Thursday, June 20, 2013

HIGH BLOOD PRESSURE or HYPERTENSION



HIGH BLOOD PRESSURE

SYMPTOMS :
There's a common misconception that people with high blood pressure, also called hypertension, will experience symptoms such as nervousness, sweating, difficulty sleeping or facial flushing. The truth is that HBP is largely a symptom less condition. If you ignore your blood pressure because you think symptoms will alert you to the problem, you are taking a dangerous chance with your life. Everybody needs to know their blood pressure numbers, and everyone needs to prevent high blood pressure from developing.
The best evidence indicates that high blood pressure does not cause headaches except perhaps in the case of hypertensive crisis (systolic/top number higher than 180 OR diastolic/bottom number higher than 110).
Except with hypertensive crisis, nosebleeds are not a reliable indicator for HBP. In one study, 17 percent of people treated for high blood pressure emergencies at the hospital had nosebleeds. However, 83 percent reported no such symptom.

Common Symptoms:
Blood spots in the eyes
Yes, blood spots in the eyes, or conjunctivitis hemorrhage, are more common in people with diabetes or high blood pressure, but neither condition causes the blood spots. Floaters in the eyes are not related to high blood pressure. However, an ophthalmologist may be able to detect damage to the optic nerve caused by untreated HBP.
  • Facial flushing
    Facial flushing occurs when blood vessels in the face dilate. The red, burning face can occur unpredictably or in response to certain triggers such as sun exposure, cold weather, spicy foods, wind, hot drinks and skin-care products. Facial flushing can also occur with emotional stress, exposure to heat or hot water, alcohol consumption and exercise, all of which can raise blood pressure temporarily. While facial flushing may occur while your blood pressure is higher than usual, HBP is not the cause of facial flushing.
  • Dizziness
    Although it is not caused by HBP, dizziness can be a side effect of some high blood pressure medications. Nonetheless, dizziness should not be ignored, especially if you notice a sudden onset. Sudden dizziness, loss of balance or coordination and trouble walking are all warning signs of a stroke. HBP is one of the leading risk factors for stroke.
Why Blood Pressure Matters
Uncontrolled high blood pressure can injure or kill you. It's sometimes called "the silent killer" because HBP has no symptoms, so you may not be aware that it's damaging your arteries, heart and other organs.
Possible health consequences that can happen over time when high blood pressure is left untreated include:
But remember, these are not symptoms of HBP. High blood pressure is a symptom less disease except in its most extreme cases known as hypertensive crisis. When BP readings rise to 180 or above for the systolic — top — number OR 110 or above for the diastolic — bottom — number, call for emergency medical treatment immediately.
DIET :
Dietary change such as a low sodium diet is beneficial. A long term (more than 4 weeks) low sodium diet in Caucasians is effective in reducing blood pressure, both in people with hypertension and in people with normal blood pressure.Also, the DASH diet, a diet rich in nuts, whole grains, fish, poultry, fruits and vegetables lowers blood pressure. A major feature of the plan is limiting intake of sodium, although the diet is also rich in potassium, magnesium, calcium, as well as protein.Different programs aimed to reduce psychological stress such a biofeedback, relaxation or meditation are advertised to reduce hypertension. However, overall efficacy is not greater than health education, with evidence being generally of low quality.
DRUGS :












Cozaar (Pro,  generic name: losartan class: angiotensin II inhibitors















Lasix (Pro, generic name: furosemide class: loop diuretics






























Zestril (Pro, generic name: lisinopr





Thursday, April 18, 2013

Heart Attack



What is a heart attack?

Your heart muscle needs oxygen to survive. A heart attack occurs when the blood flow that brings oxygen to the heart muscle is severely reduced or cut off completely (View an animation of blood flow). This happens because coronary arteries that supply the heart muscle with blood flow can slowly become narrrow from a buildup of fat, cholesterol and other substances that together are called plaque. This slow process is known as atherosclerosis . When a plaque in a heart artery breaks, a blood clot forms around the plaque. This blood clot can block the blood flow through the heart muscle. When the heart muscle is starved for oxygen and nutrients, it is called ischemia. When damage or death of part of the heart muscle occurs as a result of ischemia, it is called a heart attack or myocardial infarction (MI). About every 34 seconds, someone in the United States has a myocardial infarction (heart attack).

Signs and symptoms :

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium,[7][17] where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.
Women and older patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men).[  The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.
At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent myocardial infarctions vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus[ and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.[24] In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Risk factors

Myocardial infarction results from atherosclerosis.[  Smoking appears to be the cause of about 36% of coronary artery disease and obesity 20%. Lack of exercise has been linked to 7-12% of cases. Job stress appear to play a minor role accounting for about 3% of cases.
Risk factors for myocardial infarction include:

Diagnosis

WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
  1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
  2. Changes in serial ECG tracings
  3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

Prevention

The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:
  • Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.
  • Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
  • ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.
  • Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.
  • The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone is another option that is sometimes preferable to eplerenone due to cost.
  • Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people there is no clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. And they may increase risk in some groups.
  • Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.
DRUGS :

Medications
With each passing minute after a heart attack, more heart tissue loses oxygen and deteriorates or dies. The main way to prevent heart damage is to restore blood flow quickly.
Medications given to treat a heart attack include:
  • Aspirin. You may be given aspirin by emergency medical personnel soon after they arrive or as soon as you get to the hospital. Aspirin reduces blood clotting, thus helping maintain blood flow through a narrowed artery.
  • Thrombolytics. These drugs, also called clotbusters, help dissolve a blood clot that's blocking blood flow to your heart. The earlier you receive a thrombolytic drug following a heart attack, the greater the chance you will survive and lessen the damage to your heart.
  • Superaspirins. Doctors in the emergency room may give you other drugs that are somewhat similar to aspirin to help prevent new clots from forming. These include medications, such as clopidogrel (Plavix) and others, called platelet aggregation inhibitors.
  • Other blood-thinning medications. You'll likely be given other medications, such as heparin, to make your blood less "sticky" and less likely to form more dangerous clots. Heparin is given intravenously or by an injection under your skin and is usually used during the first few days after a heart attack.
  • Pain relievers. If your chest pain or associated pain is great, you may receive a pain reliever, such as morphine, to reduce your discomfort.
  • Nitroglycerin. This medication, used to treat chest pain (angina), temporarily opens arterial blood vessels, improving blood flow to and from your heart.
  • Beta blockers. These medications help relax your heart muscle, slow your heartbeat and decrease blood pressure making your heart's job easier. Beta blockers can limit the amount of heart muscle damage and prevent future heart attacks.
  • Cholesterol-lowering medications. Examples include statins, niacin, fibrates and bile acid sequestrants. These drugs help lower levels of unwanted blood cholesterol and may be helpful if given soon after a heart attack to improve survival.








Tuesday, April 9, 2013

Piles Treatment




What is Piles?
Piles are hemorrhoids that become inflamed. Hemorrhoids are masses, clumps, cushions of tissue in the anal canal - they are full of blood vessels, support tissue, muscle and elastic fibers.

"piles" are the swollen ones that are painful and cause problems, hemorrhoids can refer to the swollen ones (pathological hemorrhoids) or simply the normal structure. However, in most cases these days, the words piles and hemorrhoids are nearly always used interchangeably.

Piles can be of various sizes and may be internal (inside the anus) or external ones (outside the anus). Typically, internal piles occur from 2 to 4cm above the opening of the anus. External piles (perianal hematoma) occur on the outside edge of the anus. The internal ones are much more common.
According to the National Institutes of Health (NIH), USA, symptomatic hemorrhoids affect at least half the US population at some time in their lives, and approximately 5% of all adults have piles at any given time.
According to the National Health Service (NHS, UK), piles affect between 4% to 25% of the UK adult population. They are more common among adults aged between 45 and 65 years, as well as pregnant mothers.
Males and females are equally susceptible to developing troublesome hemorrhoids.

Signs and symptoms of piles:

A symptom is something the patient feels and describes, such as a pain, while a sign is something everybody can see, such as a rash.
In most cases piles are not serious and go away on their own after a few days. In fact, a considerable number of people with hemorrhoids do not experience any symptoms and do not even know they have them.
An individual with piles may experience the following symptoms:
  • A hard lump may be felt around the anus. It consists of coagulated blood, called a thrombosed external hemorrhoid. This can be extremely painful
  • After going to the toilet, a feeling that the bowels are still full
  • Bright red blood when doing a bowel movement
  • Itchiness in the anus area
  • Mucus discharge when emptying the bowels
  • Pain while defecating
  • The anus area may be red and sore
  • When passing a stool the person may strain excessively
Internal hemorrhoids - they are classified into four grades:
  • Grade 1 - there are small inflammations, usually inside the lining of the anus. They are not visible.
  • Grade 2 - larger than Grade 1 hemorrhoids, and also inside the anus. When passing a stool they may get pushed out, but soon return.
  • Grade 3 - often called 'prolapsed hemorrhoids'; these appear outside the anus. The patient may feel them hanging out. They can be pushed back in if the patient presses with his/her finger.
  • Grade 4 - these cannot be pushed back in and need to be treated by a doctor. They are large and stay outside the anus all the time.
External hemorrhoids - called perianal hematoma. These are small lumps that are located on the outside edge of the anus. They are extremely itchy and can be painful if a blood clot forms inside (thrombosed external hemorrhoid). Thrombosed external hemorrhoid requires medical treatment straight away.

= Why do piles occur?

The blood vessels around the anus and in the rectum will stretch under pressure and may swell or bulge. Inflamed veins (hemorrhoids) can develop when pressure increases in the lower rectum. This may be due to:
  • Anal intercourse
  • Chronic constipation
  • Chronic diarrhea
  • Lifting heavy weights regularly
  • Obesity/overweight
  • Pregnancy
  • Sitting on the toilet for too long
  • Straining when passing a stool
The tendency to develop hemorrhoids may also be inherited.
The risk of developing piles also grows with age.

= Diagnosing piles :

A qualified doctor can usually diagnose piles fairly rapidly after carrying out a physical examination. He/she will examine the patient's anus for swollen veins.
The doctor may ask the following questions:
  • Do any close relatives (parents, siblings) have piles?
  • Has there been any blood on the stools?
  • Has there been any mucus on the stools?
  • Has there been any recent weight loss?
  • Have bowel movements changed recently?
  • What color are the stools?
Internal hemorrhoids - the doctor may perform a DRE (digital rectal exam). The doctor may use a proctoscope - a hollow tube fitted with a light. The proctoscope allows the doctor to see the anal canal and take a small tissue sample from inside the rectum, which can be sent to the lab for analysis.
If the physician is presented with signs and symptoms which may suggest another digestive system disease, risk factors for colorectal cancer, and some other factors, he/she may recommend ordering an examination of the colon using colonoscopy.

Treatment options for piles :

In the majority of cases, piles resolve on their own without the need for any treatment. Treatments can help significantly reduce the discomfort and itching that many patients experience.
A good doctor will initially recommend some lifestyle changes.

Diet - piles can be caused by too much straining when doing bowel movements, which is the result of constipation. A change in diet can help keep the stools regular and soft. This involves eating more fiber, such as fruit and vegetables, or even switching your cereal breakfast to bran.

Water is the best drink, and the patient may be advised to increase his/her water consumption. Some experts say too much caffeine is not good.

Body weight - if the patient is obese, losing weight may help reduce the incidence and severity of hemorrhoids.
Simple things you can do yourself:
  • Try not to strain when you go to the toilet
  • Use moist toilet paper instead of dry
  • Rather than rubbing the anus area when cleaning after going to the toilet, pat instead to avoid irritation if you already have piles
Ointments, creams, pads and other OTC medications - there are some over-the-counter (OTC) medications which help soothe the redness and swelling around the anus area. Some of them contain witch hazel, hydrocortisone, or some other active ingredient which can relieve symptoms of itching and pain.

It is important to remember that they do not cure piles, they only treat the symptoms. Do not use them for more than seven consecutive days - longer periods may irritate the anus area and cause skin thinning. Unless advised to by your doctor, do not use two or more medications simultaneously.

Corticosteroids - these can reduce inflammation. However, usage must not exceed about six to seven days.
Painkillers - ask your pharmacist for suitable painkilling medications, such as acetaminophen (Tylenol, paracetamol).

Laxatives - the doctor may prescribe one if the patient suffers from constipation.

Banding - the doctor places an elastic band around the base of the pile inside the anus, cutting its blood supply. After a few days the hemorrhoids fall off. This can work for Grades 2 and 3 hemorrhoids.

Sclerotherapy - a medicine is injected into the vein to make the hemorrhoid shrink - the hemorrhoid eventually shrivels up. This is effective for Grades 2 and 3 hemorrhoids, and is a useful alternative to banding.

Infrared coagulation - also referred to as infrared light coagulation. Used for Grades 1 or 2 hemorrhoids. A device burns the hemorrhoid tissue.
Surgery - used for particularly large piles, or Grades 3 or 4 hemorrhoids. Generally, surgery is used if other procedures were not effective. Sometimes surgery is done on an outpatient basis - the patient goes home after the procedure, or he/she may have to spend the night in hospital.
  • Hemorrhoidectomy - the excess tissue that is causing the bleeding is surgically removed. This can be done in various ways. It may involve a combination of a local anesthetic and sedation, a spinal anesthetic, or a general anesthetic. This type of surgery is the most effective in completely removing piles, but there is a risk of complications, which can include difficulties passing stools, as well as urinary tract infections.
  • Hemorrhoid stapling - blood flow is blocked to the tissue of the hemorrhoid. This procedure is usually less painful than hemorrhoidectomy. However, there is a greater risk of hemorrhoid recurrence and rectal prolapse (part of the rectum sticks out of the anus).

Kidney Stone



What is the treatment for kidney stones?

Most kidney stones eventually pass through the urinary tract on their own within 48 hours, with ample fluid intake. Pain medications are used for symptom relief. When over-the-counter medications are not sufficient for pain control, narcotics may be prescribed. Intravenous pain medications can be given when nausea and vomiting are present.

There are several factors which influence the ability to pass a stone. These include the size of the person, prior stone passage, prostate enlargement, pregnancy, and the size of the stone. A 4 mm stone has an 80% chance of passage while a 5 mm stone has a 20% chance. Stones larger than 9 mm-10 mm rarely pass without specific treatment.

Some medications have been used to increase the passage rates of kidney stones. These include calcium channel blockers such as nifedipine (Adalat, Procardia, Afeditab, Nifediac) and alpha blockers such as tamsulosin (Flomax). These drugs may be prescribed to some people who have stones that do not rapidly pass through the urinary tract.

For kidney stones that do not pass on their own, a procedure called lithotripsy is often used. In this procedure, shock waves are used to break up a large stone into smaller pieces that can then pass through the urinary system.

Surgical techniques have also been developed to remove kidney stones when other treatment methods are not effective. This may be done through a small incision in the skin (percutaneous nephrolithotomy) or through an instrument known as an ureteroscope passed through the urethra and bladder up into the ureter.

Classification

Kidney stones are typically classified by their location and chemical composition.
Kidney Stone type
Population
Circumstances
Details
Calcium oxalate
80%
when urine is acidic (low pH)
Some of the oxalate in urine is produced by the body. Calcium and oxalate in the diet play a part but are not the only factors that affect the formation of calcium oxalate stones. Dietary oxalate is an organic molecule found in many vegetables, fruits, and nuts. Calcium from bone may also play a role in kidney stone formation.
Calcium phosphate
___%
when urine is alkaline (high pH)

Uric acid
5-10%
when urine is persistently acidic
Diets rich in animal proteins and purines: substances found naturally in all food but especially in organ meats, fish, and shellfish.
Struvite
10-15%
infections in the kidney
Preventing struvite stones depends on staying infection-free. Diet has not been shown to affect struvite stone formation.
Cystine
___%
rare genetic disorder
Cystine, an amino acid (one of the building blocks of protein), leaks through the kidneys and into the urine to form crystals.

Prevention

Dietary measures

Specific therapy should be tailored to the type of stones involved. Diet can have a profound influence on the development of kidney stones. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the kidneys. Current dietary recommendations to minimize the formation of kidney stones include:
  • Increasing fluid intake of citrate-rich foods (especially citrate-rich fluids such as lemonade and orange juice), with the objective of increasing urine output to more than two liters per day
  • Attempt to maintain a calcium (Ca) intake of 1000 – 1200 mg per day
  • Limiting sodium (Na) intake to less than 2300 mg per day
  • Limiting vitamin C intake to less than 1000 mg per day
  • Limiting animal protein intake to no more than two meals daily, with less than 170–230 g per day. (A positive association between animal protein consumption and recurrence of kidney stones has been shown in men.
  • Limiting consumption of foods containing high amounts of oxalate (such as spinach, strawberries, nuts, rhubarb, wheat germ, dark chocolate, cocoa, brewed tea)
Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of nephrolithiasis, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least 2 l (68 US fl oz) per day.A high fluid intake has been associated with a 40% reduction in recurrence risk.
Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream, and reducing oxalate absorption decreases kidney stone risk in susceptible people. Because of this, some nephrologists and urologists recommend chewing calcium tablets during meals containing oxalate foods. Calcium citrate supplements can be taken with meals if dietary calcium cannot be increased by other means. The preferred calcium supplement for people at risk of stone formation is calcium citrate because it helps to increase urinary citrate excretion.
Aside from vigorous oral hydration and consumption of more dietary calcium, other prevention strategies include avoidance of large doses of supplemental vitamin C and restriction of oxalate-rich foods such as leaf vegetables, rhubarb, soy products and chocolate. However, no randomized, controlled trial of oxalate restriction has yet been performed to test the hypothesis that oxalate restriction reduces the incidence of stone formation. Some evidence indicates magnesium intake decreases the risk of symptomatic nephrolithiasis.

Urine alkalinization

The mainstay for medical management of uric acid stones is alkalinization (increasing the pH) of the urine. Uric acid stones are among the few types amenable to dissolution therapy, referred to as chemolysis. Chemolysis is usually achieved through the use of oral medications, although in some cases, intravenous agents or even instillation of certain irrigating agents directly onto the stone can be performed, using antegrade nephrostomy or retrograde ureteral catheters. Acetazolamide (Diamox) is a medication that alkalinizes the urine. In addition to acetazolamide or as an alternative, certain dietary supplements are available that produce a similar alkalinization of the urine. These include sodium bicarbonate, potassium citrate, magnesium citrate, and Bicitra (a combination of citric acid monohydrate and sodium citrate dihydrate). Aside from alkalinization of the urine, these supplements have the added advantage of increasing the urinary citrate level, which helps to reduce the aggregation of calcium oxalate stones.
Increasing the urine pH to around 6.5 provides optimal conditions for dissolution of uric acid stones. Increasing the urine pH to a value higher than 7.0 increases the risk of calcium phosphate stone formation. Testing the urine periodically with nitrazine paper can help to ensure the urine pH remains in this optimal range. Using this approach, stone dissolution rate can be expected to be around 10 mm (0.39 in) of stone radius per month.

Diuretics

One of the recognized medical therapies for prevention of stones is the thiazide and thiazide-like diuretics, such as chlorthalidone or indapamide. These drugs inhibit the formation of calcium-containing stones by reducing urinary calcium excretion.[1] Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary kidney defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract.

Allopurinol

For people with hyperuricosuria and calcium stones, allopurinol is one of the few treatments that have been shown to reduce kidney stone recurrences. Allopurinol interferes with the production of uric acid in the liver. The drug is also used in people with gout or hyperuricemia (high serum uric acid levels). Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/100 ml) is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid stones; hyperuricosuria can occur in the presence of normal or even low serum uric acid. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-alkalinizing agent such as sodium bicarbonate or potassium citrate.

Management

Medical

Stone size influences the rate of spontaneous stone passage. For example, up to 98% of small stones (less than 5 mm (0.20 in) in diameter) may pass spontaneously through urination within four weeks of the onset of symptoms,but for larger stones (5 to 10 mm (0.20 to 0.39 in) in diameter), the rate of spontaneous passage decreases to less than 53%. Initial stone location also influences the likelihood of spontaneous stone passage. Rates increase from 48% for stones located in the proximal ureter to 79% for stones located at the vesicoureteric junction, regardless of stone size. Assuming no high-grade obstruction or associated infection is found in the urinary tract, and symptoms are relatively mild, various nonsurgical measures can be used to encourage the passage of a stone. Repeat stone formers benefit from more intense management, including proper fluid intake and use of certain medications. In addition, careful surveillance clearly is required to maximize the clinical course for people who are stone formers.

Analgesia

Management of pain often requires intravenous administration of NSAIDs or opioids. Orally administered medications are often effective for less severe discomfort.

Expulsion therapy

The use of medications to speed the spontaneous passage of ureteral calculi is referred to as medical expulsive therapy.[60] Several agents, including alpha adrenergic blockers (such as tamsulosin) and calcium channel blockers (such as nifedipine), have been found to be effective.[60] A combination of tamsulosin and a corticosteroid may be better than tamsulosin alone.[60] These treatments also appear to be a useful adjunct to lithotripsy.

Surgical


A lithotriptor machine is seen in an operating room; other equipment is seen in the background, including an anesthesia machine and a mobile fluoroscopic system (or "C-arm").
Most stones under 5 mm (0.20 in) pass spontaneously.[9][33] Prompt surgery may, nonetheless, be required with persons with only one working kidney, bilateral obstructing stones, a urinary tract infection and thus, it is presumed, an infected kidney, or intractable pain.[61] Beginning in the mid-1980s, less invasive treatments such as extracorporeal shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy began to replace open surgery as the modalities of choice for the surgical management of urolithiasis. More recently, flexible ureteroscopy has been adapted to facilitate retrograde nephrostomy creation for percutaneous nephrolithotomy. This approach is still under investigation, though early results are favorable.