as in bleeding or dehydration, or internally, as in extreme vasodilitation, or by loss of the ability of the heart to pump sufficient quantities of blood to those organs. The patient will exhibit central nervous system and circulatory symptoms and will require fluid replacement initially, followed secondly by medications intended to stimulate the cardiovascular system and ultimately by techniques or medications which will reverse the underlying etiology.

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Stroke is a term used to denote cessation of a portion of brain function due to acute or sub-acute injury. A more common name steeped in Medical jargon is CVA or Cerebral Vascular Accident. Injury to brain tissues, denoting a CVA, occurs when the blood supply to any part of the brain is interfered with or disturbed. This interference is caused primarily by either blockage of the blood vessel, which supplies blood to the brain, or by acute hemorrhage into the brain substance, directly, by rupture of the vessel.

SUMMARY: A STROKE or CEREBRAL VASCULAR ACCIDENT is the result of loss of blood flow to any portion of the brain, either by a blood clot that develops within the blood vessels or from a clot or fragment of a Cholesterol plaque, which breaks off, distally, and travels to one of those blood vessels, which supply the brain tissue with blood. Depending on which portion of the brain is deprived of blood will determine the clinical presentation, from slurred speech to coma to paralysis of one side of the body.

Risk factors of Strokes include Hypertension, Obesity, Inactivity, Smoking, Hardening of the Arteries, Cardiac arrhythmias, etc. Changes in life styles and treatment of reversible disease processes are the best approach to preventing and ameliorating Strokes. Diagnois at onset must differentiate between a Blood Clot and Hemorrhage. If a blood clot is implicated and the patient presents within 3 hrs. of the onset of symptoms, then thrombolytic therapy can be tried. If it’s greater than 3 hours, treatment is directed towards preventing further blood clots from forming, and aggressive rehabilitation. Hemorrhage as a cause of brain damage (Hemorrhagic Stroke) may require surgical evacuation of the bloodclot.

Interference with blood flow is caused by the formation of a blood clot in one of the vessels supplying the brain with blood. This is referred to as a thrombus. If the blood clot, piece of cholesterol plaque, or piece of heart valvular growth, travels from a distant vessel or chamber to block the blood vessel, then it is referred to as an embolus. Thrombi occur in the blood vessels when the lining of those vessels become disrupted, causing fatty and other material to migrate into the lining resulting in plaque formation. These changes are referred to as Atherosclerosis, better known as Hardening of the Arteries. As we age the arteries in our body, become longer and more torturous, resulting in blood flow turbulence, which irritates the vessel lining and predisposes it to Atherosclerosis. Other factors, listed below, can accelerate this process. This Atherosclerotic plaque eventuates into narrowing the arterial passageway and, because of numerous factors, when it ruptures, there occurs a cascade of clotting mechanisms resulting in the formation of a blood clot (Thrombus), which usually completes the blockage of the blood vessel.

Occcasionally, the thrombus may not completely occlude the vessel passageway, but a piece of the clot or even of the plaque may break off and travel downstream and block off one of the arteries, more proximal to and supplying the brain with blood. This embolus will therefore result in a STROKE. Emboli can occur from other sources besides from arterial thrombi. A bacterial or fungal growth or a blood clot on a defective or a prosthetic heart valve may fracture off and travel to the brain. In cases of an irregular heart rhythm, blood clots formed in the cardiac chambers do to eddy currents around the turbulence, may dislodge and travel to the brain. Even venous blood clots from the legs or pelvis may travel to the right side of the heart and exit into the left side of the heart through a congenital opening in the intraartrial wall and travel to the brain (Paradoxical embolus). Therefore, the two categories of blood deprivation or ISCHEMIC STROKES are Thrombotic Strokes and Embolic Strokes.

Rarely, Hemorrhage, due to acquired or congenital weakness of the blood vessel wall may occur, into the surrounding brain tissue, causing serious death of brain cells, resulting in a STROKE.

The blood vessels most frequently involved are The Carotid Arteries, the Basilar-vertebral Arteries, and the Intracranial Arteries.

EPIDEMIOLOGY

Strokes (CVAs) have been found to be the third leading cause of death in the United States. Even of the patients, who survive (approximately 2/3rds.), 50% of them will retain neurological deficits.

Beside Aging, other risks of Stroke are Hypertension, Diabetes, Hypercholesteremia, Smoking, Inactivity, Abnormal Blood Clotting Disorders, Gout, and Cardiac Arrhythmias.

CLINICAL PRESENTATION

The signs and symptoms of a CVA will vary depending on what portion of the brain has been injured by deprivation of its blood supply. In right handed persons (dominant right side), who sustain an injury in the left Broca’s speech area, there will be serious interference with their speech. They will present as Aphasic, that is, have jibberous speech. The connection between the vocal cords, etc. and the brain are cut. If the right sided speech area is injured in predominant left handed people, they will experience Aphasia. Since the opposite side of the brain controls the opposite of the body, right handed individuals will be paralyzed on the right side in left sided STOKES. The converse will be true in left handed persons with right sided STROKES.

Other symptoms and signs are Alterations in consciousness such as coma, confusion, inability to understand questions and commands, seizures, incooridination, arkward gait, partial loss of field of vision, facial weakness or asymmetry, dizziness, nausea, vertigo, vomiting, decreased sensation, loss of urinary or bowel control, etc. Any of the normal brain activities can be disrupted, depending on which vessel is blocked and what portion of the brain it supplied with blood.

A Neurological examination attempts to test all of these modalities,i.e., Cranial nerve function (I thru XII), sensory and motor activity, and reflexes.

DEGREES OF STROKE

Not all deprivation of blood flow to the brain culminates in brain death. Sometimes the blood flow is only transiently interfered with and the “stunned” brain tissue is allowed to recover, if the blood flow is reestablished quickly enough. This type of transient injury is termed:

T.I.A. (Transient cerebral Ischemic Attack)-This episode usually lasts 5 mins. or less, and the neurological signs and symptoms, such as a droopy mouth and slurred speech, will completely disseapear within 24 hrs. A T.I.A. must not be ignored, even when the symptoms disseapear, because it is often the harbinger of an impending Stroke.

R.I.N.D. (Reversible Ischemic Neurological Deficit)- This episode lasts greater than 24 hours, but resolves within 32 weeks without anly neurological residual. This too, is critical as a warning regarding a future impending permanent Stroke.

Stroke in evolution- This situation occurs when the neurological deficit becomes gradually more severe, spreading to other brain functions and intensifying the deficit of those already showing damage. This Stroke in Evolution will evolve over 2 hrs. and may continue for up to 2 days, and may progress to further damage later on.

The stable or completed Stroke is one that occurs acutely and becomes stabilized very quickly without further progression. It may, in fact, improve over the first week, as the inflammatory process receeds, and recovery may progress, especially under therapy, for the next 8 to 12 months.

DIAGNOSIS

The diagnosis of Stroke is based on the history of a sudden or recurring neurological deficit correlated by a Neurological examination which demonstrates the presence of unimpeachable neurological defects. The imperative action for the Physician, once a Stroke is suspected, is to order a Cat Scan of the Brain. This is done, even though in the first 24 hrs. it may be normal, in the presence of a thrombus or embolus, to rule out a hemorrhage. If there is no hemorrhage, which does show up almost immediately on CT scan, then the possibility of interventional therapy can be contemplated. The presence of Hemorrhage rules out the possibility of Thrombolytic therapy utililzation.

Later, an MRI or MRA, Ultrasound of the Carotid Artery and heart, EKG, cardiac rhythm monitoring, or angiogram can be done to ascertain the origin of the thromboembolis and/or the severity of the patient’s Atherosclerosis.

TREATMENT

If it is ascertained that the individual has suffered a Stroke and that Stroke is secondary to a Thromboembolis, rather than a Hemorrhage, then the possibility of breaking down that clot to re-establish the blood flow and reverse the brain damage is a definite possibility.

However, the patient must have arrived at the Emergency Room and had the correct diagnosis of a Thromboembolic Stroke within the first 3 hrs. of the onset of symptoms of the Stroke. Then he may be given t-PA (tissue plasminogen activator) which serves to try and lyse the clot.

Some authorities have used Heparin as an anticoagulant in this situation to prevent the clot from enlarging and causing more damage. The jury is still out on this approach.

Reversal and treatment of the underlying thrombembolic potentiating risk factor is then attacked, in order to prevent more Stroke episodes. An irregular heart rhythm patient (one with atrial fibrillation) is anticoagulated and later, if possible, converted to a normal heart rhythm. Patients with large thrombi in their Carotid arteries under go surgery at a later date after a period of anticoagulation and cooling off, to have the thrombus removed or bypassed. Then rehabilitation is done with great intensity.

Surgical treatment of hemorrhagic strokes is recommended in some cases, with varying results.

PREVENTION

Since we are able to identify many of the risk factors in those who are most susceptible to STROKES, the most prudent approach is to enact lifestyles and medicine to prevent Strokes. Monitoring and treating Hypertension and Diabetes will diminished the chance of Strokes.

Loss of excess weight, exercise, cessation of smoking is very helpful. Medications to prevent formation of blood clots by interfering with the normal stickyness of platelets, by the use of anti-platelet therapy has been the cornerstone in preventative treatment.
ASA-because of it’s effect in inhibiting the production of prostaglandin, it has effected the release of clot activating substances from platelets. This has been shown to reduce the risk of recurrent strokes and progression of T.I.A.’s to strokes. There is some small increased risk for hemorrhagic stroke and gastrointestinal bleeding. 81 mg appears, at present, to be the ideal dose, daily.

Ticlopidine (Ticlid)- inhibits platelet aggregation. It reduces the risk of recurrent stroke, even better than ASA.

Clopidogrel (:Plavix)- prevents fibringogen at the site of the clot which decreases platelet binding.

Warfarin (Coumadin)- is an anticoagulant and is useful in patients with cardiac arrhythmias, artificial heart valves, previous strokes, myocardial infarctions, clotting abnormalities.

References:

Chronic Care Solutions, Marymount University Arlington, Virginia, USA

SukSH, SaccoRL, et al. The Northern Manhattan Stroke Study: Stroke 2003 May 29 ( epub ahead of Print).

Stroke risk factors and stroke prevention: Semin Neurol 1998; 18(4):429-40

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Many patients complain to their physicians that they have “poor circulation.” In the old days, little could be done to help this group of patients. Often, the patient is in their 60ties or 70ties and has multiple other problems that may cloud the picture. They often have lumbar back pain and may have pain radiating down into their legs from degenerative disc disease of the spine or arthritis in their hip or knee joints. The central question remains. Can anything be done to determine if the blood vessels in their legs are diseased and symptomatic and if so can anything be done to fix the problem?

Let us start by saying that the explosion of information resulting from the development of Doppler exams, plethysmography, and echo technology has given us new hope. The entire field of vascular disease has become more scientifically based. Many vascular surgeons have established vascular labs in their offices to provide anatomic and functional information that can be used in treating patients with suspected peripheral arterial or venous disease.
If your legs hurt when you walk short distances, if your feet hurt all the time or if you are awakened from sleep with leg pain, you probably need a work-up to determine the status of your peripheral vessels. The first and perhaps the simplest test in your work-up is called a segmental pressure test or an ankle brachial index. By measuring the blood pressure at the ankle, calf and thigh in each leg and dividing that number by the systolic blood pressure in the arm, the ABI (ankle brachial index) can be determined.

Normally, the pressure at each level in the legs should be the same as the arm pressure. If it is not, a blockage or a stenosis may be present in the artery. For example if the ankle BP is 120 and the arm pressure is 120 then the ABI is 1 (120/120 = 1). If the ankle pressure is 100 and the arm pressure is 150 mm, then the ABI would decrease to 0.66 (100/150 = .66). In this case 66% of the normal blood flow would find its way to the ankle as a result of stenosis up stream from the ankle.

Due to various flow factors, a stenosis becomes more significant with exercise. So that the leg may not hurt when you are sitting in your chair, but it may begin to hurt when you walk to the mailbox. The lower the ABI score, the more severe the blockage. If the ABI gets down to the. 3 or 30% range, the leg is at risk for developing gangrene.
Another recent test is called biphasic Doppler examination. This test allows for separation and quantification of abnormal blood flow. A sound wave is bounced off the blood in your arteries and the tracing produced can help determine the extent of peripheral vascular disease. Generally accepted criteria of disease are: (i) reduction of the height of the wave of blood traveling down the artery, (ii) absence of a reversal of the wave between heart beats and (iii) a rounded peak of the wave on the tracing. Other more subtle signs which can be read by the physician to help with the diagnosis include velocity tracings and evaluation of the frequency of the signal at different levels of the artery.

The application of segmental plethymography and pulse volume recordings have added additional information to the peripheral vascular work-up. In this test, blood pressure cuffs are applied to the legs at different levels and the machine measures small volume changes in the diameter of the leg with each heart beat. The bigger the volume change, the better the blood flow is that that part of the leg. If the measurements of each segment of the leg are compared, five different degrees of severity of disease can be determined and a suspected blockage can be localized to an area of the leg. This test also works on veins and even small changes in the blood flow to the skin can be measured.
Patients with cold fingers even on warm days may have vasospastic disease in the small arteries of the fingers. This condition is called Raynaud’s disease and is found in many women with otherwise normal larger arteries. Using digital plethymography, an increased resistance to blood flow due to spasm in the artery can be measured and the patient treated with medication to dilate the artery and increase the blood flow to the fingers.

Recommendations:
1) If you have cold fingers or feet the problem may be vasospastic disease. Talk to your physician about a peripheral vascular testing program or noninvasive work-up.

2) If your legs hurt when you walk to the mail box and back, problems can be excluded and then you may benefit from a work-up. Both balloon angioplasty to open the area of stenosis without surgery and bypass surgery can be used to improve the blood flow and stop the pain.

3) If you have rest pain at night, talk to your doctor this week to make sure you don’t have total occlusion of the arteries in your legs. Finally, if it hurts, get someone to look at you. Don’t wait until the last resort is to remove the leg.

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 The aorta is the main blood vessel which brings blood from your heart to the rest of your body. As the aorta passes through the abdomen, it gives off branches to all of the internal organs. Just below the level where the arteries to kidneys come off is a special segment of aorta which can expand as we grow older to form an aneurysm or dilatation of the main vessel. The incidence of aortic aneurysm disease here in the Southeast appears to be one of the highest in the nation. Therefore a review of the pathophysiology or causes of this problem and the surgical treatment options seems to be timely.

The etiologies of aortic aneurysms have long been thought to be that of degeneration of the aortic wall, infection, dissection, smoking or splitting of the vessel wall due to high blood pressure. Although all of these causes most probably play a role, new research seems to shed light on the underlying cause. This is important news for patients with aneurysms because the clinical manifestations and natural progression of aneurysms make them serious problems that can lead to disability or death in many patients.

Beginning in 1990, scientific attention began to focus on a specific mutation of a gene that encodes for type III Procollagen. This gene exerts control over the production of collagen and elastin in the blood vessel wall. Both collagen and elastin have, as their main function, the strength of the vessel wall. Therefore, if you are born with this specific gene mutation, the aortic wall may be weak and an aneurysm may begin to grow silently as you get older. Many of the known risk factors for aortic aneurysms (such as smoking, hardening of the arteries and high blood pressure) act in non specific ways. This may be the first evidence that susceptibility to aortic aneurysms may arise from a single recessive gene and most importantly, this same gene can be transmitted by you to your offspring and successive generations.

An aneurysm is a localized irreversible dilatation of the artery. The normal size of the aorta is 2.5 cm. A 50% increase in the size of the vessel is the usual threshold for naming the aorta as having an aneurysm. The risk of rupture and death as the aneurysm enlarges can be accounted for by two factors: (1) the larger the aneurysm, the greater the loss of strength of the aortic wall. In scientific terms, the Law of LaPlace says that tension equals pressure x radius. So as the aneurysm gets bigger or the radius increases, the tension of the wall increases until the aorta ruptures. A recent study of the risk of rupture in aortic aneurysms revealed an 8% risk of rupture in aneurysms less than 4 cm. Remember, the normal size is 2.5 cm. In aneurysms between 4.1 cm and 7 cm, the risk increases to 25%. From 7.1 cm to 10 cm, it increases yet again to 45%. A new study on families of aneurysm patients has shown that first degree relatives of patients with aneurysms have a 19.2% chance of having an aneurysm vs. 2.4% chance in non aneurysm bearing families.

The presenting symptoms of an aneurysm which is about to rupture man vary. Most patients however, experience a severe abdominal pain just below the breast bone which radiates into the back. Many patients describe this pain as the sensation of being shot in the abdomen by an arrow. Abdominal aneurysms are diagnosed 70% of the time by palpation by the family doctor as part of a physical exam. Abdominal ultrasounds and CAT scans are then used to confirm the location and the size of the aneurysm. Coexisting disease is very common and must be addressed. Coronary artery disease, high blood pressure and lung disease exist in a least 50% of patients with aneurysms. Dye tests such as aortography may also be used to locate the renal artery branches and other vascular anomalies.

Recommendations:
1) If I am found to have an abdominal aneurysm I will need an ultrasound or CAT scan or both to determine its size and location.
2) If the aneurysm is 5 cm or larger and I am otherwise healthy and a candidate for surgery as determined by my cardiologist or internist, then I should get a stress echocardiogram to assess my heart function.
3) If the aneurysm is less than 5 cm and I am not symptomatic, then screening ultrasounds every 3 to 6 months should be done. Most commonly, aneurysms expand about 0.4 cm per year.
4) Finally, if surgery is recommended, the surgeon will replace the segment of aneurysm with a dacron graft and I should be back to work in about a month. Newer techniques of endovascular repair are available for selected patients and this can be determined by my surgeon.

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