Brain Diseases

Viral Hepatitis

2012-03-26T09:47:00.002-07:00

What is viral hepatitis?
Hepatitis means inflammation of the liver. Many illnesses and conditions can cause inflammation of the liver, for example, drugs, alcohol, chemicals, and autoimmune diseases. Many viruses, for example, the virus of mononucleosis and the cytomegalovirus can inflame the liver. Most viruses, however, do not primarily attack the liver; the liver is just one of several organs that the viruses affect. When doctors speak of viral hepatitis, they usually are referring to hepatitis caused by a few specific viruses that primarily attack the liver. There are several hepatitis viruses; they have been named types A, B, C, D, E, F (not confirmed), and G. As our knowledge of hepatitis viruses grows, it is likely that this alphabetical list will become longer. The most common hepatitis viruses are types A, B, and C.
The liver is located in the upper right hand side of the abdomen, mostly behind the rib cage. The liver of an adult normally weighs close to three pounds. The liver performs the following vital functions:

The liver helps purify the blood by changing harmful chemicals into harmless ones. The source of these chemicals can be external, such as medications or alcohol, or internal, such as ammonia or bilirubin. Typically, these harmful chemicals are broken down into smaller chemicals or attached to other chemicals that then are eliminated from the body in the urine or stool.
The liver produces many important substances, especially proteins that are necessary for good health. For example, it produces albumin, the protein building block of the body, as well as the proteins that cause blood to clot properly.
The liver stores many sugars, fats and vitamins until they are needed elsewhere in the body.
The liver builds smaller chemicals into larger, more complicated chemicals that are needed elsewhere in the body. An example of this type of function is the manufacture of cholesterol.

When the liver is inflamed, it does not perform these functions well, which brings about many of the symptoms, signs, and problems associated with hepatitis.

What are the common types of viral hepatitis?
Hepatitis A
Viral hepatitis A (HAV) accounts for about 150,000 of the 500,000-600,000 new cases of viral hepatitis that occur each year in the United States. The hepatitis caused by HAV is an acute illness (acute viral hepatitis) that never becomes chronic. At one time, hepatitis A was referred to as "infectious hepatitis" because it could be spread from person to person like other viral infections. Infection with hepatitis A virus can be spread through the ingestion of food or water, especially where unsanitary conditions allow water or food to become contaminated by human waste containing hepatitis A (the fecal-oral mode of transmission). Hepatitis A typically is spread among household members and close contacts through the passage of oral secretions (intimate kissing) or stool (poor hand washing). It also is common to have infection spread to customers in restaurants and among children and workers in day care centers if hand washing and sanitary precautions are not observed.
Hepatitis B
There are 200,000-300,000 new cases of viral hepatitis B (HBV) infection each year in the United States. Type B hepatitis was at one time referred to as "serum hepatitis," because it was thought that the only way hepatitis B virus (HBV) could spread was through blood or serum (the liquid portion of blood) containing the virus. It is now known that hepatitis B can spread by sexual contact, the transfer of blood or serum through shared needles in drug abusers, accidental needle sticks with needles contaminated with infected blood, blood transfusions, hemodialysis, and by infected mothers to their newborns. The infection also can be spread by tattooing, body piercing, and sharing razors and toothbrushes (if there is contamination with infected blood). About 6-10% of patients with hepatitis B develop chronic HBV infection (infection lasting at least six months and often years to decades) and can infect others as long as they remain infected. Patients with chronic hepatitis B infection also are at risk of developing cirrhosis, liver failure and liver cancer. It is estimated that there are 1.2 million people in the United States and 200-300 million people world-wide who suffer with chronic hepatitis B infection. article.
Hepatitis C
There are about 150,000 new cases of hepatitis C each year. Type C hepatitis was previously referred to as "non-A, non-B hepatitis," because the causative virus had not been identified, but it was known to be neither hepatitis A nor hepatitis B. The hepatitis C virus (HCV) usually is spread by shared needles among drug abusers, blood transfusion, hemodialysis, and needle sticks. Approximately 90% of transfusion-associated hepatitis is caused by hepatitis C. Transmission of the virus by sexual contact has been reported, but is considered rare. An estimated 50-70% of patients with acute hepatitis C infection develop chronic HCV infection. Patients with chronic hepatitis C infection can continue to infect others. Patients with chronic hepatitis C infection are at risk for developing cirrhosis, liver failure, and liver cancer. It is estimated that there are about 3.5 million people with chronic hepatitis C infection in the United States.
Types D, E, F, and G Hepatitis
There also are viral hepatitis types D, E, F (not confirmed yet), and G. The most important of these at present is the hepatitis D virus (HDV), also known as the delta virus or agent. It is a small virus that requires concomitant infection with hepatitis B to survive. HDV cannot survive on its own because it requires a protein that the hepatitis B virus makes (the envelope protein, also called surface antigen) to enable it to infect liver cells. The ways in which hepatitis D is spread are by shared needles among drug abusers, contaminated blood, and by sexual contact, essentially the same ways as for hepatitis B.
Patients who already have chronic hepatitis B infection can acquire delta virus infection at the same time as they acquire the hepatitis B infection or, alternatively, on top of a chronic hepatitis B infection. Patients with chronic hepatitis due to hepatitis B and hepatitis D viruses develop cirrhosis (severe liver scarring) rapidly. Moreover, the combination of delta and B virus infection is very difficult to treat.

Who is at risk for viral hepatitis?
People who are most at risk for developing viral hepatitis are workers in the health care professions, people with multiple sexual partners, intravenous drug users, and hemophiliacs who receive blood clotting factors. Blood transfusion, once a common means of spreading viral hepatitis, now is a rare cause of hepatitis. Viral hepatitis is generally thought to be as much as ten times more common among lower socioeconomic and poorly educated individuals. About one third of all cases of hepatitis come from an unknown or unidentifiable source. This means that you don't have to be in a high risk group in order to be infected with a hepatitis virus.
What are the symptoms and signs of viral hepatitis?
The period of time between exposure to hepatitis and the onset of the illness is called the incubation period. The incubation period varies depending on the specific hepatitis virus. Hepatitis A has an incubation period of about 15-45 days; hepatitis B from 45-160 days, and hepatitis C from 2 weeks to 6 months.
Many patients infected with hepatitis A, B, and C have few or no symptoms of illness. For those who do develop symptoms of viral hepatitis, the most common are flu- like symptoms including:

loss of appetite
nausea
vomiting
fever
weakness
tiredness
aching in the abdomen

Less common symptoms include:

dark urine
light-colored stools
fever
jaundice (a yellow appearance to the skin and white portion of the eyes)

What is the prognosis of viral hepatitis?
The prognosis of viral hepatitis for most patients is good. Symptoms of viral hepatitis such as fatigue, poor appetite, nausea, and jaundice usually subside in several weeks to months, without any specific treatment. In fact, virtually all patients with acute infection with hepatitis A and most adults (greater than 95%) with acute hepatitis B recover completely. Complete recovery from viral hepatitis means

the hepatitis virus has been completely eliminated from the liver by the body's immune system,
the inflammation in the liver subsides,
the patient develops immunity to future infection with the same virus, and
the patient cannot transmit the infection to others.

Unfortunately, not all patients with viral hepatitis infections recover completely. Five percent of patients with acute hepatitis B infection and 80% of patients with acute hepatitis C infection develop chronic hepatitis.
Acute viral hepatitis needs no specific treatment. Patients who develop chronic infection have chronic viral hepatitis and often need treatment to prevent further liver damage.
What is acute fulminant hepatitis?
Rarely, individuals with acute infections with hepatitis A and hepatitis B develop severe inflammation, and the liver fails (acute fulminant hepatitis). These patients are extremely ill with the symptoms of acute hepatitis already described and the additional problems of confusion or coma (due to the liver's failure to detoxify chemicals) and bruising or bleeding (due to a lack of blood clotting factors). In fact, up to 80% of people with acute fulminant hepatitis can die within days to weeks; therefore, it is fortunate that acute fulminant hepatitis is rare. For example, less than 0.5% of adults with acute infection with hepatitis B will develop acute fulminant hepatitis.

What is chronic viral hepatitis?
Patients infected with hepatitis B and hepatitis C can develop chronic hepatitis. Doctors define chronic hepatitis as hepatitis that lasts longer than 6 months. In chronic hepatitis, the viruses live and multiply in the liver for years or decades. For unknown reasons, these patients' immune systems are unable to eradicate the viruses. The viruses cause chronic inflammation of the liver. Chronic hepatitis can lead to the development over time of extensive liver scarring (cirrhosis), liver failure, and liver cancer. Liver failure from chronic hepatitis C infection is the most common reason for liver transplantation in the United States. Patients with chronic viral hepatitis can transmit the infection to others.
How is viral hepatitis diagnosed?
Diagnosis of viral hepatitis is based on symptoms, physical findings as well as blood tests for liver enzymes, viral antibodies, and viral genetic materials.
Symptoms and physical findings
Diagnosis of acute viral hepatitis often is easy, but diagnosis of chronic hepatitis can be difficult. When a patient reports symptoms of fatigue, nausea, abdominal pain, darkening of urine, and then develops jaundice, the diagnosis of acute viral hepatitis is likely and can be confirmed by blood tests. On the other hand, patients with chronic hepatitis due to hepatitis B and hepatitis C often have no symptoms or only mild nonspecific symptoms such as chronic fatigue. Typically, these patients do not have jaundice until the liver damage is far advanced. Therefore, these patients can remain undiagnosed for years to decades.
Blood tests
There are three types of blood tests for evaluating patients with hepatitis: liver enzymes, antibodies to the hepatitis viruses, and viral proteins or genetic material (viral DNA or RNA).
Liver enzymes. Among the most sensitive and widely used blood tests for evaluating patients with hepatitis are the liver enzymes, called aminotransferases. They include aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT). These enzymes normally are contained within liver cells. If the liver is injured (as in viral hepatitis), the liver cells spill the enzymes into the blood, raising the enzyme levels in the blood and signaling that the liver is damaged.
The normal range of values for AST is from 5 to 40 units per liter of serum (the liquid part of the blood). The normal range of values for ALT is from 7 to 56 units per liter of serum. Patients with acute viral hepatitis (for example, due to hepatitis A or hepatitis B) can develop very high AST and ALT levels (sometimes in the thousands of units per liter range). These high AST and ALT levels will become normal in several weeks or months as the patients recover completely from their acute hepatitis. In contrast, patients with chronic hepatitis B and hepatitis C infection typically have only mildly elevated AST and ALT levels, but these abnormalities can last years or decades. Since most patients with chronic hepatitis are asymptomatic (no jaundice or nausea), their mildly abnormal liver enzymes are often unexpectedly encountered on routine blood screening tests during yearly physicals or insurance physicals.
Elevated blood levels of AST and ALT only means that the liver is inflamed, and elevations can be caused by many agents other than hepatitis viruses, such as medications, alcohol, bacteria, fungus, etc. In order to prove that a hepatitis virus is responsible for the elevations, blood must be tested for antibodies to each of the hepatitis viruses as well as for their genetic material.
Viral antibodies. Antibodies are proteins produced by white blood cells that attack invaders such as bacteria and viruses. Antibodies against the hepatitis A, B, and C viruses usually can be detected in the blood within weeks of infection, and the antibodies remain detectable in the blood for decades thereafter. Blood tests for the antibodies can be helpful in diagnosing both acute and chronic viral hepatitis.
In acute viral hepatitis, antibodies not only help to eradicate the virus, but they also protect the patient from future infections by the same virus, that is the patient develops immunity. In chronic hepatitis, however, antibodies and the rest of the immune system are unable to eradicate the virus. The viruses continue to multiply and are released from the liver cells into the blood where their presence can be determined by measuring the viral proteins and genetic material. Therefore in chronic hepatitis, both antibodies to the viruses and viral proteins and genetic material can be detected in the blood.
Examples of tests for viral antibodies are:

anti-HAV (hepatitis A antibody)
antibody to hepatitis B core, an antibody directed against the inner core (nucleus) of the virus (core antigen)
antibody to hepatitis B surface, an antibody directed against the outer surface envelope of the virus (surface antigen)
antibody to hepatitis B e, an antibody directed against the genetic material of the virus (e antigen)
hepatitis C antibody-antibody against the C virus

Viral proteins and genetic material. Examples of tests for viral proteins and genetic material are:

hepatitis B surface antigen
hepatitis B DNA
hepatitis B e antigen
hepatitis C RNA

Other tests. Obstruction of the bile ducts, from either gallstones or cancer, occasionally can mimic acute viral hepatitis. Ultrasound testing can be used to exclude the possibility of gallstones or cancer.

How is viral hepatitis treated?
Treatment of acute viral hepatitis and chronic viral hepatitis are different. Treatment of acute viral hepatitis involves relieving symptoms and maintaining adequate intake of fluids. Treatment of chronic viral hepatitis involves medications to eradicate the virus and taking measures to prevent further liver damage.
Acute hepatitis
In patients with acute viral hepatitis, the initial treatment consists of relieving the symptoms of nausea, vomiting, and abdominal pain. Careful attention should be given to medications which can have adverse effects in patients with abnormal liver function. Only those medications that are considered necessary should be administered since the impaired liver is not able to eliminate drugs normally, and drugs may accumulate in the blood and reach toxic levels. In addition, sedatives and "tranquilizers" are avoided because they may accentuate the effects of liver failure on the brain and cause lethargy and coma. The patient must abstain from drinking alcohol since alcohol is toxic to the liver. It occasionally is necessary to provide intravenous fluids to prevent dehydration caused by vomiting. Patients with severe nausea and/or vomiting may need to be hospitalized for treatment and intravenous fluids.
Chronic hepatitis
Treatment of chronic infection with hepatitis B and hepatitis C usually involves medication or combinations of medications to eradicate the virus. Doctors believe that in properly selected patients, successful eradication of the viruses can stop progressive damage to the liver and prevent the development of cirrhosis, liver failure, and liver cancer. Alcohol aggravates liver damage in chronic hepatitis, and can cause more rapid progression to cirrhosis. Therefore, patients with chronic hepatitis should stop drinking alcohol. Smoking cigarettes also can aggravate liver disease and should be stopped.
Medications for chronic hepatitis C infection include:

injectable interferon
oral ribavirin

Medications for chronic hepatitis B infection include:

injectable interferon
oral lamivudine (Epivir)
oral adefovir (Hepsera)
oral entecavir (Baraclude)

Decisions regarding treatment of chronic hepatitis can be complex, and should be directed by gastroenterologists or hepatologists (doctors specially trained in treating diseases of the liver) for several reasons including:

The diagnosis of chronic viral hepatitis may not be straightforward. Sometimes a liver biopsy may have to be performed for confirmation of liver damage. Doctors experienced in managing chronic liver diseases must weigh the risk of liver biopsy against the potential benefits of the biopsy.
Not all patients with chronic viral hepatitis are candidates for treatment. Some patients need no treatment (since some patients with chronic hepatitis B and C do not develop progressive liver damage or liver cancer).
Medications for chronic infection with hepatitis B and hepatitis C are not always effective. Prolonged treatment (6 months to years) often is necessary. Even with prolonged treatment, rates of successful treatment (defined as complete and lasting eradication of the virus) often are low (usually less than 80% and often around 50%).
Some of the medications such as interferon and ribavirin can have serious side effects, and doses may have to be reduced.
There are several different strains of hepatitis C viruses with differing susceptibilities to medications. For example, hepatitis C type 3 is more likely to respond to interferon injections and ribavirin than type 1. Certain hepatitis B strains are resistant to lamivudine but respond to adefovir or entecavir.

Please read the hepatitis B and hepatitis C articles for more details in diagnosis and treatment.
Fulminant hepatitis. Treatment of acute fulminant hepatitis should be done in centers that can perform liver transplantation since acute fulminant hepatitis has a high mortality without liver transplantation.

How is viral hepatitis prevented?
Prevention of hepatitis involves measures to avoid exposure to the viruses, using immunoglobulin in the event of exposure, and vaccines. Administration of immunoglobulin is called passive protection because antibodies from patients who have had viral hepatitis are given to the patient. Vaccination is called active protection because killed viruses or noninfective components of viruses are given to stimulate the body to produce its own antibodies.
Avoidance if exposure to viruses
Prevention of viral hepatitis, like any other illness, is preferable to reliance upon treatment. Taking precautions to prevent exposure to another individual's blood (exposure to dirty needles), semen (unprotected sex), and other bodily waste (stool) will help prevent the spread of these viruses.
Use of immunoglobulins
Immune serum globulin (ISG) is human serum that contains antibodies to hepatitis A. ISG can be administered to prevent infection in individuals who have been exposed to hepatitis A. ISG works immediately upon administration, and the duration of protection is several months. ISG usually is given to travelers to regions of the world where there are high rates of hepatitis A infection and to close or household contacts of patients with hepatitis A. ISG is safe with few side effects.
Hepatitis B immune globulin or HBIG (BayHep B), is human serum that contains antibodies to hepatitis B. HBIG is made from plasma (a blood product) that is known to contain a high concentration of antibodies to the hepatitis B surface antigen. If given within 10 days of exposure to the virus, HBIG almost always is successful in preventing infection. Even if given a bit later, however, HBIG may lessen the severity of HBV infection. The protection against hepatitis B lasts for about three weeks after the HBIG is given. HBIG also is given at birth to infants born to mothers known to have hepatitis B infection. In addition, HBIG is given to individuals exposed to HBV because of sexual contact or to healthcare workers accidentally stuck by a needle known to be contaminated with blood from an infected person.
Vaccination
Hepatitis A. Two hepatitis A vaccines are available in the US, Havrix and Vaqta. Both contain inactive (killed) hepatitis A virus. For adults, two doses of the vaccine are recommended. After the first dose, protective antibodies develop in 70% of vaccine recipients in 2 weeks and more than 95% of recipients in 4 weeks. After two doses of the hepatitis A vaccine, immunity against hepatitis A infection is believed to last for many years.
Individuals at increased risk for acquiring hepatitis A and individuals with chronic liver disease (e.g., cirrhosis or chronic hepatitis C) should be vaccinated. Although individuals with chronic liver disease are not at increased risk for acquiring hepatitis A, they can develop serious (sometimes fatal) liver failure if infected with hepatitis A and, thus, they should be vaccinated.
Individuals at increased risk of acquiring hepatitis A are:

Travelers to countries where hepatitis A is common
Men who have sex with men
Illegal drug users (either injection or non-injection drug use)
Researchers working with hepatitis A or primates that are susceptible to infection with hepatitis A
Patients with clotting factor disorders who are receiving clotting factor concentrates that can transmit hepatitis A

Some local health authorities or private companies may require hepatitis A vaccination for food handlers.
Because protective antibodies take weeks to develop, travelers to countries where hepatitis A is common should be vaccinated at least 4 weeks before departure. The Centers for Disease Control (CDC) recommends immunoglobulin be given in addition to vaccination if departure is prior to 4 weeks. Immunoglobulin provides quicker protection than the vaccines, but the protection is short-lived.
Hepatitis B
For active vaccination, a harmless hepatitis B antigen is given to stimulate the body's immune system to produce protective antibodies against the surface antigen of hepatitis B. Vaccines that are currently available in the United States are made (synthesized) using recombinant DNA technology (joining DNA segments). These recombinant hepatitis B vaccines (Energix-B and Recombivax-HB) are constructed to contain only that part of the surface antigen that is very potent in stimulating the immune system to produce antibodies. The vaccine contains no viral component other than the surface antigen and is not infectious. Hepatitis B vaccines should be given in three doses with the second dose 1-2 months after the first dose, and the third dose 4-6 months after the first dose. For the best results, the vaccinations should be given in the deltoid (shoulder) muscles and not in the buttocks.
Hepatitis B vaccines are 95% effective. Five percent of vaccinated individuals will fail to develop the necessary antibodies for immunity after the three doses. Patients with weakened immunity (such as HIV infection), elderly patients, and patients undergoing kidney hemodialysis are more likely to fail to respond to the vaccines.
Hepatitis B vaccine is recommended for:

All infants
Adolescents under 18 years of age who did not receive hepatitis B vaccine as infants
People occupationally exposed to blood or body fluids
Residents and staff of institutions for the developmentally disabled
Patients receiving kidney hemodialysis
Hemophiliacs and other patients receiving clotting factor concentrates
Household contacts and sexual partners of patients infected with hepatitis B chronically
Travelers who will spend more than 6 months in regions with high rates of hepatitis B infection
Injection drug users and their sexual partners
Men who have sex with men, men or women with multiple sex partners, or recent infection with a sexually transmitted infection
Inmates of long-term correctional facilities

All pregnant women should have a blood test for the antibody to hepatitis B surface antigen. Women who test positive for hepatitis B risk transmitting the virus to their infants during labor, and, therefore, infants born to mothers with hepatitis B infection should receive HBIG in addition to hepatitis B vaccine at birth. The reason for giving both immunoglobulin and vaccine is that even though hepatitis B vaccine can offer long lasting, active immunity, immunity takes weeks or months to develop. Until active immunity develops, the short-lived, passive antibodies from the HBIG protect the infant.
Unvaccinated individuals exposed to materials infected with hepatitis B (such as healthcare workers stuck by a contaminated needle) will need HBIG in addition to hepatitis B vaccine for the same reason as infants born to mothers with hepatitis B infection.
Hepatitis C
There is currently no vaccine for hepatitis C.

Viral Hepatitis At A Glance

Many illnesses and conditions can cause inflammation of the liver (hepatitis).
Viruses that primarily attack the liver are called hepatitis viruses. There are several types of hepatitis viruses including types A, B, C, D, E, F (not yet confirmed), and G. Types A, B, and C are the most common.
Those at risk for viral hepatitis include workers in the health care profession, people with multiple sexual partners, intravenous drug abusers, and hemophiliacs. Blood transfusion is a rare cause of viral hepatitis.
All hepatitis viruses can cause acute hepatitis.
Viral hepatitis types B and C can cause chronic hepatitis.
Symptoms of acute viral hepatitis include fatigue, flu-like symptoms, dark urine, light-colored stools, fever, and jaundice. Rarely, acute viral hepatitis causes fulminant hepatic failure.
The symptoms of chronic viral hepatitis often are mild and nonspecific, and the diagnosis of chronic hepatitis often is delayed.
Chronic viral hepatitis often requires treatment in order to prevent progressive liver damage, cirrhosis, liver failure, and liver cancer
Hepatitis infections can be prevented by avoiding exposure to viruses, injectable immunoglobulins or vaccines.

Medical Author:

Dennis Lee, MD

Medical Editor:

Jay W. Marks, MD
Source:Medicinenet.com.

Kidney Failure

2012-03-26T09:13:00.002-07:00

What are the kidneys?

The kidneys play key roles in body function, not only by filtering the blood and getting rid of waste products, but also by balancing levels of electrolyte levels in the body, controlling blood pressure, and stimulating the production of red blood cells.
The kidneys are located in the abdomen toward the back, normally one on each side of the spine. They get their blood supply through the renal arteries directly from the aorta and send blood back to the heart via the renal veins to the vena cava. (The term "renal" is derived from the Latin name for kidney.)
The kidneys have the ability to monitor the amount of body fluid, the concentrations of electrolytes like sodium and potassium, and the acid-base balance of the body. They filter waste products of body metabolism, like urea from protein metabolism and uric acid from DNA breakdown. Two waste products in the blood can be measured: blood urea nitrogen (BUN) and creatinine (Cr).
When blood flows to the kidney, sensors within the kidney decide how much water to excrete as urine, along with what concentration of electrolytes. For example, if a person is dehydrated from exercise or from an illness, the kidneys will hold onto as much water as possible and the urine becomes very concentrated. When adequate water is present in the body, the urine is much more dilute, and the urine becomes clear. This system is controlled by renin, a hormone produced in the kidney that is part of the fluid and blood pressure regulation systems of the body.
Kidneys are also the source of erythropoietin in the body, a hormone that stimulates the bone marrow to make red blood cells. Special cells in the kidney monitor the oxygen concentration in blood. If oxygen levels fall, erythropoietin levels rise and the body starts to manufacture more red blood cells.

What causes kidney failure?

Kidney failure can occur from an acute situation or from chronic problems.
In acute renal failure, kidney function is lost rapidly and can occur from a variety of insults to the body. The list of causes is often categorized based on where the injury has occurred.
Prerenal causes (pre=before + renal=kidney) causes are due to decreased blood supply to the kidney. Examples of prerenal causes of kidney failure are:

hypovolemia (low blood volume) due to blood loss;
dehydration from loss of body fluid (for example, vomiting, diarrhea, sweating, fever);
poor intake of fluids;
medication, for example, diuretics ("water pills") may cause excessive water loss; and
abnormal blood flow to and from the kidney due to obstruction of the renal artery or vein.

Renal causes of kidney failure (damage directly to the kidney itself) include:

Sepsis: The body's immune system is overwhelmed from infection and causes inflammation and shutdown of the kidneys. This usually does not occur with urinary tract infections.
Medications: Some medications are toxic to the kidney, including nonsteroidal anti-inflammatory drugs like ibuprofen and naproxen. Others potentially toxic medications include antibiotics like aminoglycosides [gentamicin (Garamycin), tobramycin], lithium (Eskalith, Lithobid), iodine-containing medications such as those injected for radiology dye studies.
Rhabdomyolysis: This is a situation in which there is significant muscle breakdown in the body, and the damaged muscle fibers clog the filtering system of the kidneys. this can occur because of trauma, crush injuries, and burns. Some medications used to treat high cholesterol can cause rhabdomyolysis.
Multiple myeloma
Acute glomerulonephritis or inflammation of the glomeruli, the filtering system of the kidneys. Many diseases can cause this inflammation including systemic lupus erythematosus, Wegener's granulomatosis, and Goodpasture syndrome.

Post renal causes of kidney failure (post=after + renal= kidney) are due to factors that affect outflow of the urine:

Obstruction of the bladder or the ureters can cause back pressure because the kidneys continue to produce urine, but the obstruction acts like a dam, and urine backs up into the kidneys. When the pressure increases high enough, the kidneys are damaged and shut down.
Prostatic hypertrophy or prostate cancer may block the urethra and prevents the bladder from emptying.
Tumors in the abdomen that surround and obstruct the ureters.
Kidney stones. Usually, kidney stones affect only one kidney and do not cause kidney failure. However, if there is only one kidney present, a kidney stone may cause the lone kidney to fail.

Chronic renal failure develops over months and years. The most common causes of chronic renal failure are related to:

poorly controlled diabetes,
poorly controlled high blood pressure, and
chronic glomerulonephritis.

Less common causes of chronic renal failure include:

polycystic kidney disease,
reflux nephropathy,
kidney stones, and
prostate disease.

What are the symptoms of kidney failure?

In the beginning, kidney failure may be asymptomatic (not producing any symptoms). As kidney function decreases, the symptoms are related to the inability to regulate water and electrolyte balances, to clear waste products from the body, and to promote red blood cell production. Lethargy, weakness, shortness of breath, and generalized swelling may occur. Unrecognized or untreated, life-threatening circumstances can develop.
Metabolic acidosis, or increased acidity of the body due to the inability to manufacture bicarbonate, will alter enzyme and oxygen metabolism, causing organ failure.
Inability to excrete potassium and rising potassium levels in the serum (hyperkalemia) is associated with fatal heart rhythm disturbances (arrhythmias) including ventricular tachycardia and ventricular fibrillation.
Rising urea levels in the blood (uremia) can affect the function of a variety of organs ranging from the brain (encephalopathy) with alteration of thinking, to inflammation of the heart lining (pericarditis), to decreased muscle function because of low calcium levels (hypocalcemia).
Generalized weakness may be due to anemia, a decreased red blood cell count, because lower levels of erythropoietin produced by failing kidneys do not adequately stimulate the bone marrow. A decrease in red cells equals a decrease in oxygen-carrying capacity of the blood, resulting in decreased oxygen delivery to cells for them to do work; therefore, the body tires quickly. As well, with less oxygen, cells more readily use anaerobic metabolism (an=without + aerobic=oxygen) leading to increased amounts of acid production that cannot be addressed by the already failing kidneys.
As waste products build in the blood, loss of appetite, lethargy, and fatigue become apparent. This will progress to the point where mental function will decrease and coma may occur.
Because the kidneys cannot address the rising acid load in the body, breathing becomes more rapid as the lungs try to buffer the acidity by blowing off carbon dioxide. Blood pressure may rise because of the excess fluid, and this fluid can be deposited in the lungs, causing congestive heart failure.

How is kidney failure diagnosed?

Diagnosis of kidney failure is confirmed by blood tests measuring the buildup of waste products in the blood. BUN, creatinine, and GFR are routine blood tests used to measure the buildup of waste products in the blood. BUN and creatinine become elevated, and the glomerular filtration rate (GFR) decreases. This is the rate with which blood is filtered through the kidneys and can be calculated based upon the creatinine level, age, race, and gender.
Urine tests may be done to measure the amount of protein, detect the presence of abnormal cells, or measure the concentration of electrolytes. Protein in the urine is not normal and can be a clue that damage to the kidneys has occurred. Abnormal aggregations of red and white blood cells called casts can be seen in the urine with kidney disease. Comparing the concentrations of electrolytes in the blood and urine can help decide whether the kidneys are able to appropriately monitor and filter blood.
Other tests are used to diagnose the type of kidney failure. Abdominal ultrasound can assess the size of the kidneys and may identify whether any obstruction exists. Biopsy of the kidney uses a thin needle that is placed through the skin into the kidney itself to get bits of tissue to examine under the microscope.

What is the treatment for kidney failure?

Prevention is always the goal with kidney failure. Chronic diseases such as hypertension and diabetes are devastating because of the damage that they can do to kidneys and other organs. Lifelong diligence is important in keeping blood sugar and blood pressure within normal limits. Specific treatments are dependent upon the underlying diseases.
Once kidney failure is present, the goal is to prevent further deterioration of renal function. If ignored, the kidneys will progress to complete failure, but if underlying illnesses are addressed and treated aggressively, kidney function can be preserved, though not always improved.

Diet

Diet is an important consideration for those with impaired kidney function. Consultation with a dietician may be helpful to understand what foods may or may not be appropriate.
Since the kidneys cannot easily remove excess water, salt, or potassium, these may need to be consumed in limited quantities. Foods high in potassium include bananas, apricots, and salt substitutes.
Phosphorus is a forgotten chemical that is associated with calcium metabolism and may be elevated in the body in kidney failure. Too much phosphorus can leech calcium from the bones and cause osteoporosis and fractures. Foods with high phosphorus content include milk, cheese, nuts, and cola drinks.

Medications

Medications may be used to help control some of the issues associated with kidney failure.

Phosphorus-lowering medications (calcium carbonate [Caltrate], calcitriol [Rocaltrol], sevelamer [Renagel])
Red blood cell production stimulation (erythropoietin, darbepoetin [Aranesp])
Red blood cell production (iron supplements)
Blood pressure medications
Vitamins

Once the kidneys fail completely, the treatment options are limited to dialysis or kidney replacement by transplantation.

Dialysis

Dialysis cleanses the body of waste products in the body by use of filter systems. There are two types of dialysis; 1) hemodialysis, and 2) peritoneal dialysis.

Hemodialysis

Hemodialysis uses a machine filter called a dialyzer or artificial kidney to remove excess water and salt, to balance the other electrolytes in the body, and to remove waste products of metabolism. Blood is removed from the body and flows through tubing into the machine, where it passes next to a filter membrane. A specialized chemical solution (dialysate) flows on the other side of the membrane. The dialysate is formulated to draw impurities from the blood through the filter membrane. Blood and dialysate never touch in the artificial kidney machine.
For this type of dialysis, access to the blood vessels needs to be surgically created so that large amounts of blood can flow into the machine and back to the body. Surgeons can build a fistula, a connection between a large artery and vein in the body, usually in the arm, that causes a large amount of blood flow into the vein. This makes the vein larger and its walls thicker so that it can tolerate repeated needle sticks to attach tubing from the body to the machine. Since it takes many weeks for a fistula to mature enough to be used, significant planning is required if hemodialysis is to be considered as an option.
If the kidney failure happens acutely and there is no time to build a fistula, special catheters may be inserted into the larger blood vessels of the arm, leg, or chest. These catheters may be left in place for up to three weeks. In some diseases, the need for dialysis will be temporary, but if the expectation is that dialysis will continue for a prolonged period of time, these catheters act as a bridge until a fistula can be planned, placed, and matured.
Dialysis treatments normally occur three times a week and last a few hours at a time. Most commonly, patients travel to an outpatient center to have dialysis, but home dialysis therapy is becoming an option for some.

Peritoneal dialysis

Peritoneal dialysis uses the lining of the abdominal cavity as the dialysis filter to rid the body of waste and to balance electrolyte levels. A catheter is placed in the abdominal cavity through the abdominal wall by a surgeon and is expected to remain there for the long-term. The dialysis solution is then dripped in through the catheter and left in the abdominal cavity for a few hours and then is drained out. In that time, waste products leech from the blood normally flowing through the lining of the abdomen (peritoneum).
There are benefits and complications for each type of dialysis. Not every patient can choose which type he or she would prefer. The treatment decision depends on the patient's illness and their past medical history along with other issues. Usually, the nephrologist (kidney specialist) will have a long discussion with the patient and family to decide what will be the best option available.
Dialysis is life saving. Without it, patients whose kidneys no longer function would die relatively quickly due to electrolyte abnormalities and the buildup of toxins in the blood stream. Patients may live many years with dialysis but other underlying and associated illnesses often are the cause of death.

Kidney transplantation

If kidney failure occurs and is non-reversible, kidney transplantation is an alternative option to dialysis. If the patient is an appropriate candidate, the health care practitioner will contact an organ transplant center to arrange evaluation to see if the patient is suitable for this treatment. If so, the search for a donor begins. Sometimes, family members have compatible tissue types and, if they are willing, may donate a kidney. Otherwise, the patient will be placed on the organ transplant list that is maintained by the United Network of Organ Sharing.
Not all hospitals are capable of performing kidney transplants. The patient may have to travel to undergo their operation. The most successful programs are those that do many transplants every year.
While kidney transplants have become more routine, they still carry some risk. The patient will need to take anti-rejection medications that reduce the ability of the immune system to fight infection. The body can try to reject the kidney or the transplanted kidney may fail to work. As with any operation, there is a risk of bleeding and infection.
Kidney transplants may provide better quality of life than dialysis. After one year, 95% of transplanted kidneys are still functioning and after five years the number is 80%. It seems that the longer a patient is on dialysis, the shorter the life of the transplanted kidney.
If the transplanted kidney fails, the alternative is another kidney transplant or a return to dialysis.

What is the prognosis for someone with kidney failure?

The outlook for kidney failure depends upon the underlying condition that caused it. Kidney function may return to normal, especially if it is due to an acute obstruction and that obstruction is relieved. Other causes of decreased kidney function leading to kidney failure are due to underlying disease and occur slowly over time.
Prevention is the best chance to maintain kidney function, and controlling high blood pressure and diabetes over a lifetime can decrease the potential for progressive kidney damage. Chronic kidney failure may be managed by a primary health care practitioner or a nephrologist to help monitor electrolyte and waste product levels in the bloodstream. Major abnormalities can be life-threatening, and treatment options may be limited to dialysis or transplant.

Kidney Failure At A Glance

Kidneys are the organs that help filter waste products from the blood. They are also involved in regulating blood pressure, electrolyte balance, and red blood cell production in the body.
There are numerous causes of kidney failure, and treatment of the underlying disease may be the first step in correcting the kidney abnormality.
Some causes of kidney failure are treatable and the kidney function may return to normal. Unfortunately, kidney failure may be progressive in other situations and may be irreversible.
Symptoms of kidney failure are due to the build-up of waste products in the body that may cause weakness, shortness of breath, lethargy, and confusion. Inability to remove potassium from the bloodstream may lead to abnormal heart rhythms and sudden death. Initially, there may be no symptoms of kidney failure.
The diagnosis of kidney failure usually is made by blood tests measuring BUN, creatinine, and glomerular filtration rate (GFR).
Treatment of the underlying cause of kidney failure may return kidney function to normal. Lifelong efforts to control blood pressure and diabetes may be the best way to prevent chronic kidney disease and its progression to kidney failure. Usually, kidney function gradually decreases over time.
If the kidneys fail completely, the only treatment options available may be dialysis or transplant.

REFERENCE: eMedicine.com. Renal Failure, Acute.
<http://emedicine.medscape.com/article/777845-overview>

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Muscle Spasms

2012-03-26T09:07:00.002-07:00

What is a muscle spasm?

A muscle spasm, or muscle cramp, is an involuntary contraction of a muscle. Muscle spasms occur suddenly, usually resolve quickly, and are often painful.
A muscle spasm is different than a muscle twitch. A muscle twitch, or fasciculation, is an uncontrolled fine movement of a small segment of a larger muscle that can be seen under the skin.
Muscles are complex structures that cause movement in the body. There are three types of muscle in the body:

Heart muscle pumps blood (cardiac muscle).
Skeletal muscle moves the external body parts, like the arms and legs, and the neck, back and trunk.
Smooth muscle moves portions of hollow structures inside the body. Examples include the muscles that line the esophagus, stomach and intestine, muscles that line large arteries and the muscles of the uterus.

Skeletal muscles are anchored to bone, either directly or by a tendon. When the muscle contracts, the associated structure moves. This allows arms to lift, legs to run, and the face to smile. Most of these muscles are under willful or conscious control of the brain. This type of muscle is striated or striped with dark-colored muscles fibers containing large amounts of myoglobin, the protein that helps carry oxygen and light-colored fibers that have lesser amounts of the protein. The contraction of a skeletal muscle requires numerous steps within cells and fibers that need oxygen, electrolytes, and glucose, which are supplied by the bloodstream.
Smooth muscle is located in the walls of hollow internal structures in the body, like the arteries, intestines, bladder, and iris of the eye. They tend to circle the structure and when they contract, the hollow structure is squeezed. These muscles are involuntary and are controlled by the unconscious part of our brain function using the autonomic nervous system. The autonomic nervous system can run in the background, regulating body processes automatically for us. There is a balance between the sympathetic system (adrenergic nerves) that speed things up and the parasympathetic system (cholinergic nerves) that slow things down. These names are based on the type of chemical that is used to transmit signals at the nerve endings. Adrenaline (epinephrine from the sympathetic nervous system) allows the body to respond to stress. Imagine seeing a bear in the woods; your heart beats faster, your palms get sweaty, your eyes dilate, your hair stands on end, and your bowels move. Acetylcholine is the chemical that is the anti-adrenaline and is involved in the parasympathetic nervous system. Smooth muscle has the same basic contraction mechanism as skeletal muscle, though different proteins are involved.

What causes a muscle spasm?

There are a variety of causes of muscle spasms, and each depends upon predisposing factors, the part of the body involved, and the environment the body is working in.
Spasms may occur when a muscle is overused and tired, particularly if it is overstretched or if it has been held in the same position for a prolonged period of time. In effect, the muscle cell runs out of energy and fluid and becomes hyperexcitable and then develops a forceful contraction. This spasm may involve part of a muscle, the whole muscle, or even adjacent muscles.
Overuse as a cause of skeletal muscle spasm is often seen in athletes who are doing strenuous exercise in a hot environment. This is also an occupational issue with construction workers or others working in a hot environment. Usually, the spasms will occur in the large muscles that are being asked to do the work.
Overuse can also occur with routine daily activities like shoveling snow, or mowing or raking grass causing muscle spasms of the neck, shoulder, and back.
Unfamiliar exercise activities can also cause muscle spasms to occur. Abdominal spasms can occur when a person decides to begin working their abdominal muscles by doing situps and does too many too quickly.
Writer's cramps are similarly caused by prolonged use of the small muscles in the hand.
It is commonly thought that dehydration and depletion of electrolytes will lead to muscle spasm and cramping. Muscle cells require enough water, glucose, sodium, potassium, calcium, and magnesium to allow the proteins within them to interact and develop an organized contraction. Abnormal supply of these elements can cause the muscle to become irritable and go into spasm.
Atherosclerosis or narrowing of the arteries (peripheral artery disease) may also lead to muscle spasm and cramps, again because adequate blood supply and nutrients are not able to be delivered to the appropriate muscle. Peripheral artery disease can decrease the flow of blood to the legs causing pain with activity. There may also be associated muscle cramps.
Leg spasms are often seen related to exercise, but cramps may also be seen at night involving calf and toe muscles. Nocturnal leg cramps and restless legs syndrome are considered a type of sleep disturbance.
Systemic illnesses like diabetes, anemia (low red blood cell count), kidney disease and thyroid and other hormone issues are also potential causes of muscle spasms.
Diseases of the nervous system, such as multiple sclerosis or spinal cord injury, can be associated with muscle spasm.
Smooth muscle can also develop spasm. When a hollow structure filled with air or fluid is squeezed by the muscle spasm, significant pain can occur since the fluid or air cannot be compressed. For example, smooth muscle in the intestinal wall can go into spasm, causing waves of pain called colic. Colicky pain which tends to be rhythmic (coming and going) may also occur within the bile duct that empties the gallbladder and may develop after eating.

When kidney stones try to pass, the smooth muscles that are in the walls of the ureter that connect the kidney to the bladder, may spasm and cause significant pain. Often this type of pain is associated with nausea and vomiting.
Muscles that surround the esophagus can go into spasm when irritation occurs with reflux esophagitis or GERD.
Diarrhea can be associated with colicky pain, whereby the muscles within the colon wall spasm just before a watery bowel movement.

Dystonias are movement disorders where groups of muscles forcefully contract causing twisting and repetitive movements or the inability to have a normal posture as a result of muscle spasm and cramping. The symptoms may be very mild initially but gradually progress to become more frequent and aggressive. Occasionally, there is no progression. Examples of this type of muscle spasm include torticollis (where the neck muscles spasm and cause the head to turn to one side), blepharospasm (where there is uncontrolled blinking of the eyes), and laryngeal dystonia that affects the muscles that control speech. Dystonias may be caused by abnormally functioning neurotransmitter chemicals in the part of the brain called the basal ganglia. These chemicals (serotonin, dopamine, acetylcholine, and GABA) are required to properly send messages that begin muscle contraction. Dystonia symptoms may occur as a complication of stroke.

What are the symptoms and signs of muscle spasms?

The symptoms of muscle spasm depend upon the muscle involved and the circumstances leading up to the spasm.
Skeletal muscle spasm usually involves muscles that are being asked to do excessive work. There is acute onset of pain as the muscle contracts. A bulging muscle may be seen or felt underneath the skin where the muscle is located. Most often, the spasm resolves spontaneously after a few seconds though it may last many minutes or longer. Usually, the patient will feel the need to stretch the muscle involved, thus relieving the spasm and resolving the episode. With heat cramps, the muscle spasm may occur after the activity is completed.
A muscle fasciculation or twitch may last just a few seconds or may be a recurrent event. Usually, it's just a momentary repetitive contraction of just a few muscle fibers of a larger muscle in a localized area served by one nerve fiber. This often involves the eyelid, calf, thigh, or thumb. The fasciculations often come and go and may be related to stress or anxiety. Ingestion of stimulants like caffeine and pseudoephedrine found in over-the-counter cold medications may also cause the twitch. Medications such as albuterol (Ventolin, Proventil, AccuNeb, VoSpire, ProAir) used for the treatment of asthma and medications used to treat attention deficit disorder may be associated with twitching. These twitches are considered benign fasciculation.
However, muscle twitching may also be associated with neurologic disorders such as muscular dystrophy, amyotrophic lateral sclerosis, and myopathy (a primary muscle illness). With these diagnoses, associated symptoms include weakness, muscle wasting with loss of muscle size, and change in sensation.
Smooth muscle spasm will cause colicky pain that comes and goes. The symptoms will depend upon the organ involved.

How are muscle spasms diagnosed?

Most people have experienced a skeletal muscle spasm due to overexertion, especially in a warm environment and are able to self-diagnose. However, if the spasms are severe, last a long time, and keep recurring, the patient may present to a health-care professional for evaluation.
The diagnosis usually begins with a history and physical examination. It is helpful to know the circumstances surrounding the muscle spasms.

When did they begin? How long do they last? How frequently do they come? Is it always the same muscle group of the body involved?
Other information that is helpful includes whether there have been any recent illnesses or whether any medications have been taken, including prescription, over-the-counter, and food supplements.
Past medical history may give a clue as to the reason for the muscle cramps. These may include a history of diabetes, hypothyroidism, kidney disease, and spinal cord injury.
Work or exercise history may be of importance.

Sometimes the physical examination may be normal since the muscle spasms may not occur during the visit. However, the physical examination may useful in detecting underlying medical issues that may be helpful in making the diagnosis. For example, if the patient is complaining of leg muscle spasm, the examination may include palpating or feeling for pulses in the feet. Atherosclerosis, or hardening of the arteries, may be associated with the loss of arterial pulse in the involved extremity.
For those having pain from smooth muscle spasm, the pain may be severe enough to present to an emergency department. The history and physical examination will be directed to finding the source of the pain, while at the same time trying to control the symptoms. Kidney stone pain (renal colic) and gallbladder pain sometimes require anti-inflammatory narcotic pain medication and antinausea medication for relief. Some patients with irritable bowel condition may also present with significant intestinal spasm.
For patients with recurrent muscle spasm where the cause is not easily diagnosed by history and physical examination, testing may be needed to give direction as to potential causes.
Blood tests may or may not be indicated depending upon the situation and whether or not the diagnosis can be made by history and physical examination. Tests may include a complete blood count (CBC) looking for anemia, electrolytes (especially sodium, potassium, calcium and magnesium), glucose, and creatinine (to check for kidney function). Thyroid function tests may also be considered.
If there is concern that the spasms are due to a nerve or muscle disorder, electromyography (EMG) may be done to determine whether there may be an abnormality of the muscle, of the nerves, or both.
If there is concern about the potential for peripheral artery disease, tests of blood flow to the legs may be considered, including an ankle-brachial index (ABI) which compares blood pressures in the arms and legs and ultrasound and angiography (often using CT or MRI) to directly assess the blood vessels.

How are muscle spasms treated?

Prevention is the key to most skeletal muscle spasm episodes. Since they are often associated with dehydration and electrolyte disturbances, it is important to keep the body well hydrated. If the fluid loss is due to an illness with fever or vomiting and diarrhea, controlling the symptoms will help limit fluid loss and prevent spasms. Similarly, for those who work or exercise in a hot environment, drinking enough fluids to keep hydrated is very important.
Muscles should also be prepared for the activity that they are expected to do. Just as athletes stretch and warm up before the game, nonathletes should warm up before heavy labor, including jobs like raking, mowing, and shoveling snow.
Should a skeletal muscle go into spasm, the initial treatment is to gently stretch the muscle back to length to break the spasm cycle and resolve the acute situation.
Further treatment will depend upon the underlying cause of the muscle spasms. For muscles that have been damaged or strained, medications may be required for short-term pain relief, including anti-inflammatories (ibuprofen [Advil]), narcotics, and muscle relaxants.
The treatment of smooth muscle spasm also depends upon the underlying cause. Often, pain control will occur simultaneously with the care provider's efforts to make the diagnosis.
There is no one effective treatment for the dystonias. Medication may used to try to restore balance to the brain's neurotransmitters. The decision as to which medication to use depends upon the patient's presentation. It may take trial and error to find the right medication in the right dose to control symptoms.

Anti-Parkinsonism drugs, like trihexyphenidyl HCl (Artane) and benztropine mesylate (Cogentin), decrease acetylcholine levels.
Muscle relaxants like diazepam (Valium) and baclofen (Lioresal) affect GABA receptors.
Levodopa (Sinemet) and reserpine (Harmonyl) affect dopamine levels.
Carbamazepine (Tegretol), a seizure-control drug, may be useful in some patients.
Botulinum toxin type A (Botox) may be injected into a specific muscle to paralyze it and relieve the muscle spasm. This was initially used for blepharospasms but is now able to be used where other muscles are involved.

Muscle Spasms At A Glance

Spasms may affect many different types of muscles in the body, leading to many different symptoms and presentations.
Spasms of skeletal muscles are most common and are often due to dehydration and electrolyte abnormalities. The spasm occurs abruptly, is painful, and usually short lived. It may be relieved by gently stretching the muscle.
If muscle spasms are especially painful, if they do not resolve or if they recur, medical care should be accessed to look for potential underlying causes.
Smooth muscles that are within the walls of hollow organs in the body can go into spasm, causing significant pain. Often this pain is colicky, meaning that it comes and goes. Examples include the pain associated with diarrhea, gallbladder pain, and passing a kidney stone.
A special form of muscle spasms are the dystonias whereby an abnormality perhaps exists with the chemicals that help transmit signals within the brain. Examples include torticollis and blepharospasm. Treatment may include medications to help restore the neurotransmitter levels to normal and Botox injections to paralyze the affected muscle and relieve the spasm.

REFERENCE:

Bucholz, R.W., J.D. Heckman, and C.M. Court-Brown. Rockwood and Green's Fracture in Adults. 6th ed. Philadelphia: Lippincott, Williams & Wilkins, 2006.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR
Source:Medicinenet.com.

Cataracts

2012-03-26T08:57:00.002-07:00

Facts about cataracts

A cataract is a clouding of the lens of the eye.
Cataracts are extremely common, and most cataracts are a result of the aging process.
Although many cataracts are not significant enough to require treatment, surgical removal of cataracts is usually safe and effective, resulting in improvement of vision.
Cataract surgery should be performed when the visual loss from the cataract significantly impacts the lifestyle of the individual patient.

What is a cataract?

A cataract is an eye disease in which the clear lens of the eye becomes cloudy opaque, causing decrease in vision. Although the word cataract to describe this condition has been part of the English language only since the middle of the 16th century, the eye disease has been recognized and surgically treated since ancient times.

The lens is a portion of the eye that is normally clear. It assists in focusing rays of light entering the eye onto the retina, the light-sensitive tissue at the back of the eye. In order to get a clear image onto the retina, the portions of the eye in front of the retina, including the lens, must be clear and transparent. Once light reaches the retina, the light initiates a chemical reaction within the retina. The chemical reaction, in turn, initiates an electrical response which is carried to the brain through the optic nerve. The brain then interprets what the eye sees.
In a normal eye, light passes through the transparent lens to the retina. The lens must be clear for the retina to receive a sharp image. If the lens is cloudy from a cataract, the image striking the retina will be blurry and the vision will be blurry. The extent of the visual disturbance is dependent upon the degree of cloudiness of the lens.
Most cataracts are related to aging. Cataracts are very common in older people. By age 80, more than half of all Americans either have some degree of cataract or have already undergone cataract surgery in one or both eyes. By age 95, this percentage increases to almost 100%. A cataract can occur in either or both eyes. Individuals with a cataract in one eye usually go on to develop a cataract in the other eye as well. A cataract is not contagious and cannot spread from one eye to the other or from person to person. Cataracts do not cause the eye to tear abnormally. They are neither painful nor make the eye itchy or red.
Although vision can be restored in most people with cataracts, age-related cataracts are still the most common cause of blindness in the world, primarily because many third-world nations lack appropriate surgical services.
As life span increases in the developed world due to modern technology and new methods of treatment of acute and chronic disease, the incidence of age-related cataracts will continue to increase.

What are the different types of cataracts?

Cataracts can be classified by anatomical location within the lens, degree of clouding of the lens, or by the cause of the cataract.
The lens of the human eye is shaped similar to an M&M's candy. It has a front (anterior) part and a back (posterior) part. The central portion of the lens is called the lens nucleus, and the outer portion is called the lens capsule. Between the inner nucleus and the outer capsule is a portion of the lens called the cortex. Clouding of the lens can occur only in the nucleus, in which case the term nuclear cataract or nuclear sclerosis is used. If the clouding occurs in the lens cortex only, the cataract is termed a cortical cataract. If the loss of clarity of the lens is primarily in the capsule, the term subcapsular cataract is used. The location of the clouding can also be defined as being anterior or posterior, central, or peripheral. Often the clouding of the lens may affect multiple portions of the lens. The most common type of cataract that is related to age is sometimes termed a senile cataract. This type of cataract primarily involves the nucleus of the lens. Cataracts that develop in the posterior subcapsular area (in the rear region of the lens capsule) are more common in a younger age group.
Any degree of loss of the normal transparency of the lens is called a cataract. The more cloudy the, lens the more advanced the degree of cataract. A cataract may be mild, moderate, or severe. It may be early or advanced. If the lens is totally opaque it is termed a "mature" cataract. Any cataract that is not opaque is therefore termed an "immature" cataract. Most mature cataracts are white in color.

What are causes of cataracts?

The lens is made of mostly water and protein. The protein is arranged in a specific way that keeps the lens clear and allows light to pass through it to focus a clear image onto the retinal surface. As we age, some of the protein may clump together and start to cloud a small area of the lens. This is our understanding of the cause of an age-related cataract. Over time, the cataract may become more dense or cloud more of the lens, making it more difficult to see through. A cataract is not a growth or tumor.
There are many causes of non age-related cataracts or secondary cataracts. Secondary cataracts are a result of similar changes to the protein of the lens, also resulting in visual blurring or visual loss.
Blunt or penetrating injury to the eye may cause secondary cataracts, either immediately after the injury or some weeks to years afterward. A cataract following an injury may appear and then not increase in density (be stationary) or be progressive. Eye surgery for other conditions can also cause cataracts. Excessive exposure to ionizing radiation (X-ray), infrared radiation (as in glass blowers), or ultraviolet radiation cause secondary cataracts.
Diabetes is associated with the development of secondary cataracts. Inflammatory disease of the eye, such as iritis or uveitis, may cause or accelerate the development of cataract in the involved eye.
There are many genetic illnesses that are associated with the development of secondary cataracts. These include myotonic dystrophy, galactosemia, homocystinuria, Wilson's disease and Down syndrome, plus many others. Congenital infections with herpes simplex, rubella, toxoplasmosis, syphilis, and cytomegalic inclusion disease may also result in cataracts.
There are many medications which, when taken over a long period of time, can cause secondary cataracts. The most common of these are oral corticosteroids, such as prednisone, which are used for a wide variety of medical conditions.
The term "congenital cataract" is used when a baby is born with any clouding of the lens. This may be present in one or both eyes, be stationary or be progressive. Causes include genetic disorders or intrauterine developmental disorders, both often associated with other physical abnormalities of the baby.
Atopic dermatitis, other diseases of the skin and mucous membranes, hypothyroidism, and hyperparathyroidism are associated with the early development of cataracts.
Patients who develop cataracts in both eyes at an early age often have family members who have also developed cataracts prematurely, implying a genetic cause, even in the absence of a recognized underlying disease.

What are risk factors for cataracts?

Advanced age is a significant risk factor for the development of cataracts. A family history for early development of cataracts, the presence of diabetes, tobacco use, and prolonged exposure to sunlight are also risk factors.

What are the symptoms of cataracts?

You may not notice any symptoms with early cataracts. As a cataract becomes more advanced, decrease in clarity of vision, not fully correctable with glasses, is noticed. There is a loss of contrast sensitivity, so that shadows and color vision are less vivid. Disturbing glare may be noted as light is into the eye scattered by the cataract. Haloes may be observed around lights. Night vision will be diminished. In certain types of cataracts, double vision may be noted in the affected eye. Some patients note that they require frequent changes in their eyeglass or contact lens prescriptions and may be aware that their near vision is improving as their distance vision declines.
A cataract does not routinely cause discomfort or pain in the eye or alter the external appearance of the eye

What are the signs of cataracts?

Family members of a person affected by cataracts in both eyes may notice he or she appears not to be seeing as well as previously. The eye will appear normal to the untrained observer, unless the cataract is mature and white. In that situation the pupil of the eye, which normally appears black, will look grey or white to the observer.
The examining physician will find diminished visual acuity in the affected eye or eyes. This visual loss is not fully corrected by a change in the glasses. The lens of the eye can be easily examined by an ophthalmologist and the changes in the lens characteristic of cataract can actually be seen using a slit lamp, which is an illuminating and magnifying device used to painlessly examine the structures within the front of the eye, including the lens.

How are cataracts diagnosed?

Cataracts are relatively simple to diagnose by an ophthalmologist or an optometrist during a routine eye examination. It is important, when making the diagnosis of cataract, to also examine the entire eye for evidence of any other eye disease which may be compromising the vision. In addition to taking a medical and ocular history and visual acuity test, the ophthalmologist will check eye movements and pupillary responses, measure the pressure inside the eyes and examine the front and back of the eyes after the pupils have been dilated with drops.

What is the treatment for cataracts?

People with early cataract will find that changing their glasses, using sunglasses to decrease glare and having better lighting to read can significantly alleviate their symptoms. Magnifying lenses for close work and reading fine print may also be helpful.
Many cataracts are not bothersome, causing few symptoms. In that situation, no surgical treatment is necessary. However, the only true treatment for cataract is surgical removal of the cloudy lens. Surgery is suggested if the patient loses the ability to perform necessary activities of everyday life, such as driving, reading, or looking at computer or video screens, even with glasses, and there is the expectation that vision will improve as a result of the surgery.
Depending on a patient's specific visual needs, surgery is sometimes done on cataracts that are not very dense or surgery can wait until the cataract and the vision gets more cloudy. Patients' responses to cataracts vary. A cataract in only one eye may be disturbing to a particular patient and may not cause significant symptoms in another patient.
Cataracts usually do not harm your eye, so you can have surgery when it is convenient for you. Once you understand the benefits and risks of surgery, you can make an informed decision about whether cataract surgery is right for you. In most cases, delaying cataract surgery will not cause long-term damage to your eye or make the surgery more difficult.
If the eye has other diseases that have caused visual loss such as glaucoma, macular degeneration, diabetic retinopathy, or optic nerve damage from glaucoma, cataract surgery may not improve the vision.
Occasionally, your doctor may recommend removal of a cataract if it prevents diagnosis or treatment of another eye problem, such as macular degeneration or diabetic retinopathy.
If both eyes have cataracts and surgery is agreed upon, the surgery on the second eye is generally planned at least a week after the first eye. There is usually no harm in waiting a much longer period of time between the two eye operations.
Since the lens of the eye is necessary to accurately focus light onto the retinal surface and removal of the cataract involves removal of the lens, modern cataract surgery combines removal of the lens with placement of a new artificial lens into the eye. Measurements for the size, shape, and power of this lens will be taken at least a week prior to the surgery so that the lens can be ordered and available at the time of surgery.
More than 2 million cataract surgeries are performed annually in the United States. It is extremely safe and effective, improving vision in the vast majority of patients.

What are the different types of cataract surgery, and what risks are involved?

Cataract surgery is usually performed as an outpatient procedure under local anesthesia. Some sedation is ordinarily given intravenously just before the beginning of the surgery, which usually takes under a half-hour.
Most cataract surgery today is done through a small incision by phaco-emulsification or by other extracapsular means through a slightly larger incision. In more than 95% of cases, a new lens, known as a lens implant or intraocular lens is inserted at the same time as the cataract removal. You will not feel the new lens within the eye. Most patients need to limit their activities for only a few days and recovery time is brief.
Although modern techniques have made cataract surgery quite safe, complications can occur with any surgical procedure, including cataract extraction. These include hemorrhage, infection, loss of a portion of the cataract into the eye, displacement of the intraocular lens, glaucoma, and retinal detachment. Fortunately, all these complications are rare and usually can be managed. Blindness is a rare complication of cataract surgery.
Modern cataract surgery involves leaving a portion of the lens capsule within the eye to support the intraocular lens. This capsule may become cloudy at a later time, necessitating opening of the capsule through the use of a laser. This outpatient procedure is called a YAG laser capsulotomy. It is painless and rarely results in increased eye pressure or other eye problems.

What are complications of cataracts?

Occasionally, a very dense cataract of long-standing duration may enlarge in size and interfere with fluid drainage within the eye. In addition, a far advanced cataract may leak protein into the eye, causing inflammation of the eye. Your doctor will advise you of these possibilities and may recommend surgery to avoid these complications even if the decrease in vision is not bothering you.
The presence of a cataract may make evaluation of diseases of the retina more difficult, since the physician must look through the cataract to examine the retina.

What is the prognosis of cataracts?

The rate of progression of cataracts is usually predictable and surgery is successful in restoring vision in a large majority of cases. If other diseases are present within the eye, the degree of visual improvement will be limited by the other disease process. Ophthalmologists can usually determine this in advance.

Can cataracts be prevented?

Everyone, if they live long enough, will develop cataracts. There is no scientifically proven method that prevents the inevitable. Progression of cataracts can be slowed by avoiding large amounts of ultraviolet light, not smoking, and following a healthy diet. Wearing UV-protection sunglasses when exposed to sunlight can be helpful.

Where can people get more information on cataracts?

National Eye Institute (http://www.nei.nih.gov/health/cataract/cataract_facts.asp)
Cataracts Info Center (http://www.cataractsinfocenter.com/)
Cataract Surgery: A Patient's Guide to Cataract Treatment by Julius Shulman, MD

REFERENCES:

Cataracts InfoCenter. <http://www.cataractsinfocenter.com/>.

United States. National Eye Institute. National Institutes of Health. "Facts About Cataract." Feb. 2010. <http://www.nei.nih.gov/health/cataract/cataract_facts.asp>.

Medical Author:

Andrew A. Dahl, MD, FACS

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Pregnancy Planning

2012-03-26T08:53:00.002-07:00

Pregnancy Planning Facts

Pregnancy planning can address issues of nutrition, vitamins, body weight, exercise, and potentially harmful medications and illnesses as well as immunizations and genetic counseling.
Women who take folic acid at least four weeks prior to conception can reduce their baby's risk of birth defects of the spinal cord and skull by 70%.
Alcohol has been implicated in infertility, early miscarriage, and birth defects.
Certain acne medications and other prescription and OTC medications can cause birth defects.
Babies of older women have an increased risk of having chromosomal abnormalities.
The timing of sexual intercourse in relation to ovulation does not influence the gender of the baby.

What is pregnancy planning and why is it important?

Having a baby is one of the most important events in a woman's life. Women considering pregnancy are encouraged to start planning for the pregnancy with their doctors early. This early planning process is called pregnancy planning. The goals of pregnancy planning are to create a healthy environment for the fetus and to prevent birth defects and other pregnancy related problems to the greatest extent possible. The issues addressed during pregnancy planning include nutrition, vitamins, body weight, exercise, avoidance of certain medications and alcohol, immunizations, and genetic counseling. Even though many women will have normal pregnancies without any planning, pregnancy planning improves the chances of a smooth pregnancy and a healthy baby. Unfortunately, many more women who are anticipating conceiving do not seek prior medical consultation.
Pregnancy planning can help prevent exposure of the mother to potentially harmful medications or substances during the early days of pregnancy. The baby's organs begin developing as early as 17 days after conception, and the fertilized egg begins to grow even before the first day of the missed period. Some women continue to have light bleeding that may be mistaken for a menstrual period during the first few months of pregnancy and may not even realize that they are pregnant. Others may not recognize that they are pregnant until they experience weight gain or abdominal enlargement. By then, they may have already been exposed to medications or substances potentially harmful to the fetus.
In addition to avoiding medications and substances that are potentially harmful to the fetus, other important health issues are addressed during pre-pregnancy planning.

Conditions such as diabetes, high blood pressure, kidney disease, thyroid disease, and heart disease in the mother are controlled to optimize pregnancy outcome.
The status of the woman's immunity against German measles (rubella) and varicella (chickenpox) is also determined. Women lacking rubella antibodies are immunized before conceiving (see medical issues below). Women who are not immune to varicella (chickenpox) can be vaccinated, but should wait 30 days after vaccination before becoming pregnant.
Women who are carriers of the hepatitis B virus can be identified by blood tests, and their infants can be protected from hepatitis B infection by immunizations at the time of delivery. Women with HIV (human immunodeficiency virus) infection should take certain medications during pregnancy to decrease not only their risks but those of the fetus as well.

The effects of diet, exercise, and each of the medical conditions previously discussed will be reviewed below.

What are pregnancy symptoms?

There are both symptoms and signs of pregnancy. These symptoms and signs depend upon the time in pregnancy. In the first trimester of pregnancy, the first sign of pregnancy is most often a missed menstrual period. If a sexually active woman's periods are generally regular, missing a period for a week or more is presumptive evidence of pregnancy.
Early symptoms of pregnancy also include feelings of breast swelling and tenderness, and nausea sometimes with vomiting. "Morning sickness" does not always occur in the morning, and the nausea of pregnancy can occur at any time of day. Many women become fatigued early in pregnancy, and some may feel abdominal enlargement (bloating).
Early in pregnancy, the woman may feel she has to urinate frequently, especially at nighttime, and she may leak urine when coughing, sneezing or laughing. This is also normal later in pregnancy and is not a problem.
Other changes characteristic of pregnancy include the deepening color of the areola (area surrounding the nipple), increased body temperature, the so-called "mask of pregnancy" (darkening of skin on the forehead, bridge of the nose, or cheekbones), and a dark line going down from the middle of the central abdomen area to the pubic area. Eventually, enlargement of the abdomen is a normal feature of the growing fetus.

What is a pregnancy calculator and calendar?

A pregnancy calendar or calculator can allow a pregnant woman to understand what is happening to her body and to the developing embryo or fetus at each stage of pregnancy. Most pregnancy calendars explain the changes of pregnancy on a week-to-week level and can be found online or in print form. In many cases, pregnancy calendars contain photos or diagrams to illustrate the appearance of the fetus at each stage.

How effective are home pregnancy tests?

At-home pregnancy tests, first introduced in 1975, are very accurate and reliable when used correctly. These tests measure the presence of the hormone human chorionic gonadotropin in the urine, which, when present, is indicative of pregnancy. The same hormone is measured in blood and urine pregnancy tests available at clinics and doctors' offices. Currently, the blood test is the most specific and sensitive pregnancy test available, although urine tests have become increasingly sensitive. For example, home urine tests may be able to detect the pregnancy hormone at 8 to 9 days after conception, or a few days before the missed menstrual period.
While many manufacturers claim that their home pregnancy tests are 99% accurate, a number of factors influence the accuracy of these kits. Studies have shown that false negative results may occur when very low levels of the pregnancy hormone are present, and that home test kits from different manufacturers differ in their sensitivity for detection of the very low levels of the pregnancy hormone in the early days of pregnancy. If a woman takes a home pregnancy test too soon, the result may be negative even though she is in the first stages of pregnancy. A repeat test should always be performed a week later if a home test is negative and a woman suspects that she might be pregnant.

How can diet and nutrition affect early pregnancy?

The developing fetus receives its nutrition from the mother's blood. Therefore high fat diets and some vegetarian diets are discouraged during pregnancy because they may not provide all the nutrition needed for the developing fetus. Bulimia, anorexia nervosa and other eating disorders in the mother are addressed and treated. Weight reduction diets are avoided during pregnancy. Excess intake of sugar, alcohol, megavitamins, and caffeine are also avoided Because a "safe" amount of caffeine has never been confirmed to date, it is best to avoid caffeine entirely. Women who feel strongly that they need some coffee are advised to drink no more than one cup per day. There is no proof that 1 to 2 cups of coffee daily cause pregnancy complications.
Listeria is a type of bacteria found in contaminated food that can cause miscarriage and other problems in a fetus. Because of the danger of getting a listeria infection, pregnant women should avoid unpasteurized milk, soft cheeses, cold cuts, and undercooked or raw animal foods. In addition, fruits and vegetables should be washed completely prior to consumption.
Phenylketonuria is an inherited disease that affects the utilization of a certain protein component in foods. This disorder can be detected by a blood test. Mothers with phenylketonuria may give birth to developmentally disabled children unless their diets are strictly controlled to exclude phenylalanine.
Megavitamins contain double or even triple the recommended daily allowances of vitamins and minerals. High doses of vitamin A have been implicated in producing birth defects. The better idea is to avoid megavitamins and instead follow the recommendation that has proven benefit: take a prenatal vitamin containing folic acid.
Folic acid intake in the mother prior to, and during pregnancy has been shown to reduce the risk of birth defects involving the brain and spinal cord. The United States Public Health Service recommends folic acid for all women of child-bearing capacity. Studies have shown that if folic acid is begun at least 4 weeks prior to conception, the risk of birth defects of the spinal cord and skull can be reduced by more than 70%. In women with or even without a history of having infants with birth defects of the spinal cord or skull, folic acid should be taken one month before conception and continued through the 12th week of pregnancy. In fact, continuing prenatal vitamins through pregnancy and even through nursing is probably wise. These prenatal vitamins are available over-the-counter. If a particular brand makes you feel nauseated, simply switch to another brand or try taking the vitamin at night.
Because of the risks of mercury poisoning and nervous system damage in the fetus from contaminated fish, pregnant women are advised to eliminate consumption of certain types of fish that are known to be high in mercury, including shark, swordfish, tilefish, and king mackerel. Tuna steaks, made from large tuna, may also have high mercury levels. Canned tuna is made from smaller fish that typically have lower levels of mercury than larger fish.

How does alcohol affect pregnancy?

Alcohol has been implicated in infertility, early miscarriage, as well as in birth defects. The amount of alcohol consumption necessary to cause these problems is not known, and varies among women. Some women can drink excessively and have normal infants. Others consume considerably less alcohol but still give birth to babies with cognitive disabilities and/or other birth defects. It is generally believed that the greater the amount of alcohol consumed during pregnancy, the greater the risk of pregnancy-related problems and birth defects.
It is recommended that pregnant women avoid all consumption of alcohol. Fetal alcohol spectrum disorders are a group of conditions reflecting the possible effects of prenatal exposure to alcohol. The FASDs include fetal alcohol syndrome (FAS), alcohol-related birth defects (ARBD), and alcohol-related neurodevelopmental disabilities (ARND). Fetal alcohol syndrome (FAS) is the extreme end of the fetal alcohol spectrum disorders and is a leading cause of cognitive disabilities.

How do high blood pressure and diabetes affect pregnancy?

Elevated blood pressure (hypertension) that is present before pregnancy can interfere with growth of the fetus and increase the risk of fetal death. Therefore, controlling blood pressure with carefully chosen blood pressure medications is important during pregnancy and before conception.
In addition, underlying hypertension can increase the risk for a condition called preeclampsia, a potentially very dangerous complication of pregnancy. It is sometimes difficult for doctors to distinguish between high blood pressure alone and high blood pressure occurring from preeclampsia. For those reasons, and given the risk of birth defects from many of the blood pressure medications, women with high blood pressure who become pregnant should be followed very carefully by a medical expert who is familiar with this type of situation. Ideally, medication would be switched to a relatively safe medication before the woman even becomes pregnant.
Poorly controlled diabetes can lead to high blood sugar levels. High blood sugar levels during early pregnancy can lead to miscarriages and birth defects. Therefore, controlling diabetes is important for a good pregnancy outcome, and the blood sugar should ideally be controlled before becoming pregnant. It is important to consider that control of blood sugar during pregnancy is important, but control prior to pregnancy may be just as important.
Oral diabetes medications may be dangerous to the fetus, but insulin is not dangerous to the fetus. Insulin is the key treatment for diabetes during pregnancy. Not only is insulin safe to the baby and mother, but it also helps prevent the complications that the baby could have suffered from the mother's sugar being uncontrolled. Insulin is usually substituted for pills as soon as a woman with diabetes is considering pregnancy. The ideal time to control blood sugar is before pregnancy, because control of sugar levels even in early pregnancy (when the mother does not yet

What are examples of commonly-used medications that are dangerous in pregnancy?

Many women do not know that over-the-counter medications can be dangerous. In fact, many prescription and over-the-counter medications harm the fetus very early in pregnancy at a time that the mother does not even know she is pregnant. Even aspirin use by the mother can cause defects in the fetus. For this reason, as soon as pregnancy is being contemplated, women should avoid all over-the-counter and prescription medications until reviewed with their doctor.
Acne medications, such as isotretinoin (Accutane) can cause birth defects, and should be discontinued before conception. Since many medications and substances can affect fetal growth and development, pregnancy planning is important so that potentially harmful substances can be stopped before conceiving.
Unplanned pregnancy during oral contraceptive use is not felt to pose a significant danger to the fetus, although deliberate use of oral contraceptives during pregnancy is not advisable. Women who become pregnant during oral contraceptive use have the same risk of birth defects in their newborns as the general population of women, in the range of 2% to 3%.

How do kidney and heart disease affect pregnancy?

Because pregnancy is associated with an increase in blood volume and an increase in cardiac output as well as other changes in the circulatory system, many types of heart disease may worsen or be associated with poor outcome during pregnancy. While many mild chronic heart conditions may be well tolerated during pregnancy, other conditions pose a significant risk to mother and fetus. Women with preexisting heart disease should always consult an expert when planning a pregnancy to examine their own degree of risk, potential outcomes, and treatment options. know she is pregnant) is important for the developing baby's health.

What infections affect pregnancy?

Certain infections during early pregnancy can cause birth defects in the fetus. Rubella (German measles) virus infection during early pregnancy can cause birth defects and even miscarriages. Therefore, women of child bearing age are tested for blood antibodies against this virus. Women lacking rubella virus antibodies are susceptible to rubella infection, and should be vaccinated against this virus. Pregnancy should be avoided for one month after vaccination, due to the theoretical concern that the vaccine virus itself may cause fetal damage.
Toxoplasmosis is a small parasite that is transmitted through cat feces and raw meats, especially pork. Toxoplasmosis, like the rubella virus, can cause severe birth defects if the infection occurs during early pregnancy. Women planning pregnancy should avoid raw meat and avoid handling the cat litter box. Many people have been exposed to toxoplasmosis without even knowing it. As a result, they develop a protective immunity from the "silent" infection. Women who have a blood test that is positive for toxoplasmosis immunity can be reassured that they will not develop toxoplasmosis complications during pregnancy.
Hepatitis B is the only type of hepatitis that is known to affect the newborn infant.
Female healthcare workers, dental assistants, and others exposed to hepatitis B should receive hepatitis B vaccination to avoid chronic infection by this virus. The majority of hepatitis B virus infections resolve spontaneously without treatment. Patients whose disease resolves completely are no longer contagious. Approximately 10% of hepatitis B virus infections do not resolve, and become chronic. Patients chronically infected with hepatitis B virus may have no symptoms of liver disease early on, but they remain contagious. Over time, chronic hepatitis B infection can lead to liver cirrhosis and/or liver cancer.
Women with chronic hepatitis B infection can transmit the virus to their babies at birth. Babies infected are at risk of developing chronic liver disease, liver cirrhosis, and liver cancer in later life. Currently, infants born to mothers infected with the hepatitis B virus are given both the hepatitis B antibodies and hepatitis B vaccinations at birth for protection. Therefore, pregnant women are often tested for signs of hepatitis B infection, even if they do not have any symptoms or knowledge of past infection. The babies of infected mothers detected in this manner would receive special care at (and after) delivery.
Cytomegalovirus (CMV) is a common viral infection worldwide that often does not produce any symptoms. Women who become infected or have a reactivation of a previous infection during pregnancy may pass the infection along to their babies. Congenital CMV infection is the most common congenital viral infection. Although the majority of infected infants will not have any symptoms, up to 20% will have symptoms that may include an enlarged spleen, jaundice, or rash. Rarely, involvement of many organs may occur resulting in severe illness or disability.
Genital herpes may also result in the passage of the infection to the infant at the time of delivery. The risk of transmission is increased if the genital lesions are from a herpesvirus (HSV) infection acquired during the pregnancy, rather than simply a reactivation of previous disease. HSV infection can have multiple effects in the newborn. Disease may be limited to the eyes, skin and mouth; may be localized to the central nervous system; or may be widespread and involve many organs. Treatment involves administration of antiviral medications to the newborn and supportive care.
Parvovirus B19 is a virus that causes the condition known as Fifth disease, a common mild disease of childhood. Transmission is by droplets in the air (respiratory secretions) or through blood. Pregnant women who have not previously had fifth disease should avoid contact with those who have it because parvovirus B-19 can infect a fetus prior to birth. Although no birth defects have been reported as a result of fifth disease, it can cause the death of an unborn fetus. This occurs in less than 5% of pregnant women who become infected with the virus.
When traveling to a foreign country, it is important to determine what diseases are common, whether vaccines are needed, and whether they are safe during pregnancy. Human immunodeficiency virus (HIV) infection can be passed from a mother to her baby. The chances of this happening are decreased substantially with certain medication programs during pregnancy. Pregnant women are routinely offered testing for HIV infection. Women with previously undetected infection who are found to have HIV infection can be given special medication to try to protect the baby. At the same time, the medication may benefit the health of the mother herself.
Varicella, or chickenpox, can cause pneumonia or even death in older adults and in pregnant women. Varicella vaccine is available for women who are not immune to chickenpox. Women who had chickenpox in the past do not need a vaccine because they are immune. Women who are not sure if they are immune can receive a blood test to determine immunity status. A vaccine would be given if the blood test showed they were not immune.

What inherited (genetic) diseases can play a role in pregnancy planning?

Certain diseases, such as Tay-Sachs, sickle cell anemia, hemophilia, cystic fibrosis, and certain neurological diseases are genetically inherited. Healthy couples with family histories of these conditions may themselves be carriers of these genetic traits. Blood tests can be performed to screen for certain genetic traits prior to conceiving. Genetic counseling is given to couples who may carry genetic diseases as part of pregnancy planning.
Older women have an increased risk of having babies with chromosome abnormalities, leading to cognitive disabilities and other birth defects. Chromosomal abnormalities (like Downs syndrome ) can lead to birth defects and cognitive disabilities. Pregnant women older than 35 years may consider amniocentesis to detect these chromosomal abnormalities. During amniocentesis, amniotic fluid samples are aspirated from the womb. Chromosome analysis can be performed on fetal cells within the amniotic fluid.
Phenylketonuria is an inherited disease that affects the utilization of a certain protein component in foods. This disorder can be detected by a blood test. Mothers with phenylketonuria may give birth to developmentally disabled children unless their diets are strictly controlled to exclude phenylalanine.

Is it safe to exercise during pregnancy?

Recommendations from the American College of Obstetrics and Gynecology say that pregnant women who have an uncomplicated pregnancy should participate in at least 30 minutes of moderate exercise on most, if not all, days of the week. A few exceptions are noted: ice hockey, kickboxing, soccer, and horseback riding probably should be avoided because they are activities with higher risk of trauma to the abdomen. Also, scuba diving poses a risk of decompression sickness ("the bends") to the fetus and should be avoided. Exercise programs should be discussed with the monitoring health care professional.
Elevated temperatures can have adverse effects on the development of the fetus. Therefore, hot tubs and sauna baths should be avoided when trying to conceive and during pregnancy.

Can I travel by air during pregnancy?

The American College of Obstetrics and Gynecology guidelines say that air travel is safe for most pregnant women up to 36 weeks gestation, as long as there are no obstetric or maternal complications already diagnosed. Examples of special situations would be women with hypertension, poorly-controlled diabetes, or sickle cell disease, or women diagnosed with increased risk of premature labor. Support stockings during flight, and intermittent walking to move the legs around are recommended to minimize the chance of blood clots in the legs during prolonged flights. Travel plans should be discussed with the monitoring health care professional in high-risk pregnancies.

Can I have intercourse during pregnancy?

Intercourse during pregnancy is safe for most women. Special situations in which women might be advised to avoid intercourse include prior preterm labor, multiple miscarriages, infection, bleeding, amniotic fluid leak, and a condition called placenta previa or low placenta. (A placenta previa is when the placenta is implanted near the outlet of the uterus, so that at the time of delivery the placenta precedes the baby. Placenta previa can cause painless bleeding in the last trimester of pregnancy, and may be a reason for a C-section.)
All women are advised to avoid sexual intercourse that could put them at risk to exposure to sexually transmitted diseases.

How soon after stopping birth control can I become pregnant?

There is no evidence that there is increased risk of spontaneous abortion increases if a woman becomes pregnant in the first cycles after stopping oral contraceptive pills. Intrauterine devices (IUD's) are not harmful to the fetus. Women who get pregnant with an IUD that is still in place do not have higher change of congenital abnormalities in the fetus compared to other women. If the IUD of a woman in her 1st trimester is carefully removed by a doctor, or if it is expelled on its own in the 1st trimester, the chance of spontaneous miscarriage is not increased compared to other women.
When barrier methods such as condoms, diaphragms, cervical caps, and sponges are used, pregnancy can occur by simply discontinuing their use during a regular cycle. The same can be said for spermicidal gels and suppositories.
Medroxyprogesterone (Depo-Provera) is an injectable hormone used for contraception. The contraceptive effect of Depo-Provera may last as long as 18 months after the last injection. Normal menstrual cycles and pregnancy cannot occur until after the contraceptive effect wears off.

How do we maximize our chances of becoming pregnant?

For most couples, becoming pregnant occurs naturally. Some couples have difficulty conceiving, and ways to maximize chances of conception become important. Other parents may want to time the delivery of their babies during particular times of the year or space the birth of their babies according to a desired schedule.
The first step in maximizing the chances of conception is by estimating the time of ovulation. Ovulation is that time of the menstrual cycle wherein the egg is released from the ovary and travels towards the Fallopian tube. In women with regular menstrual cycles, ovulation usually occurs 12-14 days prior to the onset of the next menstrual flow. Simply counting back fourteen days from the expected date of the onset of next period should be the time of ovulation. The couple should have intercourse for several days before, day of, and day after the expected time of ovulation. There is usually some variation in the time of ovulation even in women with regular cycles, so a few extra days of intercourse before and after expected ovulation is advised.
If the cycles are irregular and unpredictable, estimating the time of ovulation becomes difficult, and professional assistance may be helpful. Another option for a woman with irregular cycles is the use of ovulation predictor kits available over-the-counter at most drug and grocery stores. These kits can be used to determine the approximate time of ovulation by detecting urinary hormone elevations that precede ovulation. Another approach is to have intercourse every other day throughout the menstrual cycle. This approach will take out the stress or anxiety involved in timing intercourse.
Basal body temperature timing is a technique of checking the body temperature every morning and charting the results. If the temperature rises by a certain amount and stays elevated, it can be assumed that ovulation occurred. Difficulties with this method are that it is tedious and only provides the woman with information about ovulation after it has occurred.
Ultrasound images of the ovaries can be performed to monitor the growth and collapse of the ovarian follicle during the cycle. The follicle is the fluid-filled structure that surrounds the egg, and it can easily be seen on ultrasound. This method is probably the most accurate in timing ovulation. It is also the most expensive and is usually reserved for selected couples who are experiencing difficulty in becoming pregnant.
It is important to remember that even though intercourse and ovulation coincide, pregnancy may still not be achieved in any given menstrual cycle or even after several consecutive menstrual cycles. In many situations, the failure to conceive after multiple attempts is not a reason for alarm. It is not uncommon for pregnancy to occur only after several months of consistent attempts. Couples who have experienced an inability to conceive after several cycles may consider seeking professional advice to determine if an infertility evaluation is necessary.

Can I do something to help my chances of conceiving a boy or a girl?

The ancient Greeks tied off the left testicle when attempting to conceive a boy.
French noblemen in the 18th century went one step further and actually removed the left testicle, believing that this would guarantee a male infant.
In the 19th century, the man would stand on the right bedpost and the woman would lie on her right side after intercourse in order to assure a boy!
The 20th century brought on the ideas of deep penetration, adjustment of vaginal acidity, consumption of certain foods, position, and other various methods to enhance the chances of bearing either a girl or a boy.

None of these various approaches has ever been scientifically tested. Therefore, no definite statement can be given regarding the success of these techniques, but they probably have no impact on the gender of the baby. Currently there have been a few proven laboratory techniques of increasing the percentage of male or female sperm, but these are not routinely used. These techniques either use electrical charges, or special "gels" through which the sperm have to swim. Even with these techniques, there is no guarantee that a child of the desired gender will be born. Research has refuted any relationship between the timing of sexual intercourse in relation to ovulation and the gender of the baby.

REFERENCES:

eMedicine.com. Pregnancy Diagnosis.

eMedicine.com. Common Pregnancy Complaints and Questions.

Previous contributing authors: Leon J. Baginski, MD, FACOG and Carolyn Janet Crandall, MD

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR
Source:Medicinenet.com.

Cerebral Palsy

2012-03-26T08:43:00.002-07:00

What is cerebral palsy?

Cerebral palsy (CP) is an abnormality of motor function (as opposed to mental function) and postural tone that is acquired at an early age, even before birth. Signs and symptoms of cerebral palsy usually show in the first year of life.
This abnormality in the motor system is the result of brain lesions that are non-progressive. The motor system of the body provides the ability to move and control movements. A brain lesion is any abnormality of brain structure or function. "Non-progressive" means that the lesion does not produce ongoing degeneration of the brain. It is also implies that the brain lesion is the result of a one-time brain injury, that will not occur again. Whatever the brain damage that occurred at the time of the injury is the extent of damage for the rest of the child's life.
Cerebral palsy affects approximately one to three out of every thousand children born. However, it is much higher in infants born with very low weight and in premature infants.
Interestingly, new treatment methods that resulted in an increased survival rate of low-birth weight and premature infants actually resulted in an overall increase number of children with cerebral palsy. The new technologies, however, did not change the rate of cerebral palsy in children born full term and with normal weight.

What are causes of cerebral palsy?

The term cerebral palsy does not indicate the cause or prognosis of the child with cerebral palsy. There are many possible causes of cerebral palsy.
In full term infants the cause of cerebral palsy is usually prenatal and not related to events at time of delivery; in most instances it is related to events that happened during the pregnancy while the fetus is developing inside the mother's womb.
Premature birth is a risk factor for cerebral palsy. The premature brain is at a high risk of bleeding, and when severe enough, it can result in cerebral palsy. Children that are born prematurely can also develop serious respiratory distress due to immature and poorly developed lungs. This can lead to periods of decreased oxygen delivered to the brain that might result in cerebral palsy. A poorly understood brain process observed in some premature infants is called periventricular leukomalacia. This is a disorder in which holes form in the white matter of the premature infant's brain. The white matter is necessary for the normal processing of signals that are transmitted throughout the brain, and from the brain to the rest of the body.
White matter abnormalities are observed in many cases of cerebral palsy. Nevertheless, it is important to recognize that the vast majority of premature infants, even those born very prematurely, do not suffer from cerebral palsy. There have been many advances in the field of neonatology (the care and study of problems affecting newborn infants) which have enhanced the survival of very premature infants.
Other important causes of cerebral palsy include accidents of brain development, genetic disorders, stroke due to abnormal blood vessels or blood clots, or infections of the brain.
Even though it is widely believed that the most common cause of cerebral palsy is a lack of oxygen to the brain during delivery (birth asphyxia), it is actually a very rare cause of cerebral palsy. When cerebral palsy is the result of birth asphyxia, the infant almost always suffers severe neonatal encephalopathy with symptoms during the first few days of life. These symptoms include:

seizures,
irritability,
jitteriness,
feeding and respiratory problems,
lethargy, and
coma depending on the severity.

In rare instances, obstetrical accidents during particularly difficult deliveries can cause brain damage and result in cerebral palsy. Conversely, it is very unlikely that cerebral palsy symptoms would develop after a few years of age as a result of obstetrical complications.
Child abuse during infancy can cause significant brain damage which, in turn, can lead to cerebral palsy. This abuse often takes the form of severe shaking from a frustrated parent or caregiver, causing hemorrhage in or just outside the brain. To further compound the problem, many children with developmental abnormalities are at risk for being abused. Thus, a child with cerebral palsy may be made significantly worse or even killed by a single incident of abuse.
Despite the diversity of causes of cerebral palsy, many cases remain without a defined cause. However, the enhanced ability to see the brain structure with magnetic resonance imaging (MRI) and CT scans as well as improved diagnostic capabilities for genetic disorders has made the number of such cases much lower.

What are the types of cerebral palsy?

Based upon the form of motor impairment, cerebral palsy can be divided into types:

spastic cerebral palsy,
choreoathetoid cerebral palsy, and
hypotonic cerebral palsy.

These categories are not rigid, and the majority of patients probably have a mixture of these.

What is spastic cerebral palsy?

Spastic cerebral palsy refers to a condition in which the muscle tone is increased, causing a rigid posture in one or more extremities [arm(s) or leg(s)]. This rigidity can be overcome with some force, ultimately giving way completely and suddenly -- very much like the familiar jackknife (or clasp knife). The spasticity leads to a limitation of use of the involved extremity, largely due to the inability to coordinate movements. Often the spasticity occurs on one side of the body (hemiparesis), but it can also affect the four limbs (quadriparesis) or be limited to both legs (spastic diplegia). When the condition occurs in both legs, the individual often has a scissoring posture, in which the legs are extended (straightened) and crossed.
Besides the increased muscle tone there is also increased deep tendon reflexes, impaired fine and gross motor coordination, muscle weakness, and fatigability among other problems.
Spasticity is often the result of damage to the white matter of the brain, but it can also be due to damage of gray matter.
The degree of spasticity can vary, ranging from mild to severe. Children who are mildly affected may experience few limitations of their function while severely affected children may have little to no meaningful use of the affected limb(s). Spasticity, if not properly treated, can result in contractures, which are permanent limitations in the ability of joint movement. Contractures can be greatly limiting in the care of children with cerebral palsy. Spasticity can also be quite painful, requiring medication to relax the muscle tone.
The same fundamental processes that influence spasticity of the limbs can also result in abnormalities of movement and muscle tone in other body systems. In the muscles of the head and face, for example, cerebral palsy can greatly limit the coordination and production of speech, even when the child is perfectly capable of understanding speech. There can also be limitations of chewing, swallowing, and facial and eye movements. These symptoms can be particularly troubling for afflicted children and their families.
Many patients with spastic cerebral palsy cannot control their output of urine. This inability is not necessarily due to problems in thinking but is caused by heightened reflexes of the bladder. When the bladder fills in these children, it is just like tapping on it with a reflex hammer, thus making it contract more vigorously than normal and causing a spilling of urine. This incontinence can be quite embarrassing, especially in a cognitively intact child.

What is choreoathetoid cerebral palsy?

Choreoathetoid cerebral palsy is associated with abnormal, uncontrollable, writhing movements of the arms and/or legs. Different from spastic cerebral palsy, persons with choreoathetoid cerebral palsy have variable muscle tone often with decreased muscle tone (hypotonia). Contractures of extremities are less common. The abnormal movements are activated by stress, as well as by normal emotional reactions such as laughing. Any attempt to do voluntary movements, for example extending the arm in an attempt to reach an object might result in many involuntary movements in arms, legs, trunk, and even the face. There are different types of abnormal movements. Two of the most common are choreoathetotic movement disorder with rapid, irregular, unpredictable contractions of individual or small muscles groups and dystonia with a persistent but not permanent, abnormal posture of some body parts (arms, legs, trunk) due to abnormal muscle contractions. The dystonic disorder also affects the muscle of the facial expression, swallowing, deglutition and speech, resulting in severe functional deficiencies.
These movements can be quite debilitating and greatly limit the child's ability to perform many motor tasks. Furthermore, the movements are akin to constant exercise, thereby causing the affected child to metabolize a huge number of calories. Choreoathetoid cerebral palsy is often associated with damage to specialized brain structures that are involved in movement control -- the basal ganglia. Like spastic cerebral palsy, the degree of symptom severity often varies, from mild to severely affected.

What is hypotonic cerebral palsy?

Hypotonia is diminished muscle tone. The infant or child with hypotonic cerebral palsy appears floppy -- like a rag doll. In early infancy, hypotonia can be easily seen by the inability of the infant to gain any head control when pulled by the arms to a sitting position (this symptom is often referred to as head lag). Children with severe hypotonias may have the most difficulty of all children with cerebral palsy in attaining motor skill milestones and normal cognitive development.
Hypotonic cerebral palsy is often the result of severe brain damage or malformations. It is believed that hypotonic cerebral palsy is the result of an injury or malformation at an earlier brain developmental stage than that which causes spastic or choreoathetoid cerebral palsy.
Hypotonia in infancy is a common finding in many neurological conditions, ranging from very mild abnormalities to severe or even fatal neurodegenerative or muscle disorders. It is important to note that many children with spastic cerebral palsy go through a short stage of being somewhat hypotonic in early life, before presenting the full syndrome.

What is mixed cerebral palsy?

Many (possibly most) children with cerebral palsy have multiple symptoms with combinations of the various forms of cerebral palsy. For example, children with spastic cerebral palsy often continue to have a head lag, which is representative of hypotonia. Children with choreoathetoid or hypotonic cerebral palsy often have increased deep tendon reflexes, which are suggestive of some spasticity.

What other conditions are associated with cerebral palsy?

Since cerebral palsy is indicative of damage to or malformation of the brain, it stands to reason that other symptoms that are associated with brain dysfunction can be present in children afflicted with cerebral palsy. In fact other disorders, besides the motor dysfunctions already described, are almost always seen in these patients. Some of them such as poor speech, swallowing disorders, drooling, and poor fine or gross motor coordination are the result of the motor disorder affecting specific muscles involved in those functions. Other conditions are the results of simultaneous injuries in areas of the brain besides the motor areas.
Cognitive disabilities, sometimes referred to as developmental delay, is often associated with cerebral palsy. Up to 50% of patients with cerebral palsy have cognitive disabilities. However, many of these children can be educated and lead productive lives. It is also just as important to note that many children with severe motor impairment due to cerebral palsy, as is the case with many children with the choreoathetotic or the diplegic form of cerebral palsy, are only mildly or not at all intellectually impaired.
Virtually all testing of a young child's cognitive development involves some sort of motor activity on the part of the child. If a child is capable of complex thoughts, but incapable of motor activity, the observer will not be able to detect his or her mental aptitude. Therefore, one must be very careful in assigning labels to patients with cerebral palsy. Certain features, however, are more likely to be associated with significant cognitive disabilities in the patient with cerebral palsy. These include extensive damage occurring on both sides of the brain, children with spastic quadriplegia, microcephaly (small head size), a documented genetic disorder, and a documented prenatal infection.
Seizures are a common finding in patients with cerebral palsy. Perhaps a third of all cerebral palsy patients have seizures. Seizures are caused by abnormal electrical activity of the neurons in the brain. The damaged or malformed brain is more prone to seizures. Moreover, cognitive disability is frequently associated with epileptic seizures.
The symptoms of seizures can vary depending on where in the brain they originate. Generalized seizures engage the entire cerebral cortex at once, while partial seizures only involve part of the cerebral cortex. Often, generalized seizures begin as partial seizures but spread throughout the brain rapidly. Generalized seizures may take the form of true convulsions ("grand mal"), in which the entire body jerks in a rhythmic fashion, or the form of absences ("petit mal"), which interrupt the patient's activities for a brief period, but does not cause a fall.
Other forms of generalized seizures can occur in the cerebral palsy patient. Atonic seizures cause the patient to slump suddenly to the ground or forward in their chair, resembling a marionette in which the puppeteer suddenly cut the strings. Tonic seizures are just the opposite and cause the entire body to suddenly stiffen. Both tonic and atonic seizures can result in drop attacks in which the patient falls to the ground, often resulting in injury.
Partial seizures may involve the jerking of the arm and leg on the same side of the body. Alternatively, they may be associated with strange sensory phenomena, such as flashing lights, or emotions, such as fear, depending on where in the brain the seizure occurs.
Vision deficiencies are frequently seen. Some of them, for example, strabismus ("lazy eyes") can be corrected by surgical procedures in the muscles of the eyes. Some can be corrected with eye glasses (that may be difficult to implement in non-cooperative children). In other children the visual deficiencies are the result of brain injuries to the areas of the brain that are associated with vision, rendering the child blind ("cortical blindness") even if the eyes themselves are perfectly normal. At the present time there is no treatment to improve this condition.
Children with cerebral palsy can have speech disorders of many types. Some, like poor word pronunciation (dysarthria), are the result of impairment of the peripheral mechanism of speech (poor lips, tongue, or palate coordination). In another circumstance there is brain injury in the gray matter of the brain that controls the central mechanism of speech (aphasia).
It is difficult for children with cerebral palsy to gain weight and frequently have delayed growth. This is the result of several factors including feeding disorders, gastroesophageal reflux, and in some instances, for example, children with choreoathetotic disorders, excessive caloric consumption. On the other, hand obesity could be a problem in those children with cerebral palsy that have and limited mobility.
Individuals with the choreoathetotic form of cerebral palsy might have compressed nerves or damage to the neck bones that can lead to damage to the spinal cord.
Other issues to be aware of are dental diseases, respiratory problems, urinary tract infections, osteoporosis and subsequent fractures, enuresis, encopresis, constipation.

How is a child evaluated for cerebral palsy?

Most of the information leading to the diagnosis of cerebral palsy is generally obtained from a thorough medical history and examination. The most critical tasks of the healthcare provider are to identify potentially treatable causes of a child's impairment. The healthcare provider evaluating the child with possible cerebral palsy should be experienced in neurological examination and assessment of impaired children and well-versed in the potential causes of cerebral palsy. Often, but not necessarily, this practitioner should be a pediatric neurologist. Once the examination is complete, depending on the findings, the practitioner may order laboratory tests to help in the assessment.
There is no single test to diagnose cerebral palsy. But since cerebral palsy is the result of multiple different causes, the tests performed are used to identify specific causes when possible. Other tests will be performed to assess the condition of the child (nutritional status for example) or to assess other concomitant conditions that the child might have.
Blood and urine tests may be used to identify some of the more common inborn errors of metabolism. Blood tests may also be used for chromosomal or other genetic studies. Brain imaging studies can also be used to detect structural changes in the brain. The most sensitive brain imaging study is the MRI examination. Nuclear medicine neuroimaging studies such as SPECT or PET have no place in the initial evaluation of a child with cerebral palsy, but may prove very useful in the assessment of selected candidates.
Despite all of these tests, it may not be possible to answer some of the burning questions in the mind of a parent of a neurologically impaired infant, such as "Why does my child have cerebral palsy?" or "Will my child be normal?" This is particularly true if a specific diagnosis is not reached and the child is under one year of age. Some severely impaired young infants can grow up to be independent, productive members of society, while other children, seemingly less impaired, may require care throughout their lives.
Once the diagnostic evaluation is complete, further testing may be needed in order to define the specific needs of any individual child. For example, if seizures are present or suspected, an EEG (electroencephalogram) is performed. However, this test is not needed if there are no signs of epilepsy.

How is cerebral palsy treated?

Most of the causes of cerebral palsy do not have specific, curative treatments. However, children with cerebral palsy present many medical problems that can be treated or prevented. The initial stage of treatment involves an interdisciplinary team, consisting of a pediatrician, preferable one with experience in neurodevelopmental disorders, a neurologist (or other neurological practitioner), a mental health practitioner, an orthopedic surgeon, a physical therapist, a speech therapist, and a occupational therapist. Each member of the team has important, independent contributions to make in the care of the affected child.

The physical therapist evaluates muscle tone, strength and gait (walking).
The occupational therapist reviews the child's ability to perform tasks of self-help and care -- from feeding to manual dexterity.
The speech therapist evaluates the child's ability to speak and understand speech.

Most children with neurological impairment have significant emotional distress and also require therapy from a mental health practitioner.
Virtually all states have federally-mandated programs for the assessment and treatment of children with cerebral palsy and other developmental conditions. In many states, these programs are termed "Regional Centers" and can be found in local phone books. Also Children's Hospitals usually have special clinics with experience with children with cerebral palsy. Furthermore, when a child reaches the age of 3 years, the school district may become formally involved in the review of at-risk children. These programs protect children up to the age of 21 years.
At the present time there is a vacuum in the provision of medical care for adults (young and old) with cerebral palsy living in the community settings. There are a limited number of services in adult hospitals geared to the treatment of adults with cerebral palsy or developmental disabilities.

What are specific treatment plans for cerebral palsy?

After the initial evaluation, specific treatment plans are outlined for each child:
Seizure medication
If the child has seizures, the treatment is based on the type and frequency of the seizures. Complete seizure control can often be achieved using a single medication, but some children with cerebral palsy have particularly difficult-to-control seizures. Medication can have side effects affecting the brain, ranging from sedation to hyperactivity. They can also affect liver function, white and red blood cells, and bone metabolism. Side effects are usually not harmful and resolve when the offending medication is discontinued. The goal of the treating physician should be for the child to become seizure free with few or no side effects. It must be noted that it is of no benefit to the child to be seizure-free but significantly impaired by medication side effects.
Medications for spasticity: The treatment of spasticity can involve multiple health professionals. Treatments involve the use of medications and surgical procedures to decrease the spasticity, facilitate movement, and prevent contractions. Among the most commonly medications are dantrolene sodium (Dantrium) and diazepam (Valium). Diazepam is both a muscle relaxant and a sedative. Baclofen (Lioresal) can be taken by mouth or infused continuously with an implanted pump (intrathecal infusion) directly in the cerebrospinal fluid (the liquid that bathe the spinal cord and the brain). This treatment might be specifically useful for patients with spasticity in the lower legs. The most common complications with these medications are drowsiness, sleepiness, some degree of weakness. The sedative side effects of such medications often limit their usefulness. In the case of the baclofen pump the most common complication seen in small number of patients is the infection of the catheter. Additionally, a muscle relaxing agent called botulinum toxin can be injected into tight muscles to relax them. When used prudently, this procedure may prevent surgical intervention.
Surgery
Surgery for spasticity: In the case of severe muscle spasticity, surgery may be a valuable option. Tendon release procedures, usually performed by an orthopedic surgeon, allow improved range of motion in some cases. Such procedures are usually performed on the muscles of the calf or inner thigh. A less commonly used procedure, is the dorsal rhizotomy. During this operation, the surgeon cuts some of the nerve roots that send sensory information from the muscles to the spinal cord and brain. This procedure relieves some of the spasticity and thereby helps the child walk with a more normal gait. Most neurosurgeons performing dorsal rhizotomies very carefully select only those patients whom they feel may be helped by the surgery. From time to time, other surgical interventions are required in children with cerebral palsy. In very rare cases of choreoathetoid cerebral palsy, in which the writhing movements severely limit the ability of the child to function, highly selective neurosurgical techniques can curtail these movements without significantly harming other functions.
Other surgical procedures
Ophthalmologists (eye specialists) can help strabismus by operating on the muscles that control the movement of the eye or to correct some other complications such as cataracts.
Neurosurgeons can treat intractable seizure control. Operations such as callosotomy, hemispherectomy, focal resections of areas of abnormal brain tissue responsible for the seizures, might be indicated in some cases. An alternative procedure for the treatment of epilepsy is the vagal nerve stimulation, an implantable device, that can be useful in selected patients with difficult to control seizures.
Scoliosis, or curvature of the spine, is often the result of severe hypotonia. This condition can create discomfort for the patient and difficulty for caregivers in performing the activities of daily living. Furthermore, severe scoliosis may actually restrict a patient's ability to breathe. Several surgical procedures are available in specialized centers for the correction of scoliosis.
Children who are unable to take adequate calories by mouth may require the placement of a feeding gastrostomy tube (PEG tubes) directly into the stomach.
Therapy
The treatment of spasticity can involve multiple allied healthcare professionals. Physical and occupational therapists play an important role.
Physical therapy: The extent of physical therapy depends on the degree of spasticity, hypotonia, and motor impairment. The main therapeutic effect of physical therapy is maintaining range of motion at the joints, thereby preventing contractures. Some scientists and therapists feel that physical therapy actually helps maintain the connections in the brain, although this is controversial. Other skills, such as improved gait, stance, and balance can be helped by physical therapy. A strong, proactive physical therapy program greatly aids in the life of a child with cerebral palsy.
Occupational therapy: Occupational therapy assists children with the skills needed for day-to-day life in school and at home, including eating, writing, and work skills. In early infancy, occupational therapists can provide assistance in feeding a child with a poor or uncoordinated sucking response.
Speech therapy: Speech and language pathologists are involved with the development and improvement of speech production. Using different techniques the speech pathologist helps to improve the quality and the quantity of the speech production. The role of these specialists is not limited to speech production alone, but they also teach the patients other communication techniques (sign language, use of communication boards) to facilitate the communication abilities.
Medical care
Medical care of children with cerebral palsy is often seriously hampered by the inability of the child to communicate his or her needs and sensations. Relatively common childhood illnesses in children with cerebral palsy, such as ear infections, urinary tract infections, and appendicitis, which are easily treatable in most children, may prove to be life-threatening due to delayed recognition on the part of caregivers and physicians. Each child with cerebral palsy should have a primary care practitioner that is experienced with the special medical needs of affected children.
Because physicians have offered limited hope in curing cerebral palsy, many families have turned to alternative methods in the treatment of their children. Such therapies may include diets, herbal remedies, aromas, play with animals, and hyperbaric oxygen. The scientific evidence supporting the use of diets is inadequate. Some of them such as hyperbaric oxygen therapy, which is delivered in specialized centers, can be quite expensive and has not been scientifically proven to help children with cerebral palsy. Other remedies must be investigated on a case-by-case basis. Hopefully, the family of the affected child will be able to approach their physician regarding these alternative treatments.

What is the long-term outlook for patients with cerebral palsy?

The answer is complex. Since cerebral palsy is actually a set of symptoms associated with a variety of causes, potential treatments will have to be diverse. Many scientists are now focusing on recent discoveries that suggest we will be able to replace lost or damaged brain cells. While such therapies are not yet available, it is likely that real clinical trials will begin in the next 5 to 10 years.
The more we know about the causes of cerebral palsy, the more we can do to prevent it. For example the use of folic acid in sexually active women may prevent central nervous system malformations that might lead to cerebral palsy. Avoiding the use of certain drugs during the pregnancy whether legal, such as prescribed medications, alcohol or tobacco, or illegal such as cocaine and crack, will also decrease the changes of cerebral palsy in a child.
It cannot be overemphasized that the most important person in the lives of children with cerebral palsy is their caregiver. The caregiver, whether a parent or other person, must be able to recognize a child's needs and provide for him or her in a loving, positive environment. Because of the difficulty that many children with cerebral palsy have in expressing their needs, they are at great risk for unintentional and intentional neglect as well as overt child abuse. Often, the care of children with cerebral palsy can be quite taxing emotionally and financially on the family. The appropriate care for children with cerebral palsy, therefore, must take into account mental health and financial support for families and caregivers. Many state-run programs provide out-of-home schooling as well as respite care for the caregivers, but these services often falls short of what is truly needed. Healthcare practitioners can very simply improve the lives of their patients by taking some extra time to listen to the concerns and hopes of the caregivers and provide thoughtful answers to their questions.
We must recognize that many, and possibly most, children with cerebral palsy can lead full, meaningful, and happy lives. The team of parents, caregivers, and health practitioners have the responsibility to help the child with cerebral palsy achieve this goal.

Cerebral Palsy At A Glance

Cerebral palsy (CP) is an abnormality of motor function, the ability to move and control movements.
Cerebral palsy is acquired at an early age, usually less than a year of age.
Cerebral palsy is due to a brain abnormality that does not progress in severity.
The causes of cerebral palsy include prematurity, genetic disorders, strokes, and infection of the brain.
Taking certain precautions during the pregnancy might decrease the risk of cerebral palsy.
Asphyxia, the lack of oxygen to the brain, at birth is not as common a cause of cerebral palsy as had been thought.
There are different types of cerebral palsy based on symptoms -- spastic, hypotonic, choreoathetoid and mixed types.
The best approach for diagnosis, treatment, and management is through and interdisciplinary team.
Cerebral palsy may be associated with many other medical conditions, including mental retardation or seizures. Many of these conditions can be treated with improved quality of life.
Many children with cerebral palsy have a normal intellect and have no seizures.
Treatment of cerebral palsy is for the symptoms only; there are few treatments for the underlying causes.
There are many alternative medicines promoted for the treatment of cerebral palsy that have never been proven to be helpful. Families and advocates of persons with cerebral palsy should be aware of the lack of scientific basis for these treatments.

Medical Author:

Norberto Alvarez, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Infectious Mononucleosis (Mono)

2012-03-26T08:40:00.002-07:00

Infectious mononucleosis (mono) facts

Infectious mononucleosis (mono) is a contagious illness caused by the Epstein-Barr virus (EBV).
The infection can be spread by saliva, and the incubation period for mono is four to eight weeks.
Most adults have laboratory evidence (antibodies against the EBV) indicative of a previous infection with EBV and are immune to further infection.
The symptoms of mono include fever, fatigue, sore throat, and swollen lymph nodes.
The diagnosis of mono is confirmed by blood tests.
Mono can cause liver inflammation (hepatitis) and enlargement of the spleen.
People who have had mono can continue to shed virus particles in their saliva during reactivations of the viral infection throughout their lifetime.
Vigorous contact sports should be avoided in the illness and recovery phase to prevent rupture of the spleen.

What is infectious mononucleosis?

Infectious mononucleosis, "mono," "kissing disease," and glandular fever are all terms popularly used for the very common infection caused by the Epstein-Barr virus (EBV). EBV is a member of the herpesvirus family. The characteristic symptoms of infection with EBV include fever, fatigue, malaise, and sore throat. The designation "mononucleosis" refers to an increase in a particular type of white blood cells (lymphocytes) in the bloodstream relative to the other white blood cells as a result of the EBV infection.
The disease was first described in 1889 and was referred to as "Drüsenfieber," or glandular fever. The term infectious mononucleosis was first used in 1920 when an increased number of lymphocytes were found in the blood of a group of college students who had fever and symptoms of the condition.

What is the cause of mono?

The EBV that causes mono is found throughout the world. By the time most people reach adulthood, an antibody against EBV can be detected in their blood. In the U.S., up to 95% of adults 35-40 years of age have antibodies directed against EBV. This means that most people, sometime in their lives, have been infected with EBV. The body's immune system produces antibodies to attack and help destroy invading viruses and bacteria. These specific antibodies can be detected in the blood of people who have been infected.
When infection occurs in childhood, the virus most often produces no symptoms. It is estimated that only about 10% of children who become infected with EBV develop the illness. Likewise, probably because of immunity from prior infection, adults typically do not develop the illness. Most cases of infectious mononucleosis occur in the 15-24 age group.
While there are other illnesses falling under the broad classification of mononucleosis that can cause similar symptoms (cytomegalovirus [CMV] infection is one example) and an increase in blood lymphocytes, the form caused by the EBV is by far the most common.

What are the risk factors for mono?

The EBV can infect any person. As previously discussed, the majority of people have become infected with the virus by the time that they reach adulthood, and the majority of these infections produce no symptoms or are not recognized as mono. Mono is most often diagnosed in adolescents and young adults, with a peak incidence at 15-17 years of age. However, it can also be seen in children. Generally, the illness is less severe in young children and may mimic the symptoms of other common childhood illnesses, which may explain why it is less commonly diagnosed or recognized in this younger age group.

Infectious mononucleosis symptoms and signs

How is mono transmitted or spread?

Mono is spread by person-to-person contact. Saliva is the primary method of transmitting mono, which leads to the infection of B lymphocytes in the mouth and throat. Infectious mononucleosis developed its common name of "kissing disease" from this prevalent form of transmission among teenagers. It typically takes between four to eight weeks for symptoms of mono to appear after the initial infection with EBV. A person with mono can also pass the disease by coughing or sneezing, causing small droplets of infected saliva and/or mucus to be suspended in the air which can be inhaled by others. Sharing food or beverages from the same container or utensil can also transfer the virus from one person to another since contact with infected saliva may result.
Most people have been exposed to the virus as children, and as a result of the exposure, they have developed immunity to the virus. It is of note that most people who are exposed to the EBV don't ever develop mononucleosis. The incubation period for mono, meaning the time from the initial viral infection until the appearance of symptoms, is between four and eight weeks. During an infection, a person is likely able to transmit the virus to others for at least a few weeks and possibly longer, even after symptoms have disappeared (see below).
Research has shown that, depending on the method used to detect the virus, anywhere from 20%-80% of people who have had mononucleosis and have recovered will continue to secrete the EBV in their saliva for years due to periodic "reactivations" of the viral infection. Since healthy people without symptoms also secrete the virus during reactivation episodes throughout their lifetime, isolation of people infected with EBV is not necessary. It is currently believed that these healthy people, who nevertheless secrete EBV particles, are the primary reservoir for transmission of EBV among humans.

What are the symptoms of mono?

The initial symptoms of mono are

a general lack of energy or malaise,
fatigue,
a loss of appetite,
chills.

These initial symptoms can last from one to three days before the more intense symptoms of the illness begin. The more common intense symptoms include

a severe sore throat,
fever, which may be persistent,
swollen lymph nodes (glands) in the neck area.

It is typically the severe sore throat that prompts people to contact their doctor.

What are the signs of mono?

In addition to a fever from 102 F-104 F, the most common signs of mono are

a very reddened throat and tonsils,
swollen lymph glands in the neck that typically occur on both sides.

The tonsils have a whitish coating in at least one-third of the cases. The spleen (sometimes referred to as the body's biggest lymph node) is an organ found in the left upper abdomen underneath the rib cage, which becomes enlarged or swollen in about 50% of patients with mono. An enlarged liver and abnormalities in liver function tests (blood tests) may be detected (see Complications, below). About 5% of patients have a splotchy red rash over the body, which has a similar appearance to the rash of measles. Early in the course of disease (over the first few days of illness), a temporary swelling (edema) of both upper eyelids may appear.

How is mono diagnosed?

The diagnosis of mono is suspected by the doctor based on the above symptoms and signs. Mono is confirmed by blood tests that may also include tests to exclude other possible causes of the symptoms, such as tests to rule out Strep throat. Early in the course of the mono, blood tests may show an increase in one type of white blood cell (lymphocyte). Some of these increased lymphocytes have an unusual or "atypical" appearance when viewed under a microscope, which suggests mono.
More specific blood tests, such as the monospot and heterophile antibody tests, can confirm the diagnosis of mono. These tests rely on the body's immune system to make measurable antibodies against the EBV. Unfortunately, the antibodies may not become detectable until the second or third weeks of the illness. A blood chemistry test may reveal abnormalities in liver function. Diagnostic tests performed in the laboratory may be of value to rule out other causes of sore throat and fever, including cytomegalovirus infection, Strep throat, and less common conditions such as acute HIV infection or toxoplasmosis.

What is the usual course and treatment of mono?

In most cases of mono, no specific treatment is necessary. The illness is usually self-limited and passes much the way other common viral illnesses resolve. Treatment is directed toward the relief of symptoms. Available antiviral drugs have no significant effect on the overall outcome of mono and may actually prolong the course of the illness. Occasionally, Strep throat occurs in conjunction with mono and is best treated with penicillin or erythromycin (E-Mycin, Eryc, Ery-Tab, PCE, Pediazole, Ilosone). Ampicillin (Omnipen, Polycillin, Principen) and amoxicillin (Amoxil, DisperMox, Trimox) should be avoided if there is a possibility of mono since up to 90% of patients with mono develop a rash when taking these medications. They may then be inappropriately thought to have an allergy to penicillin.
For the most part, supportive or comfort measures are all that is necessary. Acetaminophen (Tylenol) can be given for fever and any headache or body aches. A sufficient amount of sleep and rest is important. The throat soreness is worst during the first five to seven days of illness and then subsides over the next seven to 10 days. The swollen, tender lymph nodes generally subside by the third week.
A feeling of fatigue or tiredness may persist for months following the acute phase of the illness. It is recommended that patients with mono avoid participation in any contact sports for three to four weeks after the onset of symptoms to prevent trauma to the enlarged spleen. The enlarged spleen is susceptible to rupture, which can be life threatening. Cortisone medication is occasionally given for the treatment of severely swollen tonsils or throat tissues which threaten to obstruct breathing.
Patients can continue to have virus particles present in their saliva for as long as 18 months after the initial infection. When symptoms persist for more than six months, the condition is frequently called "chronic" EBV infection. However, laboratory tests generally cannot confirm continued active EBV infection in people with "chronic" EBV infection.

What are the complications of mono?

A common, but usually not serious, complication of mono is a mild inflammation of the liver, or hepatitis. This form of hepatitis is rarely serious or requires treatment. The enlargement of the spleen that occurs with mono makes traumatic rupture of the spleen a possible complication. Swelling of the throat and tonsils can also lead to airway obstruction when severe. Infection in the area of the tonsil can rarely be a serious abscess referred to as a peritonsillar abscess. Another rare complication is swelling of the throat to an extent that breathing is obstructed.
Fortunately, the more severe complications of mono are quite rare, and mono is very rarely fatal in healthy people. The rare severe complications include destruction of red blood cells (hemolytic anemia) and inflammation of the sac surrounding the heart (pericarditis), the heart muscle itself (myocarditis), and the brain (encephalitis). Mono tends to be more aggressive in patients with abnormal immune systems, such as people with AIDS or those who are taking medications that suppress immune function.
The EBV has been associated with some types of cancers, most commonly lymphomas. This occurs most frequently in people whose immune systems have been compromised due to disease or immune suppressive drugs. EBV infection has also been found to be associated with two types of cancer found in other cultures -- nasopharyngeal carcinoma (cancer of the pharynx and nose) in southern China and Burkitt's lymphoma of the jaw among children in equatorial Africa. Further, numerous studies have also found that EBV infection is associated with the development of at least one subtype of Hodgkin's disease. However, since the vast majority of people have been infected with EBV and never develop these types of tumors, EBV infection cannot be the sole cause of these cancers. The overwhelming majority of people who have had mono recover completely without any serious complications.

How can mono be prevented?

Since mono is spread from person to person, avoiding close personal contact with infected individuals and practicing excellent hygienic practices can help prevent transmission of the virus. However, since periodic reactivations of the virus infection seem to occur in healthy individuals and because many infected people who may transmit the virus to others will not have symptoms of the condition, prevention is extremely difficult. In fact, these individuals are believed to be the primary source of transmission of the virus. The fact that up to 95% of adults have antibodies to EBV suggests that prevention of the infection is difficult if not impossible. It is not known why some people develop the symptoms of mono while others appear to acquire the EBV without producing symptoms. It is possible that many infections occur and produce mild symptoms and are not recognized as mono, while other infections may not produce symptoms at all.

Conclusion

Infectious mononucleosis is usually a self-limited, although sometimes prolonged, and often uncomfortable illness. While specific treatment is rarely necessary, the potential complications make it essential that people with this illness be under the care of a physician.

REFERENCES:

Buchwald, D.S., T.D. Rea, W.J. Katon, J.E. Russo, and R.L. Ashley. "Acute Infectious Mononucleosis: Characteristics of Patients Who Report Failure to Recover." Am J Med 109.7 (2000): 531.

Cunha, Burke A. "Infectious Mononucleosis." eMedicine.com. Oct. 19, 2009. <http://emedicine.medscape.com/article/222040-overview>.

Luzuriaga, K., and J.L. Sullivan. "Infectious Mononucleosis." N Engl J Med 362.21 (2010): 1993.

Macsween, K.F., C.D. Higgins, K.A. McAulay, H. Williams, N. Harrison, A.J. Swerdlow, and D.H. Crawford. "Infectious Mononucleosis in University Students in the United Kingdom: Evaluation of the Clinical Features and Consequences of the Disease." Clin Infect Dis 50.5 (2010): 699.

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Melioidosis (Whitmore's Disease)

2012-03-26T08:35:00.002-07:00

What is melioidosis? What causes melioidosis?

Melioidosis, also called Whitmore's Disease, is an infectious disease caused by a bacterium called Burkholderia pseudomallei (previously known as Pseudomonas pseudomallei). The bacteria are found in contaminated water and soil and spread to humans and animals through direct contact with the contaminated source. The bacteria are also of some concern as a potential agent for biological warfare and biological terrorism.
Melioidosis is similar to glanders disease, which is passed to humans from infected domestic animals.

Where does melioidosis occur?

Melioidosis is most frequently reported in Southeast Asia and Northern Australia. It also occurs in South Pacific, Africa, India, and the Middle East. The bacterium that causes the disease is found in the soil, rice paddies, and stagnant waters of the area. People acquire the disease by inhaling dust contaminated by the bacteria and when the contaminated soil comes in contact with abraded (scraped) area of the skin. Infection most commonly occurs during the rainy season.
In the United States, confirmed cases range from none to five each year and occur among travelers and immigrants, according to the U.S. Centers for Disease Control and Prevention (CDC).

What are symptoms of melioidosis?

Melioidosis symptoms most commonly stem from lung disease where the infection can form a cavity of pus (abscess). The effects can range from mild bronchitis to severe pneumonia. As a result, patients also may experience fever, headache, loss of appetite, cough, chest pain, and general muscle soreness.
The effects can also be localized to infection on the skin (cellulitis) with associated fever and muscle aches. It can spread from the skin through the blood to become a chronic form of melioidosis affecting the heart, brain, liver, kidneys, joints, and eyes.
Melioidosis can be spread from person to person as well.

How is melioidosis diagnosed?

The diagnosis of melioidosis is made with a microscopic evaluation of a blood, urine, sputum, or skin-lesion sample in the laboratory. A blood test is useful to detect early acute cases of melioidosis, but it can not exclude the illness if it is negative.

How is melioidosis treated?

The treatment of melioidosis involves antibiotics and depends on the location of the disease.
For patients with more mild illness, the CDC recommends antibiotics such as imipenem, penicillin, doxycycline, amoxicillin-clavulanic acid, ceftazidime, ticarcillin-clavulanic acid, ceftriaxone, and aztreonam. Patients who are more severely ill are given a combination of two of the above for up to 12 months.
With pulmonary involvement of melioidosis, if cultures remain positive for six months, surgical removal of the lung abscess with lobectomy is considered.

Can melioidosis be prevented?

In counties where melioidosis occurs, people with compromised immune systems (such as AIDS, cancer, those undergoing chemotherapy, etc.) should avoid contact with soil and contaminated water, especially in farm areas.

What is the prognosis for melioidosis?

Untreated, melioidosis is fatal. When treated with antibiotics, severe forms of the illness have a 50% chance of recovery, but overall the mortality rate is 40%.

Melioidosis At A Glance

Melioidosis is an infectious disease caused by a bacterium, Burkholderia pseudomallei.
Melioidosis infection commonly involves the lungs.
Melioidosis is diagnosed with the help of blood, urine, sputum, or skin-lesion testing.
Melioidosis is treated with antibiotics.
The overall mortality rate is 40%.

References:

eMedicine

U.S. Centers for Disease Control and Prevention

Medical Author:

John P. Cunha, DO, FACOEP

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Hemolytic Uremic Syndrome (HUS)

2012-03-26T08:34:00.002-07:00

Hemolytic uremic syndrome (HUS) facts

Hemolytic uremic syndrome (HUS) is a condition characterized by destruction of red blood cells and kidney failure.
HUS often follows a digestive infection caused by E. coli OH157:H7, although there are other causes.
Symptoms of HUS include vomiting and diarrhea (often bloody), weakness, lethargy, and bruising (purpura). These symptoms are due to a combination of dehydration, anemia and uremia (the inability of the kidneys to clear waste products from the body).
Diagnosis of HUS is made by a combination of history, physical exam, and abnormal blood tests. There is no one test that makes the diagnosis of hemolytic uremic syndrome.
Treatment of HUS is supportive with intravenous fluids. Anemia may require blood transfusion and temporary dialysis may be necessary.
Children tend to recover from HUS, while adults with HUS may fare less well.

What is a "syndrome?"

In medicine, a syndrome defined as is a collection of symptoms (patient complaints), signs (findings on physical examination), and laboratory or imaging findings that tend to group together and be associated with a specific disease or illness.

What is hemolytic uremic syndrome (HUS)?

Hemolytic uremic syndrome (HUS) is a disease of two body systems. Hemolysis describes the destruction of red blood cells. In hemolytic uremic syndrome, blood within capillaries, the smallest blood vessels in the body, begins to clot abnormally. When red blood cells pass through the clogged capillaries, they are sheared apart and broken. (hemo=blood +lysis=destruction). The second failed system, kidney failure (uremia), occurs when urea and other waste products build up in the bloodstream because the kidneys cannot filter and dispose of them. (urea=a waste chemical + emia= in the blood).
HUS is also related to another disease caused by a similar normal clotting process within the capillaries called thrombotic thrombocytic purpura (TTP). Within the medical literature, these two conditions are often considered together. HUS is more widely known, however, because it has been discussed in the press because of its relationship to a special type of E. Coli (Escherichia coli) infection associated with food poisoning.

What causes hemolytic uremic syndrome?

While the cause of HUS has not been established with certainty, researchers believe that an abnormal inflammation reaction is stimulated in the blood stream causing platelets (the parts of the blood that form clots) to sludge in small blood vessels and form blood clots where they are not supposed to. This uses up the platelets and causes a shortage of them in the rest of the body. This abnormal reaction may be caused by a yet unidentified chemical that is produced in blood plasma (the fluid or non-cellular part of the bloodstream).
The triggering events for HUS are varied and include:

Enterohemorrhagic E. Coli is a type of bacteria that causes bloody diarrhea. E. coli is a very common type of bacteria in the body, and it is only the OH157:H7 type that causes the problem. It can be found in undercooked meat and other foods; and is one of the causes of food recalls and restaurant-related food poisoning outbreaks. This accounts for almost 90% of HUS in children. The 2011 outbreak of HUS in Germany was due to a different type of Shigela toxin-producing E. coli called 0104:H4.
Pregnancy and the early postpartum (after delivery) time period and the use of birth control pills are the more common associations with HUS.
Pneumonia caused by the Streptococcus pneumoniae bacteria is another possible precipitating factor. HUS is rare complication of this common infection. Most often, this pneumonia is treated with antibiotics as an outpatient.
Medications may be also associated with HUS, including some chemotherapy and immunosuppression drugs, birth control pills, ticlopidine (Ticlid, an anti-platelet drug) and quinine [(Quinerva, Quinite]) an anti-platelet drug].
AIDS may be associated with HUS.

Furthermore, there is an inherited type of HUS due to a gene mutation that affects the blood clotting mechanism.

What are the signs and symptoms of hemolytic uremic syndrome?

In E. coli-related HUS, gastroenteritis occurs with abdominal cramping, vomiting and profuse bloody, watery diarrhea. This may cause significant dehydration, weakness and lethargy, as well as electrolyte imbalances because of the loss of sodium, potassium, and chloride in the vomit and diarrhea. These symptoms may resolve before the onset of anemia and the kidney failure symptoms of HUS.
The anemia and uremia usually present with weakness, lethargy, and sleepiness. Purpura or small areas of bleeding in the skin may be seen because of low platelet counts.

How is hemolytic uremic syndrome diagnosed?

The healthcare provider will have a suspicion of the disease based on the history and physical examination. Abnormal laboratory tests help confirm the diagnosis. They abnormal findings include:

Hemolytic anemia: the red blood cell count is low and a peripheral blood smear, in which blood is examined under a microscope, will show that the red cells have been damaged and destroyed. This differentiates hemolysis (hemo=blood + lysis=destruction) from anemia caused by decreased production of blood cells in the bone marrow.
Thrombocytopenia: a low platelet count
Uremia: Kidney function can be measured by testing the level of waste products in the blood normally filtered by the kidney. Creatinine is a breakdown product of a muscle protein called creatine .When this level rises, it is an indication of kidney failure or uremia.
Abnormal urine findings: Blood and protein may be found in the urine when normally they are not present.
Stool cultures: Since E. coli O157:O7 is the most common cause of HUS, attempts are made to culture the bacteria from stool samples. The body usually clears the bacteria from the stool within a week, so a negative test does not exclude the disease. A positive test helps confirm HUS and will be reported to public health authorities to try to determine the source of the infection. In 2011, outbreaks in Europe were traced by public health authorities to tainted sprouts.

One of the distinguishing findings between HUS and TTP is a normal neurologic examination. The brain function is normal in HUS.

What is the treatment for hemolytic uremic syndrome?

HUS in children tends to be self-limiting, and supportive care is often all that is needed. This may include intravenous fluids for rehydration and rebalancing of electrolytes like sodium and potassium, which can be lost with the diarrhea.
Blood transfusions are only used for the most severe cases of anemia in which the hemoglobin falls below 6 or 7 g/dL (depending on age, the normal value is 11-16).
Kidney failure may be managed expectantly (by observation and supportive care), and dialysis is not often required.
Adults with HUS tend to become more ill and need more aggressive therapy than children with the condition. In addition to the supportive care discussed above, plasmapheresis or plasma exchange may be required. Since it is thought there is an abnormal chemical in the plasma stimulating the abnormal clot formation, removing the plasma and replacing it with donor plasma is helpful in treating adult HUS.
Temporary dialysis may be needed while awaiting recovery of the kidneys from the illness.

What is the prognosis of hemolytic uremic syndrome?

HUS in children tends to be self-limiting, and full recovery should be expected.
Adults do less well. Without aggressive therapy like plasmapheresis and dialysis, up to 40% of those affected may die, and 80% may have kidney impairment. With treatment, the death rate falls to 10% or less and kidney impairment to 25%.
Patients with HUS not related to a diarrheal illness have a worse prognosis than those whose illness is due to an E. coli infection.
In those patients with genetically caused HUS, relapsing illness is common as are kidney failure requiring dialysis and death.

How can hemolytic uremic syndrome be prevented?

Most cases of E. coli-related HUS can be prevented by thorough washing and cooking of food products. The vast majority of cases of HUS are caused by poor food handling from the farmer to the wholesaler and grocer. Proper washing and cooking techniques in the kitchen is the key to prevention.

REFERENCE: CDC.gov. Investigation Update: Outbreak of Shiga toxin-producing E. coli O104 (STEC O104:H4) Infections Associated with Travel to Germany.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Melissa Conrad Stöppler, MD

Rocky Mountain Spotted Fever

2012-03-26T08:31:00.002-07:00

Rocky Mountain spotted fever (RMSF) facts

Rocky Mountain spotted fever is caused by the bacterium Rickettsia rickettsii.
The bacterium is spread to humans through the bite of infected ticks, and so the disease is most common in months where ticks are active, such as summer.
Despite the name, the disease is not limited to the Rocky Mountains but rather occurs throughout most of the U.S.
Symptoms of headache, fever, and fatigue begin about a week after exposure. A few days later, a rash develops. The rash may be so mild that it is hard to see or so dramatic that it progresses to gangrene. Other possible symptoms include confusion, abdominal pain, and vomiting.
Most cases require hospitalization, and severe cases require intensive care.
The disease is diagnosed by finding high titers of antibodies in the blood or by seeing the organism under a microscope in specially stained skin biopsies.
The treatment of choice is the antibiotic doxycycline (Vibramycin, Oracea, Adoxa, Atridox). Prompt treatment improves survival and reduces complications.
Most people with RMSF recover completely over a few weeks. In severe cases, patients may have brain damage or other neurological problems that persist after treatment.
The risk of RMSF can be reduced by reducing exposure to ticks. This includes avoiding areas that have large concentrations of ticks, using insect repellents and wearing protective clothing.
Because the risk of infection increases with the duration of tick attachment, people should check themselves for ticks when they return from an outing.

What is Rocky Mountain spotted fever?

Rocky Mountain spotted fever is a bacterial infection that is transmitted to humans through the bite of a tick. Statistics show that rates of disease have been rising steadily over the past decade. Although most people recover completely, fatalities occur in approximately 0.5%-5% of cases.

Where do most cases of RMSF occur in the U.S.?

Cases of RMSF have been reported from most areas of the country, and the disease is not restricted to the Rocky Mountain region. In fact, Arkansas, Missouri, North Carolina, Oklahoma, and Tennessee account for over 60% of reported cases. In 2008, there were approximately 2,500 cases reported in the U.S., which is more than twice as many cases as were reported annually in the 1990s.

Reported incidence of RMSF per million people in 2008; NN=not reported. SOURCE: CDC.

What is the history of Rocky Mountain spotted fever?

RMSF was first described in the late 1800s in the Snake River Valley of Idaho. Initially, cases were thought to be confined to the Rocky Mountain area, but by the early 20th century, it was obvious that the disease occurred in areas throughout the country. Dr. Howard Ricketts identified the causative organism in the blood of infected people and showed that ticks could transmit the organism. Many other scientists worked to identify the characteristics of the disease and the tick vector, but it was not until the middle of the 20th century that an effective treatment was discovered. Many of the early researchers died of tick-borne infections while studying the disease.

What causes Rocky Mountain spotted fever?

RMSF is caused by a small bacterium known as Rickettsia rickettsii. R. rickettsii lives inside the cells that line the blood vessels of infected animals and humans.
The tick is the primary home or reservoir for R. rickettsii. Because ticks can also spread the organism to humans and other animals, they are sometimes referred to as vectors for transmission of RMSF. Several different types of ticks can carry R. rickettsii. For example, the American dog tick (Dermacentor variabilis) is the most common vector in the eastern, central, and Pacific U.S. In the West, the Rocky Mountain wood tick (Dermacentor andersoni) is the primary vector for RMSF. Ticks can pass the organism to their offspring, creating a new generation of infected ticks. Ticks can also be infected by feeding on an infected person or animal. Even in the woodlands and fields of high-risk areas, only a small proportion of ticks will carry R. rickettsii.

Picture of a Rocky Mountain wood tick. SOURCE: CDC/Dr. Christopher Paddock.

Picture of American dog ticks.

What are risk factors for Rocky Mountain spotted fever?

Cases of RMSF occur when the appropriate tick vector comes in contact with human populations. Risk factors include traveling to an area with a high rate of RMSF, especially in seasons when ticks are plentiful, such as summer. People at highest risk are those who frequent forested areas or fields, such as those who are hiking or camping. Even urban outdoor areas pose a risk, however. Dog ownership is a risk factor in areas where the American dog tick exists. Dogs acquire ticks while roaming outside, and these ticks can be transferred to humans during petting or other contact.
The risk of RMSF is thought to increase with the duration of tick attachment. A feeding tick can remain attached to a human for up to two weeks. Crushing an attached tick improperly may cause secretions from the tick to be injected into the skin and increase the risk of infection.
Severe disease is more common in the elderly, alcoholics, and in African Americans. The latter is at least partly due to delays in diagnosis of the typical rash in dark-skinned people. In addition, blacks are more likely to have a genetic enzyme deficiency (G6PD) that can make the disease more severe.

What are symptoms and signs of Rocky Mountain spotted fever in children and adults?

Symptoms appear within about a week of exposure to the bacteria (range two to 14 days). Initially, people feel like they have influenza (flu) with headache, high temperature, body aches, and fatigue. Other possible symptoms include abdominal pain, vomiting, and lack of appetite. Symptoms in children may be slightly different than in adults. Children may complain less of headache and more of abdominal pain, which may be severe. The eyes may be red (conjunctivitis).
A rash appears within three to five days, often starting around the wrists or ankles and then spreading to the trunk, palms, and soles. The rash starts as discrete, small red areas and resembles the rashes (exanthems) of many other viral illnesses. Over a few days, these areas may become bright red or purple and are known as petechiae, a sign of more severe disease. The petechiae may merge as the rash advances to create a diffuse redness.
In some cases, the rash may be so mild that it is missed on examination. People with dark skin often have delayed diagnosis because the rash is harder to detect. In severe cases, the skin may turn black and necrotic (meaning there is death of tissue), resembling gangrene.
Headache is often very severe and may be the presenting complaint, especially in adults. Other neurological signs that might appear include a stiff neck, difficulty hearing, confusion, and weakness or paralysis of some muscles. Severe cases may reduce the ability of the blood to clot, which causes the patient to be at risk for internal bleeding.
None of the above symptoms is specific for RMSF. Other tick-borne illnesses may cause similar symptoms, including other members of the spotted fever rickettsiosis group. Ticks may also spread other diseases such as Lyme disease.

Rocky Mountain spotted fever rash pictures. SOURCE: CDC.

How is Rocky Mountain spotted fever diagnosed?

Physicians should consider RMSF in a patient who has fever, headache, and other compatible symptoms, especially if the person has recently visited an area where the disease is known to occur. Because the disease is caused by ticks, it is seasonal and should be considered in months when ticks are active. A history of tick exposure is helpful, but it is important to remember that most ticks do not carry R. rickettsii and that many tick bites go unnoticed. The rash may appear late in the course of disease or be very mild, so it is important to think of the disease even if the rash is not present. If the facts of the case make the diagnosis appear to be likely, treatment should not be delayed to wait for the rash or results of tests.
RMSF is diagnosed through several methods. Using immunohistochemistry, a small piece of skin can be mixed with a special stain that allows the organism to show up under the microscope. Because the presence of the organism in skin may be patchy, a negative biopsy does not rule out the disease.
Blood can be tested for antibodies to the organism using techniques known as immunofluorescence (IFA) or enzyme immunoassays (ELISA or EIA). If a high concentration of antibody is found, it can be presumed that disease is present. It may take a week for antibodies to appear, so a negative titer does not completely rule out the disease. Blood can also be tested for antibodies at the onset of illness and again several weeks later to see if there is a substantial change in the titer. Other tests, such as the polymerase chain reaction (PCR) to detect the genetic material of the bacteria are available in research laboratories or from the U.S. Centers for Disease Control and Prevention (CDC) although they have not been standardized for general use.
R. rickettsii is difficult to culture and requires living host cells to grow. It is also dangerous to grow, because there have been cases of laboratory technicians getting sick while performing the culture. Only laboratories that are certified to handle this level of biohazard should attempt to culture the organism.
Most other laboratory findings are nonspecific, meaning that they cannot be used alone to make the diagnosis. White blood cell counts may be normal or increased slightly, or anemia may be present. Platelet counts may be decreased, especially in severe cases. Serum sodium levels are low in about half of patients, and liver enzyme tests in the blood may be elevated. If kidney failure occurs, the serum creatinine will be increased. If neurological symptoms occur, the spinal fluid may show increased numbers of white cells or an increased concentration of proteins.

What is the treatment for Rocky Mountain spotted fever in children and adults?

RMSF is treated with antibiotics, usually from the tetracycline class. Doxycycline is the most commonly recommended antibiotic for this purpose and is usually taken orally twice a day for seven days. An intravenous form is available for patients who are unable to tolerate the oral form.
Special comment should be made for one population in need of treatment: children. Doxycycline is not used routinely in young children (< 8 years of age) because it might cause staining of teeth, but this almost never occurs with a limited one-week course. Since the risk is minor compared to the potential severity of RMSF, both the CDC and the American Academy of Pediatrics recommend doxycycline for all children with RMSF. Similarly, doxycycline is usually not given to pregnant women because of the potential effect of the drug on fetal bones and teeth. However, the risk must be weighed against the benefit of treatment on an individual basis. If a person cannot take doxycycline, there are other possible choices, including an older agent called chloramphenicol. Chloramphenicol also has toxicities. Use of alternative agents or treatment during pregnancy warrants consultation with a specialist experienced in the area.

What are complications of Rocky Mountain spotted fever?

Complications of RMSF include kidney failure, neurological problems, bleeding, gangrene, and death. Most patients with a diagnosis of RMSF are hospitalized and severe cases require intensive care. Death occurs in approximately 0.5%-5% of treated cases and up to 20% of untreated cases.

What is the prognosis of Rocky Mountain spotted fever in children and adults?

Most people with RMSF recover completely over a few weeks. People with severe neurological symptoms may have residual difficulty with balance during walking (ataxia), blindness, and brain damage.

How can people safely remove a tick?

A tick can be removed by grasping it with tweezers very close to the skin and pulling gently. Avoid squeezing/crushing the main tick body to limit the opportunity to eject infected secretions. Do not use nail polish, petroleum jelly, or heat to try to make the tick drop off.

Can Rocky Mountain spotted fever be prevented?

The risk of RMSF can be reduced by avoiding areas where ticks are common. If a person does go into such an area, protective clothing including socks, long pants, and long sleeves will reduce that area of skin available for a tick. Insect repellents containing DEET reduce the risk of tick bites. The risk of disease increases with the duration of tick attachment, so the body should be checked carefully for ticks after returning from an outing. Because most ticks are not infected, doxycycline is not recommended after a tick bite in a person who has no symptoms.

Where can people find more information on Rocky Mountain spotted fever?

The CDC is an excellent source of information on RMSF, available online at http://www.cdc.gov/rmsf.

REFERENCE:

United States. Centers for Disease Control and Prevention. "Diagnosis and Management of Tickborne Rickettsial Diseases: Rocky Mountain Spotted Fever, Ehrlichioses, and Anaplasmosis -- United States." Morbidity and Mortality Weekly Report 55(RR04) (2006): 1-27.

Medical Author:

Mary D. Nettleman, MD, MS, MACP

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Dehydration

2012-03-26T08:21:00.002-07:00

What is dehydration?

Water is a critical element of the body, and adequate hydration is a must to allow the body to function. Up to 75% of the body's weight is made up of water. Most of the water is found within the cells of the body (intracellular space). The rest is found in the extracellular space, which consists of the blood vessels (intravascular space) and the spaces between cells (interstitial space).
Dehydration occurs when the amount of water leaving the body is greater than the amount being taken in. The body is very dynamic and always changing. This is especially true with water in the body. We lose water routinely when we:

breathe and humidified air leaves the body (this can be seen on a cold day (the breath you see in the air is water that has been exhaled);
sweat to cool the body; and
eliminate waste by urinating or having a bowel movement.

In a normal day, a person has to drink a significant amount of water to replace this routine loss.
The formula for daily fluid requirements depends upon an individual's weight. Normally, fluid and weight are calculated using the metric system; however, below is the approximation in imperial (American) units.

Body weight	Daily fluid requirements (approximate)
10 pounds	15 ounces
20 pounds	30 ounces
30 pounds	40 ounces
40 pounds	45 ounces
50 pounds	50 ounces
75 pounds	55 ounces
100 pounds	50 ounces
150 pounds	65 ounces
200 pounds	70 ounces

If you would like to calculate your body weight and daily fluid requirements using the metric system, please use this formula.

For the first 10kg (kilogram) of body weight the daily fluid intake required is 100cc per kg.
For the next 10kg of body weight, the fluid required is an additional 50 cc/kg.
For every additional kg of body weight, an additional 10cc/kg

The body is able to monitor the amount of fluid it needs to function. The thirst mechanism signals the body to drink water when the body is dry. As well, hormones like anti-diuretic hormone (ADH) work with the kidney to limit the amount of water lost in the urine when the body needs to conserve water.

What causes dehydration?

Dehydration occurs because there is too much water lost, not enough water taken in, or most often a combination of the two.

Diarrhea: Diarrhea is the most common reason for a person to lose excess amounts of water. A significant amount of water can be lost with each bowel movement. Worldwide, more than four million children die each year because of dehydration from diarrhea.
Vomiting: Vomiting can also be a cause of fluid loss. It is lost in the vomitus, but it is difficult for a person to replace water by drinking it if they have nausea and are unable to tolerate liquids.
Sweat: The body can lose significant amounts of water when it tries to cool itself by sweating. Whether the body is hot because of the environment (for example, working in a warm environment), intense exercising in a hot environment, or because a fever is present due to an infection; the body uses water in the form of sweat to cool itself. Depending upon weather conditions, a brisk walk may generate up to 16 ounces of sweat (a pound of water) to allow body cooling, and that water needs to be replaced by the thirst mechanism signaling the person to drink fluids.
Diabetes: In people with diabetes, elevated blood sugar levels cause sugar to spill into the urine and water then follows, which may cause significant dehydration. For this reason, frequent urination and excessive thirst are among the early symptoms of diabetes.
Burns: The skin acts as a protective barrier for the body and is also responsible for regulating fluid loss. Burn victims become dehydrated because the damaged skin cannot prevent fluid from seeping out of the body. Other inflammatory diseases of the skin are also associated with fluid loss.
Inability to drink fluids: The inability to drink adequately is the other potential cause of dehydration. Whether it is the lack of availability of water, intense nausea with or without vomiting, or the lack of strength to drink, this, coupled with routine or extraordinary water losses can compound the degree of dehydration.

What are the signs and symptoms of dehydration?

The body's initial responses to dehydration are thirst to increase water intake, and decreased urine output to try to conserve water loss. The urine will become concentrated and more yellow in color.
As the level of water loss increases, more symptoms can become apparent. The following are further signs and symptoms of dehydration.

Dry mouth
The eyes stop making tears
Sweating may stop
Muscle cramps
Nausea and vomiting
Heart palpitations
Lightheadedness (especially when standing)
Weakness
Decreased urine output

The body tries to maintain cardiac output (the amount of blood that is pumped by the heart to the body); and if the amount of fluid in the intravascular space is decreased, the body tries to compensate for this decrease by increasing the heart rate and making blood vessels constrict to try to maintain blood pressure and blood flow to the vital organs of the body. This coping mechanism begins to fail as the level of dehydration increases.
With severe dehydration, confusion and weakness will occur as the brain and other body organs receive less blood. Finally, coma, organ failure, and death eventually will occur if the dehydration remains untreated.

What about dehydration in children?

Millions of children die worldwide each year because of dehydration, often because of diarrhea. As well, the temperature regulation and sweat mechanism of infants are not well developed and increases their risk of heat related illness.
It is important to remember that infants and children are dependent upon others to provide them with water and nutrition. Infants cannot tell their parents or care providers when they are thirsty. Enough fluid needs to be provided so that the dehydration can be prevented. This is especially true if increased water loss occurs because of fever, vomiting or diarrhea.
In children, symptoms of dehydration increase as the level of dehydration increases.

Level of dehydration Estimated fluid loss Signs and Symptoms in Children
Level of dehydration	Estimated fluid loss	Signs and symptoms
Minimal	<3% of body weight	none
Mild to moderate	<10% of body weight	Fussy, tired, irritable child. Dry mucous membranes (mouth, tongue), increased heart rate, increased breathing rate, decreased urine output, increased thirst
Severe	10% of body weight or more	Listless, lethargic, unconscious. Too weak to cry. Sunken eyes, sunken fontanelle (soft spot of skull). Increased heart rate, weak pulses, and rapid shallow breathing. Cool, mottled skin. No urine output (dry diapers). Too weak to suckle or drink fluids.

Infants and Children respond well to fluid replacement, and often oral rehydration therapy (ORT) can treat dehydration. Small, frequent sips of fluid replacement solutions such as Pedialyte or Gatorade may be enough to prevent the need for intravenous fluids. In ORT, replacement begins with 5cc or one teaspoon of fluid every 5-10 minutes. If this is tolerated without vomiting, the amount of fluid is doubled, again providing small amounts every few minutes. However, if the child is too ill to drink or cannot tolerate even small sips of fluid, medical care should be accessed immediately.
Intravenous fluids can rehydrate the infant or child while the underlying illness is evaluated and treated. Occasionally, there is difficulty in placing an intravenous line and an intraosseous (inside the bone) needle can be placed, usually in the tibia (shin bone) that allows fluid resuscitation.
In children who are markedly dehydrated, blood tests may be used to monitor electrolytes, kidney function, and acid-base balance in the body.

How is dehydration diagnosed?

Dehydration is often a clinical diagnosis. Aside from diagnosing the reason for dehydration, the health care practitioner's examination of the patient will assess the level of dehydration. Initial evaluations may include:

Mental status tests to evaluate whether the patient is awake, alert, and oriented. Infants and children may appear listless and have whiny cries and decreased muscle tone.
Vital signs may include postural readings (blood pressure and pulse rate are taken lying down and standing). With dehydration, the pulse rate may increase and the blood pressure may drop because the blood is depleted of fluid. People taking beta blocker medications for high blood pressure, heart disease, or other indications, occasionally lose the ability to increase their heart rate as a compensation mechanism since these medications block the adrenaline receptors in the body.
Temperature may be measured to assess fever.
Skin may be checked to see if sweat is present and to assess the degree of elasticity (turgor). As dehydration progresses, the skin loses its water content and becomes less elastic. The amount of sweat is often felt in the armpit or groin, two areas that tend to have moisture normally.
The mouth can become dry and the health care practitioner may look or feel the tongue for fluid.
Infants may have additional evaluations performed, including checking for a soft spot on the skull (sunken fontanelle), assessing the suck mechanism, muscle tone, or loss of sweat in the armpits and groin. All are signs of potential significant dehydration.
Pediatric patients are often weighed during routine child visits, thus a body weight measurement may be helpful in assessing how much water has been lost with the acute illness. This is very rough estimate because all scales are not the same, and for infants and children, it is important to know what clothing they were wearing when the original weight was taken.

Laboratory testing
The purpose of blood tests is to assess potential electrolyte abnormalities (including sodium, potassium, and chloride levels) associated with the dehydration. Tests may or may not be ordered depending upon the underlying cause of dehydration, the severity of illness, the health care practitioner's assessment of their needs and resources available.
Other blood tests may be helpful in determining the level of dehydration. Hemoglobin and red blood cell counts may be elevated because the blood is more concentrated with water loss.
Kidney function tests including BUN and creatinine may be elevated, and is a sign of dehydration.
Urinalysis may be ordered to determine urine concentration, the more concentrated the urine, the more dehydrated the patient.

How is dehydration treated?

As is often the case in medicine, prevention is the important first step in the treatment of dehydration. (Please see the home treatment and prevention sections.)
Fluid replacement is the treatment for dehydration. This may be attempted by replacing fluid by mouth, but if this fails, intravenous fluid (IV) may be required. Should oral rehydration be attempted, frequent small amounts of clear fluids should be used.
Clear fluids include:

water,
clear broths,
popsicles,
Jell-O, and
other replacement fluids that may contain electrolytes (Pedialyte, Gatorade, Powerade, etc.)

Decisions about the use of intravenous fluids depend upon the health care practitioner's assessment of the extent of dehydration and the ability for the patient to recover from the underlying cause.
The success of the rehydration therapy can be monitored by urine output. When the body is dry, the kidneys try to hold on to as much fluid as possible, urine output is decreased, and the urine itself is concentrated. As treatment occurs, the kidneys sense the increased amount of fluid, and urine output increases.
Medications may be used to treat underlying illnesses and to control fever, vomiting, or diarrhea.

Can I treat dehydration at home?

Dehydration occurs over time. If it can be recognized in its earliest stages, and if its cause can be addressed, home treatment may be beneficial and adequate.
Steps a person can take at home to prevent severe dehydration include:

Individuals with vomiting and diarrhea can try to alter their diet and use medications to control symptoms to minimize water loss. Clear fluids are recommended as the diet of choice for the first 24 hours, with gradual progression to a regular diet is recommended.
Loperamide (Imodium) may be considered to control diarrhea. If the affected individual has a fever, or if there is blood in the diarrhea, medical advice should be obtained before administering medications to control diarrhea.
Acetaminophen or ibuprofen may be used to control fever.
Fluid replacements may be attempted by small, frequent amounts of clear fluids (see clear fluids information in previous section). The amount of fluid required to maintain hydration depends upon the individual's weight. The average adult needs between 2 and 3 liters of fluid per day.

If the person becomes confused or lethargic; if there is persistent, uncontrolled fever, vomiting, or diarrhea; or if there are any other specific concerns, then medical care should be accessed.
Emergency medical system (EMS) or 911 should be activated for any individual with altered mental status - confusion, lethargy, or coma.

What are the complications of dehydration?

Complications of dehydration may occur because of the dehydration, and/or because of the underlying disease or situation that causes the fluid loss.
Kidney failure
Kidney failure is a common occurrence, although if it is due to dehydration and is treated early, it is often reversible. As dehydration progresses, the volume of fluid in the blood decreases, and blood pressure may fall. This can decrease blood flow to vital organs like the kidneys, and like any organ with a decreased blood flow; it has the potential to fail to do its job.
Coma
Decreased blood supply to the brain may cause confusion and even coma. If enough organs begin to malfunction, the body itself may fail, and death can occur.
Shock
When the fluid loss overwhelms the body's ability to compensate, blood flow and oxygen delivery to the body's vital organs become inadequate and cell and organ function can begin to fail.
Heat-related illnesses and associated complications
In heat-related illness, the body's attempt to cool itself by sweating may cause dehydration to the point that muscles may go into spasm (heat cramps). It is often the muscles that are being stressed that will spasm (for example, in people who work outside in a hot environment, arm and leg muscles may spasm from lifting and moving heavy objects or equipment; in athletes, leg muscles may cramp from running). As fluid loss increases, the patient may be so dehydrated that there is not enough water to sweat and heat exhaustion or heat stroke may occur. Heat stroke is a true medical emergency and 911 or the emergency response system should be activated immediately in this situation.
Electrolyte abnormalities
In dehydration, electrolyte abnormalities may occur since important chemicals (like sodium, potassium, and chloride) are lost from the body through sweat. For example, patients with profuse diarrhea or vomiting may lose significant amounts of potassium, causing muscle weakness and heart rhythm disturbances. The doctor is often aware of the fluid and electrolyte balance in the dehydrated patient and may decide to monitor electrolyte levels by checking blood tests. Some examples of symptoms caused by abnormal electrolyte levels include muscle weakness due to low potassium, heart rhythm disturbances due to either low or high potassium, and seizures due to low (hyponatremia) or high sodium (hypernatremia). In many patients with dehydration, the kidneys are able to compensate and regulate electrolyte levels.
It is reasonable to remember that dehydration does not occur quickly, and sometimes it may take hours to slowly correct the fluid deficit and allow the electrolytes to redistribute themselves appropriately in the different spaces in the body. If rehydration is done too slowly, the patient may remain hypotensive and in shock for too long. If done too quickly, water and electrolyte concentrations within organ cells can be negatively affected, causing cells to swell and eventually die.

Can dehydration be prevented?

Environment: Dehydration due to the weather is a preventable condition. If possible, activities should not be scheduled in the heat of the day. If they are, adequate fluids should be available, and cooler, shaded areas should be used if possible. Of course, people should be monitored to make certain they are safe. Those working in hot environments need to take care to rehydrate often.

Exercise: People exercising in a hot environment need to drink adequate amounts of water. People can become dehydrated in the ocean, lakes, or pools if the water and and environmental temperatures are warm enough.
Age: The young and elderly are most at risk because of poor temperature regulation systems. During heat waves, attempts should be made to check on the elderly in their homes. During the Chicago heat wave of 1995, more than 600 people died in their homes from heat exposure.
Heat related conditions: Know the signs and symptoms of heat cramps, heat rash, heat exhaustion, and heat stroke. Preventing dehydration is one step to avoid these conditions.

Dehydration at A Glance

The body needs water to function.
Dehydration occurs when water intake is less than water loss.
Symptoms range from mild to life-threatening.
The young and the elderly are especially susceptible to dehydration.

Additional resources from WebMD Boots UK on Dehydration

REFERENCE: Fauci, Anthony S., et al. Harrison's Principles of Internal Medicine. 17th ed. United States: McGraw-Hill Professional, 2008.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Myxedema Coma

2012-03-26T08:18:00.002-07:00

What is myxedema coma?

Myxedema coma is a loss of brain function as a result of severe, longstanding low level of thyroid hormone in the blood (hypothyroidism). Myxedema coma is considered a life-threatening complication of hypothyroidism and represents the far more serious side of the spectrum of thyroid disease.

Who is affected by myxedema coma?

Myxedema coma is not common, but tends to be seen more frequently in elderly patients and in women. There is an increased incidence in the winter months, which is likely secondary to the extremes in temperature. Myxedema coma can actually result in death. Fortunately, the condition is rare.

What are the symptoms of hypothyroidism?

Before a patient develops myxedema coma, features of hypothyroidism are usually present and may have gone unsuspected for a long period of time.
These symptoms include:

fatigue,
lethargy,
mental impairment,
depression,
cold intolerance,
hoarsene6ss,
dry skin,
weight gain,
change in menstrual cycles,
constipation, and
headaches.

What causes myxedema coma?

Most patients with myxedema coma have a history of hypothyroidism, thyroid surgery, or radioactive iodine treatment for thyroid disease. Very rarely, the problem is not caused by the inability of the thyroid gland to make thyroid hormone; but rather is caused by the failure of the pituitary gland or the hypothalamus to correctly signal the thyroid gland to perform its normal functions. In this situation, the thyroid gland is normal, but it is not receiving the signals from the pituitary gland or hypothalamus to make the thyroid hormone it is capable of producing.
Picture of the Thyroid Gland

Picture of the Pituitary Gland

What are triggers of myxedema coma?

Certain factors may suddenly trigger myxedema coma in a person with poorly controlled hypothyroidism. These include:

drugs (particularly sedatives, narcotics, anesthesia, lithium (Eskalith, Lithobid), and amiodarone (Cordarone),
infections,
stroke,
trauma,
heart failure,
gastrointestinal bleeding,
hypothermia (abnormally low body temperature), and
failing to take thyroid medications as prescribed.

What are the symptoms of myxedema coma?

When a patient presents with myxedema coma the following may be present:

the body temperature is usually abnormally low (hypothermia), the core temperature may be as low as 80 F (26.6 C);
severe mental changes including hallucinations, disorientation, seizures, and ultimately, deep coma;
significant swelling (edema) all over the body with swollen eyes and thickening of the tongue,
sparse, dry hair, and loss of the outer thirds of the eyebrows;
difficulty breathing;
collections of fluid around the lungs and heart (pleural effusion and pericardial effusions);
the heart may slow down and its ability to pump blood forward can be impaired;
the gastrointestinal tract does not function well and sometimes it becomes paralyzed, thereby necessitating surgery; and
blood test abnormalities are a result of the increased fluid in the body. For example, sodium levels drop because of dilution, which is caused by the body retaining extra water.

How is myxedema coma diagnosed?

Initial laboratory evaluation usually includes a test for thyroid function (TSH, T3 and T4 levels). Other blood tests, as well as heart and lung function testing, may also be needed.

What is the treatment for myxedema coma?

Treatment may include assisting the patient to breathe and warming them to raise the body temperature to normal. Often, antibiotics are started until it is certain that an infection is not present.
The method of replacing thyroid hormone in patients with myxedema coma is controversial. Many different approaches are used. In general, initial replacement is done by intravenous infusion, since the intestinal system may not be absorbing properly.
While common hypothyroidism without myxedema is usually treated with T4 replacement (the hormone produced in greatest quantity by the thyroid gland), in the case of myxedema coma, management is different. The thyroid gland also produces a small amount of another hormone, T3. This is the more metabolically active of the two hormones. In patients who are well, T4 is converted into T3 in the bloodstream. However, patients with myxedema coma are often so sick that this conversion is impaired. As a result, many doctors choose to treat these patients with T3 initially and start T4 therapy as well. Since T4 therapy can take a month or so to work, there is usually an overlap of these two hormones. Care is taken to avoid heart rhythm abnormalities (arrhythmias) and stress on the heart, which can be caused by replacing thyroid hormone too quickly, particularly in elderly patients.
While mild thyroid disorders can be managed by primary care physicians, myxedema coma is generally managed by a thyroid specialist (endocrinologist) because treatment can be complicated and critical.

How can myxedema coma be prevented?

The ideal way to manage this condition is to prevent it from occurring in the first place. An individual with hypothyroidism should visit their doctor regularly for follow-up and blood testing to be certain that their replacement dose is appropriate.
If an individual has symptoms that concerns them, but has not been diagnosed with hypothyroidism, they should visit their health care practitioner to discuss their concerns and explore the option of testing for thyroid imbalance.

Medical Author:

Ruchi Mathur, MD, FRCP(C)

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Vitamins & Exercise Heart Attack Prevention Series

2012-03-26T08:16:00.002-07:00

Folic acid, B vitamins, and homocysteine

Homocysteine is metabolized (chemically transformed) into methionine and cysteine with the help of the B vitamins; folic acid, B12, and B6 (pyridoxine). Therefore, insufficient amounts of these B vitamins in the body can theoretically hamper the metabolic breakdown of homocysteine, and hence increase its blood levels. High levels of homocysteine in the blood (hyperhomocysteinemia) can damage the inner surface of blood vessels, promote blood clotting, and accelerate atherosclerosis.
The current state of knowledge regarding folic acid, homocysteine, and heart attacks is as follows:

The level of blood folate is an important determinant of the blood homocysteine level. Low blood folate levels are associated with high blood levels of homocysteine.
Low blood folate is common among individuals who do not take multivitamins, but unusual among those who do.
The consumption of folic acid supplements or folic acid fortified cereals can increase blood folate levels and decrease blood homocysteine levels.
In a large population study involving women, those who had the highest consumption of folic acid (usually in the form of multivitamins) had fewer heart attacks than those who consumed the least amount of folic acid.

Even though current scientific evidence suggests that taking folic acid and vitamin B supplements to lower homocysteine levels should help prevent atherosclerosis and heart attacks, conclusive proof is still lacking because:

There are no conclusive controlled studies (discussed at the beginning of this article) demonstrating that increasing folic acid intake actually prevents atherosclerosis and heart attacks.
There is no clinical study demonstrating that lowering blood levels of homocysteine actually prevents atherosclerosis and heart attacks.

There is also no official recommendation as to who should be tested for hyperhomocysteinemia. The optimal doses of the B vitamins, folic acid, B12, and B6, required to prevent and treat hyperhomocysteinemia are also uncertain. For folic acid, a daily dose of 0.8-1.0 mg is probably adequate.

What about antioxidants for heart attack prevention?

Antioxidants are food supplements that have been promoted as preventing heart disease and stroke. An important early event in the development of a cholesterol plaque in atherosclerosis is the oxidative modification of LDL cholesterol (low density lipoprotein) particles in the blood and the subsequent interaction of this modified LDL with the wall of the coronary artery. This process initiates the formation of the cholesterol plaque.
Antioxidants that block the oxidative modification of LDL have been shown to slow the progression of atherosclerosis in animal experiments. Examples of antioxidants include vitamin E and beta carotene. In humans, observational studies (studies that observe the frequency of related conditions) have found a relationship between the dietary intake of vitamin E and lower rates of heart attacks.
Observational studies provide only circumstantial evidence, however, and credible evidence is obtained only by way of controlled trials (discussed at the beginning of this article). Several controlled trials performed to date have yielded conflicting results on the benefits of antioxidant therapy. These results may possibly be due to the low doses of vitamin E used, the small number of patients in the study, or the limited duration of treatment.
The Heart Outcomes Prevention Evaluation study used a high dose (400 IU per day) of vitamin E over a span of five years in patients with significant risk factors for heart disease or stroke. This study found no difference in the occurrence of heart attack or stroke in the group treated with vitamin E versus those given the placebo. This study demonstrated that antioxidant therapy does not have any benefit in persons who have or are at high risk for having atherosclerosis.

How about exercise for heart attack prevention?

Studies of the effects of exercise in preventing heart attacks have yielded conflicting results. This is likely due to the fact that people who exercise regularly generally have healthier lifestyles and that many risk factors for heart disease can be influenced by exercise. Therefore, the specific role of exercise itself in heart attack prevention is difficult to isolate. For example, regular exercise has direct effects on weight control, blood pressure, diabetes, blood cholesterol, and smoking.

What about smoking cessation for heart attack prevention?

Smoking cessation, by whatever means, has been clearly demonstrated to reduce future heart attacks and death in patients with known coronary artery disease or who have other risk factors for the development of coronary artery disease. While many methods, both chemical and behavioral, have been used to aid smoking cessation, the initial success rate is often low, and the relapse rate is high. Certain medications that affect neurotransmitters in the brain, which are similar to agents often used to treat depression [for example, bupropion (Wellbutrin, Wellbutrin SR, Wellbutrin XL, Zyban)], have recently been demonstrated to be helpful in many patients trying to stop smoking. While effective, these agents may produce significant side effects and should only be used under the close supervision of a doctor.

Recommendations to prevent heart attacks

Eat whole, natural, and fresh foods.
Eat five to ten servings of fruits and vegetables daily and eat more peas, beans, and nuts.
Increase intake of omega-3 fatty acids by eating more fish, walnuts, flaxseed oil, and green leafy vegetables. An example of meeting the recommended intake of omega-3 fats is to eat 2 salmon portions a week or 1 gram of omega-3-fatty acid supplement daily.
Drink water, tea, non-fat dairy and red wine (two drinks or less daily for men, one drink or less daily for women).
Eat lean protein such as skinless poultry, fish, and lean cuts of red meat.
Avoid trans-fats and limit intake of saturated fats. This means avoiding fried foods, hard margarine, commercial baked goods, and most packaged and processed snack foods, high fat dairy and processed meats such as bacon, sausage, and deli meats.
Limit glycemic foods. Glycemic foods are those made with sugar and white flour, which increase blood sugar levels. Increased blood sugar levels stimulate the pancreas to release insulin. Chronically high insulin levels are believed to cause weight gain as well as atherosclerosis of the arteries.
Exercise daily.

Reference:
The HOPE and HOPE-TOO Trial Investigators. Effects of Long-term vitamin E supplementation on cardiovascular events and cancer: A randomized controlled trial. JAMA 293:1138-1347, 2005.

Medical Author:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Author:

Dennis Lee, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Tuberculosis (TB)

2012-03-26T08:14:00.002-07:00

Tuberculosis facts

Tuberculosis (TB) is an infection, primarily in the lungs (a pneumonia), caused by bacteria called Mycobacterium tuberculosis. It is spread usually from person to person by breathing infected air during close contact.
TB can remain in an inactive (dormant) state for years without causing symptoms or spreading to other people.
When the immune system of a patient with dormant TB is weakened, the TB can become active (reactivate) and cause infection in the lungs or other parts of the body.
The risk factors for acquiring TB include close-contact situations, alcohol and IV drug abuse, and certain diseases (for example, diabetes, cancer, and HIV) and occupations (for example, health-care workers).
The most common symptoms and signs of TB are fatigue, fever, weight loss, coughing, and night sweats.
The diagnosis of TB involves skin tests, chest X-rays, sputum analysis (smear and culture), and PCR tests to detect the genetic material of the causative bacteria.
Inactive tuberculosis may be treated with an antibiotic, isoniazid (INH), to prevent the TB infection from becoming active.
Active TB is treated, usually successfully, with INH in combination with one or more of several drugs, including rifampin (Rifadin), ethambutol (Myambutol), pyrazinamide, and streptomycin.
Drug-resistant TB is a serious, as yet unsolved, public-health problem, especially in Southeast Asia, the countries of the former Soviet Union, Africa, and in prison populations. Poor patient compliance, lack of detection of resistant strains, and unavailable therapy are key reasons for the development of drug-resistant TB.
The occurrence of HIV has been responsible for an increased frequency of tuberculosis. Control of HIV in the future, however, should substantially decrease the frequency of TB.

What is tuberculosis?

Tuberculosis (TB) is an infectious disease caused by bacteria whose scientific name is Mycobacterium tuberculosis. It was first isolated in 1882 by a German physician named Robert Koch who received the Nobel Prize for this discovery. TB most commonly affects the lungs but also can involve almost any organ of the body. Many years ago, this disease was referred to as "consumption" because without effective treatment, these patients often would waste away. Today, of course, tuberculosis usually can be treated successfully with antibiotics.
There is also a group of organisms referred to as atypical tuberculosis. These involve other types of bacteria that are in the Mycobacterium family. Often, these organisms do not cause disease and are referred to as "colonizers" because they simply live alongside other bacteria in our bodies without causing damage. At times, these bacteria can cause an infection that is sometimes clinically like typical tuberculosis. When these atypical mycobacteria cause infection, they are often very difficult to cure. Often, drug therapy for these organisms must be administered for one and a half to two years and requires multiple medications.

How does a person get TB?

A person can become infected with tuberculosis bacteria when he or she inhales minute particles of infected sputum from the air. The bacteria get into the air when someone who has a tuberculosis lung infection coughs, sneezes, shouts, or spits (which is common in some cultures). People who are nearby can then possibly breathe the bacteria into their lungs. You don't get TB by just touching the clothes or shaking the hands of someone who is infected. Tuberculosis is spread (transmitted) primarily from person to person by breathing infected air during close contact.
There is a form of atypical tuberculosis, however, that is transmitted by drinking unpasteurized milk. Related bacteria, called Mycobacterium bovis, cause this form of TB. Previously, this type of bacteria was a major cause of TB in children, but it rarely causes TB now since most milk is pasteurized (undergoes a heating process that kills the bacteria).

What happens to the body when a person gets TB?

When the inhaled tuberculosis bacteria enter the lungs, they can multiply and cause a local lung infection (pneumonia). The local lymph nodes associated with the lungs may also become involved with the infection and usually become enlarged. The hilar lymph nodes (the lymph nodes adjacent to the heart in the central part of the chest) are often involved.
In addition, TB can spread to other parts of the body. The body's immune (defense) system, however, can fight off the infection and stop the bacteria from spreading. The immune system does so ultimately by forming scar tissue around the TB bacteria and isolating it from the rest of the body. Tuberculosis that occurs after initial exposure to the bacteria is often referred to as primary TB. If the body is able to form scar tissue (fibrosis) around the TB bacteria, then the infection is contained in an inactive state. Such an individual typically has no symptoms and cannot spread TB to other people. The scar tissue and lymph nodes may eventually harden, like stone, due to the process of calcification of the scars (deposition of calcium from the bloodstream in the scar tissue). These scars often appear on X-rays and imaging studies like round marbles and are referred to as a granuloma. If these scars do not show any evidence of calcium on X-ray, they can be difficult to distinguish from cancer.
Sometimes, however, the body's immune system becomes weakened, and the TB bacteria break through the scar tissue and can cause active disease, referred to as reactivation tuberculosis or secondary TB. For example, the immune system can be weakened by old age, the development of another infection or a cancer, or certain medications such as cortisone, anticancer drugs, or certain medications used to treat arthritis or inflammatory bowel disease. The breakthrough of bacteria can result in a recurrence of the pneumonia and a spread of TB to other locations in the body. The kidneys, bone, and lining of the brain and spinal cord (meninges) are the most common sites affected by the spread of TB beyond the lungs.

How common is TB, and who gets it?

Over 8 million new cases of TB occur each year worldwide. In the United States, it is estimated that 10-15 million people are infected with the TB bacteria, and 22,000 new cases of TB occur each year.
Anyone can get TB, but certain people are at higher risk, including

people who live with individuals who have an active TB infection,
poor or homeless people,
foreign-born people from countries that have a high prevalence of TB,
nursing-home residents and prison inmates,
alcoholics and intravenous drug users,
people with diabetes, certain cancers, and HIV infection (the AIDS virus),
health-care workers.

There is no strong evidence for a genetically determined (inherited) susceptibility for TB.

What are the symptoms and signs of tuberculosis?

As previously mentioned, TB infection usually occurs initially in the upper part (lobe) of the lungs. The body's immune system, however, can stop the bacteria from continuing to reproduce. Thus, the immune system can make the lung infection inactive (dormant). On the other hand, if the body's immune system cannot contain the TB bacteria, the bacteria will reproduce (become active or reactivate) in the lungs and spread elsewhere in the body.
It may take many months from the time the infection initially gets into the lungs until symptoms develop. The usual symptoms that occur with an active TB infection are a generalized tiredness or weakness, weight loss, fever, and night sweats. If the infection in the lung worsens, then further symptoms can include coughing, chest pain, coughing up of sputum (material from the lungs) and/or blood, and shortness of breath. If the infection spreads beyond the lungs, the symptoms will depend upon the organs involved.

How does a doctor diagnose tuberculosis?

TB can be diagnosed in several different ways, including chest X-rays, analysis of sputum, and skin tests. Sometimes, the chest X-rays can reveal evidence of active tuberculosis pneumonia. Other times, the X-rays may show scarring (fibrosis) or hardening (calcification) in the lungs, suggesting that the TB is contained and inactive. Examination of the sputum on a slide (smear) under the microscope can show the presence of the tuberculosis-like bacteria. Bacteria of the Mycobacterium family, including atypical mycobacteria, stain positive with special dyes and are referred to as acid-fast bacteria (AFB). A sample of the sputum also is usually taken and grown (cultured) in special incubators so that the tuberculosis bacteria can subsequently be identified as tuberculosis or atypical tuberculosis. Traditionally, sputum is collected for three successive mornings and than examined. A recent study in Africa and the Middle East suggested that these specimens could be collected on the first visit and then the next morning. The study suggests that collecting specimens in fewer visits will help identify a greater population in need of treatment.
A new technology, light emitting-diode fluorescence microscopy (LED-FM), a type of smear microscopy, is more sensitive than the standard Ziehl-Neelsen AFB stain. This test is faster to perform and again may help identify patients in need of therapy quicker.
Several types of skin tests are used to screen for TB infection. These so-called tuberculin skin tests include the Tine test and the Mantoux test, also known as the PPD (purified protein derivative) test. In each of these tests, a small amount of purified extract from dead tuberculosis bacteria is injected under the skin. If a person is not infected with TB, then no reaction will occur at the site of the injection (a negative skin test). If a person is infected with tuberculosis, however, a raised and reddened area will occur around the site of the test injection. This reaction, a positive skin test, occurs about 48-72 hours after the injection. When only the skin test is positive, or evidence of prior TB is present on chest X-rays, the disease is referred to as "latent tuberculosis." This contrasts with active TB as described above, under symptoms.
If the infection with tuberculosis has occurred recently, however, the skin test can be falsely negative. The reason for a false-negative test with a recent infection is that it usually takes two to 10 weeks after the time of infection with tuberculosis before the skin test becomes positive. The skin test can also be falsely negative if a person's immune system is weakened or deficient due to another illness such as AIDS or cancer, or while taking medications that can suppress the immune response, such as cortisone or anticancer drugs.
Remember, however, that the TB skin test cannot determine whether the disease is active or not. This determination requires the chest X-rays and/or sputum analysis (smear and culture) in the laboratory. The organism can take up to six weeks to grow in culture in the microbiology lab. A special test to diagnose TB called the PCR (polymerase chain reaction) detects the genetic material of the bacteria. This test is extremely sensitive (it detects minute amounts of the bacteria) and specific (it detects only the TB bacteria). One can usually get results from the PCR test within a few days.

Is there a vaccine against tuberculosis?

Bacille Calmette Guérin, also known as BCG, is a vaccine given throughout many parts of the world. It is derived from an atypical Mycobacterium but offers some protection from developing active tuberculosis, especially in infants and children. This vaccination is believed to be important in parts of the world where TB is quite common. This is not the case in the United States, and the vaccine is not routinely administered in the U.S. When BCG has been administered, future PPD and Tine skin tests remain positive and can cause some confusion when trying to diagnose TB. It is also important to realize that even with a BCG vaccine in childhood, tuberculosis can still occur in an adult exposed to the tuberculosis bacteria, which calls into question the real utility and effectiveness of this vaccination.
A new blood test is now available that can help distinguish between a prior BCG vaccine and a positive PPD due to TB infection (QuantiFERON-TB Gold). This test involves mixing the patient's blood with substances that produce a TB-like immune response. After a period of time, the immune cells, if infected with TB, produce interferon-gamma, a protein produced by the body to defend against an infection. This test, like most, is not perfect, but with the proper clinical information can help distinguish a real TB infection from a positive reaction on the test due to a prior BCG vaccine.

What is the treatment for tuberculosis?

A person with a positive skin test, a normal chest X-ray, and no symptoms most likely has only a few TB germs in an inactive state and is not contagious. Nevertheless, treatment with an antibiotic may be recommended for this person to prevent the TB from turning into an active infection. The antibiotic used for this purpose is called isoniazid (INH). If taken for six to 12 months, it will prevent the TB from becoming active in the future. In fact, if a person with a positive skin test does not take INH, there is a 5%-10% lifelong risk that the TB will become active.
Taking isoniazid can be inadvisable (contraindicated) during pregnancy or for those suffering from alcoholism or liver disease. Also, isoniazid can have side effects. The side effects occur infrequently, but a rash can develop, and the individual can feel tired or irritable. Liver damage from isoniazid is a rare occurrence and typically reverses once the drug is stopped. Very rarely, however, especially in older people, the liver damage (INH hepatitis) can even be fatal. It is important therefore, for the doctor to monitor a patient's liver by periodically ordering blood tests called "liver function tests" during the course of INH therapy. Another side effect of INH is a decreased sensation in the extremities referred to as a peripheral neuropathy. This can be avoided by taking vitamin B6 (pyridoxine), and this is often prescribed along with INH.
A person with a positive skin test along with an abnormal chest X-ray and sputum evidencing TB bacteria has active TB and is contagious. As already mentioned, active TB usually is accompanied by symptoms, such as a cough, fever, weight loss, and fatigue.
Active TB is treated with a combination of medications along with isoniazid. Rifampin (Rifadin), ethambutol (Myambutol), and pyrazinamide are the drugs commonly used to treat active TB in conjunction with isoniazid (INH). Four drugs are often taken for the first two months of therapy to help kill any potentially resistant strains of bacteria. Then the number is usually reduced to two drugs for the remainder of the treatment based on drug-sensitivity testing that is usually available by this time in the course. Streptomycin, a drug that is given by injection, may be used as well, particularly when the disease is extensive and/or the patients do not take their oral medications reliably (termed "poor compliance"). Treatment usually lasts for many months and sometimes for years. Successful treatment of TB is dependent largely on the compliance of the patient. Indeed, the failure of a patient to take the medications as prescribed is the most important cause of failure to cure the TB infection. In some locations, the health department demands direct monitoring of patient compliance with therapy.
Surgery on the lungs may be indicated to help cure TB when medication has failed, but in this day and age, surgery for TB is unusual. Treatment with appropriate antibiotics will usually cure the TB. Without treatment, however, tuberculosis can be a lethal infection. Therefore, early diagnosis is important. Those individuals who have been exposed to a person with TB, or suspect that they have been, should be examined by a doctor for signs of TB and screened with a TB skin test.

What is drug-resistant TB?

Drug-resistant TB (TB that does not respond to drug treatment) has become a very serious problem in recent years in certain populations. For example, INH-resistant TB is seen among patients from Southeast Asia. The presence of INH-like substances in the cough syrups in that part of the world may play a role in causing the INH resistance. Drug-resistant cases are also often seen in prison populations. However, the major reason for the development of resistance is poorly managed TB care. This can result from poor patient compliance, inappropriate dosing or prescribing of medication, poorly formulated medications, and/or an inadequate supply of medication. Multidrug-resistant tuberculosis (MDR-TB) refers to organisms that are resistant to at least two of the first-line drugs, INH and Rifampin. More recently, extensively (extremely) drug-resistant tuberculosis (XDR-TB) has emerged. These bacteria are also resistant to three or more of the second-line treatment drugs.
XDR-TB is seen throughout the world but is most frequently seen in the countries of the former Soviet Union and Asia.
Preventing XDR-TB from spreading is essential. The World Health Organization (WHO) recommends improving basic TB care to prevent emergence of resistance and the development of proper laboratories for detection of resistant cases. When drug-resistant cases are found, prompt, appropriate treatment is required. This will prevent further transmission. Collaboration of HIV and TB care will also help limit the spread of tuberculosis, both sensitive and resistant strains.

What's in the future for TB?

Conceivably, TB could have been eliminated by effective treatment, vaccinations, and public-health measures by the year 2000. However, the emergence of HIV changed the whole picture. Because of HIV, a tremendous increase in the frequency (incidence) of TB occurred in the '80s and throughout the '90s. This increase in TB happened because suppression of the body's immune (defense) system by HIV allowed TB to occur as a so-called opportunistic infection. With the increasing HIV epidemic in Africa, serious concerns are being raised about the development of MDR-TB and XDR-TB in this population. Hopefully, control of HIV in the future will check this resurgence of tuberculosis.
The epidemic of HIV and TB has been a deadly combination especially on the African continent. A recent study comparing prophylactic regimens for prevention of active TB in HIV-infected individuals has shown effectiveness, however, the distribution of medication for both of these disease in the third world remains problematic.

Previous contributing author and editor:

Medical Author: Zab Mohsenifar, MD
Medical Editor: Leslie J. Schoenfield, MD, PhD

REFERENCES:

Cuevas, et al. "A Multi-Country Non-Inferiority Cluster Randomized Trial of Frontloaded Smear Microscopy for the Diagnosis of Pulmonary Tuberculosis." PloS Medicine 8.7 (2011).

Cuevas, et. al. "LED Fluorescence Microscopy for the Diagnosis of Pulmonary Tuberculosis; A Multi-Country Cross-Sectional Evaluation." PloS Medicine 8.7 (2011).

Martinson, N.A., et al. "New Regimens to Prevent Tuberculosis in Adults With HIV Infection." NEJM 365 July 7, 2011: 11-20.

United States. Centers for Disease Control and Prevention. "Guidelines for the Investigation of Contacts of Persons With Infectious Tuberculosis and Guidelines for Using the QuantiFERON-TB Gold Test for Detecting Mycobacterium tuberculosis Infection, United States." MMWR 54(No. RR-17) 2005.

United States. Centers for Disease Control and Prevention. "Updated Guidelines for Using Interferon Gamma Release Assays to Detect Mycobacterium tuberculosis Infection -- United States, 2010." MMWR 59 (No. RR-5) June 25, 2010: 1-25.

Medical Author:

George Schiffman, MD, FCCP

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Smallpox

2012-03-26T08:11:00.002-07:00

What is smallpox?

Smallpox is an infectious disease of the past that was eliminated by vaccination. The disease was caused by the variola virus, which spread from person to person. Affected people became very ill with a high fever and a characteristic rash. Up to one-third of people with smallpox died. Although the disease has been wiped out, samples of the virus still exist in high-security laboratories in the United States and Russia. This has led to concerns about use of the virus in biological warfare. For this reason, some military personnel are still vaccinated against smallpox.

What is the history of smallpox?

Smallpox is thought to have existed for more than 12,000 years. Evidence of infection can be found in mummies from ancient Egypt, including the mummy of Ramses V. Smallpox entered the New World in the 16th century, carried by European explorers and conquistadors. Because the aboriginal inhabitants had no immunity to the disease, smallpox often decimated native populations. There are even reports where infected blankets were used to intentionally infect Native American populations in the 18th century -- one of the early examples of biological warfare. During the 20th century, it is estimated that there were 300 million to 500 million deaths from smallpox worldwide, compared to 100 million from tuberculosis.
It was not until the end of the 18th century that an effective method of vaccination was developed. It was an English scientist named Edward Jenner who discovered it. Jenner observed that milkmaids often got a mild disease called cowpox and that this seemed to make them immune to smallpox. His vaccination strategy involved transferring the blister fluid from a person with cowpox to a person who had not yet had smallpox. This gave the susceptible person a cowpox infection (which was usually mild) and conveyed protection from smallpox. After a time, a virus similar to cowpox, called vaccinia, was substituted in the vaccine.
The last naturally occurring case of smallpox was in Somalia in 1977. In 1980, the World Health Organization (WHO) certified that the world was finally free of smallpox. Thus, smallpox was the first disease to be entirely eradicated. Campaigns are now under way to try to eliminate other diseases such as polio and measles.
The WHO has encouraged all member nations to destroy any remaining laboratory cultures of the virus. However, the rise of biological warfare technology led to concerns that smallpox could be weaponized and used in bioterrorism. Both the U.S. and Russia decided to retain their stockpiles in case they were needed to produce novel vaccines against a biological agent. This has understandably stirred up controversy, and the WHO is expected to renew its request to eliminate stockpiles in 2011. Supporters of retaining the cultures note that existing stocks of the virus have been used to develop and test new treatments and vaccines. The entire viral genome has been sequenced, leading to concerns that the virus may be recreated even if current stocks are destroyed.
Smallpox is a deadly disease and is on the list of potential biological weapons that are considered to pose the greatest threat to public health. Other agents on this list include anthrax, plague, smallpox, botulism, tularemia, and the viral hemorrhagic fevers, including Ebola and Marburg viruses.

What causes smallpox?

Smallpox is caused by a poxvirus called variola (Poxviridiae family of viruses). Variola is a relatively large virus that contains double-stranded DNA. The virus can be found in large numbers in many organs (skin, kidneys, spleen, liver, and other organs). Death occurs because of overwhelming toxemia, thought to be due to immune complexes trying to react to the large number of viral particles. Variola infection only occurs in humans, which was helpful in eradicating the disease. There are two strains called respectively variola major and variola minor (also known as alastrim). As implied by the names, variola major is more likely to cause serious disease and death than variola minor.

How is smallpox transmitted?

Most transmission of smallpox is directly from person to person. Large, infectious droplets of saliva are expelled during coughing or sneezing and then inadvertently inhaled by another person. This usually requires close face-to-face contact and is similar to the way that mumps, measles, and influenza are spread. On average, a single individual would infect approximately 60% of their household contacts. Infected objects, such as used silverware or heavily contaminated bedding, may carry sufficient numbers of organisms to infect another person if improperly handled, although this route of transmission is much less common.

What are smallpox symptoms and signs?

Symptoms develop seven to 17 days after exposure. Fever is the most common initial symptom and can be quite high. This is accompanied by body aches. Often, the patient is too unwell to get out of bed. Within 24 to 48 hours, a rash begins to appear everywhere on the body but especially on the legs, arms, mouth, and face. The eyes may also be affected, leading to potential blindness among survivors. Symptoms in children are similar to adults. The rash also appears on the palms and soles and goes through stages as the disease progresses. At the beginning, the rash consists of red dots that become raised. The lesions (see Figure 1) rapidly fill with fluid resembling a blister or cold sore and are known as "vesicles." The fluid in the vesicles may turn yellow, resembling pus. Rarely, the rash may start to fill with blood (hemorrhagic smallpox), which is a poor prognostic sign. After one to two weeks, the lesions scab over and eventually fall off, leaving deep scars. One of the defining features of smallpox is that all the lesions on the body are always at the same stage of development. This is in contrast to chickenpox where new lesions form while old ones are healing.

Figure 1: Picture of smallpox in a young child. SOURCE: Dr. Michael Schwartz/CDC

Approximately one-third of people with smallpox died from the infection. People who had an extensive rash were at higher risk to die. People who had only a few lesions or a milder rash had a lower risk of death. Infections caused by the variola minor strain were less severe and death occurred in only approximately 1% of cases.

How is smallpox diagnosed?

When smallpox was common, an experienced clinician could make the diagnosis simply by looking at the rash and examining the patient. Any case that occurs now will likely be a result of bioterrorism or biological warfare. In that event, misdiagnosis or delays in diagnosis could cause the infection to spread. Thus, it is still important for clinicians to be able to diagnose smallpox. The CDC has developed an online tool to help clinicians assess the likelihood that a rash is due to smallpox (http://emergency.cdc.gov.proxy1.cl.msu.edu
/agent/smallpox/diagnosis/#diagnosis).
If smallpox appears possible, public-health authorities should be notified immediately and their instructions on the protective measures for medical caregivers and others are followed carefully. They can help determine if additional testing is warranted. Material from blisters, throat swabs, and blood samples may be tested for the presence of variola DNA or cultured. These tests are done at the CDC and require prior authorization. The person(s) obtaining the specimens should have a recent smallpox vaccination (within three years) or no contraindication to immediate vaccination.

Figure 2: Picture of smallpox in a child. SOURCE: Dr. Jean Roy/CDC

What is the treatment for smallpox?

Treatment for smallpox is supportive, meaning that the patient should be kept hydrated, fever should be treated with acetaminophen (Tylenol) or a similar medication, and the patient should be closely monitoring to determine if there is a need for blood pressure support. Although there are no medications that have been proven to work against human infection, some medications have shown promise in the laboratory, including a derivative of the antiviral drug cidofovir (Vistide).

Can smallpox be prevented with a vaccine?

There is an effective vaccine for the prevention of smallpox. The vaccine is made from a virus called vaccinia. The similarity between these two names (vaccine and vaccinia) is not coincidental because smallpox was the first disease to be prevented by vaccination. In 2007, a second-generation smallpox vaccine (ACAM2000) was licensed. The vaccine contains live vaccinia virus but does not contain any smallpox virus. It is not a shot and is administered in a unique manner: a sharp, pronged piece of metal is dipped in the vaccine and then used to prick the skin of the recipient. This is done several times. If successful, the site of vaccination will develop small blisters that scab and heal, leaving a scar. This process is called scarification. While the blisters are active, the site should be kept clean, dry and covered to prevent the vaccinia virus from spreading to others.
Many older adults still have a vaccine scar on their arms from being vaccinated when they were younger. Smallpox vaccine, like other live vaccines including the yellow fever vaccine, teaches the body's immune system to remember how to make antibodies. There may still be a level of protection, even decades after vaccination. However, revaccination would be recommended in the event of a smallpox exposure. Interestingly, vaccination after exposure provides some protection against severe disease.
Vaccination is no longer recommended for the general population because the disease has been eradicated. Currently, the vaccine is given only to selected military personnel and laboratory workers who handle the smallpox virus.
Vaccination side effects are uncommon but are sometimes serious and potentially fatal. Because the vaccine contains live vaccinia virus, the virus may spread and infect the heart, causing myocarditis (infection of the heart muscle) or pericarditis (infection of the sac around the heart). This occurs in approximately one in 175 adults who are vaccinated for the first time. The vaccine can also infect the brain (encephalitis) or eye or cause a generalized rash. Vaccine complications lead to death in approximately six people for every million people who are newly vaccinated. Complications are much less common in revaccination. People with weak immune systems and those with skin conditions like eczema are at higher risk for complications. Pregnant women should not be vaccinated because of the risk of fetal death.

What is the prognosis for smallpox, and what are complications of smallpox?

Approximately one-third of people with smallpox died. Those who survived bore the scars of the disease for life. If the eye was infected, blindness was common. In the 19th century, smallpox was the leading cause of childhood blindness. It is possible that experimental medications will decrease complications and mortality rates, but this cannot be tested since human disease no longer exists. However, if the disease was reintroduced to humans (for example, by bioterrorists or other individuals), some investigators suggest the death rate may exceed one-third of the population and debilitate and scar many of those people that survive the disease.

Where can people find more information on smallpox?

The CDC web site (http://emergency.cdc.gov/agent/smallpox/index.asp) is an excellent source of information on smallpox. It provides comprehensive information on the disease and the vaccine.

Smallpox At A Glance

Smallpox is a contagious disease caused by the variola virus.
Smallpox was the first disease to be eliminated from the world through public-health efforts and vaccination.
Smallpox still poses a threat because existing laboratory strains may be used as biological weapons.
Smallpox causes high fever, prostration, and a characteristic rash. The rash usually includes blister-like lesions that occur everywhere on the body.
Approximately one-third of people with smallpox died from the disease. Survivors were scarred for life. If the eye was infected, blindness often resulted.
There are new experimental medications that might be effective in smallpox, but these have not been tested in human cases since the disease has been eradicated.
The vaccine contains a live virus called vaccinia. It is administered by dipping a pronged piece of metal into the vaccine and then pricking the skin.
The vaccine has uncommon side effects that may be fatal, including infection of the heart and brain with the vaccinia strain. Serious side effects are more common with the initial vaccine and are uncommon with second doses.
The vaccine is currently only given to selected military personnel and laboratory workers who handle the smallpox virus.

REFERENCE:

McFadden, G. "Killing a Killer: What Next for Smallpox?" PLoS Pathog 6.1 Jan. 29, 2010: e1000727.

Medical Author:

Mary D. Nettleman, MD, MS, MACP

Medical Editor:

Charles Patrick Davis, MD, PhD
Source:Medicinenet.com.

Relapsing Polychondritis

2012-03-26T08:06:00.002-07:00

Relapsing polychondritis facts

Relapsing polychondritis is an uncommon, chronic disorder of the cartilage.
Relapsing polychondritis is characterized by recurrent episodes of painful inflammation.
Relapsing polychondritis can involve all types of cartilage.
Typical cartilage tissues affected include the ears, nose, and joints.
There is no one specific test for diagnosing relapsing polychondritis.
Treatment often involves cortisone-related medications.
The course of symptoms for patients is often unpredictable.

What is relapsing polychondritis?

Relapsing polychondritis is an uncommon, chronic disorder of the cartilage that is characterized by recurrent episodes of inflammation of the cartilage of various tissues of the body. Chondritis means inflammation of cartilage. Tissues containing cartilage that can become inflamed include the ears, nose, joints, spine, and windpipe (trachea). The eyes, heart, and blood vessels, which have a biochemical makeup similar to that of cartilage, can also be affected. Relapsing polychondritis is sometimes called the red ear syndrome.

What causes relapsing polychondritis?

The cause of relapsing polychondritis is unknown. It is suspected that this condition is caused by "autoimmunity." Autoimmunity is characterized by a misdirected immune system. This results in inflammation in various tissues of the body.

What are symptoms and signs of relapsing polychondritis?

Typically, relapsing polychondritis causes sudden pain in the inflamed tissue at the onset of the disease. Common symptoms are pain, redness, swelling, and tenderness in one or both ears, the nose, throat, joints, and/or eyes. The lobe of the ear is not involved. Fever, fatigue, and weight loss often develop.
Inflammation of the ears and nose can cause deformity (saddle nose deformity and floppy ears) from weakened cartilage. Impaired hearing, balance, and nausea can be caused by inner ear inflammation.
Inflammation of the windpipe or trachea can lead to throat pain, hoarseness, and breathing difficulty. This is a potentially dangerous area of inflammation in patients with relapsing polychondritis and can require assisted breathing methods when severe.
Joint inflammation (arthritis) can cause pain, swelling, and stiffness of the joints, including of the hands, knees, ankles, wrists, and feet.
Eye inflammation can be mild or severe and can damage vision. Cataracts can be caused by the inflammation or from the cortisone used to treat relapsing polychondritis (see below).
Other tissues that can develop inflammation include the aorta (which can lead to aneurysm or aortic valve weakness), tissues in or around the heart (myocarditis and pericarditis), the skin (vasculitis), and the nerves from the brain (cranial nerve palsies).

How is relapsing polychondritis diagnosed?

Relapsing polychondritis is diagnosed when the doctor recognizes the classic pattern of cartilage involvement during the history and physical examination. The symptoms described above can suggest the disease.
There is no one specific test for diagnosing relapsing polychondritis. Blood tests that indicate inflammation, such as an elevated erythrocyte sedimentation rate (ESR), C-reactive protein, and others, are often abnormal when the disease is active.
If tissue cartilage is biopsied, the involved cartilage will demonstrate nonspecific signs of inflammation.

Can relapsing polychondritis be associated with other diseases?

Yes. The doctor will be interested in determining whether or not signs of the following diseases are present along with relapsing polychondritis: vasculitis, Wegener's granulomatosis, systemic lupus erythematosus, ankylosing spondylitis, Reiter's disease, psoriatic arthritis, rheumatoid arthritis, Behcet's disease, Churg-Strauss syndrome, polyarteritis nodosa, myelodysplasia, and others.

What medications are used to treat relapsing polychondritis?

For patients with more mild disease, nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen (Motrin), naproxen (Naprosyn), and others, can be helpful to control the inflammation. Usually, however, cortisone-related medications (steroids such as prednisone and prednisolone) are required. High-dose steroids are frequently necessary initially, especially when the eyes or breathing airways are involved. Moreover, most patient require steroids for long-term use.
Methotrexate (Rheumatrex, Trexall) has shown promise as a treatment for relapsing polychondritis in combination with steroids as well as a maintenance treatment. Studies have demonstrated that methotrexate can help reduce the steroid requirements.
Other medications that have been tried in small numbers of patients with some reports of success include cyclophosphamide (Cytoxan), dapsone, azathioprine (Imuran), penicillamine (Depen, Cuprimine), cyclosporine, anti-tumor necrosis factor (TNF) biologic medications (adalimumab [Humira], infliximab [Remicade]), and combinations of these drugs with steroids.

What is the long-term outlook (prognosis) for patients with relapsing polychondritis?

The course of symptoms for patients with relapsing polychondritis is often unpredictable.
Repeated bouts of inflammation of cartilage from relapsing polychondritis frequently leads to permanent destruction of the involved tissues and results in disability. Destruction of nose and ear cartilage results in deformity and can impair breathing when the trachea is affected.
Relapsing polychondritis is potentially dangerous and even life threatening, depending on the tissues involved. Inflammation of the cartilage of the windpipe (trachea), heart, aorta, and other blood vessels can be fatal. For some patients, however, the disease is much more limited and mild. Close monitoring of symptoms with a qualified doctor is recommended for optimal results.

REFERENCE:

Klippel, J.H., et al. Primer on the Rheumatic Diseases. New York: Springer, 2008.

Medical Author:

William C. Shiel Jr., MD, FACP, FACR

Medical Editor:

Catherine Burt Driver, MD

Source:Medicinenet.com.

Cancer

2012-03-26T08:05:00.002-07:00

What is cancer?

Cancer is the uncontrolled growth of abnormal cells anywhere in a body. The abnormal cells are termed cancer cells, malignant cells, or tumor cells. Many cancers and the abnormal cells that compose the cancer tissue are further identified by the name of the tissue that the abnormal cells originated from (for example, breast cancer, lung cancer, colon cancer). Cancer is not confined to humans; animals and other living organisms can get cancer. Below is a schematic that shows normal cell division and how when a cell is damaged or altered without repair to its system, the cell usually dies. Also shown is what can occur when such damaged or unrepaired cells do not die and become cancer cells and proliferate with uncontrolled growth; a mass of cancer cells develop. Frequently, cancer cells can break away from this original mass of cells, travel through the blood and lymph systems, and lodge in other organs where they can again repeat the uncontrolled growth cycle. This process of cancer cells leaving an area and growing in another body area is termed metastatic spread or metastatic disease. For example, if breast cancer cells spread to a bone (or anywhere else), it means that the individual has metastatic breast cancer.
There are over 200 types of cancers; most can fit into the following categories according to the National Cancer Institute:

Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs
Sarcoma: Cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue
Leukemia: Cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood
Lymphoma and myeloma: Cancers that begin in the cells of the immune system
Central nervous system cancers: Cancers that begin in the tissues of the brain and spinal cord

In the U.S., according to the National Cancer Institute in 2010, the most common cancers (excluding non-melanoma skin cancers) are listed below.

Cancer type	Estimated new cases	Estimated deaths
Bladder	70,530	14,680
Breast (female-male)	207,090-1,970	39,840-390
Colon and rectal (combined)	142,570	51,370
Endometrial	43,470	7,950
Kidney (renal cell)	53,581	11,997
Leukemia	43,050	21,840
Lung (including bronchus)	222,520	157,300
Melanoma	68,130	8,700
Non-Hodgkin lymphoma	65,540	20,210
Pancreatic	43,140	36,800
Prostate	217,730	32,050
Thyroid	44,670	1,690

The three most common cancers in men, women and children in the U.S. are as follows:

Men: Prostate, lung, and colorectal
Women: Breast, colorectal, and lung
Children: Leukemia, brain tumors, and lymphoma

The incidence of cancer and cancer types are influenced by many factors such as age, sex, race, local environmental factors, diet, and genetics. Consequently, the incidence of cancer and cancer types vary depending on these variable factors. For example, the World Health Organization (WHO) provides the following general information about cancer worldwide:

Cancer is a leading cause of death worldwide. It accounted for 7.4 million deaths (around 13% of all deaths) in 2004 (statistics published in 2009).
Lung, stomach, liver, colon, and breast cancer cause the most cancer deaths each year.
Deaths from cancer worldwide are projected to continue rising, with an estimated 12 million deaths in 2030.

Different areas of the world may have cancers that are either more or less predominant then those found in the U.S. One example is that stomach cancer is often found in Japan, while it is rarely found in the U.S.
The objective of this article is to introduce the reader to general aspects of cancers. It is designed to be an overview of cancer and cannot cover every cancer type. This article will also attempt to help guide the reader to more detailed sources about specific cancer types.

What causes cancer?

Anything that may cause a normal body cell to develop abnormally potentially can cause cancer. Many things can cause cell abnormalities and have been linked to cancer development. Some cancer causes remain unknown while other cancers may develop from more than one known cause. Some may be developmentally influenced by a person's genetic makeup. Many patients develop cancer due to a combination of these factors. Although it is often difficult or impossible to determine the initiating event(s) that cause a cancer to develop in a specific person, research has provided clinicians with a number of likely causes that alone or in concert with other causes, are the likely candidates for initiating cancer. The following is a listing of major causes and is not all-inclusive as specific causes are routinely added as research advances:
Chemical or toxic compound exposures: Benzene, asbestos, nickel, cadmium, vinyl chloride, benzidine, N-nitrosamines, tobacco or cigarette smoke (contains at least 66 known potential carcinogenic chemicals and toxins), and aflatoxin
Ionizing radiation: Uranium, radon, ultraviolet rays from sunlight, radiation from alpha, beta, gamma, and X-ray-emitting sources
Pathogens: Human papillomavirus (HPV), EBV or Epstein-Barr virus, hepatitis viruses B and C, Kaposi's sarcoma-associated herpesvirus (KSHV), Merkel cell polyomavirus, Schistosoma spp., and Helicobacter pylori; other bacteria are being researched as possible agents
Genetics: A number of specific cancers have been linked to human genes and are as follows: breast, ovarian, colorectal, prostate, skin and melanoma; the specific genes and other details are beyond the scope of this general article so the reader is referred to http://www.cancer.gov/cancertopics/genetics for more details about genetics and cancer.
It is important to point out that most everyone is exposed to cancer-causing substances (for example, sunlight, cigarette smoke, and X-rays) during their lifetime but many individuals do not develop cancer. In addition, many people have the genes that are linked to cancer but do not develop it. Why? Although researchers may not be able give a satisfactory answer for every individual, it is clear that the higher the amount or level of cancer-causing materials a person is exposed to, the higher the chance the person will develop cancer. In addition, the people with genetic links to cancer may not develop it for similar reasons (lack of enough stimulus to make the genes function). In addition, some people may have a heightened immune response that controls or eliminates cells that are or potentially may become cancer cells. There is evidence that even certain dietary lifestyles may play a significant role in conjunction with the immune system to allow or prevent cancer cell survival. For these reasons, it is difficult to assign a specific cause of cancer to many individuals.
Proving that a substance does not cause or is not related to increased cancer risk is difficult. For example, antiperspirants are considered to possibly be related to breast cancer by some investigators and not by others. The official stance by the NCI is "additional research is needed to investigate this relationship and other factors that may be involved." This unsatisfying conclusion is presented because the data collected so far is contradictive. Other claims that are similar require intense and expensive research which may never be done. Reasonable advice might be to avoid large amounts of any compounds even remotely linked to cancer, although it may be difficult to do in complex, technologically advanced modern societies.

What are cancer symptoms and signs?

Symptoms and signs of cancer depend on the type of cancer, where it is located, and/or where the cancer cells have spread. For example, breast cancer may present as a lump in the breast or as nipple discharge while metastatic breast cancer may present with symptoms of pain (if spread to bones), extreme fatigue (lungs), or seizures (brain). A few patients show no signs or symptoms until the cancer is far advanced. However, there are some signs and symptoms, although not specific, which usually occur in most cancer patients that are fairly easy for the person to detect. They are as follows:

Fever (no clear infectious source, recurrent or constant)
Fatigue (not relived by rest)
Weight loss (without trying to lose weight)
Pain (usually persistent)
Skin changes (coloration, sores that do not heal, white spots in mouth or on tongue, wart changes)
Change in bowel or bladder functions (including trouble swallowing or constipation)
Unusual bleeding (mouth, vaginal, and bladder) or discharge
Persistent cough or change in voice
Lumps or tissue masses

Anyone with these signs and symptoms should consult their doctor.
Many cancers will present with some of the above general symptoms but often have one or more symptoms that are more specific for the cancer type. For example, lung cancer may present with common symptoms of pain, but usually the pain is located in the chest. The patient may have unusual bleeding, but the bleeding usually occurs when the patient coughs. Lung cancer patients often become short of breath, and then become very fatigued.
Because there are so many cancer types (see next section) with so many nonspecific and sometimes more specific symptoms, the best way to learn about signs and symptoms of specific cancer types is to spend a few moments researching symptoms of a specific body area in question. Conversely, a specific body area can be searched to discover what signs and symptoms a person should look for in that area that is suspected of having cancer. The following examples are two ways to proceed to get information on symptoms:

Use a search engine (Google, Bing) to find links to cancer by listing the symptom followed by the term "cancer." For example, listing "blood in urine and cancer" will bring a person to web sites that list possible organs and body systems where cancer may produce the listed symptoms.
Use a search engine as above and list the suspected body area and cancer (for example, bladder and cancer), and the person will see sites that list the signs and symptoms of cancer in that area (blood in urine being one of several symptoms listed).

In addition, if the cancer type is known (diagnosed), then even more specific searches can be done listing the diagnosed cancer type and whatever may be questioned about the cancer (symptoms, tumor grades, treatments, prognosis, and many other items).
Your own research should not replace consulting a health-care provider if you ae concerned about cancer.

What are the different types of cancer?

There are over 200 types of cancer; far too numerous to include in this introductory article. However, the NCI lists several general categories (see list in first section of this article). This list is expanded below to list more specific types of cancers found in each general category; it is not all inclusive and the cancers listed in quotes are the general names of some cancers:

Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs -- "skin, lung, colon, pancreatic, ovarian cancers," epithelial, squamous and basal cell carcinomas, melanomas, papillomas, and adenomas
Sarcoma: Cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue -- "bone, soft tissue cancers," osteosarcoma, synovialsarcoma, liposarcoma, angiosarcoma, rhabdosarcoma, and fibrosarcoma
Leukemia: Cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood -- "leukemia," lymphoblastic leukemias (ALL and CLL), myelogenous leukemias (AML and CML), T-cell leukemia, and hairy-cell leukemia
Lymphoma and myeloma: Cancers that begin in the cells of the immune system -- "lymphoma," T-cell lymphomas, B-cell lymphomas, Hodgkin lymphomas, non-Hodgkin lymphoma, and lymphoproliferative lymphomas
Central nervous system cancers: Cancers that begin in the tissues of the brain and spinal cord -- "brain and spinal cord tumors," gliomas, meningiomas, pituitary adenomas, vestibular schwannomas, primary CNS lymphomas, and primitive neuroectodermal tumors

Not included in the above types listed are metastatic cancers; this is because metastatic cancer cells usually arise from a cell type listed above and the major difference from the above types is that these cells are now present in a tissue from which the cancer cells did not originally develop. Consequently, if the terms "metastatic cancer" is used, for accuracy, the tissue from which the cancer cells arose should be included. For example, a patient may say they have or are diagnosed with "metastatic cancer" but the more accurate statement is "metastatic (breast, lung, colon, or other type) cancer."

How is cancer diagnosed?

A physical exam and medical history, especially the history of symptoms, are the first steps in diagnosing cancer. In many instances, the medical caregiver will order a number of tests, most of which will be determined by the type of cancer and where it is suspected to be located in or on the person's body. In addition, most caregivers will order a complete blood count, electrolyte levels and, in some cases, other blood studies that may give additional information (for example, a PSA or prostate specific antigen test may guide the caregiver to do additional tests, such as a prostate biopsy).
Imaging studies are commonly used to help physicians detect abnormalities in the body that may be cancer. X-rays, CT and MRI scans, and ultrasound are common tools used to examine the body. Other tests such as endoscopy, which with variations in the equipment used, can allow visualization of tissues in the intestinal tract, throat, and bronchi that may be cancerous. In areas that cannot be well visualized (inside bones or some lymph nodes, for example), radionuclide scanning is often used. The test involves ingestion or IV injection of a weakly radioactive substance that can be concentrated and detected in abnormal tissue.
The preceding tests can be very good at localizing abnormalities in the body; many clinicians consider that some of the tests provide presumptive evidence for the diagnosis of cancer. However, in most patients, the definitive diagnosis of cancer is based on the examination of a tissue sample from the tissue that may be cancerous by a qualified pathologist. Some biopsy samples are relatively simple to procure (for example, skin biopsy or intestinal tissue biopsy done with an endoscope equipped with a biopsy attachment). Other biopsies may require surgery (for example, brain tissue or lymph node biopsy). In some instances, the surgery to diagnose the cancer may result in a cure if all of the cancerous tissue is removed at the time of biopsy.
The biopsy can provide more than the definitive diagnosis of cancer; it can identify the cancer type (for example, a primary or metastatic type of brain cancer) and the "stage" of the cancerous cells. The stage or cancer staging is a way for clinicians and researchers to estimate how advanced or how severe the disease is. The following section describes the general staging methods for cancers.

How is cancer staging determined?

There are a number of different staging methods used for cancers and the specific staging criteria varies among cancer types. According to the NCI, the common elements considered in most staging systems are as follows:

Site of the primary tumor
Tumor size and number of tumors
Lymph node involvement (spread of cancer into lymph nodes)
Cell type and tumor grade* (how closely the cancer cells resemble normal tissue cells)
The presence or absence of metastasis

However, there are two main methods that form the basis for the more specific or individual cancer type staging. The TMN staging is used for most solid tumors while the Roman numeral or stage grouping method is used by some clinicians and researchers on almost all cancer types.
The following is how the NCI describes the TNM staging system:

Primary tumor (T)

Regional lymph nodes (N)

Distant metastasis (M)

Consequently, a person's cancer could be listed as T1N2M0, meaning it is a small tumor (T1), but has spread to some regional lymph nodes (N2), and has no detected metastasis (M0).
The Roman numeral or stage grouping method is described by the NCI as follows:

Stage	Definition
Stage 0	Carcinoma in situ.
Stage I, Stage II, and Stage III	Higher numbers indicate more extensive disease: Larger tumor size and/or spread of the cancer beyond the organ in which it first developed to nearby lymph nodes and/or organs adjacent to the location of the primary tumor
Stage IV	The cancer has spread to another organ(s).

As mentioned above, variations of these staging methods exist. For example, some cancer registries use surveillance, epidemiology, and end results program (SEER) termed summary staging. SEER groups cancer cases into five main categories:

In situ: Abnormal cells are present only in the layer of cells in which they developed.
Localized: Cancer is limited to the organ in which it began, without evidence of spread.
Regional: Cancer has spread beyond the primary site to nearby lymph nodes or organs and tissues.
Distant: Cancer has spread from the primary site to distant organs or distant lymph nodes.
Unknown: There is not enough information to determine the stage.

Staging of cancer is important; it helps the physician to decide on the most effective therapeutic protocols, provides a basis for estimating the prognosis (outcome) for the patient, and provides a system to communicate the patient's condition to other health professionals that become involved with the patients' care.

What is the treatment for cancer?

The treatment for cancer is usually designed by a team of doctors or by the patient's oncologist and is based on the type of cancer and the stage of the cancer. Most treatments are designed specifically for each individual. In some people, diagnosis and treatment may occur at the same time if the cancer is entirely surgically removed when the surgeon removes the tissue for biopsy.
Although patients may obtain a unique treatment protocol for their cancer, most treatments have one or more of the following components: surgery, chemotherapy, radiation therapy, or combination treatments (a combination of two or all three treatments).
Individuals obtain variations of these treatments for cancer. Patients with cancers that cannot be cured (completely removed) by surgery usually will get combination therapy, the composition determined by the cancer type and stage.
Palliative therapy (medical care or treatment used to reduce disease symptoms but unable to cure the patient) utilizes the same treatments described above. It is done with the intent to extend and improve the quality of life of the terminally ill cancer patient. There are many other palliative treatments to reduce symptoms such as pain medications and antinausea medications.

What is the prognosis for cancer?

The prognosis (outcome) for cancer patients may range from excellent to poor. The prognosis is directly related to both the type and stage of the cancer. For example, many skin cancers can be completely cured by removing the skin cancer tissue; similarly, even a patient with a large tumor may be cured after surgery and other treatments like chemotherapy (note that a cure is often defined by many clinicians as a five-year period with no reoccurrence of the cancer). However, as the cancer type either is or becomes aggressive, with spread to lymph nodes or is metastatic to other organs, the prognosis decreases. For example, cancers that have higher numbers in their staging (for example, stage III or T3N2M1; see staging section above) have a worse prognosis than those with low (or 0) numbers. As the staging numbers increase, the prognosis worsens.
There are many complications that may occur with cancer; many are specific to the cancer type and stage and are too numerous to list here. However, some general complications that may occur with both cancer and its treatment protocols are listed below:

Fatigue (both cancer and treatments)
Anemia (both)
Loss of appetite (both)
Insomnia (both)
Hair loss (treatments mainly)
Nausea (both)
Lymphedema (both)
Pain (both)
Immune system depression (both)

Can cancer be prevented?

Most clinicians and researchers are convinced that many cancers can either be prevented or the risk of developing cancers can be markedly reduced. Some of the methods are simple; others are relatively extreme, depending on an individual's view.
Prevention of cancer, by avoiding its potential causes, is the simplest method. First on most clinicians and researchers list is to stop (or better, never start) smoking tobacco. Avoiding excess sunlight (by decreasing exposure or applying sunscreen) and many of the chemicals and toxins is an excellent way to avoid cancers. Avoiding contact with certain viruses and other pathogens also is likely to prevent some cancers. People who have to work close to cancer-causing agents (chemical workers, X-ray technicians, ionizing radiation researchers) should follow all safety precautions and minimize any exposure to such compounds.
There are two vaccines currently approved by the U.S. Food and Drug Administration (FDA) to prevent specific types of cancer. Vaccines against the hepatitis B virus, which is considered a cause of some liver cancers, and vaccines against human papillomavirus types 16 and 18, which, according to the NCI, are responsible for about 70% of cervical cancer. Some clinicians and researchers recommend that all people, especially young teens, be vaccinated against the human papillomavirus, but this approach is still controversial.
People with a genetic predisposition to develop certain cancers and others with a history of cancers in their genetically linked relatives currently cannot change their genetic makeup. However, some individuals who have a high possibility of developing genetically linked cancer have taken actions to prevent cancer development. For example, some young women who have had many family members develop breast cancer have elected to have their breast tissue removed even if they have no symptoms or signs of cancer development to reduce or eliminate the possibility they will develop breast cancer. Some doctors consider this as an extreme measure to prevent cancer while others do not.
Screening studies for cancer, while they do not prevent cancers, may detect them at an earlier stage when the cancer is more likely to be potentially cured with treatment. Such screening studies are breast exams, testicular exams, colon-rectal exams (colonoscopy), mammography, PSA levels, prostate exams, and others. People who have any suspicion that they may have cancer should discuss their concerns with their doctor as soon as possible. The earlier cancer is disproved or diagnosed and treated, the person will be better served.

Where can people find more information about cancer?

There are many ways a person can find more information about cancer, but if they have any immediate concerns about having cancer, their first source of information should be their doctor. In addition to the references listed at the end of this article, the following is a list of information sources that are well recognized as authorities for cancer information by most clinicians:

National Cancer Institute (http://www.cancer.gov/)
American Cancer Society (http://www.cancer.org/Cancer/index)

Cancer At A Glance

Cancer is the uncontrolled growth of abnormal cells anywhere in a body.
There are over 200 types of cancer.
Anything that may cause a normal body cell to develop abnormally potentially can cause cancer; general categories of cancer-related or causative agents are as follows: chemical or toxic compound exposures, ionizing radiation, some pathogens, and human genetics.
Cancer symptoms and signs depend on the specific type and grade of cancer; general signs and symptoms are not very specific but are as follows: fever, fatigue, weight loss, pain, skin changes, change in bowel or bladder function, unusual bleeding, persistent cough or voice change, lumps, or tissue masses
Although there are many tests to presumptively find or presumptively diagnose cancer, the definite diagnosis is made by examination of a biopsy sample of suspected cancer tissue.
Cancer staging is often determined by biopsy results and helps determine the aggressiveness of the cancer type and the extent of cancer spread; staging also helps caregivers determine treatment protocols. In general, most staging methods show that the higher the number assigned (usually between 0-4), the more aggressive the cancer type or more widespread is the cancer in the body.
Treatment protocols vary according to the type and stage of the cancer. Most treatment protocols are designed to fit the individual patient's disease. However, most treatments include at least one of the following and may include all: surgery, chemotherapy, and radiation therapy.
The prognosis of cancer can range from excellent to poor. The prognosis depends on the cancer type and its staging with those cancers known to be aggressive and those staged with higher numbers (3-4) often have a prognosis that ranges more toward poor.
Some cancers can be prevented by taking simple precautions, other cancers may have the risk of contracting them reduced by several methods, and a few may be difficult to avoid for some individuals.

REFERENCES:

Switzerland. World Health Organization. "Cancer." Feb. 2011. <http://www.who.int/mediacentre/factsheets/fs297/en/index.html>.

United States. Agency for Toxic Substances & Disease Registry. "Cancer Fact Sheet." Aug. 30, 2002. <http://www.atsdr.cdc.gov/com/cancer-fs.html>.

United States. Centers for Disease Control. "Human Papillomavirus (HPV)." Sept. 22, 2010. <http://www.cdc.gov/hpv/>.

United States. National Cancer Institute. "Cancer Genetics." <http://www.cancer.gov/cancertopics/genetics>.

United States. National Cancer Institute. "Cancer Vaccines." Aug. 4, 2010. <http://www.cancer.gov/cancertopics/factsheet/Therapy/cancer-vaccines>.

United States. National Cancer Institute. "Common Cancer Types." Nov. 4, 2010. <http://www.cancer.gov/cancertopics/types/commoncancers>.

Medical Author:

Charles Patrick Davis, MD, PhD

Medical Editor:

Jerry R. Balentine, DO, FACEP
Source:Medicinenet.com.

Tinnitus (Ringing in the Ears and Other Ear Noise)

2012-03-26T07:58:00.002-07:00

What is tinnitus?

Tinnitus is a ringing, swishing, or other type of noise that seems to originate in the ear or head. In many cases it is not a serious problem, but rather a nuisance that eventually resolves. Rarely, however, tinnitus can represent a serious health condition.
It is not a single disease, but a symptom of an underlying condition. Nearly 36 million Americans suffer from this disorder. In almost all cases, only the patient can hear the noise.

What causes tinnitus?

Tinnitus can arise in any of the following areas: the outer ear, the middle ear, the inner ear, or by abnormalities in the brain. Some tinnitus or head noise is normal. If one goes into a sound proof booth and normal outside noise is diminished, one becomes aware of these normal sounds. We are usually not aware of these normal body sounds, because outside noise masks them. Anything, such as ear wax or a foreign body in the external ear, that blocks these background sounds will cause us to be more aware of our own head sounds. Fluid, infection, or disease of the middle ear bones or ear drum (tympanic membrane) can also cause tinnitus.
One of the most common causes of tinnitus is damage to the microscopic endings of the hearing nerve in the inner ear. Advancing age is generally accompanied by a certain amount of hearing nerve impairment, and consequently chronic tinnitus.
Today, loud noise exposure is a very common cause of tinnitus, and it often damages hearing as well. Unfortunately, many people are unconcerned about the harmful effects of excessively loud noise, firearms, and high intensity music.
Some medications (for example, aspirin) and other diseases of the inner ear (Meniere's syndrome) can cause tinnitus. Tinnitus can in very rare situations be a symptom of such serious problems as a brain aneurysm or a brain tumor (acoustic tumor).

How is tinnitus evaluated?

A medical history, physical examination, and a series of special tests can help determine precisely where the tinnitus is originating. It is helpful for the doctor to know if the tinnitus is constant, intermittent or pulsating (synchronous with the heart beat, referred to as pulsatile tinnitus), or is it associated with hearing loss or loss of balance (vertigo). All patients with persisting unexplained tinnitus need a hearing test (audiogram). Patterns of hearing loss may lead the doctor to the diagnosis.
Other tests, such as the auditory brain stem response (ABR), a computerized test of the hearing nerves and brain pathways, computer tomography scan (CT scan) or, magnetic resonance imaging (MRI scan) may be needed to rule out a tumor occurring on the hearing or balance nerve. These tumors are rare, but they can cause tinnitus.

What is the treatment of tinnitus?

After a careful evaluation, your doctor may find an identifiable cause and be able to treat or make recommendations to treat the tinnitus. Once you have had a thorough evaluation, an essential part of treatment is your own understanding of the tinnitus (what has caused it, the person's specific symptoms, and options for treatment).

Tinnitus medications

In many cases, there is no specific treatment for tinnitus. It may simply go away on its own, or it may be a permanent disability that the patient will have to "live with." Some otolaryngologists (ear specialists) have recommended niacin to treat tinnitus. However, there is no scientific evidence to suggest that niacin helps reduce tinnitus, and it may cause problems with skin flushing.
The drug gabapentin (Neurontin, Gabarone), was studied in high doses, and reduced the annoyance level of the tinnitus in some patients, but did not decrease the volume of the noise, and was not found to be better than placebo.
A 2005 study in Brazil using acamprosate (Campral), a drug used to treat alcoholism, showed a nearly 87% rate of relief of symptoms. Studies of this drug for treatment of tinnitus are currently ongoing in the United States.

What are tinnitus relief remedies?

Some common and easy remedies such as the following may be of benefit to some individuals.

Reducing or avoiding caffeine and salt intake, and quitting smoking may help relieve tinnitus symptoms.
Some tinnitus patients have been found to have lower zinc levels and may benefit from zinc supplementation.
One study showed melatonin may help tinnitus sufferers, particularly those with disturbed sleep due to the tinnitus. However, this is not yet been verified in controlled studies.
Ginkgo Biloba has been touted as a natural tinnitus remedy, but controlled studies to date have not shown it to be effective.
There are some behavioral and cognitive therapies that have been successful in treating tinnitus. Seeking out a multidisciplinary program at a tinnitus center may improve chances of successful treatment. The types of therapies include tinnitus retraining therapy, masking, and behavioral therapy.

Can tinnitus be prevented?

Do not place objects in your ear such as cotton swabs (Q-tips) to clean your ear. This can cause a wax impaction against your eardrum which can cause tinnitus. Take blood pressure medicines and other prescribed medications as they are ordered by your doctor.
According to the American Tinnitus Association there are several things you can do to protect yourself from excessive noise related tinnitus:

Protect your hearing at work. Your work place should follow Occupational Safety & Health Administration (OSHA) regulations. Wear ear plugs or earmuffs and follow hearing conservation guidelines set by your employer.
When around any noise that bothers your ears (a concert, sporting event, hunting) wear hearing protection or reduce noise levels.
Even everyday noises, such as blow drying your hair or using a lawnmower, can require protection. Keep ear plugs or earmuffs handy for these activities.

Is there anything to do to lessen intensity of the tinnitus?

It is important to realize that the hearing system is one of the most delicate and sensitive mechanisms in the body. Since it is a part of the general nervous system, it is sensitive, to some degree, by anything that affects the overall health of the individual (both physical and psychological). Therefore, in order to lessen the intensity of tinnitus, it is advisable to make every effort to:

Avoid exposure to loud sounds and noises
Control blood pressure
Decrease salt intake
Avoid nerve stimulants such as coffee and colas (caffeine) and tobacco (nicotine)
Reduce anxiety
Try to stop worrying about the tinnitus. Often, the more you worry and concentrate on the noise, the louder it will become.
Get adequate rest and avoid fatigue.
Exercise
Utilize masking noise. Tinnitus is usually more bothersome when the surroundings are quiet, especially when you are in bed. A competing sound such as a ticking clock, a radio, a fan or white noise machine may help mask tinnitus. Small hearing aid like devices which generate a competitive sound may help reduce the awareness of the tinnitus.
Biofeedback may help or diminish tinnitus in some patients.
Avoid aspirin or aspirin products in large quantities

Tinnitus At A Glance

Tinnitus is abnormal ear noise.
Tinnitus can arise in any of the four sections of the ear: the outer ear, the middle ear, the inner ear, and the brain.
Persisting unexplained tinnitus is evaluated with a hearing test (audiogram).
Measures can be taken to lessen the intensity of tinnitus.

Additional resources from WebMD Boots UK on Tinnitus

REFERENCES:

Arda, H.N. et al. The role of zinc in the treatment of tinnitus. Otol Neurotol. 2003 Jan;24(1):86-9.

Azevedo, A.A. et al. Tinnitus treatment with acamprosate: double-blind study. Braz J Otorhinolaryngol. 2005 Sep-Oct;71(5):618-23. Epub 2006 Mar 31.

Megwalu, U.C. et al. The effects of melatonin on tinnitus and sleep. Otolaryngol Head Neck Surg. 2006 Feb;134(2):210-3.

Up-To-Date.com. Tinnitus.

Medical Author:

John P. Cunha, DO, FACOEP

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR
Source:Medicinenet.com.

Measles (Rubeola)

2012-03-26T07:54:00.002-07:00

What is measles?

Measles is a highly contagious viral disease that can kill you. Although an uncommon disease in the United States of America, in 2008, measles killed 164,000 children worldwide. In most people, the disease produces fever (temperature > 101 F [38.3 C]), a generalized rash that last greater than three days, cough, runny nose (coryza), and red eyes (conjunctivitis). The complications of measles that result in most deaths include pneumonia and inflammation of the brain (encephalitis).

What is rubeola?

Rubeola is the scientific name used for measles. It should not be confused with rubella (German measles).

What is rubella?

Rubella is the scientific name used of German measles, a different viral illness. While German measles is rarely fatal, it is dangerous in that it causes birth defects and can cause miscarriage and fetal death.

What are other names for measles?

Other terms have been used to describe measles. These include (erroneously) rubella, hard measles, red measles, seven-day measles, eight-day measles, nine-day measles, 10-day measles, and morbilli.

What is the history of measles?

Cases of measles were described as early as the seventh century. However, it was not until 1963 that researchers first developed a vaccine to prevent measles. Before the vaccine was made available, almost every child became infected with the virus because it is so easily spread. Before routine vaccination, there were approximately 3-4 million cases of measles and 500 deaths due to measles each year in the United States.
There were initially two types of vaccines developed against measles. One was developed from a virus that had been killed, and the other was developed using a live measles virus that was weakened (attenuated) and could no longer cause the disease. Unfortunately, the killed measles virus (KMV) vaccine was not effective in preventing people from getting the disease, and its use was discontinued in 1967. The live virus vaccine has been modified a number of times to make it safer (further attenuated) and today is extremely effective in preventing the disease. The currently used vaccine is a live attenuated vaccine.

What causes measles?

Measles is caused by the measles virus (a paramyxovirus).

How is measles spread?

Measles is spread through droplet transmission from the nose, throat, and mouth of someone who is infected with the virus. These droplets are sprayed out when the infected person coughs or sneezes. Among unimmunized people exposed to the virus, over 90% will contract the disease. The infected person is highly contagious for four days before the rash appears until four days after the rash appears. The measles virus can remain in the air (and still be able to cause disease) for up to two hours after an infected person has left a room.

How does one become immune to measles?

Anyone who has had measles is believed to be immune for life. People who have received two doses of vaccine after their first birthday have a 98% likelihood of being immune. Infants receive some immunity from their mother. Unfortunately, this immunity is not complete, and infants are at increased risk for infection until they receive the vaccination at 12 to 15 months of age.

Who is at risk for getting measles?

Those people at high risk for measles include:

children less than 1 year of age (although they have some immunity passed from their mother, it is not 100% effective);
people who have not received the proper vaccination series;
people who received immunoglobulin at the time of measles vaccination;
people immunized from 1963 until 1967 with an older ineffective killed measles vaccine.

Are measles deadly?

Measles can kill you. In 2008, approximately 164,000 people died of measles in the world. However, measles is rarely fatal in the United States. This is due to the fact that most people are immunized, which results in very infrequent outbreaks. Also, people most likely to have complications (including death) are those who are malnourished or who have weakened immune systems

What is the danger of getting measles while pregnant?

If you contract measles while you are pregnant, you may have a miscarriage, a stillbirth, or a preterm delivery. There appears to be no risk of having birth defects (unlike an infection with the rubella virus, known as German measles).

If I am exposed, how long does it take to develop symptoms?

The typical time from exposure to a person infected with measles to development of the initial symptoms is 10-12 days (the range is seven to 21 days). The rash occurs a few days after the initial symptoms (ranges from seven to 18 days from exposure).

Picture of a baby with measles. Source: CDC

What are measles symptoms and signs?

The typical case of measles actually starts with a fever, runny nose, hacking cough, and red eyes. After two to four days of these symptoms, the patient may develop spots within the mouth called Koplik's spots. These spots look like little grains of white sand surrounded by a red ring and are usually found inside the cheek toward the back of the mouth (opposite the first and second upper molars).
The skin rash (also known as an exanthem or exanthema) appears three to five days after the onset of the initial symptoms (fever, cough, runny nose, and red eyes). The rash is a flat to slightly raised (maculopapular) red rash that usually last five to six days. It begins at the hairline and then progresses to the face and upper neck. Over the next two to three days, the rash progresses downward to cover the entire body, including the hands and feet. The rash has mostly distinct lesions, but some may overlap (become confluent). Initially, these lesions will turn white when you press on them (blanch). After three to four days, they no longer will blanch. As the rash begins to fade, there will often be a fine flaking of the skin (desquamation). The rash fades in the same order that it appears.
The fever that occurs with measles is called a stepwise fever. The patient starts with a mild fever that progressively gets higher. Fevers often reach temperatures greater than 103 F (39.4 C).
Although not as common as other symptoms, some patients may have a sore throat.

What complications are seen with measles?

Approximately 30% of cases of measles have an associated complication. These complications can include diarrhea (8%), ear infections (7%), pneumonia (6%), blindness (1%), acute brain inflammation (encephalitis) (0.1%), and persistent brain inflammation (subacute sclerosing panencephalitis) (0.0001%).
Blindness associated with measles is due to a combination of poor nutrition (specifically vitamin A deficiency) and the measles infection. Prevention is the most effective treatment. In third-world countries, post-measles blindness is the leading cause of blindness, with up to 60,000 cases occurring annually.
Acute encephalitis, although rare, is extremely dangerous and results in death in approximately 15% of patients who develop it. When it occurs, acute encephalitis generally starts six days after onset of the rash. Symptoms can include fever, headache, vomiting, stiff neck, drowsiness, seizures, and coma.
Subacute sclerosing panencephalitis (SSP) is an extremely rare degenerative condition of the brain and spinal cord (central nervous system). It is believed to be caused by a chronic infection of the central nervous system with the measles virus. Typically, symptoms start years after the patient had measles (average seven years, range one month to 27 years). The patient has a slow and progressive loss of brain function, seizures, and eventually death results. There is no known treatment for SSP.
Most deaths from measles are due to pneumonia in children and encephalitis in adults. There are approximately 2.2 deaths per 1,000 people who get the measles. The people most likely to have complications (including death) are those who are malnourished or who have weakened immune systems (for example, people with AIDS or other conditions that weaken the immune system).

What is atypical measles?

Atypical measles occurs in people who received the killed measles vaccine (KMV; only used from 1963 until 1967) and who are exposed to wild-type measles virus. The KMV unfortunately sensitizes the patient to the measles virus but does not offer any protection. The disease is characterized by fever, pleural effusions, pneumonia, and swelling of the extremities. The rash of atypical measles is different from measles in that it may have an urticarial component (hives) and usually appears first on the ankles and wrists.
It is recommended by the U.S. Centers for Disease Control and Prevention (CDC) that people who may have received the KMV should receive revaccination with the live measles vaccine.
The virus can be isolated in tissue culture in the lab. Blood (serologic) tests are also available.

Picture of Koplik spots. Source: CDC

What is modified measles?

Modified measles is seen in patients who, because they were unimmunized, received immune globulin after being exposed to a patient with measles. It is also seen occasionally in young infants who have limited immunity from their mothers. The immune globulin prolongs the time from exposure to onset of symptoms (incubation period). When the symptoms do occur, they are much milder than those seen with normal measles and tend to last a shorter period of time.

How is the diagnosis of measles made?

The diagnosis of suspected measles is mostly clinical, meaning that the appearance and history of the patient suggest the diagnosis. In a person with known exposure to someone with measles or travel to a foreign country, measles should always be considered when faced with a patient who has high fever and characteristic rash. Until the rash appears, the presence of Koplik's spots should help to suggest the diagnosis. Most cases of suspected measles in the United States turn out not to be measles (see below). It is recommended that the diagnosis be confirmed using a blood test for IgM, a type of antibody against the virus. If the IgM test is positive, viral cultures should be obtained. The state and local health department should be contacted immediately for any suspected case in order to follow the correct procedures for viral culture and isolation of the patient. Further information on laboratory testing of suspected cases is available from the CDC (http://www.cdc.gov/vaccines/pubs/surv-manual/chpt07-measles.htm).

If it is not measles, what else could it be?

There are a large number of infectious diseases and other conditions that can cause some of the symptoms of measles. These include, but are not limited to, dengue fever, drug rashes, enteroviral infections, fifth disease, German measles (rubella), Kawasaki disease, Rocky Mountain spotted fever, roseola, and toxic shock syndrome. It is important that suspected cases be seen by a medical expert and appropriate laboratory tests be ordered.

What should I do if I have been exposed to measles?

People who have been appropriately vaccinated (or who have had the disease) and who are exposed to a patient with measles do not need to do anything. If an unimmunized person is exposed to a patient with measles, they should receive the vaccine as soon as possible. This may prevent the disease if given within 72 hours of exposure. Immune globulin may have some benefit if given within six days of exposure. The CDC recommends that immune globulin be utilized for household contacts of infected people, immunocompromised people, and pregnant women. It is not recommended that immune globulin be utilized to control a measles outbreak.

Is there any treatment for measles after symptoms and signs develop?

The treatment of patients with measles is mostly focused upon symptom relief. Specific complications like pneumonia may require antibiotics. Patients should be on bed rest until the fever has resolved and should remain well hydrated. In malnourished patients, vitamin A supplementation is recommended. Patients should be isolated to prevent spread of the disease.

If measles only rarely occurs in the United States, why should I get vaccinated?

Although measles only rarely occurs in the United States, it still does occur and can be fatal. In the year 2000, almost 1 million children died of the disease. Through a very intensive effort by the World Health Organization, this was decreased to only 164,000 in 2008. When the number of vaccinated individuals starts to decrease, we see the disease start to occur more frequently. This occurred from 1989 until 1991 in the U.S. During that period, there were 55,000 cases and 123 deaths from measles in the U.S. Due to a massive public-health effort, almost all children in the U.S. now receive measles vaccine before they are allowed to enter school. The number of cases of measles in the U.S. dropped to only 37 in 2004. Most cases are now from outside the U.S. (commonly from adopted children from China), although some cases occur as people in this country are exposed to the infected international traveler.

What is the prognosis for measles?

Most people who contract measles will recover completely. Only 2.2 out of 1,000 people who get measles will die. People who are malnourished or immunocompromised are more likely to have complications or die. However, it is possible for any person to die from the measles, which highlights the importance of becoming vaccinated. Almost no one who has been vaccinated has died from the disease.

How can I prevent contracting measles?

The only way to prevent measles is by receiving measles immunization: This is commonly given as a shot containing measles, mumps, and rubella vaccine (MMR) or a shot containing measles, mumps, rubella, and varicella vaccine (MMRV). The MMRV is not recommended for anyone older than 12 years of age. The current recommendation is that everyone receives two doses of the vaccine after 1 year of age. If the vaccine is received before 1 year of age, the person should receive two additional doses.
The measles vaccine is also available as a single vaccine; however, in most cases, there is no reason to utilize the measles vaccine alone without mumps and rubella vaccine. The complete schedule of recommended vaccinations is available from the CDC (http://www.cdc.gov/vaccines/recs/schedules/child-schedule.htm).

Is there any truth to the fear of getting autism from vaccines?

There is no valid scientific evidence that the measles vaccine, or any other vaccine, is the cause of autism. The possibility of an association between the measles vaccine and autism was proposed by Andrew Wakefield and colleagues in 1998. The research published by Wakefield was found to be flawed and actually forged, and the results have not been able to be repeated by other researchers. Since 1998, there have been numerous studies that have examined for such an association. None of these studies have shown any risk of autism associated with the use of the vaccine. A recent study performed in Japan after the MMR vaccine was removed from the market showed that autism continued to increase after the vaccine was no longer being utilized. Although autism is a very serious disease that warrants good research to find out its many causes, not obtaining vaccinations is potentially dangerous and not supported by the best scientific data available today.

Who should not receive measles vaccinations?

The following groups of people should not receive measles vaccinations:

People who have suffered a severe allergic reaction to either the measles vaccine or its components (gelatin or neomycin) should not receive the vaccine.
Women known to be pregnant should not receive the vaccine. Pregnancy should be avoided for four weeks after vaccination.
Severely immunocompromised patients (cancer patients or patients who are receiving large doses of corticosteroids) should not receive the vaccine. However, those leukemia patients who have been in remission for three months may receive the MMR.
Patients with severe human immunodeficiency virus (HIV) infections should not receive the vaccine. However, asymptomatic patients with HIV are considered to be safe for vaccination. The CDC has issued guidelines for vaccination based on the CD4+ T-lymphocyte counts.
People with a moderate to severe acute illness should wait until their illness resolves before receiving the vaccine.

Patients with history of thrombocytopenic purpura or thrombocytopenia (low platelets) may be at increased risk, and immunization should be decided on a case-by-case basis.

If a child has an egg allergy, can they still receive the measles vaccine?

Although the measles vaccine is made using chick embryos, there is no evidence of increased reactions in people with an egg allergy. Therefore the CDC recommends giving MMR vaccine to egg-allergic children without any prior skin testing or the use of special protocols.

What adverse reactions can occur with the measles vaccination?

Adverse reactions to measles vaccination (as part of the MMR) include fever (5%-15%), rash (5%), joint aches (5%), and low platelet count (thrombocytopenia; one instance per 30,000 doses). In adult women, up to 25% will suffer joint pain that is due to the rubella component of the vaccine. The fever usually occurs seven to 12 days after the vaccination, and the rash occurs seven to 10 days after vaccination.

Who should be revaccinated?

The following group of people should be considered unvaccinated and should receive at least one dose of vaccine:

People vaccinated before their first birthday should be revaccinated.
Anyone known to have been vaccinated with the killed measles vaccine (KMV) should be revaccinated.
Anyone vaccinated with KMV who received their dose of live measles vaccine with four months of their last dose of vaccine should be revaccinated.
Anyone vaccinated before 1968 in whom it is not known if the vaccine was KMV or not should be revaccinated.

Where can I find more information about measles?

1. http://wwwn.cdc.gov/travel/yellowBookCh4-Measles.aspx

2. http://www.cdc.gov/vaccines/pubs/
pinkbook/downloads/meas.pdf

3. http://www.cdc.gov/vaccines/pubs/surv-manual/chpt07-measles.htm

4. http://www.who.int/mediacentre/factsheets/fs286/en/

5. http://www.who.int/vaccines-documents/GlobalSummary/GlobalSummary.pdf

6. http://www.immunize.org/catg.d/p2065.pdf (autism)

Measles At A Glance

Measles is a potentially serious disease.
Measles is due to a virus that is easily spread.
Measles can be complicated by ear infections, pneumonia, or encephalitis.
Measles infection of the brain (encephalitis) can cause convulsions, mental retardation, and even death.
Measles in pregnant women can cause miscarriages or premature delivery.
Measles can be prevented through vaccination.
Each person not immunized against measles is at risk for measles and puts others at risk.

REFERENCES:

American Academy of Pediatrics. "Measles." Red Book: 2006 Report of the Committee on Infectious Diseases, 28th ed. Ed. Pickering, L.K. Elk Grove Village, IL: American Academy of Pediatrics, 2006.

Perry, R.T., and N.A. Halsey. "The Clinical Significance of Measles: A review." J Infect Dis 189 (2004): S4–16.

United States. Centers for Disease Control and Prevention. "Measles." Manual for the Surveillance of Vaccine-Preventable Diseases, 4th ed. 2008. <http://www.cdc.gov/vaccines/pubs/surv-manual/chpt07-measles.htm>.

United States. Centers for Disease Control and Prevention. "Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)." MMWR 47 (No. RR-8) 1998: 1–57.

United States. Centers for Disease Control and Prevention. "Notes from the Field: Measles Transmission Associated With International Air Travel -- Massachusetts and New York, July -- August 2010." MMWR 59.33 Aug. 2010: 1073.

United States. Centers for Disease Control and Prevention. "Use of Combination Measles, Mumps, Rubella, and Varicella Vaccine: Recommendations of the Advisory Committee on Immunization Practices (ACIP)." MMWR 59(RR03) 2010: 1-12.

World Health Organization. "Fifty-Sixth World Health Assembly. Agenda item 14.7. Reducing Global Measles Mortality." Geneva: World Health Organization, 2003. <http://www.who.int/gb/ebwha/pdf_files/WHA56/ea56r20.pdf>.

Medical Author:

Edmond Hooker, MD, DrPH

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Sudden Cardiac Arrest (Sudden Cardiac Death)

2012-03-26T07:50:00.002-07:00

Introduction to sudden cardiac arrest

A natural disaster hits, the power goes off and the lights go out. It's a common scene that plays out during hurricane and tornado seasons, and it's very similar in trying to explain sudden cardiac arrest. The heart sustains an insult, the electricity is short circuited, the heart can't pump, and the body dies.
The heart is an electrical pump, where the electricity is generated in special pacemaker cells in the upper chamber, or atrium, of the heart. This electrical spark is carried through pathways in the heart so that all the muscle cells contract at once and produce a heart beat. This pumps blood through the heart valves and into all the organs of the body so that they can do their work.
This mechanism can break down in a variety of ways, but the final pathway in sudden death is the same: the electrical system is irritated and fails to produce electrical activity that causes the heart to beat. The heart muscle can't supply blood to the body, particularly the brain, and the body dies. Ventricular fibrillation (V Fib) is the most common reason for sudden death in patients. Without a coordinated electrical signal, the bottom chambers of the heart (ventricles) stop beating and instead, jiggle like Jello. Ventricular Fibrillation is treated with electrical shock, but for it to be effective, the shock usually needs to happen within less than four to six minutes, not only for it to be effective, but also to minimize brain damage from lack of blood and oxygen supply. Automatic external defibrillators (AEDs) are commonly available in public places to allow almost anybody to treat sudden death. Less commonly, the heart can just stop beating. The absence of a heart beat is known as asystole (asystole: a=no + systole=beat).

What are the causes of sudden cardiac arrest?

Sudden death is most often caused by heart disease. When blood vessels narrow, the heart muscle can become irritated because of lack of blood supply. In heart attack (acute myocardial infarction), a blood vessel becomes completely blocked by a blood clot, and there is enough irritability of the muscle to cause ventricular fibrillation. In fact, the reason many people with chest pain are admitted to the hospital is to monitor their heart rate and rhythm for signs that might lead to ventricular fibrillation. Sudden death may also be the first presentation of heart disease.
Congestive heart failure and heart valve problems, like aortic stenosis (narrowing of the aortic valve) also increase the risk of sudden cardiac arrest.
Cardiomyopathy is a broad category of heart disease where the heart muscle does not contract properly for whatever reason. Often it is ischemic, where part of the heart muscle doesn't get an adequate blood supply for a prolonged period of time and no longer can efficiently pump blood. People whose ejection fractions (the amount of blood pumped out of the heart with each heart beat) is less than 30% are at greater risk for sudden death (a normal ejection fraction is above 50%). In some people, cardiomyopathy may develop in the absence of ischemic heart disease.
Inflammation of the heart muscle, known as myocarditis (myo=muscle + card=heart + itis= inflammation), can also cause rhythm disturbances. Diseases like sarcoidosis, amyloidosis, and infections can cause inflammation of the heart muscle.
Some people are born with electrical conducting systems that are faulty, which place them at higher risk for rhythm disturbances. Some are due to the wiring, or electrical conduction system, like Wolff-Parkinson-White syndrome, while others are due to the structural basic structural problems within the heart, like Marfan syndrome.
Pulmonary embolus, a blood clot to the lung, can also cause sudden death. Clots form in the leg or arm and may break off and flow to the lung where they decrease the lung's ability to get oxygen from the air to the body. Risk factors for blood clots include surgery, prolonged immobilization (for example, hospitalization, long car rides or plane trips), trauma, or certain diseases like cancer.
Blunt chest trauma, such is in a motor vehicle accident, may result in ventricular fibrillation. (please see commotio cordis below)

What about sudden cardiac arrest in the young?

In younger people, sudden death is a rare event, but since it often involves people involved in athletics, cases are often reported in the press. The most common cause is hypertrophic cardiomyopathy (hypertrophy=to grow abnormally large + cardio=heart + myopathy = diseased muscle). This disease is often hereditary, and the walls of the ventricle are larger than they should be. This makes the pumping chamber of the heart smaller, and the heart has to work harder to pump blood out of the heart. As well, the thickened muscle narrows the space for the blood to flow through the aortic valve and to the rest of the body. During exercise, this decreased blood flow can irritate the heart muscle itself and cause ventricular fibrillation, collapse, and sudden death.
Anomalous coronary arteries can also cause sudden death in the young. The heart is a muscle itself, and like any muscle, it needs blood supply to provide oxygen for it to work. Normally, the coronary arteries lie on the surface of the heart. Anomalous arteries dive into the heart muscle itself and may be occluded when the heart muscle that surrounds the abnormally placed artery squeezes aggressively, as with exercise, shutting off blood supply to part of the heart. This irritates the electrical system and can cause ventricular fibrillation and sudden death.
The pre-participation athletic physical examination is a useful tool to screen children and adolescents for their risk of sudden cardiac arrest.
Commotio cordis is a situation in which the heart stops when the chest is hit by an object. News stories occasionally report of baseball players who are hit in the chest by a ball and collapse because their heart stops beating. The heart sits behind the breastbone, and the electrical system can be short circuited when a direct blow is sustained.

What are the symptoms of sudden cardiac arrest?

In sudden cardiac arrest, the heart stops beating, and blood is not supplied to the body. The presentation is not subtle. Almost immediate loss of consciousness occurs, and the affected person will not be able to be aroused. The person will fall or slump over. No pulse will be able to be palpated, and there will be no signs of breathing.

What is the diagnosis for sudden cardiac arrest?

Sudden cardiac arrest is an unexpected death in a person who had no known previous diagnosis of a fatal disease or condition. The person may or may not have heart disease.

What is the treatment for sudden cardiac arrest?

The vast majority of people whose heart stops beating unexpectedly have ventricular fibrillation. The definitive treatment for this is defibrillation using electricity to shock the heart back into a regular rhythm. With technological advances, AEDs are now a routine sight wherever people congregate.
Communities which institute public CPR education, use of AEDs, and rapid activation of 911 emergency medical services have dramatically increased survival rates from sudden cardiac arrest. Unfortunately, because the brain is so sensitive to the lack of oxygen and blood flow, unless treatment occurs within four to six minutes, there is a high risk of some permanent brain damage.
Should the patient survive to be transported to the hospital, the reason for collapse and sudden death will need to be diagnosed. Regardless, the ABCs of resuscitation will be re-evaluated. Airway, Breathing, and Circulation (heart beat and blood pressure) will be supported, and admission to an intensive care unit is most likely.
Diagnostic tests may include repeated electrocardiograms (EKGs), echocardiogram (ultrasounds of the heart), and cardiac catheterization and electrophysiologic studies, in which the electrical pathways of the heart are mapped.
Recent research involving the treatment of survivors of cardiac arrest suggests that prompt institution of hypothermia (cooling of the body) may prevent or lessen the degree of brain injury.
Survivors of sudden cardiac arrest are often candidates for implantable cardiac defibrillators.

Can sudden cardiac arrest be prevented?

Death is best treated by prevention. Most sudden death is associated with heart disease, so the at-risk population remains males older than 40 years of age who smoke, have high blood pressure, and diabetes (the risk factors for heart attack). Other risks include syncope (fainting or loss of consciousness) and known heart disease.
Syncope, or loss of consciousness, is a significant risk factor for sudden death. While some reasons for passing out are benign, there is always a concern that the reason was an abnormal heart rhythm that subsequently spontaneously corrected. The fear is that the next episode will be a sudden cardiac arrest. Depending on the healthcare provider's suspicion based on the patient's history, physical examination, laboratory tests, and EKG, the healthcare practitioner may recommend inpatient or outpatient heart monitoring to try to find a clue as to whether the passing out was due to a deadly heart rhythm. Unfortunately, the potentially suspect rhythm may not recur and depending on the situation, prolonged outpatient monitoring lasting weeks and months may be necessary. Use of electrophysiologic testing may help identify high risk patients (the electrical pathways are mapped using techniques similar to heart catheterization).
In people who present to their doctor with chest pain, aside from making the diagnosis, monitoring both the heart rate and rhythm are emphasized. The purpose of watching people with chest pain in a hospital setting is to prevent sudden cardiac arrest.
Using implantable defibrillators in high risk patients, especially those with markedly decreased ejection fractions can reduce the incidence of sudden cardiac arrest. These devices are placed under the skin in the chest wall and have wires that are attached to the heart itself. When they detect ventricular fibrillation, a shock is automatically delivered to the heart, restoring a heart beat and averting sudden death.

What is the prognosis for sudden cardiac arrest?

The frequency of sudden cardiac arrest is related to the frequency of coronary artery disease. If public health initiatives work to decrease risk the factors for heart disease, the risk for sudden death should decrease as well.
In the adolescent population, increased awareness of hypertrophic cardiomyopathy and appropriate screening may decrease the frequency of sudden death.
Public education and widespread availability of AEDs will increase survival.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Sarcoidosis

2012-03-26T07:45:00.002-07:00

What is sarcoidosis?

Sarcoidosis is a disease that results from a specific type of inflammation of tissues of the body. It can appear in almost any body organ, but it starts most often in the lungs or lymph nodes.
The cause of sarcoidosis is unknown. The disease can appear suddenly and disappear. Or it can develop gradually and go on to produce symptoms that come and go, sometimes for a lifetime.
As sarcoidosis progresses, microscopic lumps of a specific form of inflammation, called granulomas, appear in the affected tissues. In the majority of cases, these granulomas clear up, either with or without treatment. In the few cases where the granulomas do not heal and disappear, the tissues tend to remain inflamed and become scarred (fibrotic).
Sarcoidosis was first identified over 100 years ago by two dermatologists working independently, Dr. Jonathan Hutchinson in England and Dr. Caesar Boeck in Norway. Sarcoidosis was originally called Hutchinson's disease or Boeck's disease. Dr. Boeck went on to fashion today's name for the disease from the Greek words "sark" and "oid," meaning flesh-like. The term describes the skin eruptions that are frequently caused by the illness.

What are symptoms of sarcoidosis?

Shortness of breath (dyspnea) and a cough that won't go away can be among the first symptoms of sarcoidosis. But sarcoidosis can also show up suddenly with the appearance of skin rashes. Red bumps (erythema nodosum) on the face, arms, or shins and inflammation of the eyes are also common symptoms.
It is not unusual, however, for sarcoidosis symptoms to be more general. Weight loss, fatigue, night sweats, fever, or just an overall feeling of ill health can also be clues to the disease.

Who gets sarcoidosis?

Sarcoidosis was once considered a rare disease. We now know that it is a common chronic illness that appears all over the world. Indeed, it is the most common of the scarring lung disorders and occurs often enough in the United States for Congress to have declared a national Sarcoidosis Awareness Day in 1990.
Anyone can get sarcoidosis. It occurs in all races and in both sexes. Nevertheless, the risk is greater if you are a young black adult, especially a black woman, or of Scandinavian, German, Irish, or Puerto Rican origin. No one knows why.
Because sarcoidosis can escape diagnosis or be mistaken for several other diseases, we can only guess at how many people are affected. The best estimate today is that about five in 100,000 white people in the United States have sarcoidosis. Among black people, it occurs more frequently, in probably 40 out of 100,000 people. Overall, there appear to be 20 cases per 100,000 in cities on the East Coast and somewhat fewer in rural locations. Some scientists, however, believe that these figures greatly underestimated the percentage of the U.S. population with sarcoidosis.
Sarcoidosis mainly affects people between 20 to 40 years of age. White women are just as likely as white men to get sarcoidosis, but the black female gets sarcoidosis two times as often as the black male. No one knows what causes sarcoidosis.
Sarcoidosis also appears to be more common and more severe in certain geographic areas. It has long been recognized as a common disease in Scandinavian countries, where it is estimated to affect 64 out of 100,000 people. But it was not until the mid '40s, when a large number of cases were identified during mass chest x-ray screening for the Armed Forces, that its high prevalence was recognized in North America.

What we know about sarcoidosis

Much about sarcoidosis remains unknown. Nevertheless, if you have the disease, you can be reassured about several things. Sarcoidosis is usually not crippling. It often goes away by itself, with most cases healing in 24 to 36 months. Even when sarcoidosis lasts longer, most patients can go about their lives as usual. Sarcoidosis is not a cancer. It is not contagious, and your friends and family will not catch it from you. Although it can occur in families, there is no evidence that sarcoidosis is passed from parents to children.

Some things we don't know about sarcoidosis

Sarcoidosis is currently thought to be associated with an abnormal immune response. It is not known whether the trigger that initiates the immune disturbance is a foreign substance, chemical, drug, virus, or some other substance.
In general, sarcoidosis appears briefly and heals naturally in 60%-70% of the cases, often without the patient knowing or doing anything about it. From 20%-30% of sarcoidosis patients are left with some permanent lung damage. In 10%-15% of the patients, sarcoidosis can become chronic.
When either the granulomas or fibrosis seriously affect the function of a vital organ—the lungs, heart, nervous system, liver, or kidneys, for example—sarcoidosis can be fatal. This occurs 5%-10% of the time. Some people are more at risk than others; no one knows why.
No one can predict how sarcoidosis will progress in an individual patient. The patient's symptoms, race, and the doctor's findings can give some clues. For example, a sudden onset of general symptoms such as weight loss of feeling poorly are usually taken to mean that the course of sarcoidosis will be relatively short and mild. Dyspnea and possibly skin sarcoidosis often indicate that the sarcoidosis will be more chronic and severe.
White patients are more likely to develop the milder form of the disease. Black people tend to develop the more chronic and severe form.
Sarcoidosis rarely develops before the age of 10 or after the age of 60. However, the illness—with or without symptoms—has been reported in younger as well as in older people. When symptoms do appear in these age groups, the symptoms are those that are more general in nature, for example, tiredness, sluggishness, coughing, and a general feeling of ill health.

How is sarcoidosis diagnosed?

Preliminary diagnosis of sarcoidosis is based on the patient's medical history, routine tests, a physical examination, and a chest x- ray.
The doctor confirms the diagnosis of sarcoidosis by eliminating other diseases with similar features. These include such granulomatous diseases as berylliosis (a disease resulting from exposure to beryllium metal), tuberculosis, farmer's lung disease (hypersensitivity pneumonitis), fungal infections, rheumatoid arthritis, rheumatic fever, and cancer of the lymph nodes (lymphoma).

What are some signs and symptoms that suggest possible sarcoidosis?

In addition to the lungs and lymph nodes, the body organs more likely than others to be affected by sarcoidosis are the liver, skin, heart, nervous system, and kidneys, in that order of frequency. Patients can have symptoms related to the specific organ affected, they can have only general symptoms, or they can be without any symptoms whatsoever. Symptoms also can vary according to how long the illness has been under way, where the granulomas are forming, how much tissue has become affected, and whether the granulomatous process is still active.
Even when there are no symptoms, a doctor can sometimes detect signs of sarcoidosis during a routine examination, usually a chest x- ray, or when checking out another complaint. The patient's age and race or ethnic group can raise an additional red flag that a sign or symptom of illness could be related to sarcoidosis. Enlargement of the salivary or tear glands and cysts in bone tissue are also among sarcoidosis signals.
The lungs are usually the first site involved in sarcoidosis. Indeed, about nine out of 10 sarcoidosis patients have some type of lung problem, with nearly one-third of these patients showing some respiratory symptoms—usually coughing, either dry or with phlegm, and dyspnea. Occasionally, patients have chest pain and a feeling of tightness in the chest.
It is thought that sarcoidosis of the lungs begins with inflammation of the alveoli (alveolitis), the tiny sac-like air spaces in the lungs where carbon dioxide and oxygen are exchanged. Alveolitis either clears up spontaneously or leads to granuloma formation. Eventually fibrosis can form, causing the lung to stiffen and making breathing even more difficult.
Eye disease occurs in about 20%-30% of patients with sarcoidosis, particularly in children who get the disease. Almost any part of the eye can be affected—the membranes of the eyelids, cornea, outer coat of the eyeball (sclera), retina, and lens. The eye involvement can start with no symptoms at all or with reddening or watery eyes. In a few cases, cataracts, glaucoma, and blindness can result.
The skin is affected in about 20% of sarcoidosis patients. Skin sarcoidosis is usually marked by small, raised patches on the face. Occasionally, the patches are purplish in color and larger. Patches can also appear on limbs, face, and buttocks.
Other symptoms include erythema nodosum, mostly on the legs and often accompanied by arthritis in the ankles, elbows, wrists, and hands. Erythema nodosum usually goes away, but other skin problems can persist.
Occasionally (1%-5%), sarcoidosis can lead to nervous system problems. For example, sarcoid granulomas can appear in the brain, spinal cord, and facial and optic nerves. Facial paralysis and other symptoms of nerve damage call for prompt treatment with medications such as high doses of cortisone (see below). Also, people with sarcoidosis can have depression that is unrelated to the activity of the disease and is felt to be, in part, because of a misdirected immune system.
Symptoms can appear suddenly and then disappear. Sometimes, however, they can continue over a lifetime.

What do laboratory tests show?

No single test can be relied on for a correct diagnosis of sarcoidosis. X-rays and blood tests are usually the first procedures the doctor will order. Pulmonary function tests often provide clues to diagnosis. Other tests may also be used, some more often than others.
Many of the tests that the doctor calls on to help diagnose sarcoidosis can also help the doctor follow the progress of the disease and determine whether the sarcoidosis is getting better or worse.
Chest x-ray
The chest x-ray is often helpful to give the doctor a picture of the lungs, heart, as well as the surrounding tissues containing lymph nodes (where infection-fighting white blood cells form) and give the first indication of sarcoidosis. For example, a swelling of the lymph glands between the two lungs can show up on an x-ray. An x-ray can also show which areas of the lung are affected.
Pulmonary function test
By performing a variety of tests called pulmonary function tests (PFT), the doctor can find out how well the lungs are doing their job of expanding and exchanging oxygen and carbon dioxide with the blood. The lungs of sarcoidosis patients cannot handle these tasks as well as they should; this is because granulomas and fibrosis of lung tissue decrease lung capacity and disturb the normal flow of gases between the lungs and the blood. One PFT procedure calls for the patient to breathe into a machine, called a spirometer. It is a mechanical device that records changes in the lung size as air is inhaled and exhaled, as well as the time it takes the patient to do this.
Blood test
Blood analyses can evaluate the number and types of blood cells in the body and how well the cells are functioning. They can also measure the levels of various blood proteins known to be involved in immunological activities, and they can show increases in serum calcium levels and abnormal liver function that often accompany sarcoidosis.
Blood tests can measure a blood substance called angiotensin converting enzyme (ACE). Because the cells that make up granulomas secrete large amounts of ACE, the enzyme levels are often high in patients with sarcoidosis. ACE levels, however, are not always high in sarcoidosis patients, and increased ACE levels can also occur in other illnesses.
Bronchoalveolar lavage
This uses an instrument called a bronchoscope—a long, narrow tube with a light at the end—to wash out, or lavage, cells and other materials from inside the lungs. This wash fluid is then examined for the amount of various cells and other substances that reflect inflammation and immune activity in the lungs. A high number of white blood cells in this fluid usually indicate an inflammation in the lungs.
Biopsy
Microscopic examination of specimens of lung tissue obtained with a bronchoscope, or of specimens of other tissues, can tell a doctor where granulomas have formed in the body and can provide the ultimate diagnosis.
Gallium scanning
In this procedure, the doctor injects the radioactive chemical element gallium-67 into the patient's vein. The gallium collects at places in the body affected by sarcoidosis and other inflammatory conditions. Two days after the injection, the body is scanned for radioactivity. Increases in gallium uptake at any site in the body indicate that inflammatory activity has developed at the site and give an idea of which tissue, and how much tissue, has been affected. However, since any type of inflammation causes gallium uptake, a positive gallium scan does not necessarily mean that the patient has sarcoidosis.
Kveim test
This test involves injecting a standardized preparation of sarcoid tissue material into the skin. On the one hand, a unique lump formed at the point of injection is considered positive for sarcoidosis. On the other hand, the test result is not always positive even if the patient has sarcoidosis.
The Kveim test is not used often in the United States because no test material has been approved for sale by the U.S. Food and Drug Administration. However, a few hospitals and clinics may have some standardized test preparation prepared privately for their own use.
Slit-lamp examination
An instrument called a slit lamp, which permits examination of the inside of the eye, can be used to detect silent damage from sarcoidosis.

How is sarcoidosis treated?

Fortunately, many patients with sarcoidosis require no treatment. Symptoms, after all, are usually not disabling and do tend to disappear spontaneously.
When therapy is recommended, the main goal is to keep the lungs and other affected body organs working and to relieve symptoms. The disease is considered inactive once the symptoms fade. After many years of experience with treating the disease, corticosteroid drugs remain the primary treatment for inflammation and granuloma formation. Prednisone is probably the corticosteroid most often prescribed today. There is no treatment at present to reverse the lung scarring (fibrosis) that might be present in advanced sarcoidosis. More than one test is needed to diagnose sarcoidosis.
Tests can also show if patients with sarcoidosis are getting better. Occasionally, a blood test will show a high blood level of calcium accompanying sarcoidosis. The reasons for this are not clear. When it does occur, the patient may be advised to avoid calcium-rich foods, vitamin D, or sunlight, or to take prednisone (this corticosteroid usually quickly reverses the condition).
Because sarcoidosis can disappear even without therapy, even doctors sometimes disagree on when to start the treatment, what dose to prescribe, and how long to continue the medicine. The doctor's decision depends on the organ system involved and how far the inflammation has progressed. If the disease appears to be severe, especially in the lungs, eyes, heart, nervous system, spleen, or kidneys, the doctor may prescribe corticosteroid.
Corticosteroid treatment usually results in improvement. Symptoms often start up again, however, when it is stopped. Treatment, therefore, may be necessary for several years, sometimes for as long as the disease remains active or to prevent relapse.
Frequent checkups are important so that the doctor can monitor the illness and, if necessary, adjust the treatment.
Corticosteroids, for example, can have side effects: mood swings, swelling, and weight gain because the treatment tends to make the body hold on to water; high blood pressure; high blood sugar; and craving for food. Long-term use can affect the stomach, skin, and bones. This situation can bring on stomach pain, an ulcer, or acne or cause the loss of calcium from bones. However, if the corticosteroid is taken in carefully prescribed low doses, the benefits from the treatment are usually far greater than the problems.
Besides corticosteroid, various other drugs have been tried, but their effectiveness has not been established in controlled studies. These drugs include chloroquine (Aralen) and D-penicillamine. Several drugs such as chlorambucil (Leukeran), azathioprine (Imuran), methotrexate (Rheumatrex, Trexall), and cyclophosphamide (Cytoxan), which might suppress alveolitis by killing the cells that produce granulomas, have also been used. None have been evaluated in controlled clinical trials, and the risk of using these drugs must be compared closely with the benefits in preventing organ damage by the disease. They are not to be used by pregnant women.
Cyclosporine, a drug used widely in organ transplants to suppress immune reaction, has been evaluated in one controlled trial. It was found to be unsuccessful. More recently, thalidomide (Thalomid) has been used successfully in a limited number of patients and seemed to improve lung function and heal skin lesions. Infliximab (Remicade) has been reported recently as effective in treating patients with sarcoidosis.
There are many unanswered questions about sarcoidosis. Identifying the agent that causes the illness, along with the inflammatory mechanisms that set the stage for the alveolitis, granuloma formation, and fibrosis that characterized the disease is the major aim of researchers of sarcoidosis. Development of reliable methods of diagnosis, treatment, and eventually, the prevention of sarcoidosis is the ultimate goal.
Originally, scientists thought that sarcoidosis was caused by an acquired state of immunological inertness (anergy). This notion was revised when the technique of bronchoalveolar lavage provided access to a vast array of cells and cell-derived mediators operating in the lungs of sarcoidosis patients. Sarcoidosis is now believed to be associated with a complex mix of immunological disturbances involving simultaneous activation, as well as depression, of certain immunological functions.
Immunological studies on sarcoidosis patients show that many of the immune functions associated with thymus-derived white blood cells, called T-lymphocytes or T-cells, are depressed. The depression of this cellular component of systemic immune response is expressed in the inability of the patients to evoke a delayed hypersensitivity skin reaction (a positive skin test), when tested by the appropriate foreign substances, or antigen, underneath the skin.
In addition, the blood of sarcoidosis patients contains a reduced number of T-cells. These T-cells do not seem capable of responding normally when treated with substances known to stimulate the growth of laboratory-cultured T-cells. Neither do they produce their normal complement of immunological mediators, cytokines, through which the cells modify the behavior of other cells.
In contrast to the depression of the cellular immune response, humoral immune response of sarcoidosis patients is elevated. The humoral immune response is reflected by the production of circulating antibodies against a variety of exogenous antigens, including common viruses. This humoral component of systemic immune response is mediated by another class of lymphocytes known as B-lymphocytes, or B-cells, because they originate in the bone marrow.
In another indication of heightened humoral response, sarcoidosis patients seem prone to develop autoantibodies (antibodies against endogenous antigens) similar to rheumatoid factors.
With access to the cells and cell products in the lung tissue compartments through the bronchoalveolar technique, it also has become possible for researchers to complement the above investigations at the blood level with analysis of local inflammatory and immune events in the lungs. In contrast to what is seen at the systemic level, the cellular immune response in the lungs seems to be heightened rather than depressed.
The heightened cellular immune response in the diseased tissue is characterized by significant increases in activated T-lymphocytes with certain characteristic cell-surface antigens, as well as in activated alveolar macrophage. This pronounced, localized cellular response is also accompanied by the appearance in the lung of an array of mediators that are thought to contribute to the disease process; these include interleukin-1, interleukin-2, B-cell growth factor, B-cell differentiation factor, fibroblast growth factor, and fibronectin. Because a number of lung diseases follow respiratory tract infections, ascertaining whether a virus can be implicated in the events leading to sarcoidosis remains an important area of research.
Some recent observations seem to provide suggestive leads on this question. In these studies, the genes of cytomegalovirus (CMV), a common disease-causing virus, were introduced into lymphocytes, and the expression of the viral genes was studied. It was found that the viral genes were expressed both during acute infection of the cells and when the virus was not replicating in the cells. However, this expression seemed to take place only when the T-cells were activated by some injurious event. In addition, the product of a CMV gene was found capable of activating the gene in alveolar macrophage responsible for the production of interleukin-1. Since interleukin-1 levels are found to increase in alveolar macrophage from patients with sarcoidosis, this suggests that certain viral genes can enhance the production of inflammatory components associated with sarcoidosis. Whether these findings implicate viral infections in the disease process in sarcoidosis is unclear.
Currently, thalidomide is being studied as a treatment for sarcoidosis. Future research with viral models may provide clues to the molecular mechanisms that trigger alterations in white blood cell (lymphocyte and macrophage) regulation leading to sarcoidosis.
For difficult to treat (refractory) sarcoidosis and sarcoidosis involving the nervous system (neurosarcoidosis), recent research using biologic medications that inhibit tumor necrosis factor (TNF-blockers) has been beneficial. The TNF-blockers used were adalimumab (Humira) and infliximab.

Living with sarcoidosis

The cause of sarcoidosis still remains unknown, so there is at present no known way to prevent or cure this disease. However, doctors have had a great deal of experience in management of the illness. It should be noted that most people with sarcoidosis lead normal lives.
If you have sarcoidosis, you can help yourself by following sensible health measures. You should not smoke. You should also avoid exposure to other substances such as dusts and chemicals that can harm your lungs.
Patients with sarcoidosis are best treated by a lung specialist or a doctor who has a special interest in sarcoidosis. Sarcoidosis specialists are usually located at major research centers.
If you have any symptoms of sarcoidosis, see your doctor regularly so that the illness can be watched and, if necessary, treated. Regular checkups with the doctor are important even if there are no symptoms present. Eye examinations by an eye specialist can detect early eye inflammation from sarcoidosis.
Although severe sarcoidosis can reduce the chances of becoming pregnant, particularly for older women, many young women with sarcoidosis have given birth to healthy babies while on treatment. Patients planning to have a baby should discuss the matter with their doctor. Medical checkups all through pregnancy and immediately thereafter are especially important for sarcoidosis patients. In some cases, bed rest is necessary during the last three months of pregnancy. In addition to family and close friends, a number of local lung organizations, other nonprofit health organizations, and self-help groups are available to help patients cope with sarcoidosis. By keeping in touch with them, you can share personal feelings and experiences. Members also share specific information on the latest scientific advances, where to find a sarcoidosis specialist, and how to improve one's self-image.
Information above was contributed, in part, by the generosity of National Institutes of Health.

Where can a person find more information on sarcoidosis?

Current sarcoidosis research and clinical trials
National Heart, Lung, and Blood Institute (NHLBI)
Division of Lung Diseases
5333 Westward Avenue
Room 6A16
Bethesda, MD 20892
If you are interested in participating on NHLBI clinical studies of sarcoidosis, have your physician write to:
National Heart, Lung, and Blood Institute
Pulmonary Branch
9000 Rockville Pike
Building 10, Room 6D06
Bethesda, MD 20892
Information and publications for patients and families
National Institute of Allergy and Infectious Diseases
9000 Rockville Pike
Building 31, 7A32
Bethesda, MD 20892
Sarcoidosis Family Aid and Research Foundation
460A Central Avenue
East Orange, NJ 07018
Many local chapters of the American Lung Association host support groups for sarcoidosis patients. The address and telephone number of the chapter nearest to you should be in your local telephone directory. Or you can write or call the association's national headquarters:
American Lung Association
1740 Broadway
New York, NY 10019-4374
(212) 315-8700

Sarcoidosis At A Glance

Sarcoidosis is a disease that causes inflammation of body tissues.
The cause of sarcoidosis is not known.
Sarcoidosis commonly affects the lungs and skin.
Diagnosis is suggested by the patient's medical history, routine tests, a physical examination, and a chest x- ray.
Many patients with sarcoidosis require no treatment.
For more severe disease, cortisone-related medications are used. Other treatments are considered, as above, depending on what areas of the body are affected and to what degree.

References:
American College of Rheumatology, National Meeting, 2007.

Medical Author:

William C. Shiel Jr., MD, FACP, FACR

Source:Medicinenet.com.

Naegleria fowleri

2012-03-26T07:42:00.002-07:00

Naegleria fowleri infection facts

Naegleria fowleri is an amoeba that lives predominately in warm, fresh water.
Naegleria fowleri is acquired by people when infected water is forcibly aspirated into the nose. This can occur through recreational swimming, diving, or during sports like water skiing.
Once acquired, the amoeba travels into the brain, causing primary amoebic meningoencephalitis (PAM).
PAM is very rare, and there are only a few cases reported each year in the United States.
People with PAM initially experience changes in smell or taste. The disease advances rapidly, causing fever, stiff neck, and coma.
Infection is diagnosed by examining spinal fluid under the microscope to identify the amoeba. Naegleria fowleri may also be grown in the laboratory, although this takes several days. Newer tests based on PCR technology are being developed.
The treatment of choice is an intravenous drug called amphotericin B. Amphotericin B may also be instilled directly into the brain.
More than 95% of cases of PAM are fatal despite treatment.

What is Naegleria fowleri?

Naegleria fowleri is an amoeba that lives in fresh water and soil. The organism goes through three stages in its life cycle: cysts, flagellates, and trophozoites. It is the trophozoite form that causes human disease. Naegleria are "thermophilic," meaning that they prefer warmer water. However, the cysts are able to survive for months in very cold water. Thus, Naegleria infection is found both in tropical and temperate climates.
Although there are many species of Naegleria, including Naegleria gruberi, only Naegleria fowleri causes human infection. There are other free-living amoebas that cause human disease, including Acanthamoeba.

Picture of Naegleria fowleri surrounded by white cells in spinal fluid; Source: CDC

What causes a Naegleria fowleri infection?

N. fowleri is a water-borne disease. Exposure occurs when people come into contact with warm, fresh water usually through swimming, diving, water skiing, or other recreational activity. Although contact with infected water is common, symptomatic disease caused by N. fowleri is rare. It is common for people in the southern U.S. to have antibodies showing evidence of past exposure even when they have no history of symptoms or disease.
The danger of serious infection comes when water containing Naegleria fowleri is forced in into the nose and nasal mucosa. The parasite then migrates through the olfactory nerves and enters the brain. The initial step of infection can occur when diving or inadvertently aspirating water during swimming. Rarely, under-chlorinated swimming pools have been implicated in transmission. Because Naegleria fowleri can be present in untreated well water, there is a small but real chance of transmission to young children during bathing. Naegleria fowleri has also caused disease in adults who inject water into the nose as part of ritual ablutions related to religious practices.

What are risk factors for Naegleria fowleri infection?

The major risk factor for infection is recreational exposure to warm fresh water, especially if there is a history of aspiration of water into the nose. A review of cases in the U.S. by Yoder, et al. showed that there were 111 reported cases of primary amoebic encephalitis between 1962 and 2008. Living in the southern States is a risk factor for infection, because the water is warmer and more conducive to growth of the amoeba. A frequently asked question is when infections most commonly occur. The answer is that the organism is most active in summer months, even in the southern states. Most cases occur in previously healthy young males (median age of 12 years).

What are symptoms and signs of a Naegleria fowleri infection?

After entering the nose, the amoeba travels into the brain along the olfactory nerve and through membranes to enter the brain. Once there, it causes primary amoebic meningoencephalitis (meaning inflammation of the brain and the lining around the brain). In the popular press, Naegleria fowleri is sometimes called the brain-eating amoeba, and meningoencephalitis is sometimes referred to as Naegleriasis.
Symptoms usually appear within five days after exposure but can be delayed up to two weeks. Patients may initially notice changes in smell or taste. Fever, headache, loss of appetite, and nausea follow quickly. The patient becomes confused or semiconscious and finally comatose. Physical examination shows fever and a stiff neck (meningismus).

How is a Naegleria fowleri infection diagnosed?

A spinal tap will be done to examine the spinal fluid. Infection is diagnosed by seeing the amoeba under the microscope. Traditional Gram staining is not used to detect Naegleria because the heat used in the fixation process destroys the organism. Although not specific to Naegleria, the spinal fluid often has a mild elevation in the levels of proteins and a mild decrease in glucose, along with a high white cell count, and is often bloody in the later stages of disease.
Because rapid diagnosis is critical, examination of the spinal fluid is imperative. The organism can also be cultured in the laboratory using on a plate that is coated with bacteria for the amoeba to eat. The culture takes a few days. Newer tests are becoming available that use polymerase chain reaction (PCR) technology to detect amoebic DNA in spinal fluid.

What is the treatment for a Naegleria fowleri infection?

Because Naegleria meningoencephalitis is rare, there are no studies comparing one treatment regimen to another.
The treatment of choice is amphotericin B, which is an intravenous drug usually used for fungal infections. In addition to intravenous treatment, amphotericin B can be instilled directly into the brain (intrathecally).
Other drugs such as rifampin (Rifadin), voriconazole (Vfend), or miltefosine (Miltex) have activity against Naegleria fowleri and may sometimes be used in combination with amphotericin B. However, there is no scientific data available to determine the clinical efficacy of these medications and no official recommendation for their use.

Can Naegleria fowleri infections be prevented?

Infection with Naegleria fowleri can be prevented by avoiding aspiration of fresh water into the nose. Although there have been investigations of how to reduce the risk of disease, it is not possible to eliminate the amoeba from all freshwater sources. Standard chlorination of swimming pools is sufficient to eliminate the organism. Untreated well water should not be forced into the nose or used to irrigate the nose.

What is the prognosis of a Naegleria fowleri infection?

The prognosis for infected patients is very poor. More than 95% of infections are fatal despite treatment. Survivors may have residual neurological problems, such as seizure disorders.

Where can people find additional information about Naegleria fowleri infections?

The CDC is a good source of information on Naegleria infections: http://www.cdc.gov/parasites/Naegleria/faqs.html.

REFERENCE:

Yoder, J.S., B.A. Eddy, G.S. Visvesvara, L. Capewell, and M.J. Beach. "The Epidemiology of Primary Amoebic Meningoencephalitis in the USA, 1962-2008." Epidemiol Infect. 138.7 July 2010: 968-975.

Medical Author:

Mary D. Nettleman, MD, MS, MACP

Medical Editor:

Charles Patrick Davis, MD, PhD

Source:Medicinenet.com.

Biorhythms

2012-03-26T07:40:00.002-07:00

What are biologic rhythms?

What are biologic rhythms? In essence, they're the rhythms of life. All forms of life on earth, including our bodies, respond rhythmically to the regular cycles of the sun, moon, and seasons.
For example, as night turns into day, vital body functions, including heart rate and blood pressure, speed up in anticipation of increased physical activity. These and other predictable fluctuations in body function, taking place during specific time cycles, are our biologic rhythms. They are regulated by "biologic clock" mechanisms located in the brain.
Although biologic rhythms can be "reprogrammed" by environmental influences (such as when a person regularly works the night shift and sleeps during the day), they are genetically "hard-wired" into our cells, tissues, and organs.
Medical chronobiologists have found that biologic rhythms can affect the severity of disease symptoms, diagnostic test results, and even the body's response to drug therapy. Now these investigators are working to discover how the rhythms of life can be used to improve the practice of medicine - and your health.
These time-related medical observations, and others still in the exciting process of discovery, are rooted in chronobiology (chronos - time; bios - life; logos - science), the study of biologic rhythms.

How does the "body clock" affects symptoms of illness?

Among the various biologic rhythm cycles that medical chronobiologists study, the 24-hour day/night-activity/rest cycle is considered a key chronobiologic factor in medical diagnosis and treatment. Formally known as the circadian rhythm, it's also referred to as the "body clock."
Why is the 24-hour body clock so important?
Because so many of our normal body functions follow daily patterns of speeding up and slowing down, intensifying and diminishing, in alignment with circadian rhythm. Interestingly, so do the symptoms of a number of chronic disorders:
Allergic rhinitis: (nasal inflammation associated with hay fever) Symptoms of sneezing, runny nose, and stuffy nose are typically worse in the early waking hours than later during the day.
Asthma: In most patients, symptoms are more than 100 times as likely to occur in the few hours prior to awakening than during the day.
Stable angina: Chest pain and electrocardiographic (ECG, EKG) abnormalities are most common during the first 4 to 6 hours after awakening.
Prinzmetal's angina: ECG abnormalities are most common during sleep; chest pain can occur even while at rest.
Heart attack: Heart attack most commonly occurs in the early waking hours.
Stroke: Strokes most commonly occur in the early waking hours.
Hypertension: The highest blood pressure readings typically occur from late morning to middle afternoon; lowest occur during early sleep. Therapy now exists that works with your body clock; consult your physician about this treatment. Clinical studies are underway to further this research.
Rheumatoid arthritis: RA symptoms are most intense upon awakening.
Osteoarthritis: Symptoms of osteoarthritis worsen in the afternoon and evening.
Ulcer disease: The pain typically occurs after stomach emptying, following daytime meals, and in the very early morning, disrupting sleep.
Epilepsy: Seizures often occur only at particular times of the day or night; individual patterns differ among patients.

What are examples of specific diseases affected by biorhythms?

Angina

Angina is chest pain or pressure due to an insufficient supply of oxygenated blood to the heart muscle.

Oxygenated blood is normally delivered to the heart muscle by arteries to the heart (coronary arteries).
Inadequate oxygenation of heart muscle (ischemia) can occur because of either narrowing or spasm of the coronary arteries.
Narrowing of the coronary arteries (coronary artery disease or CAD) is usually caused by arteriosclerosis (cholesterol deposits on the inner wall of the arteries).
In patients with narrowed coronary arteries, factors that increase work demand and oxygen consumption of the heart (such as exercise, excitement, increased blood pressure and heart rate) can precipitate heart muscle ischemia and angina.

Patients who develop angina only during stress or physical exertion have stable, exertional angina. When a coronary artery becomes critically narrowed, heart muscle ischemia or angina can occur with minimal or no exertion. These patients have unstable angina, and are at imminent risk of heart attack (myocardial infarction). A heart attack occurs when a diseased coronary artery becomes completely obstructed by a blood clot, leading to irreversible death of heart muscle. During the early hours of a heart attack, irregular heart rhythms can occur which commonly cause sudden cardiac death.
Heart ischemia resulting in angina can be caused by spasm of the coronary arteries. This is a rare condition called vasospastic angina (also known as Prinzmetal's angina) and is not associated with exertion.
It has been known for some time that the symptoms of ischemic heart disease are more common in the morning hours than at any other time of day.

Patients experience episodes of stable angina with lower levels of exertion in the morning than in the afternoon.
The occurrence of episodes of vasospastic angina is higher in the morning than in the afternoons.
In patients with CAD, electrocardiogram (ECG) changes indicative of heart muscle ischemia are seen more frequently in the morning than in the afternoon.

Heart attack

Over one million Americans suffer a heart attack annually. Over four hundred thousand of these heart attack victims die as a result. Many of the heart attack deaths are due to sudden ventricular fibrillation occurring before the patient can reach any medical assistance or the emergency room. Ventricular fibrillation and other heart electrical disturbances can be treated with medications once the patient reaches the hospital. Therefore, 90% to 95% of those heart attack patients who make it to the hospital survive.
Heart attack (myocardial infarction) is the irreversible death of heart muscle due to complete blockage of a coronary artery, usually by a blood clot forming on a cholesterol plaque.

A coronary artery is an artery supplying blood to the heart muscle.
A cholesterol plaque is an abnormal, hard thick deposit on the artery wall.
The condition whereby cholesterol plaque deposits on coronary arteries is called coronary artery disease (CAD).
CAD leads to narrowing of these coronary arteries, thus impairing the normal oxygen supply to the heart.
Coronary artery narrowing can cause angina, chest pain or pressure due to an insufficient supply of oxygenated blood (ischemia) to the heart muscle.
During a heart attack, heart muscle dies when a diseased coronary artery becomes completely blocked by a blood clot. Heart attack can cause chest pain, heart pump failure, and electrical disturbances in the heart.
Electrical disturbances in the heart can cause ventricular fibrillation (a chaotic heart rhythm). A heart undergoing ventricular fibrillation simply quivers, and is incapable of pumping oxygenated blood to the rest of the body and the brain. Permanent brain damage usually occurs unless oxygenated blood is restored to the brain within minutes.

Numerous studies, including the classic Framingham study, have shown that the incidence pattern of sudden cardiac death parallels those of hypertension, heart muscle ischemia, angina, and heart attack - a 70% greater risk between the hours of 7 a.m. and 9 a.m., compared to the rest of the day.
Stroke resulting from ischemia occurs more frequently in the morning than at any other time of day. Like heart attack, ischemic stroke refers to permanent death of brain tissue because of blockage of the artery supplying blood to the brain, usually by a blood clot.

High blood pressure (hypertension)

Hypertension or high blood pressure is a silent killer. Early high blood pressure produces no symptoms or discomfort. However, untreated long-term high blood pressure can lead to strokes, heart diseases, kidney disease, and eye damage. Medical scientists now know that a person's blood pressure varies according to the time of day (circadian rhythm). Such variations may have important implications in the diagnosis, treatment, and monitoring of patients with high blood pressure.
It is important to understand a critical distinction: Circadian rhythms do not cause clinical hypertension in normotensives (people with normal blood pressure). Circadian rhythms do, however, result in a cyclic worsening of hypertension in hypertensive patients.
In the majority of individuals - normotensive and hypertensive - blood pressure rises rapidly in the early morning hours, the time when most individuals wake up and begin their day. This morning rise in blood pressure is not caused by the act of getting out of bed and beginning activity. It is a genetically preset system that automatically increases a person's blood pressure at that time.
For example, if a person goes to sleep at around 10 p.m., beginning in the very early morning - sometime between 3 a.m. and 5 a.m. – the blood pressure begins to rise and continues to rise through the morning.
This increase, which is accompanied by an increase in heart rate, corresponds to the following biologic changes, which are also governed by circadian rhythms:

Increased secretion of catecholamines, particularly norepinephrine, into the bloodstream.
Increased plasma renin activity.

Catecholamines, norepinephrine, and renin are natural hormones produced by the kidneys and adrenal glands (small glands located near the top of both kidneys). These hormones cause tightening of blood vessels in the body (vasoconstriction). Vasoconstriction causes resistance to blood flow and elevates blood pressure.
The vasoconstricting effects of catecholamines may also be enhanced in the morning by the high levels of certain hormones which interact with catecholamines and increase their effects. Many high blood pressure medications are designed to counteract the vasoconstrictive effects of these hormones.
In the late morning or early afternoon, the natural rise in blood pressure reaches its peak. After that, blood pressure declines, falling 15 to 20 mmHg between about 8 p.m. and 2 a.m., the time at which blood pressure is normally at its lowest point.
The blood pressure pattern just described is typical of some individuals, whether the individual is hypertensive or normotensive. These people are referred to as "dippers." In other individuals (called "nondippers"), there is no nightly decline in blood pressure. The blood pressure in these people remains high, even during sleep.
Disease of the heart and blood vessels (cardiovascular disease), including hypertension and the syndromes of ischemic heart disease (angina, heart attack, sudden death), also follow circadian rhythms. This pattern makes sense when you consider that heart rate and blood levels of enzymes and catecholamines that strongly influence blood pressure and heart function follow circadian rhythms.

Hay fever (allergic rhinitis)

Allergic rhinitis (hay fever) is a very common condition, affecting 17.6 million Americans annually. The symptoms of allergic rhinitis (sneezing, runny nose, nasal congestion, and itchy eyes) occur when an allergic individual is exposed to allergens. Allergens are tiny proteins that stimulate the allergic reaction. Common allergens include:

pollens from ragweed, trees, and grasses;
mold spores;
animal proteins; and
mites.

The best way to treat allergic rhinitis is to avoid the allergens. Skin testing is often performed to identify the allergens which cause allergic reactions in a given individual. Scientists now believe that the symptoms of allergic rhinitis, and even the skin testing results, can vary according to the time of day.
For sufferers of allergic rhinitis, the major symptoms of sneezing, runny nose, and stuffy nose are typically worse upon arising than during the middle of the activity span of a given day.

Asthma

Asthma is a common breathing problem, affecting 16.1 million Americans. Asthma is a disease of the lung airways (bronchi). Narrowing of the openings of the airways (caused by spasm, swelling of the tissue lining, and/or mucus accumulation) can lead to shortness of breath, wheezing, or coughing.
Causes of asthma attacks include:

allergies,
cold air,
air pollutants,
drugs,
cigarette smoke,
molds,
exercise, and
infections.

Asthma attacks (rapid worsening of symptoms) typically occur in episodes. Intervals between attacks can be days, weeks, or years. With severe asthma, attacks can occur daily. Scientists now believe that asthma attacks vary according to the time of day.
The occurrence of asthma attacks is not random during the day. Asthma symptoms are frequently worse at night (nocturnal) for a majority of asthma sufferers. A group of active asthma patients recorded the occurrence of acute asthma attacks, manifested by dyspnea (difficulty breathing) and wheezing, during a medication trial.
The incidence of asthma attacks was more than 100 times greater during nighttime sleep, especially around 4 a.m., than it was during the middle of the day.

Can the "body clock" affect diagnostic testing?

The body clock's powerful influence can also be seen in the way it affects diagnostic test results. These results can vary significantly, possibly producing inaccurate readings, depending on the time of day when a test is done.
Consider how the body clock affects blood pressure. Blood pressure isn't constant throughout the day and night; it normally rises in the morning, remains elevated during the day and early evening, and decreases to its lowest level during sleep. So a single reading taken during the day may not give a true picture of whether blood pressure is within the normal range or requires treatment. Some doctors now ask patients to wear special monitoring devices that provide a complete 24-hour blood pressure pattern by recording blood pressures a number of times during the day.
The body clock also affects skin testing for allergies. Results are lower in the morning, considerably higher in the evening, and greatest just before bedtime.
The body clock may complicate testing for asthma severity. Airway patency, or degree of openness, is poorest during the night and best during midday and evening. The same is generally true for forced expiratory volume and peak expiratory flow readings, which can be up to 50% higher at midday and in the afternoon than overnight or when the patient wakes up. Unless these circadian rhythms are taken into account, daytime evaluation of asthma patients could result in underestimating the severity of the disease.
What's being done to help doctors obtain the most accurate results from diagnostic tests likely to be affected by the body clock?
Just heightening their awareness of the problem helps. In addition, medical chronobiologists are working to develop test interpretation guidelines for doctors that take circadian rhythms into account.

Can drug therapy be matched to the "body clock?"

The time of day also can affect the way our bodies respond to medical therapy, especially drug therapy. Investigators working in a special area of chronobiology, called chronotherapeutics or chronotherapy, are studying these effects. Their goal is to come up with new medications, or improve existing ones, that make the most of what we know about how the body clock works.
Already there is evidence that taking medication "by the clock" helps the drugs work better and reduces their side effects. Currently, some doctors are prescribing nighttime administration of medication for patients with ulcer disease or asthma (which worsen at night), rheumatoid arthritis (which worsens in the early morning hours), and high cholesterol levels (most of the body's cholesterol production occurs at night). For patients with osteoarthritis, which worsens in the afternoon and evening, some doctors are prescribing midday medication.
Drugs that may be given "by the clock" include corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), antihistamines, theophyllines, and anticancer drugs.
These lists are growing as chronobiology, chronotherapy, and the diagnostic and treatment methods derived from them are slowly accepted by the medical community. However, the broad acceptance of chronobiology in medicine is expected to take (excuse the expression) time.

Chronobiology: marking time, making progress

Although chronobiology is not new to medical science, it's still in the process of being accepted by the medical community. That's because most doctors are not taught about chronobiology - in fact, they are taught something that seems to contradict it!
What are doctors taught?
Homeostasis - the concept that body functions are in a constant "steady state" throughout the day and night, and that the goal of treatment is restoring or maintaining this "steady state." Even the treatment itself may have this goal, for example, a prescribed drug is given in a way ("every 4 hours") that theoretically will ensure a steady level of it in the patient's bloodstream. Obviously, this view contrasts sharply with diagnosing and treating illness chronobiologically - "by the clock."
Fortunately, although chronobiology is not yet taught in medical schools, doctors are increasingly taking biologic rhythms into account in diagnosing and treating illness. They are recognizing that whereas homeostatic mechanisms keep the body functioning continuously on a moment-to-moment basis (for example, by maintaining breathing and heartbeat), biologic rhythms program the body "in advance" for coping with its predictably changing needs, such as varying energy requirements, during specific time cycles.
The time is coming, medical experts say, when chronobiology, and particularly the body clock, will play a vital role in many areas of medical practice. In some of those areas, as we've seen, that time is now.
If you are taking medication for a medical condition, consider keeping a record of the timing and intensity of your symptoms for a few days and showing it to your doctor; he or she may want to adjust your therapy to align more with your body clock. Who knows, maybe now is your time to get more into the rhythm of life!

References:

The right time? Chronopharmacology - a new science. Nursing RSA Verpleging. 1992;7:23-27. Pharmacology.

Smolensky MH, D'Alonzo GE. Medical chronobiology: concepts and applications. Am Rev Respir Dis.1993;147:S2-S 19.

Time of day medicine dose is taken may boost its efficacy, cut toxicity. JAMA. 1996;275:1 143-1 144. Medical News & Perspectives.

American Heart Association; "Know the Facts, Get the Stats 2007."

Centers for Disease Control, National Center for Health Statistics; "Allergies/Hay Fever."

Centers for Disease Control, National Center for Health Statistics; "Asthma."

Medical Author:

William C. Shiel Jr., MD, FACP, FACR

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Men's Health

2012-03-26T07:36:00.003-07:00

Introduction to men's health

The average life expectancy of a man born in the United State in 2007 is 75 years and 5 months. The life expectancy for a man has increased dramatically in the past 50 years. How long we live is important; however, the quality of life is equally important. The ability to enjoy life to its fullest requires investing time and effort into health maintenance and disease prevention. This investment pays dividends almost immediately and it is never too late to begin. A person who was 65 years old in 2007 could expect to live to age 82, and a 75 year old could expect 10 more years of life.
Our bodies are incredibly complex machines that require fuel components (food, water, and air) to grow, function, and repair itself. Like any machine, the body requires routine maintenance to make it last a long time and to function well throughout a person's life expectancy. Using the body as it was intended and minimizing abuse also increases its ability to perform. When we buy a car, we expect to routinely change the oil, filters, rotate the tires, and avoid driving too aggressively to keep the car running smoothly and last a certain length of time. As in life, accidents happen and cosmetic injuries occur, but it is the "guts" of a car, the engine, transmission, and brakes that will decide if it will be happily driving down the road or sitting in the junkyard.
Our bodies suffer through illnesses and accidents and many are unavoidable. Taking care of your body also includes scheduled maintenance and screening examinations to detect illnesses at an early stage, which increases the potential for cure and a return to health. Learning to listen to the body's warning signs and symptoms is the same as paying attention to the check engine light in your car, neither should not be ignored.
A healthy lifestyle is not just an absence of disease but an opportunity to enjoy the years of life available to each person. Medical care can help the body maintain its performance as it ages. A longer life expectancy should not be considered a jail sentence to inactivity. But as the body ages, there is an expected and normal physiologic change in some of the hormones in the male body.

Prostate problems

The prostate is a unique male organ. It is located beneath the bladder and connects it to the penis. Its function is to produce part of the seminal fluid that is alkaline, which helps lengthen the life span of semen when it enters the vagina. The prostate also has involuntary muscles that contract to help expel semen during ejaculation.
A common condition in men that is part of the normal aging process is benign prostatic hypertrophy (BPH or enlarged prostate). The urethra is a tube that passes through the prostate and drains the bladder. A man with an enlarged prostate (BPH) often has difficulty emptying the bladder because the urethra is being compressed by prostatic tissue. This compression of the urethra makes it difficult for the bladder to generate enough pressure to overcome the obstruction (enlarged prostate). Over time, the bladder itself begins to weaken making urination even more difficult.
Symptoms of BPH include:

Urinary frequency (urinating more often)
Urinary urgency (the feeling that he has to empty the bladder urgently or risk wetting himself)
Urinary hesitancy (difficulty starting the urine stream)
Urinary straining (requiring more pressure or bearing down to empty the bladder)
Poor urine stream and dribbling

Treatment of BPH (which may include medications or surgery) depends upon the man, any underlying medical conditions, and the severity of symptoms.

Testosterone

Sexual health and function are important parts of a healthy lifestyle. The ability to participate in sexual intercourse depends upon the brain, hormones, nerves, and blood vessels that supply the penis. A variety of mechanisms and feedback loops need to work for an erection to occur. There are numerous causes of erectile dysfunction (ED, impotence) including:

diabetes,
peripheral vascular disease,
spinal cord injury, and
multiple sclerosis.

Impotence is also a complication of prostate cancer treatment including surgery and radiation.
Smoking is an independent risk factor for developing impotence.
Treatment of erectile dysfunction depends upon the cause but may include medications (for example, tadalafil [Cialis], sildenafil [Viagra], and vardenafil [Levitra, Staxyn], testosterone replacement therapy and, for some men, prosthetic devices surgically inserted into the penis.
Testosterone levels that are required for puberty, muscle, and bone development in young adulthood gradually decrease over a man's lifetime (sometimes referred to as Low T). Testosterone levels need to be at a certain level to maintain body and brain function. Numerous theories exist about the use of testosterone therapy routinely in older men, but these theories have not been widely accepted. There are however, a few health care practitioners that use testosterone to "prevent aging."

Top 10 diseases that kill men

"Know your enemy and know yourself and you can fight a hundred battles without disaster."

Sun Tzu. Chinese General. 500BC

Most of the common diseases that affect men are potentially preventable, but one needs to know their enemy. Interestingly, the presence of some diseases increases the likelihood that another will occur. Heart disease, stroke, peripheral vascular disease, and dementia all share the same risk factors:

smoking,
high blood pressure,
high cholesterol, and
family history.

1. Heart disease

Heart disease is the number one killer of men in the United States.
The heart is like any other muscle, requiring blood to supply oxygen and nutrients for it to function. The heart's needs are provided by the coronary arteries, which begin at the base of the aorta and spread across the surface of the heart, branching out to all areas of the heart muscle.
Angina
The coronary arteries are at risk for narrowing as cholesterol deposits, called plaques, build up inside the artery. If the arteries narrow enough, blood supply to the heart muscle may be compromised (slowed down), and this slowing of blood flow to the heart causes pain, or angina.
Angina symptoms include:

chest pressure with radiation down the arm and to the jaw,
shortness of breath,
sweating,
indigestion,
nausea,
a decreased ability to do routine activities.

This heart pain is often referred to as "anginal equivalent."
Heart attack
A heart attack (myocardial infarction) occurs when a plaque ruptures, allowing a blood clot to form, which can be life-threatening. The blood clot completely obstructs the artery, stopping blood flow to part of the heart muscle, and that portion of muscle dies.
Abnormal heart rhythms and sudden cardiac arrest
The heart is an electrical pump composed of heart muscle and cells that produce and conduct electrical signals. Heart muscle cells can become irritable because they have lost blood supply and may, in addition, cause electrical abnormalities or short circuits that prevent the heart muscle from pumping which can result in sudden cardiac death.
Heart disease risk factors
The major risk factors for heart disease (and stroke and peripheral vascular disease) include smoking, high blood pressure, high cholesterol, diabetes, and family history. While one cannot control their family history, the other factors can be controlled and the risks minimized. These are life-long obligations to decrease the risk of heart disease.

2. Cancers

Lung cancer is the number one killer among cancers in men, and most are preventable. Smoking causes 90% of all lung cancers and while the number of smokers in the United States has decreased in the past generation, 20% of teenagers smoke and will be the future victims of lung cancer. It is harder to stop smoking than it is to stop many other addictions; nicotine in tobacco is a very addictive drug. Tobacco in its various forms including smokeless or chewing tobacco is related to a variety of other cancers including cancer of the mouth, throat and larynx.
Prostate cancer affects the prostate gland. Prostate cancer is the most common cancer among men, and is a disease of aging and is rarely seen in men younger than 50 years of age. Often prostate cancer causes no symptoms and is diagnosed with routine screening tests including a rectal examination to feel the prostate and a PSA (prostate specific antigen) blood test. The cure rate for prostate cancer has increased since the wide spread use of PSA testing began but it still accounts for 10% of cancer deaths among men.
Colon and rectal cancers tie with prostate cancer as the second most common cause of cancer deaths in men. There are few symptoms in the early stages of colon and rectal cancers, thus the diagnosis is often made by routinely screening the stool for occult blood (blood that is not visible to the naked eye but can be found by testing the stool sample) and undergoing routine screening colonoscopy.
Testicular cancer accounts for only about 1% of cancer in men in the US, but usually occurs in younger men (ages 15 to 39); men can help detect this disease by doing a testicular exam routinely and reporting any testicle abnormalities or symptoms (lumps, swelling, pain) to their health care practitioner.
Living a healthy lifestyle decreases the potential risk of developing cancer. Regular exercise, a healthy diet, and avoiding toxins in the environment (including smoking and secondhand smoke) are positive lifestyle changes that the average person can control during their lifetime.

3. Injuries

Accidents happen and the key to minimizing the risk of death is to use common sense and avoid potentially dangerous situations.

Simple actions like wearing a seatbelt while in a car, wearing a helmet when cycling, skiing, skateboarding, or other activities where head injuries occur help decrease risk of death in an accident.
Driving while impaired on drugs or alcohol is never acceptable and causes a dangerous situation not only for the driver but for those around him. Impairment driving includes not only alcohol but also medications that can cause sedation, including over-the-counter cold and sleep medications. It also includes driving when tired or sleepy. Many authorities on impaired drivers consider texting and cell phone use impaired driving.
Most accidents happen around the house and routine prevention can help decrease those accidents. Easy fixes include making sure that floors aren't slippery or wet, stair railings are secure, and walks and driveways are well maintained and well lit at night. Smoke and carbon monoxide detectors can only work if their batteries are fresh.

4. Stroke (cerebrovascular accident, CVA)

A stroke (cerebrovascular accident [CVA]), occurs when blood supply to part of the brain is disrupted, causing brain cells to die. Blood flow can be compromised by a variety of mechanisms. This can occur because blood supply has been cut off (ischemia) or because there has been bleeding in the brain (hemorrhage). Ischemic strokes occur due to a variety of reasons including the gradual narrowing of a blood vessel in the brain, debris that can break off from the carotid artery in the neck, or from a blood clot that embolizes (or travels) from the heart.
The risk factors for stroke are the same as for heart disease: smoking, high blood pressure, high cholesterol, and family history.
A TIA (transient ischemic attack, mini-stroke) is a stroke that improves, usually quickly. A person develops stroke like symptoms (weakness of one side of the body or face, vision loss, speech difficulty) but it resolves spontaneously within a few minutes or hours. This situation should never be ignored since it is a major warning sign that an impending stroke may occur.

5. COPD (chronic obstructive pulmonary disease)

Emphysema and chronic bronchitis are the two types of chronic obstructive pulmonary disease (COPD) and both are most commonly caused by smoking. Due to the toxins in smoke, the lung tissue is damaged and loses its ability to transfer oxygen from the inhaled air into the blood stream. Symptoms of COPD include shortness of breath and wheezing. COPD increases the risk of lung infection including pneumonia.

6. Diabetes

The pancreas makes insulin to help cells use glucose for energy. Diabetes describes the situation where insulin function in the body is abnormal.

Type 1 diabetes usually occurs in people younger than 40 where the body's immune system destroys the insulin producing cells in the pancreas.
More than 80% of people with diabetes have type 2 diabetes.

Poorly controlled diabetes increases blood sugar levels in the bloodstream and in the long-term, affects the small blood vessels in the body, which can lead to multi-organ failure. Poorly controlled diabetes can cause vascular disease leading to heart attacks, strokes, limb amputations, kidney failure, blindness, and nerve damage (diabetic neuropathy).
Diabetes prevention and control include eating a well balanced diet, maintaining a healthy weight, and routinely exercising, and keeping active.

7. Influenza and pneumonia

A healthy lifestyle and healthy body makes for a strong immune system that can fight common infections like influenza (flu). It is important to follow public health recommendations for routine immunizations to reduce the risk of contracting the flu, and its complications such as pneumonia. However, pneumonia is not limited to just viral causes. Bacterial pneumonia is ranked with influenza as one of the major causes of death in men by many researchers. Fortunately, a pneumococcal vaccine has proven effective in preventing one of the most common bacterial causes of pneumonia, Streptococcus pneumoniae.

8. Suicide

Mens sana in copore sano: a healthy mind in a healthy body

Thoughts of self harm are not normal. They should not be ignored by a man, family, or friends, and should be considered an emergency situation. Depression can become overwhelming and potentially life-threatening. Men with depression may be able to function reasonably well on a day to day basis and may be reluctant to seek help. It may take a crisis situation to finally get a man to agree to get medical, psychological, and counseling assistance.
Symptoms of depression may be subtle and arise slowly. They can include:

difficulty concentrating or completing projects
lack of energy
difficulty sleeping or sleeping too much
change in appetite (some people stop eating while others overeat)
feelings of hopelessness or worthlessness
excessive sadness or feelings of emptiness
thoughts of suicide or self harm

9. Kidney disease

The kidneys filter impurities from the blood and dispose of them in the urine. They are also important in maintaining electrolyte balance in the blood. Even in healthy people, aging gradually decreases the efficiency of kidney function. Kidney failure is often a result of years of poorly controlled high blood pressure and diabetes.
In the United States, approximately 26 million people have chronic kidney disease.

10. Alzheimer's disease

Dementia and Alzheimer's disease describes a gradual loss of cognition and intellectual ability including language, attention, memory, and problem solving is an otherwise healthy person. The cause is unknown and there is no cure. Recommendations to decrease the risk of dementia include avoiding smoking, and keeping blood pressure, high cholesterol, and diabetes under control. Physical and mental fitness may help prevent dementia; keeping socially active may also help. Recurrent head injuries are associated with dementia.

The checklist: How to stay healthy

Being proactive about your health is an important starting point in maintaining health. Some steps are self-evident but a person may need help in taking the first step. The ability to recognize that living healthy is a life-long commitment is an important key to longevity. Nobody is perfect, and the ultimate goal is to have more good habits than bad. Failing to meet a goal does not give permission to quit trying. Doing well one day is not a license to stray the next.
Here is a checklist to promote a healthier lifestyle and living a longer, healthier life.

Stop smoking
Maintain a healthy weight
Engage in some type of physical activity every day
Eat a heart healthy diet
Maintain good control of blood pressure, cholesterol, and diabetes
Get routine medical care and physical examinations
Get recommended screenings for prostate and colon cancer
Perform routine home testicle exams
Keep mentally active
Maintain close relationships with a circle of friends
Seek help if you have symptoms of depression

REFERENCES:

CDC.gov. Leading Causes of Death in Males United States, 2006.
<http://www.cdc.gov/men/lcod/index.htm>

CDC.gov. Pneumococcal Disease In-Short.
<http://www.cdc.gov/vaccines/vpd-vac/pneumo/in-short-both.htm>

CDC.gov. Life expectancy at birth, at 65 years of age, and at 75 years of age, by race and sex: United States, selected years 1900-2007.
<http://www.cdc.gov/nchs/data/hus/hus2009tables/Table024.pdf>

CDC.gov. Lung Cancer Risk Factors.
<http://www.cdc.gov/cancer/lung/basic_info/risk_factors.htm>

National Kidney Foundation.org. Chronic Kidney Disease (CKD).
<http://www.kidney.org/kidneydisease/ckd/index.cfm>

Sun Tzu. (n.d.). Great-Quotes.com. Retrieved December 12, 2011, from Great-Quotes.com Web site.
<http://www.great-quotes.com/quote/964523>

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Charles Patrick Davis, MD, PhD
Source:Medicinenet.com.

Cirrhosis (Cirrhosis of the Liver)

2012-03-26T07:33:00.002-07:00

What is cirrhosis?

Cirrhosis is a complication of many liver diseases that is characterized by abnormal structure and function of the liver. The diseases that lead to cirrhosis do so because they injure and kill liver cells, and the inflammation and repair that is associated with the dying liver cells causes scar tissue to form. The liver cells that do not die multiply in an attempt to replace the cells that have died. This results in clusters of newly-formed liver cells (regenerative nodules) within the scar tissue. There are many causes of cirrhosis; they include chemicals (such as alcohol, fat, and certain medications), viruses, toxic metals (such as iron and copper that accumulate in the liver as a result of genetic diseases), and autoimmune liver disease in which the body's immune system attacks the liver.

Why does cirrhosis cause problems?

The liver is an important organ in the body. It performs many critical functions, two of which are producing substances required by the body, for example, clotting proteins that are necessary in order for blood to clot, and removing toxic substances that can be harmful to the body, for example, drugs. The liver also has an important role in regulating the supply to the body of glucose (sugar) and lipids (fat) that the body uses as fuel. In order to perform these critical functions, the liver cells must be working normally, and they must have an intimate relationship with the blood since the substances that are added or removed by the liver are transported to and from the liver by the blood.
The relationship of the liver to the blood is unique. Unlike most organs in the body, only a small amount of blood is supplied to the liver by arteries. Most of the liver's supply of blood comes from the intestinal veins as the blood returns to the heart. The main vein that returns blood from the intestines is called the portal vein. As the portal vein passes through the liver, it breaks up into increasingly smaller and smaller veins. The tiniest veins (called sinusoids because of their unique structure) are in close contact with the liver cells. In fact, the liver cells line up along the length of the sinusoids. This close relationship between the liver cells and blood from the portal vein allows the liver cells to remove and add substances to the blood. Once the blood has passed through the sinusoids, it is collected in increasingly larger and larger veins that ultimately form a single vein, the hepatic vein that returns the blood to the heart.
In cirrhosis, the relationship between blood and liver cells is destroyed. Even though the liver cells that survive or are newly-formed may be able to produce and remove substances from the blood, they do not have the normal, intimate relationship with the blood, and this interferes with the liver cells' ability to add or remove substances from the blood. In addition, the scarring within the cirrhotic liver obstructs the flow of blood through the liver and to the liver cells. As a result of the obstruction to the flow of blood through the liver, blood "backs-up" in the portal vein, and the pressure in the portal vein increases, a condition called portal hypertension. Because of the obstruction to flow and high pressures in the portal vein, blood in the portal vein seeks other veins in which to return to the heart, veins with lower pressures that bypass the liver. Unfortunately, the liver is unable to add or remove substances from blood that bypasses it. It is a combination of reduced numbers of liver cells, loss of the normal contact between blood passing through the liver and the liver cells, and blood bypassing the liver that leads to many of the manifestations of cirrhosis.
A second reason for the problems caused by cirrhosis is the disturbed relationship between the liver cells and the channels through which bile flows. Bile is a fluid produced by liver cells that has two important functions: to aid in digestion and to remove and eliminate toxic substances from the body. The bile that is produced by liver cells is secreted into very tiny channels that run between the liver cells that line the sinusoids, called canaliculi. The canaliculi empty into small ducts which then join together to form larger and larger ducts. Ultimately, all of the ducts combine into one duct that enters the small intestine. In this way, bile gets to the intestine where it can help with the digestion of food. At the same time, toxic substances contained in the bile enter the intestine and then are eliminated in the stool. In cirrhosis, the canaliculi are abnormal and the relationship between liver cells and canaliculi is destroyed, just like the relationship between the liver cells and blood in the sinusoids. As a result, the liver is not able to eliminate toxic substances normally, and they can accumulate in the body. To a minor extent, digestion in the intestine also is reduced.

What are the symptoms and signs of cirrhosis?
Patients with cirrhosis may have few or no symptoms and signs of liver disease. Some of the symptoms may be nonspecific, that is, they don't suggest that the liver is their cause. Some of the more common symptoms and signs of cirrhosis include:

Yellowing of the skin (jaundice) due to the accumulation of bilirubin in the blood
Fatigue
Weakness
Loss of appetite
Itching
Easy bruising from decreased production of blood clotting factors by the diseased liver.

Patients with cirrhosis also develop symptoms and signs from the complications of cirrhosis that are discussed next.
What are the complications of cirrhosis?
Edema and ascites
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and water in the body. The excess salt and water first accumulates in the tissue beneath the skin of the ankles and legs because of the effect of gravity when standing or sitting. This accumulation of fluid is called edema or pitting edema. (Pitting edema refers to the fact that pressing a fingertip firmly against an ankle or leg with edema causes an indentation in the skin that persists for some time after release of the pressure. Actually, any type of pressure, such as from the elastic band of a sock, may be enough to cause pitting.) The swelling often is worse at the end of a day after standing or sitting and may lessen overnight as a result of the loss of the effects of gravity when lying down. As cirrhosis worsens and more salt and water are retained, fluid also may accumulate in the abdominal cavity between the abdominal wall and the abdominal organs. This accumulation of fluid (called ascites ) causes swelling of the abdomen, abdominal discomfort, and increased weight.
Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow. Normally, the abdominal cavity contains a very small amount of fluid that is able to resist infection well, and bacteria that enter the abdomen (usually from the intestine) are killed or find their way into the portal vein and to the liver where they are killed. In cirrhosis, the fluid that collects in the abdomen is unable to resist infection normally. In addition, more bacteria find their way from the intestine into the ascites. Therefore, infection within the abdomen and the ascites, referred to as spontaneous bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening complication. Some patients with SBP have no symptoms, while others have fever, chills, abdominal pain and tenderness, diarrhea, and worsening ascites.
Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart from the intestines and raises the pressure in the portal vein (portal hypertension). When pressure in the portal vein becomes high enough, it causes blood to flow around the liver through veins with lower pressure to reach the heart. The most common veins through which blood bypasses the liver are the veins lining the lower part of the esophagus and the upper part of the stomach.
As a result of the increased flow of blood and the resulting increase in pressure, the veins in the lower esophagus and upper stomach expand and then are referred to as esophageal and gastric varices; the higher the portal pressure, the larger the varices and the more likely a patient is to bleed from the varices into the esophagus or stomach.
Bleeding from varices usually is severe and, without immediate treatment, can be fatal. Symptoms of bleeding from varices include vomiting blood (the vomitus can be red blood mixed with clots or "coffee grounds" in appearance, the latter due to the effect of acid on the blood), passing stool that is black and tarry due to changes in the blood as it passes through the intestine (melena), and orthostatic dizziness or fainting (caused by a drop in blood pressure especially when standing up from a lying position).
Bleeding also may occur from varices that form elsewhere in the intestines, for example, the colon, but this is rare. For reasons yet unknown, patients hospitalized because of actively bleeding esophageal varices have a high risk of developing spontaneous bacterial peritonitis.
Hepatic encephalopathy

Some of the protein in food that escapes digestion and absorption is used by bacteria that are normally present in the intestine. While using the protein for their own purposes, the bacteria make substances that they release into the intestine. These substances then can be absorbed into the body. Some of these substances, for example, ammonia, can have toxic effects on the brain. Ordinarily, these toxic substances are carried from the intestine in the portal vein to the liver where they are removed from the blood and detoxified.
As previously discussed, when cirrhosis is present, liver cells cannot function normally either because they are damaged or because they have lost their normal relationship with the blood. In addition, some of the blood in the portal vein bypasses the liver through other veins. The result of these abnormalities is that toxic substances cannot be removed by the liver cells, and, instead, the toxic substances accumulate in the blood.
When the toxic substances accumulate sufficiently in the blood, the function of the brain is impaired, a condition called hepatic encephalopathy. Sleeping during the day rather than at night (reversal of the normal sleep pattern) is among the earliest symptoms of hepatic encephalopathy. Other symptoms include irritability, inability to concentrate or perform calculations, loss of memory, confusion, or depressed levels of consciousness. Ultimately, severe hepatic encephalopathy causes coma and death.
The toxic substances also make the brains of patients with cirrhosis very sensitive to drugs that are normally filtered and detoxified by the liver. Doses of many drugs that normally are detoxified by the liver have to be reduced to avoid a toxic buildup in cirrhosis, particularly sedatives and drugs that are used to promote sleep. Alternatively, drugs may be used that do not need to be detoxified or eliminated from the body by the liver, for example, drugs that are eliminated by the kidneys.
Hepatorenal syndrome

Patients with worsening cirrhosis can develop the hepatorenal syndrome. This syndrome is a serious complication in which the function of the kidneys is reduced. It is a functional problem in the kidneys, that is, there is no physical damage to the kidneys. Instead, the reduced function is due to changes in the way the blood flows through the kidneys themselves. The hepatorenal syndrome is defined as progressive failure of the kidneys to clear substances from the blood and produce adequate amounts of urine even though some other important functions of the kidney, such as retention of salt, are maintained. If liver function improves or a healthy liver is transplanted into a patient with hepatorenal syndrome, the kidneys usually begin to work normally. This suggests that the reduced function of the kidneys is the result of the accumulation of toxic substances in the blood when the liver fails. There are two types of hepatorenal syndrome. One type occurs gradually over months. The other occurs rapidly over a week or two.
Hepatopulmonary syndrome

Rarely, some patients with advanced cirrhosis can develop the hepatopulmonary syndrome. These patients can experience difficulty breathing because certain hormones released in advanced cirrhosis cause the lungs to function abnormally. The basic problem in the lung is that not enough blood flows through the small blood vessels in the lungs that are in contact with the alveoli (air sacs) of the lungs. Blood flowing through the lungs is shunted around the alveoli and cannot pick up enough oxygen from the air in the alveoli. As a result the patient experiences shortness of breath, particularly with exertion.
Hypersplenism

The spleen normally acts as a filter to remove older red blood cells, white blood cells, and platelets (small particles that are important for the clotting of blood.). The blood that drains from the spleen joins the blood in the portal vein from the intestines. As the pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow of blood from the spleen. The blood "backs-up" and accumulates in the spleen, and the spleen swells in size, a condition referred to as splenomegaly. Sometimes, the spleen is so swollen that it causes abdominal pain.
As the spleen enlarges, it filters out more and more of the blood cells and platelets until their numbers in the blood are reduced. Hypersplenism is the term used to describe this condition, and it is associated with a low red blood cell count (anemia), low white blood cell count (leucopenia), and/or a low platelet count (thrombocytopenia). The anemia can cause weakness, the leucopenia can lead to infections, and the thrombocytopenia can impair the clotting of blood and result in prolonged bleeding.
Liver cancer (hepatocellular carcinoma)

Cirrhosis due to any cause increases the risk of primary liver cancer (hepatocellular carcinoma). Primary refers to the fact that the tumor originates in the liver. A secondary liver cancer is one that originates elsewhere in the body and spreads (metastasizes) to the liver.
The most common symptoms and signs of primary liver cancer are abdominal pain and swelling, an enlarged liver, weight loss, and fever. In addition, liver cancers can produce and release a number of substances, including ones that cause an increased in red blood cell count (erythrocytosis), low blood sugar (hypoglycemia), and high blood calcium (hypercalcemia ).

What are the common causes of cirrhosis?

Alcohol is a very common cause of cirrhosis, particularly in the Western world. The development of cirrhosis depends upon the amount and regularity of alcohol intake. Chronic, high levels of alcohol consumption injure liver cells. Thirty percent of individuals who drink daily at least eight to sixteen ounces of hard liquor or the equivalent for fifteen or more years will develop cirrhosis. Alcohol causes a range of liver diseases; from simple and uncomplicated fatty liver (steatosis), to the more serious fatty liver with inflammation (steatohepatitis or alcoholic hepatitis), to cirrhosis.

Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases that, like alcoholic liver disease, ranges from simple steatosis, to nonalcoholic steatohepatitis (NASH), to cirrhosis. All stages of NAFLD have in common the accumulation of fat in liver cells. The term nonalcoholic is used because NAFLD occurs in individuals who do not consume excessive amounts of alcohol, yet, in many respects, the microscopic picture of NAFLD is similar to what can be seen in liver disease that is due to excessive alcohol. NAFLD is associated with a condition called insulin resistance, which, in turn, is associated with the metabolic syndrome and diabetes mellitus type 2. Obesity is the most important cause of insulin resistance, metabolic syndrome, and type 2 diabetes. NAFLD is the most common liver disease in the United States and is responsible for 24% of all liver disease. In fact, the number of livers that are transplanted for NAFLD-related cirrhosis is on the rise. Public health officials are worried that the current epidemic of obesity will dramatically increase the development of NAFLD and cirrhosis in the population.

Cryptogenic cirrhosis (cirrhosis due to unidentified causes) is a common reason for liver transplantation. It is termed cryptogenic cirrhosis because for many years doctors have been unable to explain why a proportion of patients developed cirrhosis. Doctors now believe that cryptogenic cirrhosis is due to NASH (nonalcoholic steatohepatitis) caused by long standing obesity, type 2 diabetes, and insulin resistance. The fat in the liver of patients with NASH is believed to disappear with the onset of cirrhosis, and this has made it difficult for doctors to make the connection between NASH and cryptogenic cirrhosis for a long time. One important clue that NASH leads to cryptogenic cirrhosis is the finding of a high occurrence of NASH in the new livers of patients undergoing liver transplant for cryptogenic cirrhosis. Finally, a study from France suggests that patients with NASH have a similar risk of developing cirrhosis as patients with long standing infection with hepatitis C virus. (See discussion that follows.) However, the progression to cirrhosis from NASH is thought to be slow and the diagnosis of cirrhosis typically is made in patients in their sixties.

Chronic viral hepatitis is a condition where hepatitis B or hepatitis C virus infects the liver for years. Most patients with viral hepatitis will not develop chronic hepatitis and cirrhosis. For example, the majority of patients infected with hepatitis A recover completely within weeks, without developing chronic infection. In contrast, some patients infected with hepatitis B virus and most patients infected with hepatitis C virus develop chronic hepatitis, which, in turn, causes progressive liver damage and leads to cirrhosis, and, sometimes, liver cancers.

Inherited (genetic) disorders result in the accumulation of toxic substances in the liver which lead to tissue damage and cirrhosis. Examples include the abnormal accumulation of iron (hemochromatosis) or copper (Wilson's disease). In hemochromatosis, patients inherit a tendency to absorb an excessive amount of iron from food. Over time, iron accumulation in different organs throughout the body causes cirrhosis, arthritis, heart muscle damage leading to heart failure, and testicular dysfunction causing loss of sexual drive. Treatment is aimed at preventing damage to organs by removing iron from the body through bloodletting (removing blood). In Wilson disease, there is an inherited abnormality in one of the proteins that controls copper in the body. Over time, copper accumulates in the liver, eyes, and brain. Cirrhosis, tremor, psychiatric disturbances and other neurological difficulties occur if the condition is not treated early. Treatment is with oral medication that increases the amount of copper that is eliminated from the body in the urine.

Primary biliary cirrhosis (PBC) is a liver disease caused by an abnormality of the immune system that is found predominantly in women. The abnormal immunity in PBC causes chronic inflammation and destruction of the small bile ducts within the liver. The bile ducts are passages within the liver through which bile travels to the intestine. Bile is a fluid produced by the liver that contains substances required for digestion and absorption of fat in the intestine, as well as other compounds that are waste products, such as the pigment bilirubin. (Bilirubin is produced by the breakdown of hemoglobin from old red blood cells.). Along with the gallbladder, the bile ducts make up the biliary tract. In PBC, the destruction of the small bile ducts blocks the normal flow of bile into the intestine. As the inflammation continues to destroy more of the bile ducts, it also spreads to destroy nearby liver cells. As the destruction of the hepatocytes proceeds, scar tissue (fibrosis) forms and spreads throughout the areas of destruction. The combined effects of progressive inflammation, scarring, and the toxic effects of accumulating waste products culminates in cirrhosis.

Primary sclerosing cholangitis (PSC) is an uncommon disease found frequently in patients with ulcerative colitis . In PSC, the large bile ducts outside of the liver become inflamed, narrowed, and obstructed. Obstruction to the flow of bile leads to infections of the bile ducts and jaundice and eventually causes cirrhosis. In some patients, injury to the bile ducts (usually as a result of surgery) also can cause obstruction and cirrhosis of the liver.

Autoimmune hepatitis is a liver disease caused by an abnormality of the immune system that is found more commonly in women. The abnormal immune activity in autoimmune hepatitis causes progressive inflammation and destruction of liver cells (hepatocytes), leading ultimately to cirrhosis.

Infants can be born without bile ducts (biliary atresia) and ultimately develop cirrhosis. Other infants are born lacking vital enzymes for controlling sugars that leads to the accumulation of sugars and cirrhosis. On rare occasions, the absence of a specific enzyme can cause cirrhosis and scarring of the lung (alpha 1 antitrypsin deficiency).

Less common causes of cirrhosis include unusual reactions to some drugs and prolonged exposure to toxins, as well as chronic heart failure (cardiac cirrhosis). In certain parts of the world (particularly Northern Africa), infection of the liver with a parasite (schistosomiasis) is the most common cause of liver disease and cirrhosis.

How is cirrhosis diagnosed and evaluated?
The single best test for diagnosing cirrhosis is biopsy of the liver. Liver biopsies, however, carry a small risk for serious complications, and, therefore, biopsy often is reserved for those patients in whom the diagnosis of the type of liver disease or the presence of cirrhosis is not clear. The possibility of cirrhosis may be suggested by the history, physical examination, or routine testing. If cirrhosis is present, other tests can be used to determine the severity of the cirrhosis and the presence of complications. Tests also may be used to diagnose the underlying disease that is causing the cirrhosis. The following are some examples of how doctors discover, diagnose and evaluate cirrhosis:

In taking a patient's history, the physician may uncover a history of excessive and prolonged intake of alcohol, a history of intravenous drug abuse, or a history of hepatitis. These pieces of information suggest the possibility of liver disease and cirrhosis.

Patients who are known to have chronic viral hepatitis B or C have a higher probability of having cirrhosis.

Some patients with cirrhosis have enlarged livers and/or spleens. A doctor can often feel (palpate) the lower edge of an enlarged liver below the right rib cage and feel the tip of the enlarged spleen below the left rib cage. A cirrhotic liver also feels firmer and more irregular than a normal liver.

Some patients with cirrhosis, particularly alcoholic cirrhosis, have small red spider-like markings (telangiectasias) on the skin, particularly on the chest, that are made up of enlarged, radiating blood vessels. These spider telangiectasias also can be seen in individuals without liver disease, however.

Jaundice (yellowness of the skin and of the whites of the eyes due to elevated bilirubin in the blood) is common among patients with cirrhosis, but jaundice can occur in patients with liver diseases without cirrhosis and other conditions such as hemolysis (excessive break down of red blood cells).

Swelling of the abdomen (ascites) and/or the lower extremities (edema) due to retention of fluid is common among patients with cirrhosis though other diseases can cause them commonly, e.g., congestive heart failure.

Patients with abnormal copper deposits in their eyes or certain types of neurologic disease may have Wilson's disease, a genetic disease in which there is abnormal handling and accumulation of copper throughout the body, including the liver, that can lead to cirrhosis.

Esophageal varices may be found unexpectedly during upper endoscopy (EGD), and they strongly suggesting cirrhosis.

Computerized tomography (CT or CAT) or magnetic resonance imaging (MRI) scans and ultrasound examinations of the abdomen done for reasons other than evaluating the possibility of liver disease may unexpectedly detect enlarged livers, abnormally nodular livers, enlarged spleens, and fluid in the abdomen that suggest cirrhosis.

Advanced cirrhosis leads to a reduced level of albumin in the blood and reduced blood clotting factors due to the loss of the liver's ability to produce these proteins. Thus, reduced levels of albumin in the blood or abnormal bleeding suggest cirrhosis.

Abnormal elevation of liver enzymes in the blood (such as ALT and AST) that are obtained routinely as part of yearly health examinations suggests inflammation or injury to the liver from many causes as well as cirrhosis.

Patients with elevated levels of iron in their blood may have hemochromatosis, a genetic disease of the liver in which iron is handled abnormally and which leads to cirrhosis.

Auto-antibodies (antinuclear antibody, anti-smooth muscle antibody and anti-mitochondrial antibody) sometimes are detected in the blood and may be a clue to the presence of autoimmune hepatitis or primary biliary cirrhosis, both of which can lead to cirrhosis.

Liver cancer (hepatocellular carcinoma) may be detected by CT and MRI scans or ultrasound of the abdomen. Liver cancer most commonly develops in individuals with underlying cirrhosis.

If there is an accumulation of fluid in the abdomen, a sample of the fluid can be removed using a long needle. The fluid then can be examined and tested. The results of testing may suggest the presence of cirrhosis as the cause of the fluid.

How is cirrhosis treated?
Treatment of cirrhosis includes 1) preventing further damage to the liver, 2) treating the complications of cirrhosis, 3) preventing liver cancer or detecting it early, and 4) liver transplantation.
Preventing further damage to the liver

Consume a balanced diet and one multivitamin daily. Patients with PBC with impaired absorption of fat soluble vitamins may need additional vitamins D and K.

Avoid drugs (including alcohol) that cause liver damage. All patients with cirrhosis should avoid alcohol. Most patients with alcohol induced cirrhosis experience an improvement in liver function with abstinence from alcohol. Even patients with chronic hepatitis B and C can substantially reduce liver damage and slow the progression towards cirrhosis with abstinence from alcohol.

Avoid nonsteroidal antiinflammatory drugs (NSAIDs, e.g., ibuprofen). Patients with cirrhosis can experience worsening of liver and kidney function with NSAIDs.

Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not all patients with cirrhosis due to chronic viral hepatitis are candidates for drug treatment. Some patients may experience serious deterioration in liver function and/or intolerable side effects during treatment. Thus, decisions to treat viral hepatitis have to be individualized, after consulting with doctors experienced in treating liver diseases (hepatologists).

Remove blood from patients with hemochromatosis to reduce the levels of iron and prevent further damage to the liver. In Wilson's disease, medications can be used to increase the excretion of copper in the urine to reduce the levels of copper in the body and prevent further damage to the liver.

Suppress the immune system with drugs such as prednisone and azathioprine (Imuran) to decrease inflammation of the liver in autoimmune hepatitis.

Treat patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA), also called ursodiol (Actigall). Results of an analysis that combined the results from several clinical trials showed that UDCA increased survival among PBC patients during 4 years of therapy. The development of portal hypertension also was reduced by the UDCA. It is important to note that despite producing clear benefits, UDCA treatment primarily retards progression and does not cure PBC. Other medications such as colchicine and methotrexate also may have benefit in subsets of patients with PBC.

Immunize patients with cirrhosis against infection with hepatitis A and B to prevent a serious deterioration in liver function. There are currently no vaccines available for immunizing against hepatitis C.

Treating the complications of cirrhosis
Edema and ascites. Retention of salt and water can lead to swelling of the ankles and legs (edema) or abdomen (ascites) in patients with cirrhosis. Doctors often advise patients with cirrhosis to restrict dietary salt (sodium) and fluid to decrease edema and ascites. The amount of salt in the diet usually is restricted to 2 grams per day and fluid to 1.2 liters per day. In most patients with cirrhosis, however, salt and fluid restriction is not enough, and diuretics have to be added.
Diuretics are medications that work in the kidneys to promote the elimination of salt and water into the urine. A combination of the diuretics spironolactone (Aldactone) and furosemide can reduce or eliminate the edema and ascites in most patients. During treatment with diuretics, it is important to monitor the function of the kidneys by measuring blood levels of blood urea nitrogen (BUN) and creatinine to determine if too much diuretic is being used. Too much diuretic can lead to kidney dysfunction that is reflected in elevations of the BUN and creatinine levels in the blood.
Sometimes, when the diuretics do not work (in which case the ascites is said to be refractory), a long needle or catheter is used to draw out the ascitic fluid directly from the abdomen, a procedure called abdominal paracentesis. It is common to withdraw large amounts (liters) of fluid from the abdomen when the ascites is causing painful abdominal distension and/or difficulty breathing because it limits the movements of the diaphragms.
Another treatment for refractory ascites is a procedure called transjugular intravenous portosystemic shunting (TIPS, see below).
Bleeding from varices. If large varices develop in the esophagus or upper stomach, patients with cirrhosis are at risk for serious bleeding due to rupture of these varices. Once varices have bled, they tend to rebleed and the probability that a patient will die from each bleeding episode is high (30%-35%). Therefore, treatment is necessary to prevent the first (initial) bleeding episode as well as rebleeding. Treatments include medications and procedures to decrease the pressure in the portal vein and procedures to destroy the varices.

Propranolol (Inderal), a beta blocker, is effective in lowering pressure in the portal vein and is used to prevent initial bleeding and rebleeding from varices in patients with cirrhosis. Another class of oral medications that lowers portal pressure is the nitrates, for example, isosorbide dinitrate ( Isordil). Nitrates often are added to propranolol if propranolol alone does not adequately lower portal pressure or prevent bleeding.

Octreotide (Sandostatin) also decreases portal vein pressure and has been used to treat variceal bleeding.

During upper endoscopy (EGD), either sclerotherapy or band ligation can be performed to obliterate varices and stop active bleeding and prevent rebleeding. Sclerotherapy involves infusing small doses of sclerosing solutions into the varices. The sclerosing solutions cause inflammation and then scarring of the varices, obliterating them in the process. Band ligation involves applying rubber bands around the varices to obliterate them. (Band ligation of the varices is analogous to rubber banding of hemorrhoids.) Complications of sclerotherapy include esophageal ulcers, bleeding from the esophageal ulcers, esophageal perforation, esophageal stricture (narrowing due to scarring that can cause dysphagia), mediastinitis (inflammation in the chest that can cause chest pain), pericarditis (inflammation around the heart that can cause chest pain), and peritonitis (infection in the abdominal cavity). Studies have shown that band ligation may be slightly more effective with fewer complications than sclerotherapy.

Transjugular intrahepatic portosystemic shunt (TIPS) is a non-surgical procedure to decrease the pressure in the portal vein. TIPS is performed by a radiologist who inserts a stent (tube) through a neck vein, down the inferior vena cava and into the hepatic vein within the liver. The stent then is placed so that one end is in the high pressure portal vein and the other end is in the low pressure hepatic vein. This tube shunts blood around the liver and by so doing lowers the pressure in the portal vein and varices and prevents bleeding from the varices. TIPS is particularly useful in patients who fail to respond to beta blockers, variceal sclerotherapy, or banding. (TIPS also is useful in treating patients with ascites that do not respond to salt and fluid restriction and diuretics.) TIPS can be used in patients with cirrhosis to prevent variceal bleeding while the patients are waiting for liver transplantation. The most common side effect of TIPS is hepatic encephalopathy. Another major problem with TIPS is the development of narrowing and occlusion of the stent, causing recurrence of portal hypertension and variceal bleeding and ascites. The estimated frequency of stent occlusion ranges from 30%-50% in 12 months. Fortunately, there are methods to open occluded stents. Other complications of TIPS include bleeding due to inadvertent puncture of the liver capsule or a bile duct, infection, heart failure, and liver failure.

A surgical operation to create a shunt (passage) from the high-pressure portal vein to veins with lower pressure can lower blood flow and pressure in the portal vein and prevent varices from bleeding. One such surgical procedure is called distal splenorenal shunt (DSRS). It is appropriate to consider such a surgical shunt for patients with portal hypertension who have early cirrhosis. (The risks of major shunt surgery in these patients is less than in patients with advanced cirrhosis.) During DSRS, the surgeon detaches the splenic vein from the portal vein, and attaches it to the renal vein. Blood then is shunted from the spleen around the liver, lowering the pressure in the portal vein and varices and preventing bleeding from the varices.

Hepatic encephalopathy. Patients with an abnormal sleep cycle, impaired thinking, odd behavior, or other signs of hepatic encephalopathy usually should be treated with a low protein diet and oral lactulose. Dietary protein is restricted because it is a source of the toxic compounds that cause hepatic encephalopathy. Lactulose, which is a liquid, traps the toxic compounds in the colon. Consequently, they cannot be absorbed into the blood stream and cause encephalopathy. To be sure that adequate lactulose is present in the colon at all times, the patient should adjust the dose to produce 2-3 semiformed bowel movements a day. (Lactulose is a laxative, and the adequacy of treatment can be judged by loosening or increasing frequency of stools.) If symptoms of encephalopathy persist, oral antibiotics such as neomycin or metronidazole (Flagyl), can be added to the treatment regimen. Antibiotics work by blocking the production of the toxic compounds by the bacteria in the colon.
Hypersplenism. The filtration of blood by an enlarged spleen usually results in only mild reductions of red blood cells (anemia), white blood cells (leukopenia) and platelets (thrombocytopenia) that do not require treatment. Severe anemia, however, may require blood transfusions or treatment with erythropoietin or epoetin alfa (Epogen, Procrit), hormones that stimulate the production of red blood cells. If the numbers of white blood cells are severely reduced, another hormone called granulocyte-colony stimulating factor is available to increase the numbers of white blood cells. An example of one such factor is filgrastim (Neupogen).
No approved medication is available yet to increase the number of platelets. As a necessary precaution, patients with low platelets should not use aspirin or other nonsteroidal antiinflammatory drugs (NSAIDS) since these drugs can hinder the function of platelets. If a low number of platelets is associated with significant bleeding, transfusions of platelets usually should be given. Surgical removal of the spleen (called splenectomy) should be avoided, if possible, because of the risk of excessive bleeding during the operation and the risk of anesthesia in advanced liver disease.
Spontaneous bacterial peritonitis (SBP). Patients suspected of having spontaneous bacterial peritonitis usually will undergo paracentesis. Fluid that is removed is examined for white blood cells and cultured for bacteria. Culturing involves inoculating a sample of the ascites into a bottle of nutrient-rich fluid that encourages the growth of bacteria, thus facilitating the identification of even small numbers of bacteria. Blood and urine samples often are obtained as well for culturing because many patients with spontaneous bacterial peritonitis also will have infection in their blood and urine. In fact, many doctors believe that infection may have begun in the blood and the urine and spread to the ascitic fluid to cause spontaneous bacterial peritonitis. Most patients with spontaneous bacterial peritonitis are hospitalized and treated with intravenous antibiotics such as ampicillin, gentamycin, and one of the newer generation cephalosporin. Patients usually treated with antibiotics include:

Patients with blood, urine, and/or ascites fluid cultures that contain bacteria.
Patients without bacteria in their blood, urine, and ascitic fluid but who have elevated numbers of white blood cells (neutrophils) in the asciticfluid(>250 neutrophils/cc). Elevated neutrophil numbers in ascitic fluid often means that there is bacterial infection. Doctors believe that the lack of bacteria with culturing in some patients with increased neutrophils is due either to a very small number of bacteria or ineffective culturing techniques.

Spontaneous bacterial peritonitis is a serious infection. It often occurs in patients with advanced cirrhosis whose immune systems are weak, but with modern antibiotics and early detection and treatment, the prognosis of recovering from an episode of spontaneous bacterial peritonitis is good.
In some patients oral antibiotics (such as Cipro or Septra) can be prescribed to prevent spontaneous bacterial peritonitis. Not all patients with cirrhosis and ascites should be treated with antibiotics to prevent spontaneous bacterial peritonitis, but some patients are at high risk for developing spontaneous bacterial peritonitis and warrant preventive treatment:

Patients with cirrhosis who are hospitalized for bleeding varices have a high risk of developing spontaneous bacterial peritonitis and should be started on antibiotics early during the hospitalization to prevent spontaneous bacterial peritonitis
Patients with recurring episodes of spontaneous bacterial peritonitis
Patients with low protein levels in the ascitic fluid (Ascitic fluid with low levels of protein is more likely to become infected.)

Prevention and early detection of liver cancer
Several types of liver disease that cause cirrhosis are associated with a particularly high incidence of liver cancer, for example, hepatitis B and C, and it would be useful to screen for liver cancer since early surgical treatment or transplantation of the liver can cure the patient of cancer. The difficulty is that the methods available for screening are only partially effective, identifying at best only 50% of patients at a curable stage of their cancer. Despite the partial effectiveness of screening, most patients with cirrhosis, particularly hepatitis B and C, are screened yearly or every six months with ultrasound examination of the liver and measurements of cancer-produced proteins in the blood, e.g. alpha fetoprotein.
Liver transplantation
Cirrhosis is irreversible. Many patients' liver function will gradually worsen despite treatment and complications of cirrhosis will increase and become difficult to treat. Therefore, when cirrhosis is far advanced, liver transplantation often is the only option for treatment. Recent advances in surgical transplantation and medications to prevent infection and rejection of the transplanted liver have greatly improved survival after transplantation. On average, more than 80% of patients who receive transplants are alive after five years. Not everyone with cirrhosis is a candidate for transplantation. Furthermore, there is a shortage of livers to transplant, and there usually is a long (months to years) wait before a liver for transplanting becomes available. Therefore, measures to retard the progression of liver disease and treat and prevent complications of cirrhosis are vitally important.

What is new and in the future for cirrhosis?
Progress in the management and prevention of cirrhosis continues. Research is ongoing to determine the mechanism of scar formation in the liver and how this process of scarring can be interrupted or even reversed. Newer and better treatments for viral liver disease are being developed to prevent the progression to cirrhosis. Prevention of viral hepatitis by vaccination, which is available for hepatitis B, is being developed for hepatitis C. Treatments for the complications of cirrhosis are being developed or revised and tested continually. Finally, research is being directed at identifying new proteins in the blood that can detect liver cancer early or predict which patients will develop liver cancer.

Cirrhosis At A Glance

Cirrhosis is a complication of liver disease which involves loss of liver cells and irreversible scarring of the liver.
Alcohol and viral hepatitis B and C are common causes of cirrhosis, although there are many other causes.
Cirrhosis can cause weakness, loss of appetite, easy bruising, yellowing of the skin (jaundice), itching, and fatigue.
Diagnosis of cirrhosis can be suggested by the history, physical examination and blood tests, and can be confirmed by liver biopsy.
Complications of cirrhosis include edema and ascites, spontaneous bacterial peritonitis, bleeding from varices, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, hypersplenism, and liver cancer.
Treatment of cirrhosis is designed to prevent further damage to the liver, treat complications of cirrhosis, and preventing or detecting liver cancer early.
Transplantation of the liver is becoming an important option for treating patients with advanced cirrhosis.

Medical Author:

Dennis Lee, MD

Medical Editor:

Jay W. Marks, MD

Source:Medicinenet.com.