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INTRODUCTION-

Kidney stones, or renal calculi, are solid masses made of crystals. Kidney stones usually originate in your kidneys. However, they can develop anywhere along your urinary tract, which consists of these parts:

• kidneys
• ureters
• bladder
• urethra

Kidney stones are one of the most painful medical conditions. The causes of kidney stones vary according to the type of stone.

Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting, hematuria, and, possibly, chills and fever due to secondary infection. Diagnosis is based on urinalysis and radiologic imaging, usually noncontrast helical CT. Treatment is with analgesics, antibiotics for infection, medical expulsive therapy, and, sometimes, shock wave lithotripsy or endoscopic procedures.

About 1/1000 adults in the US is hospitalized annually because of urinary calculi, which are also found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.

Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting, hematuria, and, possibly, chills and fever due to secondary infection. Diagnosis is based on urinalysis and radiologic imaging, usually noncontrast helical CT. Treatment is with analgesics, antibiotics for infection, medical expulsive therapy, and, sometimes, shock wave lithotripsy or endoscopic procedures.

About 1/1000 adults in the US is hospitalized annually because of urinary calculi, which are also found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.

Urolithiasis is a common disease, estimated to affect 11% of men and 7% of women in their lifetime. More than 1 million patients with suspected urolithiasis present to an emergency department (ED) each year in the United States.  Ureterolithiasis causes severe unilateral colicky flank pain, and patients usually present within hours of onset. The pain may radiate from the flank anteromedially toward the groin into the genitals and may be accompanied by nausea, vomiting, and hematuria. Passage of a urinary stone is the single most common cause of acute ureteral obstruction and affects as many as 12% of the population. The pain may be some of the most severe pain that humans experience, and complications of stone disease may result in severe infection, renal failure, or, in rare cases, death.

Types of kidney stones-

Not all kidney stones are made up of the same crystals. The different types of kidney stones include:

Calcium

Calcium stones are the most common. They’re often made of calcium oxalate (though they can consist of calcium phosphate or maleate). Eating fewer oxalate-rich foods can reduce your risk of developing this type of stone. High-oxalate foods include:

• potato chips
• peanuts
• chocolate
• beets
• spinach

However, even though some kidney stones are made of calcium, getting enough calcium in your diet can prevent stones from forming.

Uric acid

This type of kidney stone is more common in men than in women. They can occur in people with gout or those going through chemotherapy.

This type of stone develops when urine is too acidic. A diet rich in purines can increase urine’s acidic level. Purine is a colorless substance in animal proteins, such as fish, shellfish, and meats.

Struvite

This type of stone is found mostly in women with urinary tract infections (UTIs). These stones can be large and cause urinary obstruction. They result from a kidney infection. Treating an underlying infection can prevent the development of struvite stones.

Cystine

Cystine stones are rare. They occur in both men and women who have the genetic disorder cystinuria. With this type of stone, cystine — an acid that occurs naturally in the body — leaks from the kidneys into the urine.

CAUSES-

About 85% of calculi in the US are composed of calcium, mainly calcium oxalate (see table Composition of Urinary Calculi); 10% are uric acid; 2% are cystine; most of the remainder are magnesium ammonium phosphate (struvite).

General risk factors include disorders that increase urinary salt concentration, either by increased excretion of calcium or uric acid salts, or by decreased excretion of urinary citrate.For calcium calculi, risk factors vary by population. The main risk factor in the US is hypercalciuria, a hereditary condition present in 50% of men and 75% of women with calcium calculi; thus, patients with a family history of calculi are at increased risk of recurrent calculi. These patients have normal serum calcium, but urinary calcium is elevated > 250 mg/day (> 6.2 mmol/day) in men and > 200 mg/day (> 5.0 mmol/day) in women.

ypocitruria (urinary citrate < 350 mg/day [1820 micromol/day]), present in about 40 to 50% of calcium calculi–formers, promotes calcium calculi formation because citrate normally binds urinary calcium and inhibits the crystallization of calcium salts.

About 5 to 8% of calculi are caused by renal tubular acidosis. About 1 to 2% of patients with calcium calculi have primary hyperparathyroidism. Rare causes of hypercalciuria are sarcoidosis, vitamin D intoxication, hyperthyroidism, multiple myeloma, metastatic cancer, and hyperoxaluria.

Hyperoxaluria (urinary oxalate > 40 mg/day [> 440 micromol/day]) can be primary or caused by excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes, chronic pancreatic or biliary disease) or ileojejunal (eg, bariatric) surgery.

Other risk factors include taking high doses of vitamin C (ie, > 2000 mg/day), a calcium-restricted diet (possibly because dietary calcium binds dietary oxalate), and mild hyperuricosuria. Mild hyperuricosuria, defined as urinary uric acid > 800 mg/day (> 5 mmol/day) in men or > 750 mg/day (> 4 mmol/day) in women, is almost always caused by excess intake of purine (in proteins, usually from meat, fish, and poultry); it may cause calcium oxalate calculus formation (hyperuricosuric calcium oxalate nephrolithiasis).

Uric acid calculi most commonly develop as a result of increased urine acidity (urine pH < 5.5), or rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more commonly, provide a nidus on which calcium or mixed calcium and uric acid calculi can form.

Cystine calculi occur only in the presence of cystinuria.

Magnesium ammonium phosphate calculi (struvite, infection calculi) indicate the presence of a urinary tract infection caused by urea-splitting bacteria (eg, Proteus species, Klebsiella species). The calculi must be treated as infected foreign bodies and removed in their entirety. Unlike other types of calculi, magnesium ammonium phosphate calculi occur 3 times more frequently in women.

Rare causes of urinary calculi include indinavir, melamine, triamterene, and xanthine.

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Pathophysiology-

Urinary calculi may remain within the renal parenchyma or renal collecting system or be passed into the ureter and bladder. During passage, calculi may irritate the ureter and may become lodged, obstructing urine flow and causing hydroureter and sometimes hydronephrosis. Common areas of lodgment include the following:

• Ureteropelvic junction
• Distal ureter (at the level of the iliac vessels)
• Ureterovesical junction

Larger calculi are more likely to become lodged. Typically, a calculus must have a diameter > 5 mm to become lodged. Calculi ≤ 5 mm are likely to pass spontaneously.

Even partial obstruction causes decreased glomerular filtration, which may persist briefly after the calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow declines, further worsening renal function. Generally, however, in the absence of infection, permanent renal dysfunction occurs only after about 28 days of complete obstruction.

Secondary infection can occur with long-standing obstruction, but most patients with calcium-containing calculi do not have infected urine.

SIGN AND SYMPTOM-

Kidney stones are known to cause severe pain. Symptoms of kidney stones may not occur until the stone begins to move down the ureters. This severe pain is called renal colic. You may have pain on one side of your back or abdomen.

In men, pain may radiate to the groin area. The pain of renal colic comes and goes, but can be intense. People with renal colic tend to be restless.

Other symptoms of kidney stones can include:

• blood in the urine (red, pink, or brown urine)
• vomiting
• nausea
• discolored or foul-smelling urine
• chills
• fever
• frequent need to urinate
• urinating small amounts of urine

In the case of a small kidney stone, you may not have any pain or symptoms as the stone passes through your urinary tract.

Large calculi remaining in the renal parenchyma or renal collecting system are often asymptomatic unless they cause obstruction and/or infection. Severe pain, often accompanied by nausea and vomiting, usually occurs when calculi pass into the ureter and cause acute obstruction. Sometimes gross hematuria also occurs.

Pain (renal colic) is of variable intensity but is typically excruciating and intermittent, often occurs cyclically, and lasts 20 to 60 minutes. Nausea and vomiting are common. Pain in the flank or kidney area that radiates across the abdomen suggests upper ureteral or renal pelvic obstruction. Pain that radiates along the course of the ureter into the genital region suggests lower ureteral obstruction. Suprapubic pain along with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or bladder calculus (see Obstructive Uropathy: Symptoms and Signs).

On examination, patients may be in obvious extreme discomfort, often ashen and diaphoretic. Patients with renal colic may be unable to lie still and may pace, writhe, or constantly shift position. The abdomen may be somewhat tender on the affected side as palpation increases pressure in the already-distended kidney (costovertebral angle tenderness), but peritoneal signs (guarding, rebound, rigidity) are lacking.

For some patients, the first symptom is hematuria or either gravel or a calculus in the urine. Other patients may have symptoms of a urinary tract infection, such as fever, dysuria, or cloudy or foul-smelling urine.

RISK FACTORS –

The greatest risk factor for kidney stones is making less than 1 liter of urine per day. This is why kidney stones are common in premature infants who have kidney problems. However, kidney stones are most likely to occur in people between the ages of 20 and 50.

Different factors can increase your risk of developing a stone. In the United States, white people are more likely to have kidney stones than black people.

Sex also plays a role. More men than women develop kidney stones, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

A history of kidney stones can increase your risk. So does a family history of kidney stones.

Other risk factors include:

• dehydration
• obesity
• a diet with high levels of protein, salt, or glucose
• hyperparathyroid condition
• gastric bypass surgery
• inflammatory bowel diseases that increase calcium absorption
• taking medications such as triamterene diuretics, antiseizure drugs, and calcium-based antacids

DIAGNOSIS-

• Clinical differential diagnosis
• Urinalysis
• Imaging
• Determination of calculus composition

The symptoms and signs may suggest other diagnoses, such as

• Peritonitis (eg, due to appendicitis, ectopic pregnancy, or pelvic inflammatory disease): Pain is usually constant, and patients lie still because movement worsens pain; patients often also have rebound tenderness or rigidity.
• Cholecystitis: May cause colicky pain, usually in the epigastrium or right upper quadrant, often with Murphy sign.
• Bowel obstruction: May cause colicky abdominal pain and vomiting, but the pain is usually bilateral and not located primarily in the flank or along the ureter.
• Pancreatitis: May cause upper abdominal pain and vomiting, but the pain is usually constant, may be bilateral, and is usually not along the flank or ureter.

With most of these disorders, urinary symptoms are uncommon and other symptoms may suggest which organ system is actually involved (eg, vaginal discharge or bleeding in pelvic disorders among females). Dissecting aortic aneurysm must be considered, particularly in the elderly, because, if a renal artery is affected, it can cause hematuria, pain that radiates along a ureteral distribution, or both. Other considerations in the general evaluation of acute abdominal pain are discussed elsewhere (see Acute Abdominal Pain: Evaluation).Patients suspected of having a calculus causing colic require urinalysis and usually an imaging study. If a calculus is confirmed, evaluation of the underlying disorder, including calculus composition testing, is required.

Urinalysis

Macroscopic or microscopic hematuria is common, but urine may be normal despite multiple calculi. Pyuria with or without bacteria may be present. Pyuria suggests infection, particularly if combined with suggestive clinical findings, such as foul-smelling urine or a fever. A calculus and various crystalline substances may be present in the sediment. If so, further testing is usually necessary because the composition of the calculus and crystals cannot be determined conclusively by microscopy. The only exception is when typical hexagonal crystals of cystine are found in a concentrated, acidified specimen, confirming cystinuria.

Imaging tests

Noncontrast helical CT is the initial imaging study. This study can detect the location of a calculus as well as the degree of obstruction. Moreover, helical CT may also reveal another cause of the pain (eg, aortic aneurysm). For patients who have recurrent calculi, cumulative radiation exposure from multiple CT scans is a concern. However, the routine use of low-dose renal CT can meaningfully reduce cumulative radiation dose with little loss of sensitivity. For patients with typical symptoms, ultrasonography or plain abdominal x-rays can usually confirm presence of a calculus with minimal or no radiation exposure. MRI may not identify calculi.

Although most urinary calculi are demonstrable on plain x-ray, neither their presence nor their absence obviates the need for more definitive imaging, so this study can be avoided except in some patients with suspected recurrent calculi. Both renal ultrasonography and excretory urography (previously called intravenous urography) can identify calculi and hydronephrosis. However, ultrasonography is less sensitive for small or ureteral calculi in patients without hydronephrosis, and excretory urography is time consuming and exposes the patient to the risk of IV contrast agents. These studies are generally used when helical CT is unavailable.

Identifying the cause

The calculus is obtained by straining the urine (or, if necessary, during operative removal) and sent to the laboratory for stone analysis. Some calculi are brought in by patients. Urine specimens that show microscopic crystals are sent for crystallography.

In patients with a single calcium calculus and no additional risk factors for calculi, evaluation to exclude hyperparathyroidism is sufficient. Evaluation entails urinalysis and determination of plasma calcium concentration on 2 separate occasions. Predisposing factors, such as recurrent calculi, a diet high in animal protein, or use of vitamin C or D supplements, should be sought.

Patients with a strong family history of calculi, conditions that might predispose to calculi formation (eg, sarcoidosis, bone metastases, multiple myeloma), or conditions that would make it difficult to treat calculi (eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and risk factors. This evaluation should include serum electrolytes, uric acid, and calcium on 2 separate occasions. Follow-up determination of parathyroid hormone levels is done if necessary. Urine tests should include routine urinalysis and 2 separate 24-hour urine collections to determine urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, and creatinine. For further information on the medical management of kidney stones, see the guideline of the American Urological Association.

Diagnosis references

• Zilberman DE, Tsivian M, Lipkin ME, et al: Low dose computerized tomography for detection of urolithiasis—its effectiveness in the setting of the urology clinic. J Urol 185(3):910-914, 2011.
• Pearle MS, Goldfarb DS, Assimos DG, et al: Medical management of kidney stones—AUA guideline. J Urology 92(2):316-24, 2014.

PREVENTION-

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Proper hydration is a key preventive measure. drinking enough water to pass about 2.6 quarts of urine each day. Increasing the amount of urine you pass helps flush the kidneys.

You can substitute ginger ale, lemon-lime soda, and fruit juice for water to help you increase your fluid intake. If the stones are related to low citrate levels, citrate juices could help prevent the formation of stones.

Eating oxalate-rich foods in moderation and reducing your intake of salt and animal proteins can also lower your risk of kidney stones.

Your doctor may prescribe medications to help prevent the formation of calcium and uric acid stones. If you’ve had a kidney stone or you’re at risk for a kidney stone, speak with your doctor and discuss the best methods of prevention.

In a patient who has passed a first calcium calculus, the likelihood of forming a 2nd calculus is about 15% at 1 year, 40% at 5 years, and 80% at 10 years. Drinking large amounts of fluids—8 to 10 ten-ounce (300-milliliter) glasses a day—is recommended for prevention of all stones. Recovery and analysis of the calculus, measurement of calculus-forming substances in the urine, and the clinical history are needed to plan other prophylactic measures.

In < 3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, potassium citrate, and increased fluid intake may reduce their calculus production rate.

For hypercalciuria, patients may receive thiazide diuretics (eg, chlorthalidone 25 mg orally once a day or indapamide 1.25 mg orally once a day) to lower urine calcium excretion and thus prevent urinary supersaturation with calcium oxalate. Patients are encouraged to increase their fluid intake to ≥ 3 L/day. A diet that is low in sodium and high in potassium is recommended. Even with a high potassium intake, supplementation with potassium citrate is recommended to prevent hypokalemia. Restriction of dietary animal protein is also recommended.

For patients with hypocitruria, potassium citrate (20 mEq [20 mmol/L] orally twice a day) enhances citrate excretion. A normal calcium intake (eg, 1000 mg or about 2 to 3 dairy servings per day) is recommended, and calcium restriction is avoided. Oral orthophosphate has not been thoroughly studied. Alternative alkaline agents (eg, sodium or potassium bicarbonate) can be used to enhance citrate excretion.

Hyperoxaluria prevention varies. Patients with small-bowel disease can be treated with a combination of high fluid intake, calcium loading (usually in the form of calcium citrate 400 mg orally twice a day with meals), cholestyramine, and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine 100 to 200 mg orally once a day, possibly by increasing transaminase activity, because this activity is responsible for the conversion of glyoxylate, the immediate oxalate precursor, to glycine.

In hyperuricosuria, intake of animal protein should be reduced. If the diet cannot be changed, allopurinol 300 mg each morning lowers uric acid production. For uric acid calculi, the urine pH must be increased to between 6 and 6.5 by giving an oral alkalinizing drug that contains potassium (eg, potassium citrate 20 mEq [20 mmol/L] twice a day) along with increased fluid intake.

Infection with urea-splitting bacteria requires culture-specific antibiotics and complete removal of all calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin) may be necessary. In addition, acetohydroxamic acid can be used to reduce the recurrence of struvite calculi.

To prevent recurrent cystine calculi, urinary cystine levels must be reduced to < 250 mg cystine/L of urine. Any combination of increasing urine volume along with reducing cystine excretion (eg, with alpha-mercaptopropionylglycine [tiopronin] or penicillamine) should reduce the urinary cystine concentration.

TREATMENT-

• Analgesia
• Facilitate calculus passage, eg, with alpha-receptor blockers such as tamsulosin (described as medical expulsive therapy)
• For persistent or infection-causing calculi, complete removal using primarily endoscopic techniques

Analgesia

Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl. Ketorolac 30 mg IV is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron 10 mg IV).

Medical expulsive therapy

Although increasing fluids (either oral or IV) has traditionally been recommended, increased fluid administration has not been proven to speed the passage of calculi. Patients with calculi < 1 cm in diameter who have no infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be treated at home with analgesics and alpha-receptor blockers (eg, tamsulosin 0.4 mg orally once a day) to facilitate calculus passage. Calculi that have not passed within 6 to 8 weeks typically require removal. In patients with infection and obstruction, initial treatment is relief of obstruction with a ureteral stent and treatment of the infection followed by removal of calculi as soon as possible.

Pain relief may require narcotic medications. The presence of infection requires treatment with antibiotics. Other medications include:

• allopurinol (Zyloprim) for uric acid stones
• thiazide diuretics to prevent calcium stones from forming
• sodium bicarbonate or sodium citrate to make the urine less acidic
• phosphorus solutions to prevent calcium stones from forming
• ibuprofen (Advil) for pain
• acetaminophen (Tylenol) for pain
• naproxen sodium (Aleve) for pain

Calculus removal

The technique used for removal depends on the location and size of the calculus. Techniques include shock wave lithotripsy and, to ensure complete removal or for larger calculi, endoscopic techniques. Endoscopic techniques may involve rigid or flexible ureteroscopes (endoscopes) and may involve direct-vision removal (basketing), fragmentation with some sort of lithotripsy device (eg, pneumatic, ultrasonic, laser), or both.

For symptomatic calculi < 1 cm in diameter in the renal collecting system or proximal ureter, shock wave lithotripsy is a reasonable first option for therapy.

For larger calculi or if shock wave lithotripsy is unsuccessful, ureteroscopy (done in a retrograde fashion) with holmium laser lithotripsy is usually used. Sometimes removal is possible using an endoscope inserted anterograde through the kidney. For renal stones > 2 cm, percutaneous nephrolithotomy, with insertion of a nephroscope directly into the kidney, is the treatment of choice.

For midureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of choice. Shock wave lithotripsy is an alternative.

For distal ureteral calculi, endoscopic techniques (ureteroscopy), such as direct removal and use of intracorporeal lithotripsy (eg, holmium laser, pneumatic), are considered by many to be the procedures of choice. Shock wave lithotripsy can also be used.

Calculus dissolution

Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged alkalinization of the urine with potassium citrate 20 mEq (20 mmol/L) orally 2 to 3 times a day, but chemical dissolution of calcium calculi is not possible and of cystine calculi is difficult.

Lithotripsy

Extracorporeal shock wave lithotripsy uses sound waves to break up large stones so they can more easily pass down the ureters into your bladder. This procedure can be uncomfortable and may require light anesthesia. It can cause bruising on the abdomen and back and bleeding around the kidney and nearby organs.

Ureteroscopy

When a stone is stuck in the ureter or bladder, your doctor may use an instrument called a ureteroscope to remove it.

A small wire with a camera attached is inserted into the urethra and passed into the bladder. The doctor then uses a small cage to snag the stone and remove it. The stone is then sent to the laboratory for analysis.

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INTRODUCTION-

An aneurysm occurs when an artery’s wall weakens and causes an abnormally large bulge. This bulge can rupture and cause internal bleeding. Although an aneurysm can occur in any part of your body, they’re most common in the:

• brain
• aorta
• legs
• spleen

About 13,000 deathsTrusted Source occur each year in the United States from aortic aneurysms.

brain aneurysm (AN-yoo-riz-um) is a bulge or ballooning in a blood vessel in the brain. It often looks like a berry hanging on a stem.

A brain aneurysm can leak or rupture, causing bleeding into the brain (hemorrhagic stroke). Most often a ruptured brain aneurysm occurs in the space between the brain and the thin tissues covering the brain. This type of hemorrhagic stroke is called a subarachnoid hemorrhage.

A ruptured aneurysm quickly becomes life-threatening and requires prompt medical treatment.

Most brain aneurysms, however, don’t rupture, create health problems or cause symptoms. Such aneurysms are often detected during tests for other conditions.

Treatment for an unruptured brain aneurysm may be appropriate in some cases and may prevent a rupture in the future. Talk with your caregiver to ensure you understand the best options for your specific needs.

CAUSES-

Although the exact cause of an aneurysm is unclear, certain factors contribute to the condition.

For example, damaged tissue in the arteries can play a role. The arteries can be harmed by blockages, such as fatty deposits. These deposits can trigger the heart to pump harder than necessary to push blood past the fatty buildup. This stress can damage the arteries because of the increased pressure.

Atherosclerotic disease

Atherosclerotic disease can also lead to an aneurysm. People with atherosclerotic disease have a form of plaque buildup in their arteries. Plaque is a hard substance that damages the arteries and prevents blood from flowing freely.

High blood pressure

High blood pressure may also cause an aneurysm. The force of your blood as it travels through your blood vessels is measured by how much pressure it places on your artery walls. If the pressure increases above a normal rate, it may enlarge or weaken the blood vessels.

Blood pressure for an adult is considered normal at or below 120/80 mm Hg, or millimeters of mercury.

A significantly higher blood pressure can increase the risk for heart, blood vessel, and circulation problems. Higher-than-normal blood pressure doesn’t necessarily put you at risk for an aneurysm.

TYPES-

An aneurysm may occur anywhere in your body, but these are the most common locations of aneurysms:

Aorta

The aorta is the largest blood vessel in the body. It begins at the left ventricle of the heart and travels down the abdomen where it splits off into both legs. The aorta is a common site for arterial aneurysms.

• Aneurysms in the chest cavity are called thoracic aortic aneurysms.
• Abdominal aortic aneurysms are the most common type. In rare cases, both the chest and abdomen can be affected by arterial damage.

Brain

Aneurysms in the brain can be any size. These often form in the blood vessels that lie deep within the brain. They also may not present any symptoms or signs. You may not even know you have an aneurysm. Brain aneurysms of this type may cause bleeding in as many as 3 percent of people.

Other areas

You can also have an aneurysm in the artery behind your knee, in your spleen, or in your intestines.

SYMPTOM-

Symptoms of an aneurysm vary with each type and location. It’s important to know that aneurysms that occur in the body or brain generally don’t present signs or symptoms until they rupture.

Aneurysms that occur near the surface of the body may show signs of swelling and pain. A large mass may also develop. The symptoms of ruptured aneurysms anywhere in the body can include:

• bleeding
• increased heart rate
• pain
• feeling dizzy or lightheaded

Serious complications from aneurysms can cause death if you don’t get emergency care.

Ruptured aneurysm

A sudden, severe headache is the key symptom of a ruptured aneurysm. This headache is often described as the “worst headache” ever experienced.

Common signs and symptoms of a ruptured aneurysm include:

• Sudden, extremely severe headache
• Nausea and vomiting
• Stiff neck
• Blurred or double vision
• Sensitivity to light
• Seizure
• A drooping eyelid
• Loss of consciousness
• Confusion

‘Leaking’ aneurysm

In some cases, an aneurysm may leak a slight amount of blood. This leaking (sentinel bleed) may cause only a:

• Sudden, extremely severe headache

A more severe rupture often follows leaking.

‘Leaking’ aneurysm

In some cases, an aneurysm may leak a slight amount of blood. This leaking (sentinel bleed) may cause only a:

• Sudden, extremely severe headache

A more severe rupture often follows leaking.

Unruptured aneurysm

An unruptured brain aneurysm may produce no symptoms, particularly if it’s small. However, a larger unruptured aneurysm may press on brain tissues and nerves, possibly causing:

• Pain above and behind one eye
• A dilated pupil
• Change in vision or double vision
• Numbness of one side of the face

When to see a doctor

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Seek immediate medical attention if you develop a:

• Sudden, extremely severe headache

If you’re with someone who complains of a sudden, severe headache or who loses consciousness or has a seizure, call 911 or your local emergency number.

Brain aneurysms develop as a result of thinning artery walls. Aneurysms often form at forks or branches in arteries because those sections of the vessel are weaker.

Although aneurysms can appear anywhere in the brain, they are most common in arteries at the base of the brain.

DIAGNOSIS-

The diagnostic tools used to find arterial damage often depend on the location of the problem. Your doctor may refer you to a specialist like a cardiothoracic or vascular surgeon.

CT scans and ultrasound methods are common tools used to diagnose or find blood vessel irregularities. CT scans use X-rays to examine the inside of your body. This allows your doctor to see the condition of the blood vessels, as well as any blockages, bulges, and weak spots that may be inside the blood vessels.

RISK FACTOR-

A number of factors can contribute to weakness in an artery wall and increase the risk of a brain aneurysm or aneurysm rupture. Brain aneurysms are more common in adults than in children and more common in women than in men.

Some of these risk factors develop over time; others are present at birth.

Risk factors that develop over time

These include:

• Older age
• Cigarette smoking
• High blood pressure (hypertension)
• Drug abuse, particularly the use of cocaine
• Heavy alcohol consumption

Some types of aneurysms may occur after a head injury (dissecting aneurysm) or from certain blood infections (mycotic aneurysm).

Risk factors present at birth

Selected conditions that date to birth can be associated with an elevated risk of developing a brain aneurysm. These include:

• Inherited connective tissue disorders, such as Ehlers-Danlos syndrome, that weaken blood vessels
• Polycystic kidney disease, an inherited disorder that results in fluid-filled sacs in the kidneys and usually increases blood pressure
• Abnormally narrow aorta (coarctation of the aorta), the large blood vessel that delivers oxygen-rich blood from the heart to the body
• Cerebral arteriovenous malformation (brain AVM), an abnormal connection between arteries and veins in the brain that interrupts the normal flow of blood between them
• Family history of brain aneurysm, particularly a first-degree relative, such as a parent, brother, sister, or child.

COMPLICATION-

When a brain aneurysm ruptures, the bleeding usually lasts only a few seconds. The blood can cause direct damage to surrounding cells, and the bleeding can damage or kill other cells. It also increases pressure inside the skull.

If the pressure becomes too elevated, the blood and oxygen supply to the brain may be disrupted to the point that loss of consciousness or even death may occur.

Complications that can develop after the rupture of an aneurysm include:

• Re-bleeding. An aneurysm that has ruptured or leaked is at risk of bleeding again. Re-bleeding can cause further damage to brain cells.
• Vasospasm. After a brain aneurysm ruptures, blood vessels in your brain may narrow erratically (vasospasm). This condition can limit blood flow to brain cells (ischemic stroke) and cause additional cell damage and loss.
• Hydrocephalus. When an aneurysm rupture results in bleeding in the space between the brain and surrounding tissue (subarachnoid hemorrhage) — most often the case — the blood can block circulation of the fluid surrounding the brain and spinal cord (cerebrospinal fluid). This condition can result in an excess of cerebrospinal fluid that increases pressure on the brain and can damage tissues (hydrocephalus).
• Hyponatremia. Subarachnoid hemorrhage from a ruptured brain aneurysm can disrupt the balance of sodium in the blood. This may occur from damage to the hypothalamus, an area near the base of the brain. A drop in blood-sodium levels (hyponatremia) can lead to swelling of brain cells and permanent damage.

PREVENTION-

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Eating a healthy diet containing plenty of fruits, whole grains, and vegetables may help prevent an aneurysm from forming. Meat and poultry low in saturated fat and cholesterol are also good options for protein. Low-fat dairy products are also beneficial.

Regular exercise, especially cardio, can encourage healthy blood circulation and blood flow through the heart, arteries, and other blood vessels.

If you smoke tobacco products, now is the time to quit. Eliminating tobacco can decrease your risk for an aneurysm.

You should also see your doctor for annual checkups.

TREATMENT-

Treatment typically depends on the location and type of aneurysm.

For example, a weak area of a vessel in your chest and abdomen may require a type of surgery called an endovascular stent graft. This minimally invasive procedure may be chosen over traditional open surgery because it involves repairing and reinforcing damaged blood vessels. The procedure also reduces the chance of infection, scarring, and other problems.

Other treatments can include medications that treat high blood pressure and high cholesterol. Certain types of beta-blockers may also be prescribed to lower blood pressure. Lowering your blood pressure may keep your aneurysm from rupturing.

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INTRODUCTION-

A thrombus is a blood clot in the circulatory system. It attaches to the site at which it formed and remains there, hindering blood flow.

Doctors describe the development of a thrombus as thrombosis.

A thrombus is most likely to occur in people who are immobile and in those with a genetic predisposition to blood clotting.

A thrombus can also form after damage occurs in an artery, vein, or surrounding tissue.In this article, we look at blood clotting and the different types of thrombi. We also look at the symptoms, diagnosis, and treatment of a thrombus.

TYPES-

Thrombosis occurs when blood clots block your blood vessels. There are 2 main types of thrombosis:

• Venous thrombosis is when the blood clot blocks a vein. Veins carry blood from the body back into the heart.
• Arterial thrombosis is when the blood clot blocks an artery. Arteries carry oxygen-rich blood away from the heart to the body.

A blood clot is usually a normal physical response to injury.

It quickly forms a plug that can reduce or prevent bleeding. However, a thrombus can cause severe health problems, as it interrupts the function of a blood vessel.

A section of a blood clot that breaks free from the thrombus and circulates in the bloodstream is called an embolus.

An embolus moves through the vascular system until it lodges in a different part of the body.

An embolus is a dangerous and potentially fatal complication of thrombosis. It is especially dangerous if it reaches the heart, lungs, or brain (embolism).

Doctors categorize thrombi based on the type of blood vessel in which they develop:

When a thrombus forms in an artery, such as in the heart or brain, it is called an arterial thrombosis.

When a thrombus occurs in a vein, it is called a venous thrombosis. When this happens in the deep veins of the leg, it is called deep vein thrombosis (DVT).

CAUSES-

Clotting occurs due to a series of chemical reactions between blood cells known as platelets and proteins called clotting factors.

When a person is in good health, the body regulates the clotting process according to its needs.

However, a clot can form more easily when a person:

• uses tobacco
• has high cholesterol
• has obesity or is overweight
• has cancer
• has diabetes
• is stressed
• has an inactive lifestyle

Venous thrombosismay be caused by:

• Disease or injury to the leg veins
• Not being able to move around (immobility) for any reason
• A broken bone (fracture)
• Certain medicines
• Obesity
• Inherited disorders, or a greater likelihood of having a certain disorder based on your genes
• Autoimmune disorders that make it more likely your blood will clot
• Medicines that increase your risk of clotting (such as certain birth control medicines)

Arterial thrombosismay be caused by a hardening of the arteries, called arteriosclerosis. This happens when fatty or calcium deposits cause artery walls to thicken. This can lead to a buildup of fatty material (called plaque) in the artery walls. This plaque can suddenly burst (rupture), followed by a blood clot.

Arterial thrombosis can occur in the arteries that supply blood to the heart muscle (coronary arteries). This can lead to a heart attack. When arterial thrombosis occurs in a blood vessel in the brain, it can lead to a stroke.

Some of these factors also increase the risk of atherosclerosis, a condition wherein fatty plaque deposits line the blood vessels and clog them.

Atherosclerosis makes blood clots more likely to block the arteries and the veins.

SYMPTOM-

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Each person’s symptoms may vary. Symptoms may include:

• Pain in one leg (usually the calf or inner thigh)
• Swelling in the leg or arm
• Chest pain
• Numbness or weakness on one side of the body
• Sudden change in your mental state

The symptoms of thrombosis may look like other blood disorders or health problems. Always see your healthcare provider for a diagnosis.

Deep vein thrombosis signs and symptoms can include:

Swelling in the affected leg. Rarely, there’s swelling in both legs.

• Pain in your leg. The pain often starts in your calf and can feel like cramping or soreness.
• Red or discolored skin on the leg.
• A feeling of warmth in the affected leg.

Deep vein thrombosis can occur without noticeable symptoms.

When to see a doctor

If you develop signs or symptoms of deep vein thrombosis, contact your doctor.

If you develop signs or symptoms of a pulmonary embolism — a life-threatening complication of deep vein thrombosis — seek immediate medical attention.

The warning signs and symptoms of a pulmonary embolism include:

• Sudden shortness of breath
• Chest pain or discomfort that worsens when you take a deep breath or when you cough
• Feeling lightheaded or dizzy, or fainting
• Rapid pulse
• Coughing up blood

Symptoms of arterial thrombosis

A thrombus in an artery can result in:

• unstable angina, which is a type of chest pain
• heart attack
• ischemic stroke
• peripheral arterial limb ischemia, a condition that significantly reduces blood flow to the limbs

These conditions all require prompt medical attention.

People should seek emergency treatment if they experience any of the following symptoms:

• chest pain
• shortness of breath
• drooping on the lower half of the face
• a sudden loss of strength in one arm or leg
• a limb that has become cold, pale, and painful

Diagnosis

Doctors use several different methods to diagnose the presence of a thrombus. For example, they may use:

• Duplex ultrasound: This is the most common test for diagnosing DVT. A duplex ultrasound uses sound waves to create images of the blood flowing through the arteries and veins.
• A D-dimer test: This test measures the levels of a substance in the blood that results from the breakdown of blood clots. High levels of this substance may indicate the presence of DVT or another type of blood clot. However, the test is not definitive. If the result is normal and few risk factors are present, a person does not have a high risk of DVT.
• Venography: For venography, a doctor will inject a dye into a vein in the affected leg. This dye makes the vein visible on some types of X-ray, such as a fluoroscopy. If the scan shows a slower-than-usual blood flow through the vein, a thrombus may be present.
• MRI and CT scans: These scans create detailed images of organs, tissues, and blood vessels.
• A VQ scan: This is a nuclear imaging study. It uses a radioactive substance called a radiotracer to reveal, on a scan, the flow of air and blood within the lungs.

A doctor may request blood tests to check for a genetic blood clotting disorder. This may be necessary in cases of repeated unexplained blood clots.Thrombi in the liver, kidney, or brain may develop due to an inherited clotting disorder.

RISK FACTOR-

Many of the risk factors for venous and arterial thrombosis are the same.

Risk factors for venous thrombosis may include:

• A family history of a blood clot in a vein deep in the body, called a deep vein thrombosis (DVT)
• A history of DVT
• Hormone therapy or birth control pills
• Pregnancy
• Injury to a vein, such as from surgery, a broken bone, or other trauma
• Lack of movement, such as after surgery or on a long trip
• Inherited blood clotting disorders
• A central venous catheter
• Older age
• Smoking
• Being overweight or obese
• Some health conditions, such as cancer, heart disease, lung disease, or Crohn’s disease

Risk factors for arterial thrombosis may include:

• Smoking
• Diabetes
• High blood pressure
• High cholesterol
• Lack of activity and obesity
• Poor diet
• Family history of arterial thrombosis 
• Lack of movement, such as after surgery or on a long trip
• Older age

Many factors can increase your risk of developing deep vein thrombosis (DVT). The more you have, the greater your risk of DVT. Risk factors include:

• Inheriting a blood-clotting disorder. Some people inherit a disorder that makes their blood clot more easily. This condition on its own might not cause blood clots unless combined with one or more other risk factors.
• Prolonged bed rest, such as during a long hospital stay, or paralysis. When your legs remain still for long periods, your calf muscles don’t contract to help blood circulate, which can increase the risk of blood clots.
• Injury or surgery. Injury to your veins or surgery can increase the risk of blood clots.
• Pregnancy. Pregnancy increases the pressure in the veins in your pelvis and legs. Women with an inherited clotting disorder are especially at risk. The risk of blood clots from pregnancy can continue for up to six weeks after you have your baby.
• Birth control pills (oral contraceptives) or hormone replacement therapy. Both can increase your blood’s ability to clot.
• Being overweight or obese. Being overweight increases the pressure in the veins in your pelvis and legs.
• Smoking. Smoking affects blood clotting and circulation, which can increase your risk of DVT.
• Cancer. Some forms of cancer increase substances in your blood that cause your blood to clot. Some forms of cancer treatment also increase the risk of blood clots.
• Heart failure. This increases your risk of DVT and pulmonary embolism. Because people with heart failure have limited heart and lung function, the symptoms caused by even a small pulmonary embolism are more noticeable.
• Inflammatory bowel disease. Bowel diseases, such as Crohn’s disease or ulcerative colitis, increase the risk of DVT.
• A personal or family history of deep vein thrombosis or pulmonary embolism. If you or someone in your family has had one or both of these, you might be at greater risk of developing a DVT.
• Age. Being older than 60 increases your risk of DVT, though it can occur at any age.
• Sitting for long periods of time, such as when driving or flying. When your legs remain still for hours, your calf muscles don’t contract, which normally helps blood circulate. Blood clots can form in the calves of your legs if your calf muscles don’t move for long periods.

COMPLICATION-

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Thrombosis can block the blood flow in both veins and arteries. Complications depend on where the thrombosis is located. The most serious problems include stroke, heart attack, and serious breathing problems.

A serious complication associated with deep vein thrombosis is pulmonary embolism.

Pulmonary embolism

A pulmonary embolism occurs when a blood vessel in your lung becomes blocked by a blood clot (thrombus) that travels to your lung from another part of your body, usually your leg.

A pulmonary embolism can be life-threatening. It’s important to watch for signs and symptoms of a pulmonary embolism and seek medical attention if they occur. Signs and symptoms of a pulmonary embolism include:

• Sudden shortness of breath
• Chest pain or discomfort that worsens when you take a deep breath or when you cough
• Feeling lightheaded or dizzy, or fainting
• Rapid pulse
• Coughing up blood

Postphlebitic syndrome

A common complication that can occur after deep vein thrombosis is known as postphlebitic syndrome, also called postthrombotic syndrome. Damage to your veins from the blood clot reduces blood flow in the affected areas, which can cause:

• Persistent swelling of your legs (edema)
• Leg pain
• Skin discoloration
• Skin sores

PREVENTION-

You can reduce your risk of thrombosis by:

• Being active
• Getting back to activity as soon as possible after surgery
• Exercising your legs during long trips
• Quitting smoking
• Losing weight
• Managing other health problems such as diabetes, high blood pressure, and high cholesterol

Measures to prevent deep vein thrombosis include:

• Avoid sitting still. If you have had surgery or have been on bed rest for other reasons, try to get moving as soon as possible. If you’re sitting for a while, don’t cross your legs, which can hamper blood flow. If you’re traveling a long distance by car, stop every hour or so and walk around. If you’re on a plane, stand or walk occasionally. If you can’t do that, exercise your lower legs. Try raising and lowering your heels while keeping your toes on the floor, then raising your toes with your heels are on the floor.
• Make lifestyle changes. Lose weight and quit smoking.
• Exercise. Regular exercise lowers your risk of blood clots, which is especially important for people who sit a lot or travel frequently.

It is not always possible to prevent a thrombus. However, people can take steps to reduce their risk.

For example, a person can:

• avoid or quit tobacco smoking
• prevent excessive weight gain or lose weight to avoid obesity
• adopt a healthful diet
• exercise regularly

It is particularly important for a person to move around as much as possible after a surgical procedure or during long distance travel.

Those with a higher risk of developing a blood clot may also require anticoagulant therapy alongside medications to reduce blood pressure and blood cholesterol levels.

TREATMENT-

The aim of treating a thrombus is to achieve the following quickly and effectively:

• gain control over the symptoms
• restore the blood flow
• reduce and remove the thrombus

Doctors typically recommend the following treatments to deal with the effects of thrombi:

Surgery

Surgery for the effects of thrombosis will always be a medical emergency.

The procedure can involve directly accessing and unblocking an affected artery. In other cases, the surgeon will divert blood flow or completely bypass the blocked artery.

Inferior vena cava filters

Inferior vena cava (IVC) filters are small mesh devices that a surgeon can put in the inferior vena cava (a large vein), usually under local anesthetic.

The IVC filter traps fragments of the blood clot and prevents them from reaching the heart and lungs.

An IVC filter can be permanent, and doctors typically combine this treatment with anticoagulation medication therapy where possible. However, a surgeon may remove the IVC filter if the person’s risk of a blood clot declines.

Anticoagulants

Anticoagulants, or blood thinners, have a misleading name; they do not give the blood a thinner consistency.

Instead, they reduce the risk of a clot forming, which can reduce the size of a thrombus.

When taking anticoagulant medications, a person should visit a specialized anticoagulant management service instead of a primary care physician.

If anticoagulants are not effective, or if a person does not tolerate them well, a doctor will consider other treatment options.

Compression stockings

Doctors may recommend that people wear compression stockings while taking anticoagulant therapy for DVT.

The stockings help prevent calf pain and swelling, as well as reduce the risk of complications.

A person should wear compression stockings for as long as their doctor recommends.

Raising the affected leg

As well as wearing compression stockings, people should try to keep the affected leg elevated above hip level during the night.

This can relieve pressure in the veins, improve blood circulation, and help prevent complications.

Exercise

Once a doctor has prescribed compression stockings, they will usually recommend more frequent walking to stimulate blood circulation.

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INTRODUCTION-

Most of the nerves in your body are covered with a protective layer called myelin. It’s a lot like the insulation on electric wires. It helps messages from your brain move quickly and smoothly through your body, the way electricity flows from a power source.

Demyelinating disorders are any conditions that damage myelin. When this happens, scar tissue forms in its place. Brain signals can’t move across scar tissue as quickly, so your nerves don’t work as well as they should.

The peripheral nerves consist of bundles of long neuronal axons as they exit the central nervous system (CNS). Some peripheral nerves are wrapped in a myelin sheath generated by Schwann cells, whereas others are unmyelinated. Peripheral nerves serve different motor, sensory, and autonomic functions. The term peripheral neuropathy is usually used to describe symmetric and universal damage to adjacent nerves. The damage and clinical manifestations are usually located distally with a proximal progression. Several disorders can damage peripheral nerves and cause peripheral neuropathy; it is important to differentiate actual neuropathy from other disorders that can have a similar clinical presentation.

Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes mellitus, hypothyroidism, and nutritional deficiencies. The diagnosis requires careful clinical assessment, judicious laboratory testing, and electrodiagnostic studies or nerve biopsy if the diagnosis remains unclear. A systematic approach begins with localization of the lesion to the peripheral nerves, identification of the underlying etiology, and exclusion of potentially treatable causes. Initial blood tests should include a complete blood count, comprehensive metabolic profile, and measurement of erythrocyte sedimentation rate and fasting blood glucose, vitamin B₁₂, and thyroid-stimulating hormone levels; specialized tests should be ordered if clinically indicated. Lumbar puncture and cerebrospinal fluid analysis may be helpful in the diagnosis of Guillain-Barré syndrome and chronic inflammatory demyelinating neuropathy. Electrodiagnostic studies, including nerve conduction studies and electromyography, can help in the differentiation of axonal versus demyelinating or mixed neuropathy. Treatment should address the underlying disease process, correct any nutritional deficiencies, and provide symptomatic treatment.

Symptoms and Signs-

A host of symptoms and signs that reflect sensory, motor, and autonomic nerve fiber dysfunction are typical of peripheral neuropathies, and some combinations of symptoms and signs may be recognized as specific syndromes of peripheral nerve disease. Sensory symptoms include sensory loss, often described by patients as a sense of numbness or a “Novocain-like” feeling. In most generalized polyneuropathies, these symptoms begin in the most distal extent of the longest sensory fibers (i.e., those that subserve sensation in the toes and feet). The pathologic changes in most of these polyneuropathies are those of a distal-to-proximal axonal degeneration that have been referred to as distal axonopathies or dying-back neuropathies. Similar symptoms may be seen in hereditary or acquired demyelinating polyneuropathies.

Sensory Symptoms

Typically, all sensory modalities are affected to some extent, including light touch, pain, thermal sensation, vibratory sense, and joint position sense. As the disease progresses, sensory loss ascends the lower extremities, typically in a symmetrical fashion. When the sensory loss is at or above the level of the knee, the axons supplying the distal fingertips begin to be involved, and the length-dependent process then begins in the upper extremities. In addition to sensory loss, patients often complain of paresthesias and dysesthesias, often characterized by a sense of numbness, tingling, prickling, and pins-and-needles sensations. They might also complain of intense bandlike sensations and feelings of pressure.

The sensory examination often discloses a distal-to-proximal loss of the various sensory modalities. In certain polyneuropathies, pain predominates in the clinical picture, and the sensory examination tends to disclose deficits predominantly of pain and thermal sensation, conforming to an SFN. On occasion, when significant proprioceptive deafferentation occurs, patients are found to have altered joint position sense that can manifest as an ataxia or tremor of the affected limbs and an imbalance of gait and station.

Pain is a serious symptom for many patients. It may be described as a dull aching sensation, an intense burning sensation or, occasionally, as intermittent lancinating pulses of pain. On occasion, patients notice that their skin is hypersensitive to tactile stimulation such as from the touch of bed sheets or clothing or from standing on their feet. Some patients note an exaggerated painful sensation resulting from any stimulus to the affected area, a form of pain termed allodynia.

Weakness

Impairment of motor function typically produces weakness in a distal-to-proximal gradient consistent with a length-dependent axonal degeneration. As with sensory loss, weakness begins in the toes, and as the polyneuropathy progresses, it ascends up the distal lower extremities to the level of the knees, at which time motor involvement in the hands may be observed. Similar patterns of weakness may be seen in demyelinating polyneuropathies. However, in the acquired segmental demyelinating polyneuropathies such as CIDP and related disorders, proximal muscle weakness resulting from root involvement may be observed outside the proximal-to-distal gradient of the dying-back mechanism. This pattern of involvement is termed a polyradiculoneuropathy.

Axonal degenerative polyneuropathies tend to produce weakness along with muscle atrophy, but atrophy is much less conspicuous in segmental demyelinating polyneuropathies because in these disorders the axon remains in continuity with the muscle, preventing denervation atrophy. The most common symptom in polyneuropathy is weakness in dorsiflexion of the feet at the ankles. This can result in a partial or complete foot drop that typically causes the feet to slap while walking and predisposes the patient to stumble and fall when the toes catch on an uneven surface.

Tendon reflexes are usually depressed or absent in a distal-to-proximal pattern of involvement, with the lower extremities affected more than the upper extremities. An exception to this is in SFN, in which the large-caliber sensory afferent fibers from muscle spindles are relatively preserved and the tendon reflexes might remain intact.

Autonomic Symptoms

In some polyneuropathies, typically in SFN, autonomic fibers are also affected. In these disorders, a variety of autonomic symptoms may be present, although certainly the most dramatic and incapacitating is orthostatic hypotension, which causes postural light- headedness, syncope, or both. However, orthostatic hypotension typically occurs only with advanced autonomic involvement.

Earlier in the course of autonomic neuropathy, patients might notice reduced or absent sweating (i.e., anhidrosis) often in a distal-to-proximal gradient. Some patients complain of excessive sweating confined to the head and neck region. This is most often secondary to anhidrosis in the limbs and thorax and reflects compensatory hyperhidrosis in the restricted areas that maintain normal sweating.

Other autonomic symptoms include dryness of the eyes and mouth and gastrointestinal dysmotility, often manifested by alternating constipation and diarrhea or by early satiety from gastroparesis. In addition, patients may have urinary bladder dysfunction caused by an atonic bladder, which results in overflow incontinence. In men, erectile dysfunction can represent an early autonomic symptom, reflecting parasympathetic autonomic nervous system involvement.

Other Symptoms and Signs

Various limb deformities and trophic changes may be observed in chronic polyneuropathies. Pes cavus, characterized by high arches and hammer toes and the clawfoot deformity, are typical foot deformities in hereditary polyneuropathies with childhood onset. These deformities are a result of progressive weakness and atrophy of intrinsic foot muscles. A similar claw-like deformity may be observed in the hand.

Autonomic involvement of a limb may, at times, cause the affected area to appear warm, red, and swollen and at other times pale and cold because of abnormal regulation of small vessels as a result of autonomic denervation. Various trophic changes can occur including tight, shiny skin.

In patients who have had severe sensory loss in the limbs, the affected areas may be subject to incidental traumas, including burns, pressure sores, and other injuries that are not perceived by the patient. In these patients, repeated injuries and traumas can result in chronic infections, sometimes leading to osteomyelitis.

In peripheral nerve disorders that are focal and asymmetrical, sensory and motor—and occasionally autonomic—symptoms and signs may conform to a specific peripheral nerve distribution. For example, in carpal tunnel syndrome, patients might complain of intermittent numbness and tingling in the median nerve distribution in the hand or, as the entrapment progresses, atrophy and weakness of the thenar muscle group. In the mononeuritis multiplex syndrome, multiple individual peripheral nerves may be affected, and the sensory, motor, and autonomic symptoms and signs will be distributed in a multifocal pattern conforming to numerous individual peripheral nerve lesions. On occasion, some peripheral nerve disorders cause generalized sensory and motor fiber involvement with asymmetrical and focal features.

Prevalence and Risk Factors-

Peripheral nerve disorders are relatively common conditions that affect 2.4% of the population. However, the prevalence increases to 8.0% with advancing age.

The most common generalized polyneuropathy is diabetic sensorimotor polyneuropathy, which may be present in as many as 66% of type 1 diabetes patients and in nearly 59% of type 2 diabetes patients.Even higher prevalence rates have been reported depending on the criteria used to diagnose polyneuropathy. Considering that the prevalence rate of diabetes is approximately 1.3%, this common complication of diabetes could affect nearly 1% of the general population.

The most common genetic sensorimotor polyneuropathy is Charcot-Marie-Tooth disease type 1a, which has a prevalence of approximately 30 per 100,000 population. Carpal tunnel syndrome, caused by chronic entrapment of the median nerve in the carpal tunnel, is the most common mononeuropathy, with a prevalence estimated to be between 3% and 5% of adults.

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Diagnosis

Diagnosis begins by recognizing typical symptoms of peripheral nerve disease and identifying the pattern of peripheral nerve involvement. For example, if the symptoms are highly restricted and focal, they might conform to the distribution of an individual peripheral nerve or, possibly, to an individual root. More-diffuse involvement of an entire limb might be caused by involvement of the brachial or lumbosacral plexus. Alternatively, if generalized symptoms are distributed in an asymmetrical and focal fashion, they may be consistent with a mononeuritis multiplex picture or possibly a polyradiculoneuropathy or polyradiculopathy syndrome. Most often, peripheral neuropathies produce symptoms that are generalized and relatively symmetrical, conforming to a distal-to-proximal gradient typical of a distal axonopathy.

History and Physical Examination

As soon as their distribution is recognized, the symptoms should be analyzed to determine which fiber types appear to be involved (i.e., sensory, motor, autonomic). In addition, the temporal profile of the disorder (i.e., chronic, subacute, acute) is noted. The neurologic examination is then helpful in confirming signs of sensory, motor, or autonomic dysfunction and in documenting the pattern and fiber type involved. These clinical features, which can be derived solely from the history and physical examination, are valuable for characterizing the nature of the peripheral nerve syndrome, which is essential in constructing a differential diagnosis.

Electrodiagnostic Studies

Another important component to the evaluation of peripheral nerve disease is electrodiagnostic studies, primarily nerve conduction studies and the needle electrode examination. Electrodiagnostic testing can document the presence of peripheral nerve disease, define the distribution and pattern of various sensory and motor fibers, and characterize the underlying pathologic processes (i.e., wallerian degeneration, axonal degeneration, segmental demyelination, or some mixture of these pathologic reactions). Characterizing the electrodiagnostic features, particularly whether the process is axonal or demyelinating, adds additional information.⁴

Medical Studies

Other special studies include lumbar puncture for cerebrospinal fluid analysis, which may be useful in diagnosing inflammatory or infectious causes of polyneuropathy, in evaluating acquired demyelinating polyneuropathies such as those in GBS and CIDP, and in a variety of immune-mediated polyneuropathies.

Nerve biopsy, typically sural nerve biopsy, is most often recommended in patients with asymmetrical or focal polyneuropathies in whom a diagnosis of vasculitis is being considered. In addition, biopsies may be used to assist in the diagnosis of some inflammatory, infectious, and metabolic polyneuropathies. Nerve biopsy can help to establish the pathologic basis of the polyneuropathy when electrodiagnostic studies cannot conclusively distinguish an axonal from an acquired segmental demyelinating disorder.

Special autonomic studies, particularly those that measure cardiovascular autonomic reflexes (including heart rate response to deep breathing, heart rate and blood pressure responses to the Valsalva maneuver, and heart rate and blood pressure responses to head-up-tilt) may also be valuable in documenting autonomic cardiovascular involvement. Various tests of sudomotor function including the sympathetic skin response, quantitative sudomotor axon reflex test, and thermoregulatory sweat testing can provide valuable information regarding the extent and distribution of sudomotor impairment in polyneuropathy.

Skin biopsy to measure epidermal nerve fiber density is also a helpful test for the diagnosis of SFN. Quantitative sensory testing is a technique that allows precise measurement of sensory perception thresholds of various fiber types, which can also be helpful in assessing peripheral neuropathy, especially SFN, in which the electrodiagnostic studies are often normal.

Laboratory Studies

By recognizing the peripheral nerve syndrome and appreciating the potential differential diagnosis, one may systematically perform appropriate medical tests to explore the various possible causes. The most common peripheral nerve syndrome is the generalized sensorimotor polyneuropathy with electrodiagnostic features of a distal axonopathy. For this disorder, it is usually appropriate to pursue a history of toxin exposure (see Tables 2 and 3) and alcoholism with nutritional deficiency. It is also reasonable to perform routine laboratory screening studies including a complete blood cell count; erythrocyte sedimentation rate; a blood chemistry panel encompassing hepatic function, renal function, and electrolytes; thyroid function studies; and vitamin B₁₂ level.

It is important to screen patients for diabetes mellitus. In the past, a fasting blood sugar or hemoglobin A_1c, or both, was often performed, but recent reports suggest that impaired glucose tolerance detected on a glucose tolerance test might provide more meaningful information regarding diabetes as a potential cause for polyneuropathy.⁵

Screening the serum and urine with protein electrophoresis with immunofixation is also important in assessing patients with generalized polyneuropathy. In one series, the only laboratory tests that were helpful in establishing a precise cause for the polyneuropathy were vitamin B₁₂, serum protein electrophoresis with immunofixation, and serum glucose.Additional laboratory and radiographic studies may be considered pending the specific clinical features, and may include chest radiograph, skeletal bone survey, antinuclear antibodies, rheumatoid factor, and angiotensin-converting enzyme level.

In patients with an aggressive, evolving polyneuropathy or a specific paraneoplastic syndrome, additional testing for an occult malignancy is often performed, usually in conjunction with autoantibodies, especially anti-Hu. A variety of autoantibodies have been associated with different polyneuropathy syndromes. The most useful of these include anti-GM₁ antibodies in the setting of MMNCB, anti-Hu antibodies in the context of a sensory neuronopathy, and anti-myelin-associated glycoprotein antibodies in acquired demyelinating polyneuropathy with predominately sensory features and with a distal pattern of involvement. Most of the other antibodies are much less specific, and their roles in the mechanism of the polyneuropathies are less certain. Thus, the precise value of performing panels of antibody tests is unclear at this time.

Lumbar puncture is often reserved for patients with possible immune-mediated polyneuropathies, particularly those with demyelinating features on electrodiagnostic testing. However, CSF studies are also often assessed in cryptogenic axonal degeneration polyneuropathies and in patients with possible infectious or inflammatory disorders.

Epidemiology

One study estimated that the prevalence of peripheral neuropathy in the family medicine setting is 8 percent in persons 55 years and older. The prevalence in the general population may be as high as 2.4 percent. A community-based study estimated the prevalence of peripheral neuropathy in patients with type 2 diabetes mellitus to be 26.4 percent.

TREATMENT-

Medical Treatment

Specific therapies for polyneuropathy are based on the precise etiologic diagnosis. In disorders attributed to underlying medical conditions, management is focused on the medical disorder. For example, optimizing glycemic control in diabetic polyneuropathy often stabilizes or improves the polyneuropathy.

In patients with idiopathic immune-mediated polyneuropathies, including GBS, CIDP, and MMNCB, specific immune-modulating therapies are often recommended.^8,11 For GBS, intravenous gamma globulin (IVIg), typically administered at a dosage of 400 mg/kg daily for 5 consecutive days, is initiated early in the patient’s course. Alternatively, plasmapheresis may also be instituted as initial therapy.

Treatment of CIDP may begin with corticosteroid therapy. However, chronic IVIg or plasmapheresis, or both, are usually effective and obviate the need for long-term steroid therapy. Alternative therapies including azathioprine, cyclophosphamide, cyclosporine, mycophenolate mofetil, methotrexate, and rituximab have also been used in patients who have not responded to initial standard therapies.

Toxic polyneuropathies are managed by discontinuing the offending drug or removing the industrial toxin from the patient’s environment.

Management of hereditary polyneuropathies includes education of the affected family members regarding the nature and genetic features of the disorder and judicious screening of family members at risk.

Supportive Therapy

For all patients, and particularly for those without a specific or treatable cause, therapy focuses on supportive measures. This may include the use of various physical therapy and occupational therapy modalities including bracing and aids to ambulation. An ankle-foot orthosis may be effective in improving ambulation in a patient with foot drop. In patients with severe sensory loss in the feet and lower extremities, careful daily foot inspection for signs of trauma and infection are essential to prevent serious infections and other complications.

Pain Management

In patients who have associated pain, particularly patients with SFN, specific neuropathic pain management is instituted. Neuropathic pain typically does not respond to simple analgesics, and its potential chronicity precludes narcotic therapy as a first choice. Typically, patients with SFN and other painful polyneuropathies respond to drugs known to be effective for neuropathic pain, including tricyclic antidepressants and a variety of antiepileptic drugs and membrane stabilizers.

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INTRODUCTION-

Brain and spinal cord lesions have an increasing social and economic importance. Accidental trauma of various kinds is the main cause of mortality of children and young adults in developed countries. Only cardiac disease and cancer surpass the number of death caused by accidents and, examining the number of potential work years lost, CNS lesions surpass all other problems. Most brain and spinal cord injuries cause chronic incapacity and frequently occur to individuals under 45 years of age. Edema and other acute events can be efficiently treated and CNS lesions may not be mortal, but are incurable.

Traumatic Brain Injury (TBI) is a disruption in the normal function of the brain that can be caused by a blow, bump or jolt to the head, the head suddenly and violently hitting an object or when an object pierces the skull and enters brain tissue. Observing one of the following clinical signs constitutes alteration in the normal brain function:

• Loss of or decreased consciousness
• Loss of memory for events before or after the event (amnesia)
• Focal neurological deficits such as muscle weakness, loss of vision, change in speech
• Alteration in mental state such as disorientation, slow thinking or difficulty concentrating

Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Mild cases may result in a brief change in mental state or consciousness. Severe cases may result in extended periods of unconsciousness, coma, or even death.

he final outcome of CNS injury depend on the area damaged and the extent of the lesion, but the best present therapies can offer is relief of the symptoms and rehabilitation. This review examines the present state of functional repair of experimental central nervous system trauma.

TRAUMA-

Cellular infiltrates in the CSF of victims of CNS trauma are indistinguishable from the cells seen in subarachnoid hemorrhage and destructive lesions of other etiologies. Thus, red blood cells and macrophages containing hemosiderin or myelin debris are the most common manifestations of trauma in CSF. Patients with sinus and basilar skull fractures with tears in the meninges are at risk for developing leakage of sinus contents into the SAS. The CSF in this setting contains a marked acute inflammatory reaction. Bacteria and other elements, such as fragments of Candida and ciliated respiratory epithelial cells from the sinus lining, may also be seen.

Key features of trauma•

Red blood cells; and•

Macrophages containing hemosiderin or myelin debris.

The Problem

Traumatic brain injury (TBI) remains a major health problem with serious socio-economic consequences. Although its incidence is decreasing in most western countries according to some estimates, severe TBI will become the third most common cause of death and disability globally by the year 2020.

In 1996, 3740 deaths from serious injuries were recorded in the United Kingdom. The death rate for all ages from a head injury in the United Kingdom is 9 deaths per 100,000 population per year, or 1% of all deaths, or 15-20% of deaths of persons aged 5-35 years

CAUSES-

Brain trauma can be caused by a direct impact or by acceleration alone. In addition to the damage caused at the moment of injury, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury. These processes, which include alterations in cerebral blood flow and the pressure within the skull, contribute substantially to the damage from the initial injury.

TYPES-

Brain injuries can be classified into mild, moderate, and severe categories. The Glasgow Coma Scale (GCS), the most commonly used system for classifying TBI severity, grades a person’s level of consciousness on a scale of 3–15 based on verbal, motor, and eye-opening reactions to stimuli. It is generally agreed that a TBI with a GCS of 13 or above is mild, 9–12 is moderate, and 8 or below is severe.

TBIs can cause “mass lesions,” w an area of localized injury such as hematomas and contusions that increase pressure within the brain. Summarized below are different types of sequelae deveoped from TBIs:

Hematoma: A hematoma is a blood clot within the brain or on its surface. Hematomas may occur anywhere within the brain. An epidural hematoma is a collection of blood between the dura mater (the protective covering of the brain) and the inside of the skull. A subdural hematoma is a collection of blood between the dura mater and the arachnoid layer, which sits directly on the surface of the brain.

Contusion: A cerebral contusion is bruising of brain tissue. When examined under a microscope, cerebral contusions are comparable to bruises in other parts of the body. They consist of areas of injured or swollen brain mixed with blood that has leaked from arteries, veins, or capillaries. Most commonly, contusions are at the base of the front parts of the brain, but may occur anywhere.

Intracerebral Hemorrhage: An intracerebral hemorrhage (ICH) describes bleeding within the brain tissue, may be related to other brain injuries, especially contusions. The size and location of the hemorrhage helps determine whether it can be removed surgically.

Subarachnoid Hemorrhage: Subarachnoid hemorrhage (SAH) is caused by bleeding into the subarachnoid space. It appears as diffuse blood spread thinly over the surface of the brain and commonly after TBI. Most cases of SAH associated with head trauma are mild. Hydrocephalus may result from severe traumatic SAH.

Diffuse Injuries: TBIs can produce microscopic changes that do not appear on CT scans and are scattered throughout the brain. This category of injuries, called diffuse brain injury, may occur with or without an associated mass lesion.

Diffuse Axonal Injury: Axonal injury refers to impaired function and gradual loss of axons.These long extensions of nerve cells enable them to communicate with each other. If enough axons are harmed in this way, the ability of nerve cells to communicate with each other and to integrate their function may be lost or greatly impaired, possibly leaving a patient with severe disabilities.

Ischemia: Another type of diffuse injury is ischemia or insufficient blood supply to certain parts of the brain. A decrease in blood supply to very low levels may occur commonly in a significant number of TBI patients. This is crucial since a brain that has just undergone a traumatic injury is especially sensitive to slight reductions in blood flow. Changes in blood pressure during the first few days after head injury can also have an adverse effect.

Skull Fractures: Linear skull fractures or simple breaks or “cracks” in the skull may accompany TBIs.

Possible forces, strong enough to cause a skull fracture may damage the underlying brain. Skull fractures may be alarming, if found on a patient evaluation. Fractures at the base of the skull are problematic since they can cause injury to nerves, arteries, or other structures. If the fracture extends into the sinuses, a leakage of cerebrospinal fluid (CSF) from the nose or ears may occur. Depressed skull fractures, in which part of the bone presses on or into the brain, can also occur.

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SYMPTOM-

Symptoms vary greatly depending on the severity of the head injury. They may include any of the following:

• Vomiting
• Lethargy
• Headache
• Confusion
• Paralysis
• Coma
• Loss of consciousness
• Dilated pupils
• Vision changes (blurred vision or seeing double, unable to tolerate bright light, loss of eye movement, blindness)
• Cerebrospinal fluid (CSF) (clear or blood-tinged) appear from the ears or nose
• Dizziness and balance concerns
• Breathing problems
• Slow pulse
• Slow breathing ratewith an increase in blood pressure
• Ringing in the ears or changes in hearing
• Cognitive difficulties
• Inappropriate emotional responses
• Speech difficulties (slurred speech, inability to understand and/or articulate words)
• Difficulty swallowing
• Body numbness or tingling
• Droopy eyelid or facial weakness
• Loss of bowel control or bladder control

If a TBI is suspected, call 911 immediately or take the person to an emergency room.

Side Effects and Complications

Subdural hematoma is a possible result of traumatic head injury: In this image, the single arrow marks spread of the subdural haematoma and the double arrow marks the midline shift.

TBI can cause a host of physical, cognitive, social, emotional, and behavioral effects, and the outcome can range from complete recovery to permanent disability or death. The 20^th century saw critical developments in diagnosis and treatment that decreased death rates and improved outcome. Some of the current imaging techniques used for diagnosis and treatment include CT scans (computed tomography) and MRIs (magnetic resonance imaging). Depending on the injury, treatment required may be minimal or may include interventions such as medications, emergency surgery or surgery years later. Physical therapy, speech therapy, recreation therapy, and occupational therapy may be employed for rehabilitation.

Complications are distinct medical problems that may arise as a result of the TBI. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings), and minimally conscious state. Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke. Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire). The risk of post-traumatic seizures increases with severity of trauma and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas.

TESTING AND DIAGNOSIS-

Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because we cannot do much to reverse the initial brain damage caused by trauma, medical providers try to stabilize an individual with TBI and focus on preventing further injury.

First, the cardiac and pulmonary function is assessed. Next, a quick examination of the entire body is performed, followed by a complete neurological examination. The neurological examination includes an assessment utilizing the Glasgow Coma Scale (GCS). In addition to the GCS, also tested is the ability of the pupils to become smaller in bright light. In patients with large mass lesions or with high intracranial pressure (ICP), one or both pupils may be very wide or “blown.” The presence of a wide or dilated pupil on only one side suggests a large mass lesion may be present. Brainstem reflexes including gag and corneal (blink) may also be tested.

Radiological Tests

A computed tomography scan (CT or CAT scan) is the gold standard for the radiological assessment of a TBI patient. A CT scan is easy to perform and an excellent test for detecting the presence of blood and fractures, the most crucial lesions to identify in medical trauma cases. Plain x-rays of the skull are recommended by some as a way to evaluate patients with only mild neurological dysfunction. However, most centers in the U.S. have readily available CT scanning, a more accurate test, rendering the routine use of skull x-rays for TBI patients to decline.

Magnetic resonance imaging (MRI) is not commonly used for acute head injury since it takes longer to perform a MRI than a CT. Because it is difficult to transport an acutely-injured patient from the emergency room to a MRI scanner, the use of MRI is impractical. However, once a patient is stabilized, MRI may demonstrate the existence of lesions that were not detected on the CT scan. This information is generally more useful for determining prognosis than for influencing treatment.

TREATMENT-

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Surgery–

Many patients with moderate or severe head injuries head directly from the emergency room to the operating room. In many cases, surgery is performed to remove a large hematoma or contusion that is significantly compressing the brain or raising the pressure within the skull. After surgery, these patients are under observation in the intensive care unit (ICU).

Other head-injured patients may not head to the operating room immediately, instead are taken from the emergency room to the ICU. Since contusions or hematomas may enlarge over the first hours or days after head injury, immediate surgery is not recommended on these patients until several days after their injury. Delayed hematomas may be discovered when a patient’s neurological exam worsens or when their ICP increases. On other occasions, a routine follow-up CT scanto determine whether a small lesion has changed in size indicates that the hematoma or contusion has enlarged significantly. In these cases, the safest approach is to remove the lesion before it enlarges and causes neurological damage.

During surgery, the hair over the affected part of the head is usually shaved. After the scalp incision, the removed bone is extracted in a single piece or flap, then replaced after surgery unless contaminated. The dura mater is carefully cut to reveal the underlying brain. After any hematoma or contusion is removed, the neurosurgeon ensures the area is not bleeding. He or she then closes the dura, replaces the bone and closes the scalp. If the brain is very swollen, some neurosurgeons may decide not to replace the bone until the swelling decreases, which may take up to several weeks. The neurosurgeon may elect to place an ICP monitor or other types of monitors if these were not already in place. The patient is returned to the ICU for observation and additional care.

Non-Surgical Treatments

At present, medication administered to prevent nerve damage or promote nerve healing after TBI not available. The primary goal in the ICU is to prevent any secondary injury to the brain. The “primary insult” refers to the initial trauma to the brain, whereas the “secondary insult” is any subsequent development that may contribute to neurological injury. For example, an injured brain is especially sensitive and vulnerable to decreases in blood pressure otherwise well tolerated. One way to avoid secondary insults is to attempt normal or slightly elevated blood pressure levels. Likewise, increases in ICP, decreases in blood oxygenation, increases in body temperature, increases in blood glucose and many other disturbances can potentially worsen neurological damage. The major role of ICU management is the prevention of secondary insults in head-injured patients.

Various monitoring devices may assist health care personnel in caring for the patient. Placement of an ICP monitor into the brain can help detect excessive swelling. One commonly used type of ICP monitor is a ventriculostomy, a narrow, flexible, hollow catheter that is passed into the ventricles, or fluid spaces in the center of the brain, to monitor ICP and drain CSF if ICP increases. Another commonly used type of intracranial pressure monitoring device involves placement of a small fiberoptic catheter directly into the brain tissue. Additional catheters may be added to measure brain temperature and brain tissue oxygenation. Placement of an oxygen sensor into the jugular vein can detect how much oxygen the brain is using. This may be related to the degree of brain damage. Many other monitoring techniques currently under investigation to determine whether they can help improve outcome after head injury or provide additional information about caring for TBI patients.

Rehabilitation

Once head-injured patients leave the acute-care hospital, some benefit from a rehabilitation program. Prime candidates for rehabilitation are patients with less severe initial injuries or those that started to show significant improvement.

In some cases, transfer to a rehabilitation hospital or to the rehabilitation service of a large hospital may expedite further recovery. For more severely injured patients or those with slow recovery, constant vigilance is required to prevent the gradual onset of problems with joint mobility, skin integrity, respiratory status, infection and many other physiological functions. Patients with moderate or mild injuries, or severely injured patients who have improved sufficiently, are likely candidates for outpatient therapy.

Most head-injury rehabilitation centers emphasize compensatory strategies to help patients learn to reach the maximum level of function allowed by their impairments. The concept of cognitive retraining, a controversial concept, which presumes that at least some of the brain’s cognitive capacity can be restored by constant repetition of certain simple tasks, is also emphasized at many centers. Head injury rehabilitation centers work with patients’ families to educate them about realistic expectations and best help their injured family member.

General Head Injury Prevention Tips

• Wear a seatbelt every time you drive or ride in a motor vehicle.
• Never drive while under the influence of drugs, alcohol or ride as a passenger with anyone who is under the influence.
• Keep firearms unloaded in a locked cabinet or safe, and store ammunition in a separate, secure location.
• Remove hazards in the home that may contribute to falls. Secure rugs and loose electrical cords, put away toys, use safety gates and install window guards. Install grab bars and handrails if you are frail or elderly.

Sports and Recreation Head Injury Prevention Tips

• For specific sports, 100 percent of the time, buy and use helmets or protective headgear approved by the American Society for Testing and Materials (ASTM).
• Supervise younger children at all times.
• Do not allow younger children to use sporting equipment or play sports unsuitable for their age.
• Avoid the use of playgrounds with hard surfaces.
• Follow all rules and warning signs at water parks, swimming pools and public beaches.
• Do not dive in water less than 12 feet deep or in above-ground pools. Check the depth – and check for debris in the water before diving.
• Wear appropriate clothing for the sport.
• Do not wear any clothing that can interfere with your vision.
• Do not participate in sports when you are ill or very tired.
• Obey all traffic signals, and be aware of drivers when cycling or skateboarding.
• Avoid uneven or unpaved surfaces when cycling, skateboarding or in-line skating.
• Perform regular safety checks of sports fields, playgrounds and equipment.
• Discard and replace damaged sporting equipment or protective gear
• Never slide head-first when stealing a base.

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INTRODUCTION-

Leprosy, also known as Hansen’s disease, is a chronic infectious disease caused by Mycobacterium leprae. The disease mainly affects the skin, the peripheral nerves, mucosal surfaces of the upper respiratory tract and the eyes. Leprosy is known to occur at all ages ranging from early infancy to very old age. Leprosy is curable and early treatment averts most disabilities.

Leprosy is an infectious disease that causes severe, disfiguring skin sores and nerve damage in the arms, legs, and skin areas around the body. The disease has been around since ancient times, often surrounded by terrifying, negative stigmas and tales of leprosy patients being shunned as outcasts. Outbreaks of leprosy have affected, and panicked, people on every continent. The oldest civilizations of China, Egypt, and India feared leprosy was an incurable, mutilating, and contagious disease.

However, leprosy is actually not that contagious. You can catch it only if you come into close and repeated contact with nose and mouth droplets from someone with untreated leprosy. Children are more likely to get leprosy than adults.

Today, about 180,000 people worldwide are infected with leprosy, according to the World Health Organization, most of them in Africa and Asia. About 100 people are diagnosed with leprosy in the U.S. every year, mostly in the South, California, Hawaii, and some U.S. territories.

CAUSES-

Leprosy is caused by a slow-growing type of bacteria called Mycobacterium leprae (M. leprae). Leprosy is also known as Hansen’s disease, after the scientist who discovered M. leprae in 1873

SYMPTOM-

Leprosy primarily affects the skin and the nerves outside the brain and spinal cord, called the peripheral nerves. It may also strike the eyes and the thin tissue lining the inside of the nose.

The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away after several weeks or months. The skin sores are pale-colored.

Nerve damage can lead to:

• Loss of feeling in the arms and legs
• Muscle weakness

It usually takes about 3 to 5 years for symptoms to appear after coming into contact with the leprosy-causing bacteria. Some people do not develop symptoms until 20 years later. The time between contact with the bacteria and the appearance of symptoms is called the incubation period. Leprosy’s long incubation period makes it very difficult for doctors to determine when and where a person with leprosy got infected.

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DIAGNOSIS-

Clinical signs are easy to observe. In a country or area with a high incidence of leprosy, an individual should be regarded as having leprosy if he or she shows ONE of the following cardinal signs:

• skin lesion consistent with leprosy and with definite sensory loss, with or without thickened nerves
• positive skin smears

The skin lesion can be single or multiple, usually less pigmented than the surrounding normal skin. Sometimes the lesion is reddish or copper-coloured. A variety of skin lesions may be seen but macules (flat), papules (raised), or nodules are common. Sensory loss is a typical feature of leprosy. The skin lesion may show loss of sensation to pin pick and/or light touch. Thickened nerves, mainly peripheral nerve trunks constitute another feature of leprosy. A thickened nerve is often accompanied by other signs as a result of damage to the nerve. These may be loss of sensation in the skin and weakness of muscles supplied by the affected nerve. In the absence of these signs, nerve thickening by itself, without sensory loss and/or muscle weakness is often not a reliable sign of leprosy.

Leprosy can be classified on the basis of clinical manifestations and skin smear results. In the classification based on skin smears, patients showing negative smears at all sites are said to have paucibacillary leprosy (PB), while those showing positive smears at any site are said to have multibacillary leprosy (MB).

TREATMENT

Leprosy is curable with a combination of drugs known as multidrug therapy (MDT), as the treatment of leprosy with only one antileprosy drug (monotherapy) will result in development of drug resistance to that drug. The combination of drugs used in the MDT depends on the classification of the disease. Rifampicin, the most important antileprosy medicine, is included in the treatment of both types of leprosy. For the treatment of patients with multibacillary leprosy, WHO recommends a combination of rifampicin, clofazimine and dapsone; for patients with paucibacillary leprosy, MDT uses a combination of rifampicin and dapsone.

Access to treatment

Multidrug therapy (MDT), first recommended by a WHO Expert Committee in 1984, rapidly became the standard treatment of leprosy and has been supplied by WHO free of charge to all endemic countries since 1995.

As a major supplier of very close to 100% of global MDT needs, WHO works closely with donors and manufacturers to plan the manufacture, procurement and shipment of the MDT drugs having the maximum available shelf life, at the time most appropriate for each national programme. WHO also arranges independent laboratory testing of the drugs at the manufacturer’s own expense in order to ensure that the finished WHO product is the best available for national programmes. Such testing is considered essential to maintain the confidence of national programmes in the donated product.

In order to meet emergency requests for MDT, WHO maintains at the donor’s expense, substantial buffer stocks at the manufacturing plant. Currently these buffer stocks are equivalent to around 40% of global annual requirements but vary depending on perceived need. To ensure a rapid response to requests for smaller emergency supplies, WHO maintains additional buffer stocks at its headquarters in Geneva and Regional Office in Manila. Response times from WHO Geneva are typically 48 hours and most despatches are made via courier.

he Global Leprosy Strategy

In 2016 WHO launched the Global Leprosy Strategy 2016–2020: Accelerating towards a leprosy-free world, which aims to reinvigorate efforts to control leprosy and avert disabilities, especially among children still affected by the disease in endemic countries.

The strategy emphasizes the need to sustain expertise and increase the number of skilled leprosy staff, improve the participation of affected persons in leprosy services and reduce visible deformities as well as stigmatization associated with the disease. It also calls for renewed political commitment and enhanced coordination among partners while highlighting the importance of research and improved data collection and analysis.

The key interventions needed to achieve the targets include:

• detecting cases early before visible disabilities occur, with a special focus on children as a way to reduce disabilities and reduce transmission;
• targeting detection among higher risk groups through campaigns in highly endemic areas or communities; and
• improving health care coverage and access for marginalized populations.

Endemic countries need to include other strategic interventions in their national plans to meet the new targets, namely:

• screening all close contacts of persons affected by leprosy;
• promoting a shorter and uniform treatment regimen; and
• incorporating specific interventions against stigmatization and discrimination.

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INTRODUCTION-

Tenosynovitis is inflammation of a tendon and its sheath. Most acute cases of flexor tenosynovitis (FT)—which involves disruption of normal flexor tendon function in the hand—result from infection. However, FT also can develop secondary to acute or chronic inflammation from a noninfectious cause, such as diabetes, overuse, or arthritis.

tenosynovitis is a painful condition affecting the tendons on the thumb side of your wrist. If you have de Quervain’s tenosynovitis, it will probably hurt when you turn your wrist, grasp anything or make a fist.

Although the exact cause of de Quervain’s tenosynovitis isn’t known, any activity that relies on repetitive hand or wrist movement — such as working in the garden, playing golf or racket sports, or lifting your baby — can make it worse.

A tendon is a type of fibrous tissue that connects your muscles to your bones. These tissues help control actions such as running, jumping, grasping, and lifting. Without tendons, you wouldn’t be able to control the movement of your body.

A protective sheath known as the synovium covers tendons. This sheath produces synovial fluid, which keeps the tendon lubricated.

Injury to the tendon may result in the malfunction of the sheath. If this occurs, the sheath may fail to make synovial fluid or may not make enough fluid. This can cause inflammation or swelling of the sheath. This condition is known as tendon sheath inflammation. It’s also sometimes called tenosynovitis.

CAUSES-

Tendon sheath inflammation is typically the result of injury to the tendon or surrounding muscle or bone. It’s not limited to athletes and appears in people who perform a variety of repetitive-motion activities, such as assembly-line work, weeding, and typing. People working in certain jobs appear to have greater risk of it than others, including:

• carpenters
• dentists
• musicians
• office workers

It’s most common in the tendons of the wrist, hands, and feet. Injury can result from:

• repetitive-stress activities
• prolonged physical activities, such as running
• standing in the same position for long periods of time
• sudden sprains and strains

Tendon sheath inflammation can also be due to underlying health conditions. Examples of conditions that can result in this condition include:

• rheumatoid arthritis
• scleroderma
• gout
• diabetes
• reactive arthritis, such as Reiter’s syndrome
• gonorrhea

The cause of the disease can’t be determined in some people. In rare cases, tendon sheath inflammation is due to an infection that resulted from a cut or puncture to the tendon.

SYMPTOM-

Symptoms of tenosynovitis include:

• Pain near the base of your thumb
• Swelling near the base of your thumb
• Difficulty moving your thumb and wrist when you’re doing something that involves grasping or pinching
• A “sticking” or “stop-and-go” sensation in your thumb when moving it

If the condition goes too long without treatment, the pain may spread further into your thumb, back into your forearm or both. Pinching, grasping and other movements of your thumb and wrist aggravate the pain.

When to see a doctor

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Consult your doctor if you’re still having problems with pain or function and you’ve already tried:

• Not using your affected thumb
• Applying cold to the affected area
• Using nonsteroidal anti-inflammatory drugs, such as ibuprofen (Advil, Motrin IB, others) and naproxen (Aleve)

DIAGNOSIS-

Diagnosis of tendon sheath inflammation will require a physical exam of the affected area. Your doctor will check to see if redness and swelling are present. Your doctor may also ask you to move the affected area to see if pain is present.

In some cases, your doctor may order an ultrasound or MRI scan to confirm a diagnosis or rule out other possible causes such as arthritis.

Risk factors

Risk factors for de Quervain’s tenosynovitis include:

• Age. If you’re between the ages of 30 and 50, you have a higher risk of developing de Quervain’s tenosynovitis than do other age groups, including children.
• Sex. The condition is more common in women.
• Being pregnant. The condition may be associated with pregnancy.
• Baby care. Lifting your child repeatedly involves using your thumbs as leverage and may also be associated with the condition.
• Jobs or hobbies that involve repetitive hand and wrist motions. These may contribute to de Quervain’s tenosynovitis.

Complications

Untreated de Quervain’s tenosynovitis might make it hard to use your hand and wrist properly and limit your wrist’s range of motion.

Untreated de Quervain’s tenosynovitis might make it hard to use your hand and wrist properly and limit your wrist’s range of motion.

PREVENTION-

Tendon sheath inflammation is preventable if you avoid excessive movements or motions that are repetitive or forceful. Muscle strengthening around the site of the joint can also help prevent this type of injury, as well as stretching and range-of-motion exercises.

If you cut your hands, wrists, or feet, proper cleaning of the wound will help prevent infection and the possible development of tendon sheath inflammation.

TREATMENT-

The treatment for tendon sheath inflammation focuses on reducing inflammation and pain. One strategy is to rest the affected area and stop the activities that caused the initial injury. Your doctor may recommend the use of a brace or splint to immobilize the affected area.

Applying heat or cold may also help reduce swelling and pain. Other therapies that your doctor may recommend are:

• massage
• stretching the affected area
• transcutaneous electrical nerve stimulation (TENS)
• ultrasound

Your doctor may also prescribe medications for tendon sheath inflammation. Over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil), or injectable corticosteroids are other options.

Injection of the tendon sheath with a steroid is usually successful (in noninfectious cases) and occasionally surgery is necessary to release the tendon sheath about the tendon. If your condition was caused by an infection, your doctor may prescribe antibiotics to fight the infection.

If your condition is due to an underlying health issue, such as rheumatoid arthritis or gout, treatment may also include medications to treat these disorders.

Once the tendon heals, your doctor may recommend exercises or physical therapy to help strengthen the muscle. Strengthening the muscle will help protect the tendon from injury in the future. If you have recurring tendon sheath inflammation, your doctor may recommend surgery to correct the problem.

PHYSICAL THERAPY

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Ice/Heat Packs – Heat can help relax and loosen tight musculature, and ice can be used to help relieve inflammation of the extensor sheath.

Massage – Deep tissue massage at the thenar eminence can help relax tight musculature that causes pain. (See video). Graston Technique of manual soft tissue mobilization along with the eccentric exercise is also helpful. Graston technique includes breaking down fascia restriction, stretching connective tissue and promoting better healing environment.

Stretching – Stretching the thenar eminence muscles into thumb extension and abduction can relax and lengthen this tight musculature that causes pain.

Increasing Strength

• Resisted finger and thumb extension
• Palm up position – for thumb extension and abduction strength
• Thumb up position – for thumb extension and abduction strength
• Resisted radial deviation
• In thumb up position
• Resisted supination
• In thumb up position
• Resisted thumb opposition
• In thumb up position

Improving Range of Motion Stretching as explained above can be used to improve range of motion. Ice/Heat packs can relax tight musculature so that you can attain a bigger range of motion.

Mobilization with movement has shown effectiveness in decreasing the pain, improving range of motion and improving the function of a patient with De-Quervain tenosynovitis. The therapist provides a manual radial glide of the proximal row of carpals, then asked the patient to move her thumb into radial abduction-adduction. Mobilization with movement performed for 3 sets of 10 repetitions and followed by eccentric hammer curl exercise with theraband and high voltage electrical stimulation has shown effective result after 6 months followup,

Kinesio-taping Technique can also be used to decrease pain and improve function.

Therapeutic Ultrasound has also better outcome in pain reduction and healing.

Decreasing Swelling To decrease swelling you can use:

• Thumb splinting
• Corticosteroid injections
• NSAIDs
• Ice/heat packs
• Massage
• Stretching

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INTRODUCTION-

Primary nonspecific ulceration of the small intestine is a unique and characteristic lesion. The ulcer, usually single, occurs in the wall of the ileum or jejunum and is frequently accompanied by an annular ring of fibrous tissue. Perforation, although not common, does occur. The presenting symptoms are generally those of small-bowel obstruction, and the treatment is surgical.

This lesion was first described by Mattew Baillie in 1805, and since then has rarely been described in the medical literature. A review in 1963¹ produced only 170 case reports.

During the summer of 1964, a few scattered cases were reported describing a similar small intestinal lesion occurring in patients being treated with various formulations of potassium chloride or a diuretic for oral administration. In September and November 1964 two publications appeared, one by Lindholmer, Nyman, and Raf from Stockholm, and the other by Baker, Schrader, and Hitchcock from Minneapolis.

Ulcers of the small and large intestine are rare, yet they are responsible for a broad spectrum of disease. Ulcers can occur singly, as in solitary rectal ulcer syndrome, or diffusely, as in enteropathy-associated T-cell lymphoma. Clinical presentations vary widely with location and degree of intestinal involvement, ranging from anemia and hypoproteinemia to abdominal pain, hemorrhage, obstruction, and perforation.

This chapter is divided into two sections. The first section covers isolated intestinal ulcers, including nonspecific solitary ulcers of the small intestine, solitary rectal ulcer syndrome, stercoral ulcers, and ulcerations induced by nonsteroidal anti-inflammatory drugs (NSAIDs). The second section covers syndromes of diffuse intestinal ulceration, including ulcerative enteritis, refractory celiac disease types I and II, and enteropathy-associated T-cell lymphoma (EATL).

Because of the length and relative inaccessibility of the small intestine, diagnosis of small intestinal ulcerative diseases has been challenging. Currently, however, video-capsule endoscopy enables the entire small intestine to be viewed with clarity, and double-balloon enteroscopy offers the opportunity to evaluate the small intestine visually, obtain biopsy specimens, and provide a variety of endoscopic therapies.

SYMPTOM-

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Patients with nonspecific ulcers of the small intestine can present with acute or chronic gastrointestinal bleeding, symptoms of small bowel obstruction, abdominal pain, or perforation. Symptoms may be present from a few days to many years before diagnosis.

most presenting in the fifth and sixth decades of life; no gender predominance was found. The most common presenting symptom was intermittent small bowel obstruction (63%). Physical findings ranged from nonspecific abdominal tenderness and distention to an acute abdomen resulting from intestinal perforation. Laboratory evaluation was notable only for anemia in one half of the patients. Radiologic studies localized the ulcer in a minority of patients.

TREATMENT-

All patients were treated with segmental resection; only two patients had recurrent ulceration, 2 and 10 years after initial diagnosis and resection. Ischemia, central nervous system disease, infection, trauma, and hormonal influences all have been put forth as possible causes of primary nonspecific ulcerations, but the cause or causes still remains unknown. In the absence of more recent reviews, it is impossible to determine the current incidence rate of these ulcer.

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INTRODUCTION-

Gastritis is an inflammation of the protective lining of the stomach. Acute gastritis involves sudden, severe inflammation. Chronic gastritis involves long-term inflammation that can last for years if it’s left untreated.

Erosive gastritis is a less common form of the condition. It typically doesn’t cause much inflammation, but can lead to bleeding and ulcers in the lining of the stomach.

Gastritis is an inflammation, irritation, or erosion of the lining of the stomach. It can occur suddenly (acute) or gradually (chronic).

Gastritis is a general term for a group of conditions with one thing in common: inflammation of the lining of the stomach. The inflammation of gastritis is most often the result of infection with the same bacterium that causes most stomach ulcers. Regular use of certain pain relievers and drinking too much alcohol also can contribute to gastritis.

Gastritis may occur suddenly (acute gastritis), or appear slowly over time (chronic gastritis). In some cases, gastritis can lead to ulcers and an increased risk of stomach cancer. For most people, however, gastritis isn’t serious and improves quickly with treatment.

CAUSES-

Weakness in your stomach lining allows digestive juices to damage and inflame it, causing gastritis. Having a thin or damaged stomach lining raises your risk for gastritis.

A gastrointestinal bacterial infection can also cause gastritis. The most common bacterial infection that causes it is Helicobacter pylori. It’s a bacterium that infects the lining of the stomach. The infection is usually passed from person to person, but can also be transmitted through contaminated food or water.

Certain conditions and activities may increase your risk for developing gastritis. Other risk factors include:

• extreme alcohol consumption
• routine use of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and aspirin
• cocaine use
• age, because the stomach lining thins naturally with age
• tobacco use

Other less common risk factors include:

• stress caused by severe injury, illness, or surgery
• autoimmune disorders
• digestive disorders like Crohn’s disease
• viral infections

Gastritis can be caused by irritation due to excessive alcohol use, chronic vomiting, stress, or the use of certain medications such as aspirin or other anti-inflammatory drugs. It may also be caused by any of the following:

• Helicobacter pylori (H. pylori): A bacteria that lives in the mucous lining of the stomach; without treatment, the infection can lead to ulcers, and in some people, stomach cancer.
• Bile reflux: A backflow of bile into the stomach from the bile tract (that connects to the liver and gallbladder)
• Infections caused by bacteria and viruses

If gastritis is left untreated, it can lead to a severe loss of blood and may increase the risk of developing stomach cancer

SYMPTOM-

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Gastritis doesn’t cause noticeable symptoms in everyone. The most common symptoms are:

• nausea
• vomiting
• a feeling of fullness in your upper abdomen, particularly after eating
• indigestion

Nausea or recurrent upset stomach Abdominal bloatingAbdominal pain Vomiting Indigestion Burning or gnawing feeling in the stomach between meals or at night Hiccups

If you have erosive gastritis, you might experience different symptoms, including:

• black, tarry stool
• vomiting blood or material that looks like coffee grounds

When to see a doctor

Nearly everyone has had a bout of indigestion and stomach irritation. Most cases of indigestion are short-lived and don’t require medical care. See your doctor if you have signs and symptoms of gastritis for a week or longer. Tell your doctor if your stomach discomfort occurs after taking prescription or over-the-counter drugs, especially aspirin or other pain relievers.

If you are vomiting blood, have blood in your stools or have stools that appear black, see your doctor right away to determine the cause.

DIAGNOSIS-

To diagnose gastritis, your doctor will review your personal and family medical history, perform a thorough physical evaluation, and may recommend any of the following tests:

• Upper endoscopy. An endoscope, a thin tube containing a tiny camera, is inserted through your mouth and down into your stomach to look at the stomach lining. The doctor will check for inflammation and may perform a biopsy, a procedure in which a tiny sample of tissue is removed and then sent to a laboratory for analysis.
• Blood tests. The doctor may perform various blood tests, such as checking your red blood cell count to determine whether you have anemia, which means that you do not have enough red blood cells. He or she can also screen for H. pylori infection and pernicious anemia with blood tests.
• Fecal occult blood test (stool test). This test checks for the presence of blood in your stool, a possible sign of gastritis.

Risk factors

Factors that increase your risk of gastritis include:

• Bacterial infection. Although infection with Helicobacter pylori is among the most common worldwide human infections, only some people with the infection develop gastritis or other upper gastrointestinal disorders. Doctors believe vulnerability to the bacterium could be inherited or could be caused by lifestyle choices, such as smoking and diet.
• Regular use of pain relievers. Common pain relievers — such as aspirin, ibuprofen (Advil, Motrin IB, others) and naproxen (Aleve, Anaprox) — can cause both acute gastritis and chronic gastritis. Using these pain relievers regularly or taking too much of these drugs may reduce a key substance that helps preserve the protective lining of your stomach.
• Older age. Older adults have an increased risk of gastritis because the stomach lining tends to thin with age and because older adults are more likely to have H. pylori infection or autoimmune disorders than younger people are.
• Excessive alcohol use. Alcohol can irritate and erode your stomach lining, which makes your stomach more vulnerable to digestive juices. Excessive alcohol use is more likely to cause acute gastritis.
• Stress. Severe stress due to major surgery, injury, burns or severe infections can cause acute gastritis.

Your own body attacking cells in your stomach. Called autoimmune gastritis, this type of gastritis occurs when your body attacks the cells that make up your stomach lining. This reaction can wear away at your stomach’s protective barrier.

Autoimmune gastritis is more common in people with other autoimmune disorders, including Hashimoto’s disease and type 1 diabetes. Autoimmune gastritis can also be associated with vitamin B-12 deficiency.

Other diseases and conditions. Gastritis may be associated with other medical conditions, including HIV/AIDS, Crohn’s disease and parasitic infections.

Complications

Left untreated, gastritis may lead to stomach ulcers and stomach bleeding. Rarely, some forms of chronic gastritis may increase your risk of stomach cancer, especially if you have extensive thinning of the stomach lining and changes in the lining’s cells.

Tell your doctor if your signs and symptoms aren’t improving despite treatment for gastritis.

Prevention

Preventing H. pylori infection

It’s not clear how H. pylori spreads, but there’s some evidence that it could be transmitted from person to person or through contaminated food and water. You can take steps to protect yourself from infections, such as H. pylori, by frequently washing your hands with soap and water and by eating foods that have been cooked completely.

TREATMENT-

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The treatment for gastritis depends on the cause of the condition. If you have gastritis caused by NSAIDs or other drugs, avoiding those drugs may be enough to relieve your symptoms. Gastritis as a result of H. pylori is routinely treated with antibiotics that kill the bacteria.

In addition to antibiotics, several other types of medication are used to treat gastritis:

Proton pump inhibitors

Medications called proton pump inhibitors work by blocking cells that create stomach acid. Common proton pump inhibitors include:

• omeprazole (Prilosec)
• lansoprazole (Prevacid)
• esomeprazole (Nexium)

However, long-term use of these medications, especially at high doses, can lead to an increased risk of spine, hip, and wrist fractures. It can also lead to increased risk of renal failure, dementia, and nutrient deficiencies.

Speak to your doctor before beginning one of these medications to create a treatment plan that is right for you.

Acid reducing medications

Medications that reduce the amount of acid your stomach produces include:

• famotidine (Pepcid)

By lowering the amount of acid that’s released into your digestive tract, these medications relieve the pain of gastritis and allow your stomach lining to heal.

Antacids

Your doctor may recommend that you use antacids for rapid relief of gastritis pain. These medications can neutralize the acid in your stomach.

Some antacids may cause diarrhea or constipation, so talk to your doctor if you experience any of these side effects.

Probiotics

Probiotics have been shown to help replenish digestive flora and heal gastric ulcers. However, there’s no evidence that they have any impact on acid secretion. There are currently no guidelines supporting the use of probiotics in ulcer management.

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INTRODUCTION-

neumoconiosis is one of a group of interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs.

Because you are likely to encounter these dusts only in the workplace, pneumoconiosis is called an occupational lung disease.

Pneumoconiosis usually take years to develop. Because your lungs can’t get rid of all these dust particles, they cause inflammation in your lungs that can eventually lead to scar tissue.

Pneumoconiosis is a lung disease that affects miners, builders, and other workers who breathe in certain kinds of dust on the job.

Over time, the dust gathers in your lungs, and you may find it hard to get enough air.

You may hear other people call pneumoconiosis “black lung disease” or “popcorn lung.” There’s no cure, but treatments can make it easier for you to breathe and go about your regular activities

TYPE-

The disease appears in different forms, depending on the type of dust you inhale. One of the most common forms is black lung disease, also known as miner’s lung. It’s caused by breathing in coal dust. Another is brown lung, which comes from working around dust from cotton or other fibers. Other types of dusts that can cause pneumoconiosis include silica and asbestos. Diacetyl, the compound used to give movie popcorn its buttery flavor, also can lead to the disease. This is known as popcorn lung. 

Pneumoconiosis can be simple or complicated. Simple pneumoconiosis causes a small amount of scar tissue. The tissue may appear on an X-ray as round, thickened areas called nodules. This type of the disease is sometimes called coal worker pneumoconiosis, or CWP. Complicated pneumoconiosis is known as progressive massive fibrosis, or PMF. Fibrosis means that a lot of scarring is present in the lungs.

For either simple or complicated pneumoconiosis, the damage causes the loss of blood vessels and air sacs in your lungs. The tissues that surround your air sacs and air passages become thick and stiff from scarring. Breathing becomes increasingly difficult. This condition is called interstitial lung disease.

Types of dust that may cause pneumoconiosis include:

• coal dust from drilling into rock when mining
• asbestos fibers, often from insulation or roofing
• cotton dust, usually from textile manufacturing
• silica, often from sand and rock at a foundry
• beryllium, a lightweight metal used in electronics and aerospace industries
• aluminum oxide, cobalt, and talc

CAUSES-

Pneumoconiosis doesn’t show up overnight. It happens after you’ve spent years in a place where you breathe in fine mineral or chemical dust, such as silica, coal dust, or asbestos. When the specks of dust build up in your lungs, the immune system — your body’s defense against germs — swings into action. It sees the dust particles as invaders and tries to destroy them.

Your lung tissue often gets inflamed during this process. As a result, scar tissue may form in your lungs, just as it would after an injury. Since scar tissue is less stretchy than regular lung tissue, it may become harder for you to take a full, deep breath.

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SYMPTOM-

Symptoms of pneumoconiosis often depend on how severe the disease is. Simple CWP may have no or few symptoms and show up only on an X-ray. PMF may cause mild to severe difficulty breathing. Symptoms may include:

• Cough
• Lots of phlegm
• Shortness of breath

DIAGNOSIS-

Many employers offer a routine check for lung diseases, such as a chest X-ray or breathing test, if employees are exposed to harmful dust in the workplace.

If a person has symptoms of pneumoconiosis, a doctor will complete a physical examination and ask about medical history, including whether the person has been exposed to dust particles. A more detailed examination may be carried out by a doctor specializing in the lungs, known as a pulmonologist.

A chest X-ray or CT scan can reveal inflammation, excess fluid, or scarring in the lungs. A test may also be done to check how much oxygen is reaching the blood from the lungs. Sometimes a biopsy may be needed to rule out other diseases.

RISK FACTOR-

There are clear risk factors for pneumoconiosis and a range of jobs that are more likely to bring people into contact with harmful dust.

Some examples of occupations that may bring workers into contact with dust particles that cause pneumoconiosis include:

• plumbers, roofers, and builders who work with asbestos
• coal miners
• textile workers

Working with dust particles does not mean that a person will develop pneumoconiosis. Many steps can be taken to protect workers.

The Occupational Safety and Health Act (OSHA) is a law that instructs employers to make sure that their workplace is “free from recognized hazards,” which includes exposure to harmful dust.

Steps that can be taken to help prevent pneumoconiosis in the workplace include:

• keeping levels of dust down
• ventilating a workspace properly
• providing regular medical examinations
• making sure workers wear a face mask and protective clothing
• washing hands and face before eating or drinking

Being exposed to high levels of dust or working in unsafe conditions for a long time will increase the risk of pneumoconiosis. Smoking can also make someone more vulnerable to developing the condition.

Who’s at risk

Being exposed to dust that can cause  pneumoconiosis, in an everyday setting, is not enough to cause the disease. But you could be at risk if you’ve worked around or directly with these dusts. Studies show that about 16 percent of American coal miners may eventually develop interstitial fibrosis from coal dust. Other dust exposures that may put you at risk include working with asbestos fibers or silica dust. Your risk may also be increased by:

• Smoking
• Being exposed to a high level of dust
• Being exposed for a long time

Complications

The main complication is when simple pneumoconiosis progresses to PMF. These are other possible complications:

• Progressive respiratory failure
• Lung cancer
• Tuberculosis (but this is now rare)
• Heart failure caused by pressure inside the lungs

Prevention

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Prevention is important because the disease cannot be treated or reversed. The Occupational Safety and Health Administration sets standard prevention rules for workers at risk for pneumoconiosis. These are common prevention measures:

• Wearing a mask
• Washing areas of skin that come in contact with dust
• Safe removal of dust from clothing
• Washing your face and hands thoroughly before eating, drinking, or taking any medications
• Not smoking
• Letting your doctor and your employer know about any symptoms of pneumoconiosis
• Getting regular chest X-rays and physical exams

TREATMENT –

There isn’t any treatment that can remove the specks of mineral dust in your lungs. Instead, most treatments try to keep your lungs working.

You may need to stop doing the work that led to your pneumoconiosis. If you’re a smoker, your doctor will recommend you quit to improve your lung health.

Your doctor may prescribe an inhaled medication such as a bronchodilator or corticosteroid. Bronchodilators open up your airways if you have trouble breathing, while corticosteroids can curb airway inflammation.

If your tests show low levels of oxygen in your blood, your doctor may suggest you get “supplemental oxygen therapy.” In this treatment, you breathe in extra oxygen through a mask or prongs in your nose. The oxygen you get this way is stored in a tank or some other kind of device. Some people use this treatment throughout the day, while others may need it only

There isn’t any treatment that can remove the specks of mineral dust in your lungs. Instead, most treatments try to keep your lungs working.

You may need to stop doing the work that led to your pneumoconiosis. If you’re a smoker, your doctor will recommend you quit to improve your lung health.

Your doctor may prescribe an inhaled medication such as a bronchodilator or corticosteroid. Bronchodilators open up your airways if you have trouble breathing, while corticosteroids can curb airway inflammation.

If your tests show low levels of oxygen in your blood, your doctor may suggest you get “supplemental oxygen therapy.” In this treatment, you breathe in extra oxygen through a mask or prongs in your nose. The oxygen you get this way is stored in a tank or some other kind of device. Some people use this treatment throughout the day, while others may need it only

If your tests show low levels of oxygen in your blood, your doctor may suggest you get “supplemental oxygen therapy.” In this treatment, you breathe in extra oxygen through a mask or prongs in your nose. The oxygen you get this way is stored in a tank or some other kind of device. Some people use this treatment throughout the day, while others may need it only at night.

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