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Monday 25 June 2012

YOGA for SCIATICA Pt1and Pt-2

Saturday 23 June 2012

Low Blood Pressure (Hypotension)

What is low blood pressure?

Blood pressure is the force exerted by circulating blood on the walls of blood vessels. It constitutes one of the critically important signs of life or vital signs which include heart beat, breathing, and temperature. Blood pressure is generated by the heart pumping blood into the arteries modified by the response of the arteries to the flow of blood.
An individual's blood pressure is expressed as systolic/diastolic blood pressure, for example, 120/80.The systolic blood pressure (the top number) represents the pressure in the arteries as the muscle of the heart contracts and pumps blood into them. The diastolic blood pressure (the bottom number) represents the pressure in the arteries as the muscle of the heart relaxes following its contraction. Blood pressure always is higher when the heart is pumping (squeezing) than when it is relaxing.
The range of systolic blood pressure for most healthy adults falls between 90 and 120 millimeters of mercury (mm Hg). Normal diastolic blood pressure ranges between 60 and 80 mm Hg. Current guidelines define normal blood pressure range as lower than 120/80. Blood pressures over 130/80 are considered high. High blood pressure increases the risk of developing:
Low blood pressure (hypotension) is pressure so low it causes symptoms or signs due to the low flow of blood through the arteries and veins. When the flow of blood is too low to deliver enough oxygen and nutrients to vital organs such as the brain, heart, and kidney, the organs do not function normally and may be temporarily or permanently damaged.
Unlike high blood pressure, low blood pressure is defined primarily by signs and symptoms of low blood flow and not by a specific blood pressure number. Some individuals routinely may have blood pressures of 90/50 with no symptoms and therefore do not have low blood pressure. However, others who normally have higher blood pressures may develop symptoms of low blood pressure if their blood pressure drops to 100/60.

How is blood pressure generated?

During relaxation of the heart (diastole) the left ventricle of the heart fills with blood returning from the lungs. The left ventricle then contracts and pumps blood into the arteries (systole). The blood pressure in the arteries during contraction of the ventricle (systolic pressure) is higher because blood is being actively ejected into the arteries. It is lower during relaxation of the ventricle (diastolic pressure) when no blood is being ejected into the arteries. The pulse that we can feel when we place our fingers over an artery is caused by the contraction of the left ventricle and the ejection of blood.
Blood pressure is determined by two factors: 1) The amount of blood pumped by the left ventricle of the heart into the arteries, and 2) the resistance to the flow of blood caused by the walls of the arterioles (smaller arteries).
Generally, blood pressure tends to be higher if more blood is pumped into the arteries or if the arterioles are narrow and/or stiff. (Narrow and/or stiff arterioles, by resisting the flow of blood, increase blood pressure.) Arterioles may become narrower when the muscles surrounding them contract. Arterioles may become stiff and narrow when older patients develop atherosclerosis.
Blood pressure tends to be lower if less blood is being pumped into the arteries or if the arterioles are larger and more flexible and, therefore, have less resistance to the flow of blood.

How does the body maintain normal blood pressure?

The body has mechanisms to alter or maintain blood pressure and blood flow. There are sensors that sense blood pressure in the walls of the arteries and send signals to the heart, the arterioles, the veins, and the kidneys that cause them to make changes that lower or increase blood pressure. There are several ways in which blood pressure can be adjusted - by adjusting the amount of blood pumped by the heart into the arteries (cardiac output), the amount of blood contained in the veins, the arteriolar resistance, and the volume of blood.

  • The heart can speed up and contract more frequently and it can eject more blood with each contraction. Both of these responses increase the flow of blood into the arteries and increase blood pressure.
  • The veins can expand and narrow. When veins expand, more blood can be stored in the veins and less blood returns to the heart for pumping into the arteries. As a result, the heart pumps less blood, and blood pressure is lower. On the other hand, when veins narrow, less blood is stored in the veins, more blood returns to the heart for pumping into the arteries, and blood pressure is higher.
  • The arterioles can expand and narrow. Expanded arterioles create less resistance to the flow of blood and decrease blood pressure, while narrowed arterioles create more resistance and raise blood pressure.
  • The kidney can respond to changes in blood pressure by increasing or decreasing the amount of urine that is produced. Urine is primarily water that is removed from the blood. When the kidney makes more urine, the amount (volume) of blood that fills the arteries and veins decreases, and this lowers blood pressure. If the kidneys make less urine, the amount of blood that fills the arteries and veins increases and this increases blood pressure. Compared with the other mechanisms for adjusting blood pressure, changes in the production of urine affect blood pressure slowly over hours and days. (The other mechanisms are effective in seconds.)
For example, low blood volume due to bleeding (such as a bleeding ulcer in the stomach or from a severe laceration from an injury) can cause low blood pressure. The body quickly responds to the low blood volume and pressure by the following adjustments which all increase blood pressure:

  • The heart rate increases and the forcefulness of the heart's contractions increase thus pumping more blood through the heart.
  • Veins narrow to return more blood to the heart for pumping.
  • Blood flow to the kidneys decreases to reduce the formation of urine and thereby increases the volume of blood in the arteries and veins.
  • Arterioles narrow to increase resistance to blood flow
These adaptive responses will keep the blood pressure in the normal range unless blood loss becomes so severe that the responses are overwhelmed

Is low blood pressure bad for your health?

People who have lower blood pressures have a lower risk of stroke, kidney disease, and heart disease. Athletes, people who exercise regularly, people who maintain ideal body weight, and non-smokers tend to have lower blood pressures. Therefore, low blood pressure is desirable as long as it is not low enough to cause symptoms and damage to the organs in the body.

What are low blood pressure signs and symptoms?

When blood pressure is not sufficient to deliver enough blood to the organs of the body, the organs do not work properly and can be temporarily or permanently damaged. For example, if insufficient blood flows to the brain, brain cells do not receive enough oxygen and nutrients, and a person can feel lightheaded, dizzy, or even faint.
Going from a sitting or lying position to a standing position often brings out symptoms of low blood pressure. This occurs because standing causes blood to "settle" in the veins of the lower body, and this can lower the blood pressure. If the blood pressure is already low, standing can make the low pressure worse, to the point of causing symptoms. The development of lightheadedness, dizziness, or fainting upon standing caused by low blood pressure is called orthostatic hypotension. Normal individuals are able to compensate rapidly for the low pressure created by standing with the responses discussed previously and do not develop orthostatic hypotension.
When there is insufficient blood pressure to deliver blood to the coronary arteries (the arteries that supply blood to the heart's muscle), a person may develop chest pain (a symptom of angina) or even a heart attack.
When insufficient blood is delivered to the kidneys, the kidneys fail to eliminate wastes from the body, for example, urea (BUN) and creatinine, and increases in their levels in the blood occur.
Shock is a life-threatening condition where persistently low blood pressure causes organs such as kidney(s), liver, heart, lung, and brain to fail rapidly

What are the causes of low blood pressure?

Conditions that reduce the volume of blood, reduce cardiac output (the amount of blood pumped by the heart), and medications are frequent reasons for low blood pressure.
  • Dehydration is common among patients with prolonged nausea, vomiting, and diarrhea. Large amounts of water are lost when vomiting and with diarrhea, especially if the person does not drink adequate amounts of fluid to replace the depleted water.
Other causes of dehydration include exercise, sweating, fever, and heat exhaustion, or heat stroke. Individuals with mild dehydration may experience only thirst and dry mouth. Moderate to severe dehydration may cause orthostatic hypotension (manifested by lightheadedness, dizziness, or fainting upon standing). Prolonged and severe dehydration can lead to shock, kidney failure, confusion, acidosis (too much acid in the blood), coma, and even death.
  • Moderate or severe bleeding can quickly deplete an individual's body of blood, leading to low blood pressure or orthostatic hypotension. Bleeding can result from trauma, surgical complications, or from gastrointestinal abnormalities such as ulcers, tumors, or diverticulosis. Occasionally, the bleeding may be so severe and rapid (for example, bleeding from a ruptured aortic aneurysm) that it causes shock and death rapidly.
  • Severe inflammation of organs inside the body such as acute pancreatitis can cause low blood pressure. In acute pancreatitis, fluid leaves the blood vessels to enter the inflamed tissues around the pancreas as well as the abdominal cavity, concentrating blood and reducing its volume.
Causes of low blood pressure due to heart disease
  • Weakened heart muscle can cause the heart to fail and reduce the amount of blood it pumps. One common cause of weakened heart muscle is the death of a large portion of the heart's muscle due to a single, large heart attack or repeated smaller heart attacks. Other examples of conditions that can weaken the ability of the heart to pump blood include medications that are toxic to the heart, infections of the muscle of the heart by viruses (myocarditis), and diseases of the heart's valves such as aortic stenosis.
  • Pericarditis is an inflammation of the pericardium (the sac surrounding the heart). Pericarditis can cause fluid to accumulate within the pericardium and compress the heart, restricting the ability of the heart to fill and pump blood.
  • Pulmonary embolism is a condition in which a blood clot in a vein (deep vein thrombosis) breaks off and travels to the heart and eventually the lung. A large blood clot can block the flow of blood into the left ventricle from the lungs and severely diminish the blood returning to the heart for pumping. Pulmonary embolism is a life-threatening emergency.
  • A slow heart rate (bradycardia) can decrease the amount of blood pumped by the heart. The resting heart rate for a healthy adult is between 60 and 100 beats/minute. Bradycardia (resting heart rates slower than 60 beats/minute) does not always cause low blood pressure. In fact, some highly trained athletes can have resting heart rates in the 40s and 50s (beats per minute) without any symptoms. (The slow heart rates are offset by more forceful contractions of the heart that pump more blood than in non-athletes.) But in many patients bradycardia can lead to low blood pressure, lightheadedness, dizziness, and even fainting.
Several common reasons for bradycardia include: 1) sick sinus syndrome, 2) heart block, and 3) drug toxicity. Many of these conditions occur in the elderly.
  1. Sick sinus syndrome: Sick sinus syndrome occurs when the diseased electrical system of the heart cannot generate signals fast enough to maintain a normal heart rate.


  2. Heart block: Heart block occurs when the specialized tissues that transmit electrical current in the heart are damaged by heart attacks, degeneration from atherosclerosis, and medications. Heart block prevents some or all of the electrical signals from reaching parts of the heart, and this prevents the heart from contracting as well as it otherwise would.


  3. Drug toxicity: Drugs such as digoxin (Lanoxin) or beta blockers for high blood pressure, can slow the transmission of electricity in the heart chemically and can cause bradycardia and hypotension (see section below "Medications that cause low blood pressure").
  • An abnormally fast heart rate (tachycardia) also can cause low blood pressure. The most common example of tachycardia causing low blood pressure is atrial fibrillation. Atrial fibrillation is a disorder of the heart characterized by rapid and irregular electrical discharges from the muscle of the heart causing the ventricles to contract irregularly and (usually) rapidly. The rapidly contracting ventricles do not have enough time to fill maximally with blood before the each contraction, and the amount of blood that is pumped decreases in spite of the faster heart rate. Other abnormally rapid heart rhythms such as ventricular tachycardia also can produce low blood pressure, sometimes even life-threatening shock.
Medications that cause low blood pressure
  • Medications such as calcium channel blockers, beta blockers, and digoxin (Lanoxin) can slow the rate at which the heart contracts. Some elderly people are extremely sensitive to these medications since they are more likely to have diseased hearts and electrical conduction tissues. In some individuals, the heart rate can become dangerously slow even with small doses of these medications.
  • Medications used in treating high blood pressure (such as ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, and alpha-blockers) can excessively lower blood pressure and result in symptomatic low blood pressure especially among the elderly.
  • Alcohol and narcotics also can cause low blood pressure.
Other conditions that cause low blood pressure

  • Vasovagal reaction is a common condition in which a healthy person temporarily develops low blood pressure, slow heart rate, and sometimes fainting. A vasovagal reaction typically is brought on by emotions of fear or pain such as having blood drawn, starting an intravenous infusion, or by gastrointestinal upset. Vasovagal reactions are caused by activity of the involuntary (autonomic) nervous system, especially the vagus nerve, which releases hormones that slow the heart and widen the blood vessels. The vagus nerve also controls digestive tract function and senses activity in the digestive system. Thus, some people can have a vasovagal reaction from straining at a bowel movement or vomiting.
  • Postural (orthostatic) hypotension is a sudden drop in blood pressure when an individual stands up from a sitting, squatting, or supine (lying) position. When a person stands up, gravity causes blood to settle in the veins in the legs so that less blood returns to the heart for pumping, and, as a result, the blood pressure drops. The body normally responds automatically to the drop in blood pressure by increasing the rate at which the heart beats and by narrowing the veins to return more blood to the heart. In patients with postural hypotension, this compensating reflex fails to occur, resulting low blood pressure and its symptoms. Postural hypotension can occur in persons of all ages but is much more common among the elderly, especially in those on medications for high blood pressure and/or diuretics. Other causes of postural hypotension include dehydration, adrenal insufficiency (discussed later), prolonged bed rest, diabetes that has caused damage to the autonomic nerves, alcoholism with damage to the autonomic nerves, and certain rare neurological syndromes (for example, Shy-Drager syndrome) that damage the autonomic nerves.
  • Another form of postural hypotension occurs typically in young healthy individuals. After prolonged standing, the individual's heart rate and blood pressure drop, causing dizziness, nausea, and often fainting. In these individuals, the autonomic nervous system wrongly responds to prolonged standing by directing the heart to slow down and the veins to dilate.
  • Micturition syncope is a temporary drop in blood pressure and loss of consciousness brought about by urinating. This condition typically occurs in elderly patients and may be due to the release by the autonomic nerves of hormones that lower blood pressure.
  • Adrenal insufficiency, for example, due to Addison's disease, can cause low blood pressure. Addison's disease is a disorder in which the adrenal glands (small glands next to the kidneys) are destroyed. The destroyed adrenal glands can no longer produce sufficient adrenal hormones (specifically cortisol) necessary to maintain normal bodily functions. Cortisol has many functions, one of which is to maintain blood pressure and the function of the heart. Addison's disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and, sometimes, darkening of the skin.
  • Septicemia is a severe infection in which bacteria (or other infectious organisms such as fungi) enter the blood. The infection typically originates in the lungs (as pneumonia), bladder, or in the abdomen due to diverticulitis or gallstones. The bacteria then enter the blood where they release toxins and cause life-threatening and profound low blood pressure (septic shock), often with damage to several organs.
  • Anaphylaxis (anaphylactic shock) is a potentially fatal allergic reaction to medications such as penicillin, intravenous iodine used in some X-ray studies, foods such as peanuts, or bee stings (insect stings). In addition to a severe drop in blood pressure, individuals may also experience hives as well as wheezing due to constriction of the airways, and a swollen throat which cause difficulty breathing. The shock is caused by enlargement of blood-containing blood vessels and escape of water from the blood into the tissues.
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    How is low blood pressure diagnosed and evaluated?

    In some individuals, particularly relatively healthy ones, symptoms of weakness, dizziness, and fainting raise the suspicion of low blood pressure. In others, an event often associated with low blood pressure, for example a heart attack has occurred to cause the symptoms.
    Measuring blood pressure, in both the lying (supine) and standing positions usually is the first step in diagnosing low blood pressure. In patients with symptomatic low blood pressure, there often is a marked drop in blood pressure upon standing, and patients may even develop orthostatic symptoms. The heart rate often increases greatly. Once low blood pressure has been identified as the cause of symptoms, the goal is to identify the cause of the low blood pressure. Sometimes the causes are readily apparent (such as loss of blood due to trauma, or sudden shock after receiving x-ray dyes containing iodine). At other times, the cause may be identified by testing:
  • CBC (complete blood count). CBC may reveal anemia from blood loss or elevated white blood cells due to infection.
  • Cortisol levels can be measured to diagnose adrenal insufficiency and Addison's disease.
  • Blood and urine cultures can be performed to diagnose septicemia and bladder infections, respectively.
  • Electrocardiograms (EKG) can detect abnormally slow or rapid heart beats, pericarditis, and heart muscle damage from either previous heart attacks or a reduced supply of blood to the heart muscle that has not yet caused a heart attack.
  • Holter monitor recordings are used to diagnose intermittent episodes of abnormal heart rhythms. If abnormal rhythms occur intermittently, a standard EKG performed at the time of a visit to the doctor's office may not show the abnormal rhythm. A Holter monitor is a continuous recording of the heart's rhythm for 24 hours that often is used to chart and diagnose intermittent episodes of bradycardia or tachycardia.
  • Patient-activated event recorder. If the episodes of bradycardia or tachycardia are infrequent, a 24-hour Holter recording may not capture these sporadic episodes. In this situation, a patient can wear a patient-activated event recorder for up to four weeks. The patient presses a button to start the recording when he or she senses the onset of an abnormal heart rhythm or symptoms possibly caused by low blood pressure. The doctor then analyzes the recordings at a later date to identify the abnormal episodes.
  • Echocardiograms are examinations of the structures and motion of the heart using ultrasound. Echocardiograms can detect pericardial fluid due to pericarditis, the extent of heart muscle damage from heart attacks, diseases of the heart valves, and rare tumors of the heart.
  • Tilt-Table tests are used to evaluate patients suspected of having postural hypotension or syncope due to abnormal function of the autonomic nerves. During a tilt-table test, the patient lies on an examining table with an intravenous infusion administered while the heart rate and blood pressure are monitored. The table then is tilted upright for 15 minutes to 45 minutes. Heart rate and blood pressure are monitored every few minutes. The purpose of the test is to try to reproduce postural hypotension.  Sometimes a doctor may administer epinephrine (Adrenalin, Isuprel) intravenously to induce postural hypotension.

How is low blood pressure treated?

Low blood pressure in healthy subjects without symptoms or organ damage needs no treatment. However, all patients with symptoms possibly due to low blood pressure should be evaluated by a doctor. (Patients who have had a major drop in blood pressure from their usual levels even without the development of symptoms also should be evaluated.) The doctor needs to identify the cause of the low blood pressure; remedies will depend on the cause. For example, if a medication is causing the low blood pressure, the dose of medication may have to be reduced or the medication stopped, though only after consulting the doctor. Self-adjustment of medication should not be done.

  • Dehydration is treated with fluids and minerals (electrolytes). Mild dehydration without nausea and vomiting can be treated with oral fluids and electrolytes. Moderate to severe dehydration usually is treated in the hospital or emergency room with intravenous fluids and electrolytes.
  • Blood loss can be treated with intravenous fluids and blood transfusions. Continuous and severe bleeding needs to be treated immediately.
  • Septic shock is an emergency and is treated with intravenous fluids and antibiotics.
  • Blood pressure medications or diuretics are adjusted, changed, or stopped by the doctor if they are causing low blood pressure symptoms.
  • Bradycardia may be due to a medication. The doctor may reduce, change or stop the medication. Bradycardia due to sick sinus syndrome or heart block is treated with an implantable pacemaker.
  • Tachycardia is treated depending on the nature of the tachycardia. Atrial fibrillation can be treated with oral medications, electrical cardioversion, or a catheterization procedure called pulmonary vein isolation. Ventricular tachycardia can be controlled with medications or with an implantable defibrillator.
  • Pulmonary embolism and deep vein thrombosis is treated with blood thinners, intravenous initially with heparin, and oral warfarin (Coumadin) later.
  • Pericardial fluid can be removed by a procedure called pericardiocentesis.
  • Postural hypotension can be treated with changes in diet such as increasing water and salt intake*, increasing intake of caffeinated beverages (because caffeine constricts blood vessels), using compression stockings to compress the leg veins and reduce the pooling of blood in the leg veins, and in some patients, the use of a medication called midodrine (ProAmatine). The problem with ProAmatine is that while it increases blood pressure in the upright position, the supine blood pressure may become too high, thus increasing the risk of strokes. Mayo Clinic researchers found that a medication used to treat muscle weakness in myasthenia gravis called pyridostigmine (Mestinon) increases upright blood pressure but not supine blood pressure. Mestinon, an anticholinesterase medication, works on the autonomic nervous system, especially when a person is standing up. Side effects include minor abdominal cramping or increased frequency of bowel movements. *Note: Increasing salt intake can lead to heart failure in patients with existing heart disease and should not be undertaken without consulting a doctor.
  • Postprandial hypotension refers to low blood pressure occurring after meals. Ibuprofen (Motrin) or indomethacin (Indocin) may be beneficial.

source:medicinenet.com

Congestive Heart Failure

Congestive heart failure facts

  • Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to meet the body's needs.
  • Many disease processes can impair the pumping efficiency of the heart to cause congestive heart failure.
  • The symptoms of congestive heart failure vary, but can include fatigue, diminished exercise capacity, shortness of breath, and swelling.
  • The diagnosis of congestive heart failure is based on knowledge of the individual's medical history, a careful physical examination, and selected laboratory tests.
  • The treatment of congestive heart failure can include lifestyle modifications, addressing potentially reversible factors, medications, heart transplant, and mechanical therapies.
  • The course of congestive heart failure in any given patient is extremely variable.

What is congestive heart failure?

Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to deliver oxygen rich blood to the body. Congestive heart failure can be caused by:
  1. diseases that weaken the heart muscle,
  2. diseases that cause stiffening of the heart muscles, or
  3. diseases that increase oxygen demand by the body tissue beyond the capability of the heart to deliver adequate oxygen-rich blood.
The heart has two atria (right atrium and left atrium) that make up the upper chambers of the heart, and two ventricles (left ventricle and right ventricle) that make up the lower chambers of the heart. The ventricles are muscular chambers that pump blood when the muscles contract. The contraction of the ventricle muscles is called systole.
Many diseases can impair the pumping action of the ventricles. For example, the muscles of the ventricles can be weakened by heart attacks, infections (myocarditis) or toxins (alcohol, some chemotherapy agents). The diminished pumping ability of the ventricles due to muscle weakening is called systolic dysfunction. After each ventricular contraction (systole) the ventricle muscles need to relax to allow blood from the atria to fill the ventricles. This relaxation of the ventricles is called diastole.
Diseases such as hemochromatosis (iron overload) or amyloidosis can cause stiffening of the heart muscle and impair the ventricles' capacity to relax and fill; this is referred to as diastolic dysfunction. The most common cause of this is longstanding high blood pressure resulting in a thickened (hypertrophied) heart. Additionally, in some patients, although the pumping action and filling capacity of the heart may be normal, abnormally high oxygen demand by the body's tissues (for example, with hyperthyroidism or anemia) may make it difficult for the heart to supply an adequate blood flow (called high output heart failure).
In some individuals one or more of these factors can be present to cause congestive heart failure. The remainder of this article will focus primarily on congestive heart failure that is due to heart muscle weakness, systolic dysfunction.
Congestive heart failure can affect many organs of the body. For example:
  • The weakened heart muscles may not be able to supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. This diminished kidney function can cause the body to retain more fluid.
  • The lungs may become congested with fluid (pulmonary edema) and the person's ability to exercise is decreased.
  • Fluid may likewise accumulate in the liver, thereby impairing its ability to rid the body of toxins and produce essential proteins.
  • The intestines may become less efficient in absorbing nutrients and medicines.
  • Fluid also may accumulate in the extremities, resulting in edema (swelling) of the ankles and feet.
Eventually, untreated, worsening congestive heart failure will affect virtually every organ in the body.
Picture of the heart and valves, left and right ventricles, left and right atria

Picture of the heart and valves, left and right ventricles, left and right atria

What causes congestive heart failure?

Many disease processes can impair the pumping efficiency of the heart to cause congestive heart failure. In the United States, the most common causes of congestive heart failure are:
Less common causes include viral infections of the stiffening of the heart muscle, thyroid disorders, disorders of the heart rhythm, and many others.
It should also be noted that in patients with underlying heart disease, taking certain medications can lead to the development or worsening of congestive heart failure. This is especially true for those drugs that can cause sodium retention or affect the power of the heart muscle. Examples of such medications are the commonly used nonsteroidal anti-inflammatory drugs (NSAIDs), which include ibuprofen (Motrin and others) and naproxen (Aleve and others) as well as certain steroids, some medication for diabetes (such as rosiglitazone [Avandia] or pioglitazone [Actos]), and some calcium channel blockers.

What are the symptoms of congestive heart failure?

The symptoms of congestive heart failure vary among individuals according to the particular organ systems involved and depending on the degree to which the rest of the body has "compensated" for the heart muscle weakness.
  • An early symptom of congestive heart failure is fatigue. While fatigue is a sensitive indicator of possible underlying congestive heart failure, it is obviously a nonspecific symptom that may be caused by many other conditions. The person's ability to exercise may also diminish. Patients may not even sense this decrease and they may subconsciously reduce their activities to accommodate this limitation.
  • As the body becomes overloaded with fluid from congestive heart failure, swelling (edema) of the ankles and legs or abdomen may be noticed. This can be referred to as "right sided heart failure" as failure of the right sided heart chambers to pump venous blood to the lungs to acquire oxygen results in buildup of this fluid in gravity-dependent areas such as in the legs. The most common cause of this is longstanding failure of the left heart, which may lead to secondary failure of the right heart. Right-sided heart failure can also be caused by severe lung disease (referred to as "cor pulmonale"), or by intrinsic disease of the right heart muscle (less common)
  • In addition, fluid may accumulate in the lungs, thereby causing shortness of breath, particularly during exercise and when lying flat. In some instances, patients are awakened at night, gasping for air.
  • Some may be unable to sleep unless sitting upright.
  • The extra fluid in the body may cause increased urination, particularly at night.
  • Accumulation of fluid in the liver and intestines may cause nausea, abdominal pain, and decreased appetite.

How is congestive heart failure diagnosed?

The diagnosis of congestive heart failure is most often a clinical one that is based on knowledge of the patient's pertinent medical history, a careful physical examination, and selected laboratory tests.
A thorough patient history may disclose the presence of one or more of the symptoms of congestive heart failure described above. In addition, a history of significant coronary artery disease, prior heart attack, hypertension, diabetes, or significant alcohol use can be clues.
The physical examination is focused on detecting the presence of extra fluid in the body (breath sounds, leg swelling, or neck veins) as well as carefully characterizing the condition of the heart (pulse, heart size, heart sounds, and murmurs).
Useful diagnostic tests include the electrocardiogram (ECG) and chest X-ray to detect previous heart attacks, arrhythmia, heart enlargement, and fluid in and around the lungs. Perhaps the single most useful diagnostic test is the echocardiogram, in which ultrasound is used to image the heart muscle, valve structures, and blood flow patterns. The echocardiogram is very helpful in diagnosing heart muscle weakness. In addition, the test can suggest possible causes for the heart muscle weakness (for example, prior heart attack, and severe valve abnormalities). Virtually all patients in whom the diagnosis of congestive heart failure is suspected should ideally undergo echocardiography early in their assessment.
Nuclear medicine studies assess the overall pumping capability of the heart and examine the possibility of inadequate blood flow to the heart muscle. Heart catheterization allows the arteries to the heart to be visualized with angiography (using dye inside of the blood vessels that can be seen using X-ray methods). During catheterization the pressures in and around the heart can be measured and the heart's performance assessed. In rare cases, a biopsy of the heart tissue may be recommended to diagnose specific diseases. This biopsy can often be accomplished through the use of a special catheter device that is inserted into a vein and maneuvered into the right side of the heart.
Another helpful diagnostic test is a blood test called a BNP or B-type natriuretic peptid level. This level can vary with age and gender but is typically elevated from heart failure and can aid in the diagnosis, and can be useful in following the response to treatment of congestive heart failure.
The choice of tests depends on each patient's case and is based on the suspected diagnoses.

What is the treatment of congestive heart failure?


Lifestyle modifications

After congestive heart failure is diagnosed, treatment should be started immediately. Perhaps the most important and yet most neglected aspect of treatment involves lifestyle modifications. Sodium causes an increase in fluid accumulation in the body's tissues. Because the body is often congested with excess fluid, patients become very sensitive to the levels of intake of sodium and water. Restricting salt and fluid intake is often recommended because of the tendency of fluid to accumulate in the lungs and surrounding tissues. An American "no added salt" diet can still contain 4 to 6 grams (4000 to 6000 milligrams) of sodium per day. In individuals with congestive heart failure, an intake of no more than 2 grams (2000 milligrams) of sodium per day is generally advised. Reading food labels and paying close attention to total sodium intake is very important. Severe restriction of alcohol consumption also is advised.
Likewise, the total amount of fluid consumed must be regulated. Although many people with congestive heart failure take diuretics to aid in the elimination of excess fluid, the action of these medications can be overwhelmed by an excess intake of water and other fluids. The maxim that "drinking eight glasses of water a day is healthy" certainly does not apply to patients with congestive heart failure. In fact, patients with more advanced cases of congestive heart failure are often advised to limit their total daily fluid intake from all sources to 2 quarts. The above guidelines for sodium and fluid intake may vary depending on the severity of congestive heart failure in any given individual and should be discussed with their physician.
An important tool for monitoring an appropriate fluid balance is the frequent measurement of body weight. An early sign of fluid accumulation is an increase in body weight. This may occur even before shortness of breath or swelling in the legs and other body tissues (edema) is detected. A weight gain of two to three pounds over two to three days should prompt a call to the physician, who may order an increase in the dose of diuretics or other methods designed to stop the early stages of fluid accumulation before it becomes more severe.
Aerobic exercise, once discouraged for congestive heart failure patients, has been shown to be beneficial in maintaining overall functional capacity, quality of life, and perhaps even improving survival. Each person's body has its own unique ability to compensate for the failing heart. Given the same degree of heart muscle weakness, individuals may display widely varying degrees of limitation of function. Regular exercise, when tailored to the person's tolerance level, appears to provide significant benefits and should be used only when the individual is compensated and stable.
Addressing potentially reversible factors

Depending on the underlying cause of congestive heart failure, potentially reversible factors should be explored. For example:
  • In certain persons whose congestive heart failure is caused by inadequate blood flow to the heart muscle, restoration of the blood flow through coronary artery surgery or catheter procedures (angioplasty, intracoronary stenting) may be considered.
  • Congestive heart failure that is due to severe disease of the valves may be alleviated by valve surgery in appropriate patients.
  • When congestive heart failure is caused by chronic, uncontrolled high blood pressure (hypertension), aggressive blood pressure control will often improve the condition.
  • Heart muscle weakness that is due to longstanding, severe alcohol abuse can improve significantly with abstinence from drinking.
  • Congestive heart failure that is caused by other disease states may be similarly partially or completely reversible by appropriate measures
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    Medications

    Until recently, the selection of medications available for the treatment of congestive heart failure was frustratingly limited and focused mainly on controlling the symptoms. Medications have now been developed that both improve symptoms, and, importantly, prolong survival.
    Angiotensin Converting Enzyme (ACE) Inhibitors

    ACE inhibitors have been used for the treatment of hypertension for more than 20 years. This class of drugs has also been extensively studied in the treatment of congestive heart failure. These medications block the formation of angiotensin II, a hormone with many potentially adverse effects on the heart and circulation in patients with heart failure. In multiple studies of thousands of patients, these drugs have demonstrated a remarkable improvement of symptoms in patients, prevention of clinical deterioration, and prolongation of survival. In addition, they have been recently been shown to prevent the development of heart failure and heart attacks. The wealth of the evidence supporting the use of these agents in heart failure is so strong that ACE inhibitors should be considered in all patients with heart failure, especially those with heart muscle weakness.
    Possible side effects of these drugs include:
  • a nagging, dry cough,
  • low blood pressure,
  • worsening kidney function and electrolyte imbalances, and
  • rarely, true allergic reactions.
When used carefully with proper monitoring, however, the majority of individuals with congestive heart failure tolerate these medications without significant problems. Examples of ACE inhibitors include:
For those individuals who are unable to tolerate the ACE inhibitors, an alternative group of drugs, called the angiotensin receptor blockers (ARBs), may be used. These drugs act on the same hormonal pathway as the ACE inhibitors, but instead block the action of angiotensin II at its receptor site directly. A small, early study of one of these agents suggested a greater survival benefit in elderly congestive heart failure patients as compared to an ACE inhibitor. However, a larger, follow-up study failed to demonstrate the superiority of the ARBs over the ACE inhibitors. Further studies are underway to explore the use of these agents in congestive heart failure both alone and in combination with the ACE inhibitors.
Possible side effects of these drugs are similar to those associated with the ACE inhibitors, although the dry cough is much less common. Examples of this class of medications include:
Beta-blockers
Certain hormones, such as epinephrine (adrenaline), norepinephrine, and other similar hormones, act on the beta receptor's of various body tissues and produce a stimulative effect. The effect of these hormones on the beta receptors of the heart is a more forceful contraction of the heart muscle. Beta-blockers are agents that block the action of these stimulating hormones on the beta receptors of the body's tissues. Since it was assumed that blocking the beta receptors further depressed the function of the heart, beta-blockers have traditionally not been used in persons with congestive heart failure. In congestive heart failure, however, the stimulating effect of these hormones, while initially useful in maintaining heart function, appears to have detrimental effects on the heart muscle over time.
However, studies have demonstrated an impressive clinical benefit of beta-blockers in improving heart function and survival in individuals with congestive heart failure who are already taking ACE inhibitors. It appears that the key to success in using beta-blockers in congestive heart failure is to start with a low dose and increase the dose very slowly. At first, patients may even feel a little worse and other medications may need to be adjusted.
Possible side effects include:
  • fluid retention,
  • low blood pressure,
  • low pulse, and
  • general fatigue and lightheadedness.
Beta-blockers should generally not be used in people with certain significant diseases of the airways (for example, asthma, emphysema) or very low resting heart rates. While carvedilol (Coreg) has been the most thoroughly studied drug in the setting of congestive heart failure, studies of other beta-blockers have also been promising. Research comparing carvedilol directly with other beta-blockers in the treatment of congestive heart failure is ongoing. Long acting metoprolol (Toprol XL) is also very effective in individuals with congestive heart failure.
Digoxin
Digoxin (Lanoxin) has been used in the treatment of congestive heart failure for hundreds of years. It is naturally produced by the foxglove flowering plant. Digoxin stimulates the heart muscle to contract more forcefully. It also has other actions, which are not completely understood, that improve congestive heart failure symptoms and can prevent further heart failure. However, a large-scale randomized study failed to demonstrate any effect of digoxin on mortality.
Digoxin is useful for many patients with significant congestive heart failure symptoms, even though long-term survival may not be affected. Potential side effects include:
These side effects, however, are generally a result of toxic levels in the blood and can be monitored by blood tests. The dose of digoxin may also need to be adjusted in patients with significant kidney impairment.
Diuretics
Diuretics are often an important component of the treatment of congestive heart failure to prevent or alleviate the symptoms of fluid retention. These drugs help keep fluid from building up in the lungs and other tissues by promoting the flow of fluid through the kidneys. Although they are effective in relieving symptoms such as shortness of breath and leg swelling, they have not been demonstrated to positively impact long-term survival.
Nevertheless, diuretics remain key in preventing deterioration of the patient's condition thereby requiring hospitalization. When hospitalization is required, diuretics are often administered intravenously because the ability to absorb oral diuretics may be impaired, when congestive heart failure is severe. Potential side effects of diuretics include:
It is important to prevent low potassium levels by taking supplements, when appropriate. Such electrolyte disturbances may make patients susceptible to serious heart rhythm disturbances. Examples of various classes of diuretics include:
One particular diuretic has been demonstrated to have surprisingly favorable effects on survival in congestive heart failure patients with relatively advanced symptoms. Spironolactone (Aldactone) has been used for many years as a relatively weak diuretic in the treatment of various diseases. Among other things, this drug blocks the action of the hormone aldosterone.
Aldosterone has many theoretical detrimental effects on the heart and circulation in congestive heart failure. Its release is stimulated in part by angiotensin II (see ACE inhibitors, above). In patients taking ACE inhibitors, however, there is an "escape" phenomenon in which aldosterone levels can increase despite low levels of angiotensin II. Medical researchers have found that spironolactone (Aldactone) can improve the survival rate of patients with congestive heart failure. In that the doses used in the study were relatively small, it has been theorized that the benefit of the drug was in its ability to block the effects of aldosterone rather than its relatively weak action as a diuretic (water pill). Possible side effects of this drug include elevated potassium levels and, in males, breast tissue growth (gynecomastia).
Another aldosterone inhibitor is eplerenone (Inspra).

Heart transplant

In some cases, despite the use of optimal therapies as described above, the patient's condition continues to deteriorate due to progressive heart failure. In selected patients, heart transplantation is a viable treatment option. Candidates for heart transplantation are generally under age 70 and do not have severe or irreversible diseases affecting the other organs. Additionally, a transplant is done only when it is clear that the patient's prognosis is poor with continued medical treatment of the heart condition. Transplant patients require close medical follow-up while taking the necessary drugs that suppress the immune system, and because of the risk of rejection of the transplanted heart. They also must be monitored for possible development of coronary artery disease in the transplanted heart.
Although there are thousands of patients on waiting lists for a heart transplant at any given time, the number of operations performed each year is limited by the number of available donor organs. For these reasons, heart transplantation is a realistic option in only a small subset of the large numbers of patients with congestive heart failure.

Other mechanical therapies

Given the limitations associated with heart transplantation, much attention has recently been directed towards the development of mechanical assist devices that are designed to assume part or all of the pumping function of the heart. There are several devices available for clinical use and many more are actively being developed. For instance, there are currently left ventricular assist devices that are approved for use as a temporary mode of circulatory support in very ill patients until a transplant can be performed. Studies examining the possible role of these mechanical assist devices on a long term basis as permanent self-contained implants are ongoing. They may often be used for longer periods of time in older patients who may not be heart transplant candidates. The current major limitation of these devices is the risk of infection, especially at the site where the device exits the body through the skin to communicate with its external power source.
A less invasive modality, which can be placed without surgery, is the biventricular pacemaker. This device has proved valuable in appropriate types of patients with heart failure and impaired ventricles by improving the synchrony of contraction.

What is the long term prognosis for patients with congestive heart failure?

Congestive heart failure is generally a progressive disease with periods of stability punctuated by episodic clinical exacerbations. The course of the disease in any given individual, however, is extremely variable. Factors involved in determining the long term outlook (prognosis) for a given patient include:
  • the nature of the underlying heart disease,
  • the response to medications,
  • the degree to which other organ systems are involved and the severity of other accompanying conditions,
  • the person's symptoms and degree of impairment, and
  • other factors that remain poorly understood.
With the availability of newer drugs to potentially favorably affect the progression of disease, the prognosis in congestive heart failure is generally more favorable than that observed just 10 years ago. In some cases, especially when the heart muscle dysfunction has recently developed, a significant spontaneous improvement is not uncommonly observed, even to the point where heart function becomes normal.
Heart failure is often graded on a scale of I to IV based on the patient's ability to function.
  1. Class I is patients with a weakened heart but without limitation or symptoms.
  2. Class II is only limitation at heavier workloads.
  3. Class III is limitation at everyday activity.
  4. Class IV is severe symptoms at rest or with any degree of effort.
The prognosis of heart failure patients is very closely associated with the functional class.
An important issue in congestive heart failure is the risk of heart rhythm disturbances (arrhythmias). Of those deaths that occur in individuals with congestive heart failure, approximately 50% are related to progressive heart failure. Importantly, the other half are thought to be related to serious arrhythmias. A major advance has been the finding that nonsurgical placement of automatic implantable cardioverter/defibrillators (AICD) in individuals with severe congestive heart failure (defined by an ejection fraction below 30%-35%) can significantly improve survival, and has become the standard of care in most such individuals.
In some people with severe heart failure and certain ECG abnormalities, the left and right side of the heart don't beat in rhythm, and inserting a device called a biventricular pacer can significantly reduce symptoms

What are the areas of new research in congestive heart failure?

Despite the significant advances in drug therapy for congestive heart failure over the past 20 years, many exciting developments are under active study. New classes of medications are being tested in clinical trials, including the calcium sensitizing agents, vasopeptidase inhibitors, and natriuretic peptides. As was the case with the ACE inhibitors and beta-blockers, the potential use of these drugs is based on theoretical considerations that have resulted from an increased understanding of the processes both underlying and resulting from heart failure. Additionally, gene therapy that is targeted toward certain genes thought to contribute to heart failure is being tested.
These developments have justified an unprecedented optimism in the treatment of congestive heart failure. The majority of individuals, with appropriate lifestyle measures and medical regimens, can maintain active, fulfilling lifestyles. The range of treatment options has been significantly strengthened by drugs such as the ACE inhibitors and beta-blockers. In the future, we will surely see the addition of many more and equally potent interventions.
source:medicinenet.com


Thursday 14 June 2012

Degenerative Disc Disease and Sciatica


Degenerative disc disease & sciatica facts


  • The discs of the spine serve as "cushions" between each vertebral segment.
  • The discs are designed somewhat like a jelly donut.
  • Degeneration (deterioration) of the disc makes the disc more susceptible to herniation (rupture), which can lead to localized or radiating pain.
  • Sciatica can result from disc herniation when nerves in the low back are irritated.

How is the spine designed?


The vertebrae are the bony building blocks of the spine. Between each of the largest part of the vertebrae are the discs. Ligaments are situated around the spine and discs. The spine has seven vertebrae in the neck (cervical vertebrae), 12 vertebrae in the mid-back (thoracic vertebrae), and five vertebrae in the low back (lumbar vertebrae). In addition, in the mid-buttock beneath the fifth lumbar vertebra, are five sacral vertebrae -- usually fused as the sacrum bone followed by the tailbone (coccyx).

What is the purpose of the spine and its discs?


The bony spine is designed so that vertebrae "stacked" together can provide a movable support structure. The spine also protects the spinal cord (nervous tissue that extends down the spinal column from the brain) from injury. Each vertebra has a spinous process, which is a bony prominence behind the spinal cord that shields the cord's nerve tissue. The vertebrae also have a strong bony "body" in front of the spinal cord to provide a platform suitable for weight-bearing.
The discs are pads that serve as "cushions" between each vertebral body that serve to minimize the impact of movement on the spinal column. Each disc is designed like a jelly donut with a central softer component (nucleus pulposus). With injury or degeneration, this softer component can sometimes rupture (herniate) through the surrounding outer ring (annulus fibrosus) and irritate adjacent nervous tissue. Ligaments are strong fibrous soft tissues that firmly attach bones to bones. Ligaments attach each of the vertebrae and surround each of the discs. When ligaments are injured as the disc degenerates, localized pain in the area affected can result.
Picture of herniated disc between L4 and L5

Picture of herniated disc between L4 and L5

Cross-section picture of herniated disc between L4 and L5

What causes degenerative disc disease?


As we age, the water and protein content of the cartilage of the body changes. This change results in weaker, more fragile, and thin cartilage. Because both the discs and the joints that stack the vertebrae (facet joints) are partly composed of cartilage, these areas are subject to wear and tear over time (degenerative changes). The gradual deterioration of the disc between the vertebrae is referred to as degenerative disc disease, sometimes abbreviated DDD. Wear of the facet cartilage and the bony changes of the adjacent joint is referred to as degenerative facet joint disease or osteoarthritis of the spine. Trauma injury to the spine can also lead to degenerative disc disease.
Degeneration of the disc is medically referred to as spondylosis. Spondylosis can be noted on X-ray tests or MRI scanning of the spine as a narrowing of the normal "disc space" between the adjacent vertebrae.

What are the symptoms of degenerative disc disease?


Degeneration of the disc tissue makes the disc more susceptible to herniation. Degeneration of the disc can cause local pain in the affected area. Any level of the spine can be affected by disc degeneration. When disc degeneration affects the spine of the neck, it is referred to as cervical disc disease. When the mid-back is affected, the condition is referred to as thoracic disc disease. Disc degeneration that affects the lumbar spine can cause chronic low back pain (referred to as lumbago) or irritation of a spinal nerve to cause pain radiating down the leg (sciatica). Lumbago causes pain localized to the low back and is common in older people. Degenerative arthritis (osteoarthritis) of the facet joints that can be detected with plain X-ray testing is also a cause of localized lumbar pain. The pain from degenerative disc or joint disease of the spine is usually treated conservatively with intermittent heat, rest, rehabilitative exercises, and medications to relieve pain, muscle spasm, and inflammation.

Cross-section picture of herniated disc between L4 and L5

What causes degenerative disc disease?


As we age, the water and protein content of the cartilage of the body changes. This change results in weaker, more fragile, and thin cartilage. Because both the discs and the joints that stack the vertebrae (facet joints) are partly composed of cartilage, these areas are subject to wear and tear over time (degenerative changes). The gradual deterioration of the disc between the vertebrae is referred to as degenerative disc disease, sometimes abbreviated DDD. Wear of the facet cartilage and the bony changes of the adjacent joint is referred to as degenerative facet joint disease or osteoarthritis of the spine. Trauma injury to the spine can also lead to degenerative disc disease.
Degeneration of the disc is medically referred to as spondylosis. Spondylosis can be noted on X-ray tests or MRI scanning of the spine as a narrowing of the normal "disc space" between the adjacent vertebrae.

What are the symptoms of degenerative disc disease?


Degeneration of the disc tissue makes the disc more susceptible to herniation. Degeneration of the disc can cause local pain in the affected area. Any level of the spine can be affected by disc degeneration. When disc  degeneration affects the spine of the neck, it is referred to as cervical disc disease. When the mid-back is affected, the condition is referred to as thoracic disc disease. Disc degeneration that affects the lumbar spine can cause chronic low back pain (referred to as lumbago) or irritation of a spinal nerve to cause pain radiating down the leg (sciatica). Lumbago causes pain localized to the low back and is common in older people. Degenerative arthritis (osteoarthritis) of the facet joints that can be detected with plain X-ray testing is also a cause of localized lumbar pain. The pain from degenerative disc or joint disease of the spine is usually treated conservatively with intermittent heat, rest, rehabilitative exercises, and medications to relieve pain, muscle spasm, and inflammation.

What are radiculopathy and sciatica? What are the symptoms?


Radiculopathy refers to nerve irritation caused by damage to the disc between the vertebrae. This occurs because of degeneration ("wear and tear") of the outer ring of the disc or because of traumatic injury, or both. Weakness of the outer ring leads to disc bulging and disc herniation. As a result, the central softer portion of the disc can rupture through the outer ring of the disc and abut the spinal cord or its nerves as they exit the bony spinal column.
When nerves are irritated in the neck from degenerative disc disease, the condition is referred to as cervical radiculopathy. This can lead to painful burning or tingling sensations in the arms. When nerves are irritated in the low back from degenerative disc disease, the condition is called lumbar radiculopathy, and it often causes the commonly recognized "sciatica" pain that shoots down a lower extremity. This condition can be preceded by a localized low-back aching. Sciatica pain can follow a "popping" sensation at onset and be accompanied by numbness and tingling. The pain commonly increases with movements at the waist and can increase with coughing or sneezing. In more severe instances, lumbar radiculopathy can be accompanied by incontinence of the bladder and/or bowels.

How are degenerative disc disease, radiculopathy, and sciatica diagnosed?


Degenerative disc disease, radiculopathy, and sciatica are suspected when the symptoms described above are noted. The doctor can sometimes detect signs of irritated nerves during the examination. For example, increased radiating pain when the lower extremity is lifted supports the diagnosis of lumbar radiculopathy. Nerve testing (EMG/electromyogram and NCV/nerve conduction velocity) of the lower extremities can be used to detect the nerve irritation. The actual disc herniation can be detected with radiology testing, such as CAT or MRI scanning.

How is radiculopathy treated?


The treatment of degenerative disc disease, radiculopathy, and sciatica ranges from nonsurgical (medical) management to surgery. Medical management of radiculopathy includes patient education of the condition, medications to relieve pain and muscles spasm, cortisone injection around the spinal cord (epidural injection), physical therapy (heat, exercises, massage, ultrasound, electrical stimulation), and rest (not strict bed rest, but avoiding reinjury). With unrelenting pain, severe impairment of function, or incontinence (which can indicate spinal cord irritation), surgery may be necessary. The operation performed depends on the overall status of the spine and the age and health of the patient. Procedures include removal of the herniated disc with laminotomy (producing a small hole in the bone of the spine surrounding the spinal cord), laminectomy (removal of the bony wall adjacent to the nerve tissues), by needle technique through the skin (percutaneous discectomy), disc-dissolving procedures (chemonucleolysis), and others.

What is bony encroachment and spinal stenosis?


Any condition that results in movement or growth of the bony vertebrae of the spine can limit the space (encroachment) for the adjacent spinal cord and nerves. Causes of bony encroachment of the spinal nerves include foramen narrowing (narrowing of the portal through which the spinal nerve passes from the spinal column, out of the spinal canal to the body), spondylolisthesis (slipping of one vertebra relative to another), and spinal stenosis (narrowing of the spinal canal causing by compression of the nerve roots or spinal cord by bony spurs or other soft tissues in the spinal canal). For example, lumbar spinal nerve compression in these conditions can lead to sciatica pain that radiates down the lower extremities.
Spinal stenosis (narrowing of the spinal canal) can occur at any level of the spine, but it's most common in the lumbar spine of the low back. Symptoms depend on the level affected. For example, lumbar spinal stenosis can cause lower-extremity pains that worsen with walking and are relieved by resting (mimicking poor circulation of the lower extremities).
Treatment of these conditions varies (depending on the severity and condition of the patient) from rest to epidural cortisone injection and surgical decompression by removing the bone that is compressing the nervous tissue.

What is the outlook (prognosis) of degenerative disc disease, radiculopathy, and sciatica?


The outlook of degenerative disc disease, radiculopathy, and sciatica depends on the severity of the condition, its precise cause, and the interventions used to treat the patient. When patients respond to conservative treatments, the result can be complete healing. Surgical repairs can require rehabilitation physical therapy.

Can degenerative disc disease, radiculopathy, and sciatica be prevented?


Avoiding injury can prevent these conditions. When the disease already exists, aggravation of existing symptoms can be avoided by limiting stressing or overusing the involved spine.
source:medicinenet.com