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Cirrhosis Management Prevention in Futures

Progress in the hepatic cirrhosis prevention and management of cirrhosis continues. Research is underway to determine the mechanism of scar formation in the liver and how the healing process can be halted or even reversed. The newest and best treatments for viral diseases of the liver are being developed to prevent progression to cirrhosis. Prevention of viral hepatitis by vaccination, which is available for hepatitis B, is in development for hepatitis C. The treatment of complications of cirrhosis are continuously developed and tested. Finally, the research aims to identify new proteins in the blood can detect liver cancer early or predict which patients will develop liver cancer.

Hepatic Cirrhosis Disease Brief Information

• Cirrhosis disease is a liver complication disease leading to loss of liver cells and irreversible scarring of the liver.
• Alcohol and viral hepatitis C and hepatitis C are common causes of cirrhosis, although there are many other causes.
• Cirrhosis can cause bruising, weakness, loss of appetite, yellowing of the skin (jaundice), fatigue and itching.
• The cirrhosis diagnosis can be suggested by history, blood tests and physical examination, and can be confirmed by liver biopsy.
• The complications of liver cirrhosis are edema and ascites, variceal bleeding, spontaneous bacterial peritonitis, hepatic encephalopathy, hypersplenism, hepatorenal syndrome, Hepatopulmonary syndrome and liver cancer.
• Treatment of cirrhosis is designed to prevent more damage to the liver, treatment of complications of cirrhosis, and prevention or early detection of liver cancer.
• Liver transplantation is becoming an important option for treating patients with advanced cirrhosis.

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Some Cirrhosis Treatment Complications Part 2

In Complications of Cirrhosis Treatment Part 1, you have learen more detail information about bleeding from varices, also edema and ascites. And now, in Some Cirrhosis Treatment Complications Part 2 I will give information more details about Hepatic encephalopathy, Hypersplenism, Spontaneous bacterial peritonitis (SBP)

Hepatic Encephalopathy

Patients with an abnormal sleep cycle, thought disorders, bizarre behavior, or other signs of hepatic encephalopathy usually be treated with a low protein diet and oral lactulose. The dietary protein is limited because it is a source of toxic compounds that cause hepatic encephalopathy. Lactulose, which is a liquid, the pitfalls of toxic compounds in the colon. Therefore, can be absorbed into the bloodstream and cause encephalopathy. To ensure that adequate lactulose present in the colon, at any time, patient dose should be used to produce semi-formed stools per day 2.3. (Lactulose is a laxative, and the adequacy of treatment may be tried by the looseness or increased stool frequency.) Encephalopathy If symptoms persist, oral antibiotics such as neomycin or metronidazole (Flagyl) can be added to the system. Antibiotics by blocking the production of toxic compounds by bacteria in the colon.

Hypersplenism

The filtration of blood by an enlarged spleen usually means that the cuts only mild symptoms of red blood cells (anemia), white blood cells (leukopenia) and platelets (thrombocytopenia), which do not require treatment. Severe anemia, however, may need blood transfusions or treatment with erythropoietin or epoetin alfa (Epogen, Procrit), hormones that stimulate red blood cell production. If the number of white blood cells are significantly reduced, another factor stimulating hormone called granulocyte colony is available to increase the number of white blood cells. An example of one of these factors is filgrastim (Neupogen).

There is no approved drug is still available to increase the number of platelets. As a precaution necessary, patients with low platelet count should not use aspirin or other antiinflammatory drugs (NSAIDs), because these drugs may affect platelet function. If a low number of platelets is associated with significant bleeding, platelet transfusions should be given normally. Surgical removal of the spleen (called splenectomy) should be avoided if possible because of the risk of excessive bleeding during surgery and the risk of anesthesia in advanced liver disease.

Spontaneous Bacterial Peritonitis (SBP)

Patients with suspected spontaneous bacterial peritonitis usually covered by paracentesis. The liquid that is extracted is examined for white blood cells and for bacteria. Culture is the inoculation of a sample of ascites in a bottle of fluid containing nutrients that promote growth of bacteria, facilitating the identification of even small amounts of bacteria. The blood and urine samples are often obtained for both culture, since many patients with spontaneous bacterial peritonitis has also infection in the blood and urine. In fact, many doctors believe the infection may have begun in the blood and urine and spread to cause ascites spontaneous bacterial peritonitis. Most patients with spontaneous bacterial peritonitis were hospitalized and treated with intravenous antibiotics such as ampicillin, gentamicin, and one of the most recent generations cephalosporins. In general, patients treated with antibiotics as follows:

• Patients with blood, urine and / or ascites fluid cultures containing bacteria.
• Patients without bacteria in the blood, urine and ascites, but who have a high number of white blood cells (neutrophils) in asciticfluid (> 250 neutrophils / cc). High number of neutrophils in the ascitic fluid usually means that there is a bacterial infection. Doctors believe that the absence of bacteria to grow in some patients with increased neutrophils is due either to a very small number of bacteria or inefficient farming techniques.

Spontaneous bacterial peritonitis is a serious infection. It often occurs in patients with advanced cirrhosis, whose immune system is weakened, but with modern antibiotics and early detection and treatment, the prognosis for recovery from an episode of spontaneous bacterial peritonitis is good.

In some patients, oral antibiotics (like Cipro or Septra) can be prescribed to prevent spontaneous bacterial peritonitis. All patients with cirrhosis and ascites should be treated with antibiotics to prevent spontaneous bacterial peritonitis, but some patients are at high risk for spontaneous bacterial peritonitis and justify preventive treatment :

• Patients with cirrhosis who were hospitalized for variceal bleeding are at high risk for spontaneous bacterial peritonitis and should be released in early antibiotics during hospitalization to prevent spontaneous bacterial peritonitis
• Patients with recurrent episodes of spontaneous bacterial peritonitis
• Patients with low protein content in ascites (accumulation of ascites with low protein is more susceptible to infection)

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Complications of Cirrhosis Treatment Part 1

The treatment complications of cirrhosis include Edema and Ascites, Bleeding from Varices, Hepatic encephalopathy, Hypersplenism, Spontaneous bacterial peritonitis (SBP). In Complications of Cirrhosis Treatment Part 1, I will give more detail information about edema and ascites, also bleeding from varices.

Edema and Ascites

The salt and water retention can lead to swollen ankles and legs (edema) or abdomen (ascites) in patients with cirrhosis. Doctors often advise patients with cirrhosis of limiting the intake of salt (sodium) and fluid to reduce edema and ascites. The amount of salt in the diet is generally limited to 2 grams per day and the liquid to 1.2 liters per day. In most patients with cirrhosis, however, salt and fluid restriction is not enough, and diuretics should be added.

Diuretics are drugs that act on the kidneys to promote excretion of salt and water in urine. A combination of the diuretic spironolactone (Aldactone) and furosemide can reduce or eliminate the edema and ascites in most patients. During treatment with diuretics, it is important to monitor kidney function by measuring blood levels of blood urea nitrogen (BUN) and creatinine to determine if a diuretic is used too. Too many diuretics can cause kidney dysfunction leading to elevated urea and creatinine in blood.

Sometimes when diuretics are not working (in this case, is known as refractory ascites), a long needle or catheter is used to make the ascitic fluid directly into the abdomen, a procedure called abdominal paracentesis. It is common to remove large quantities (liters) of fluid in the abdomen when ascites is abdominal distention causing pain and / or difficulty breathing, as it restricts the movement of the diaphragm.

Another treatment of refractory ascites is a procedure known as porto-systemic shunt transjugular intravenous TIPS.

Bleeding from Varices

If large varices develop in the stomach, esophagus or superior in patients with cirrhosis are at risk of serious bleeding due to rupture of these varices. Once varices have bled, they tend to bleed and the likelihood that patients die each episode of bleeding is high (30% -35%). Therefore, treatment is needed to prevent the episode (original) first bleeding and rebleeding. Treatments include medications and procedures to reduce the pressure in the portal vein and procedures to destroy varicose veins.

* Propranolol (Inderal), a beta blocker, is effective in reducing the pressure in the portal vein and is used to prevent the initial hemorrhage and rebleeding of varices in patients with cirrhosis. Another class of oral drugs that lower portal pressure is nitrates, eg isosorbide dinitrate (Isordil). Nitrates are often added to propranolol, while propranolol alone is not enough to reduce portal pressure and prevent bleeding.

* Octreotide (Sandostatin) also reduces the pressure of the portal vein and is used to treat variceal bleeding.

* During upper endoscopy (EGD) or sclerotherapy or ligation can be performed to remove varicose veins and stop the bleeding and prevent rebleeding. Sclerotherapy involves injecting small doses of sclerosing solution into varicose veins. Sclerosing solutions cause inflammation and scarring and varicose veins, erasing in the process. Band ligation is the use of rubber bands around the varices to erase. (Ligation of varicose veins is similar to rubber bands of hemorrhoids.) Complications of sclerotherapy: esophageal ulcers, bleeding ulcers of the esophagus perforation, esophagus, esophageal stricture (narrowing due to scarring that can cause) , dysphagia, mediastinitis (inflammation of the lungs that can cause chest pain), pericarditis (inflammation around the heart can cause chest pain), and peritonitis (infection of the abdominal cavity). Studies have shown that ligation may be slightly more effective with fewer complications than sclerotherapy.

* Transjugular intrahepatic portosystemic shunt (TIPS) is a surgical procedure to relieve pressure in the portal vein. TIPS is performed by a radiologist inserts a catheter (tube) into a vein in the neck to the inferior vena cava and hepatic vein in the liver. The stent then so that one end is in the high pressure portal vein and the other is in the low-pressure hepatic vein. This blood will not pass through the tube around the liver and therefore decreases the pressure in the portal vein and varicose veins and prevents bleeding varices. TIPS is particularly useful in patients unresponsive to beta-blockers, sclerotherapy of varicose veins or bands. (TIPS is also useful in the treatment of patients with ascites do not respond to salt and fluid restriction and diuretics.) TIPS can be used in patients with cirrhosis to prevent variceal bleeding while patients are awaiting transplant hepático. The most common side effect of TIPS is hepatic encephalopathy. Another major problem is the development advice of narrowing and occlusion of the stent, causing the recurrence of portal hypertension and variceal bleeding and ascites. The ranges of estimated frequency of stent occlusion in 30% -50% in 12 months. Fortunately, there are ways to open occluded stents. Other complications include bleeding boards due to accidental perforation of the capsule of the liver or bile duct, infection, heart failure and liver failure.

* A surgical operation to create a bypass (step) of the vein portal vein high pressure to low pressure can reduce blood flow and portal vein pressure and prevent variceal bleeding. The surgery is called distal splenorenal shunt (DSRS). To consider a bypass surgery in patients with portal hypertension who have early cirrhosis. (The risks of bypass surgery for these patients is lower in patients with advanced cirrhosis.) During DSRS, the surgeon separates the splenic vein, portal vein and attached to the renal vein. Blood is diverted from the spleen to the liver, lowering blood pressure in the portal vein and varices and prevention of variceal bleeding.

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The Most Frequent Cirrhosis Causes

There are some causes of cirrhosis, such as alcohol, non-alcoholic fatty liver disease (NAFLD), cryptogenic cirrhosis, chronic viral hepatitis, Inherited disorders, primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, biliary atresia, and cardiac chronic heart failure as cirrhosis causes problems.

• Alcohol cause hepatic cirrhosis

Alcohol is a very common cause of cirrhosis, especially in the western world. The development of cirrhosis depends on the amount and regularity of alcohol consumption. Chronic high levels of alcohol consumption for liver cell damage. Thirty percent of people drinking daily for at least eight to sixteen ounces of hard liquor or the equivalent of fifteen or more years will develop cirrhosis. Alcohol causes a range of diseases of the liver to be simple and uncomplicated fatty liver (steatosis), to more severe fatty liver with inflammation (nonalcoholic steatohepatitis or hepatitis), cirrhosis.

• Non-alcoholic Fatty Liver Disease (NAFLD)

NAFLD, better known as Non-Alcoholic Fatty Liver Disease refers to a broad spectrum of liver diseases such as alcoholic liver disease, ranging from simple steatosis to non-alcoholic steato-hepatitis (NASH) to cirrhosis. All stages of NAFLD have in common the accumulation of fat in liver cells. The term is used because NAFLD nonalcoholic occurs in people who do not consume excessive amounts of alcohol, however, in many respects, the microscopic image of non-alcoholic fatty liver is similar to what can be seen in liver disease caused by excessive alcohol consumption. Is NAFLD associated with a condition called insulin resistance, which in turn is associated with metabolic syndrome and type 2 diabetes mellitus. Obesity is a major cause of insulin resistance, metabolic syndrome, type 2 diabetes. NAFLD is the most common liver disease in the United States and is responsible for 24% of all liver diseases. In fact, the number of livers that are transplanted from non-alcoholic fatty liver, cirrhosis is related to the increase. The public health administrators that the current epidemic of obesity dramatically increases the development of nonalcoholic fatty liver and cirrhosis in the population.

• Cryptogenic cirrhosis (cirrhosis due to unidentified causes)

Cirrhosis due to unidentified causes, better known as Cryptogenic-Cirrhosis is a common reason for liver transplantation. It’s called cryptogenic cirrhosis because for years doctors have been unable to explain why a proportion of patients with cirrhosis developed. Doctors now believe that cryptogenic cirrhosis 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 estimated to disappear with the onset of cirrhosis, and this makes it difficult for physicians to establish the link between NASH and cryptogenic cirrhosis long. An important clue leading to NASH cryptogenic cirrhosis is the discovery of a large number of Nash in the new liver of patients undergoing liver transplantation in cryptogenic cirrhosis. Finally, a French study suggests that patients with NASH have a similar risk of developing cirrhosis patients with long-term infection with hepatitis C. (See below). However, it is expected that progression to cirrhosis from NASH to be slow and the diagnosis of cirrhosis is usually performed in patients in the sixties.

• Chronic Viral Hepatitis

Viral hepatitis chronic is a condition where chronic hepatitis B or chronic hepatitis C affects the liver for years. Most patients with viral hepatitis develop chronic hepatitis and cirrhosis. For example, most patients infected with hepatitis A recover completely within a few weeks without developing chronic infection. However, some patients infected with hepatitis B and most patients infected with hepatitis C develop chronic hepatitis, which in turn leads to progressive liver disease leading to cirrhosis and sometimes liver cancer.

• Inherited (genetic) disorders

Inherited genetic disorders that cause the accumulation of toxic substances in the liver, leading 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 too much iron from food. Over time, iron accumulation in various organs in the body causes cirrhosis, arthritis, heart muscle damage leading to heart failure, and testicular dysfunction causing loss of sexual appetite. Treatment aims to prevent organ damage from the removal of iron in the body by bleeding (blood removal). In Wilson’s disease, is an inherited abnormality in one of the proteins that control copper in the body. Over time, copper accumulates in the liver, eyes and brain. Cirrhosis, tremor, psychiatric disorders and other neurological disorders occur if the condition is not treated quickly. Treatment with oral medication that increases the amount of copper from the body in urine.

• Primary biliary cirrhosis (PBC)

PBC, better known as Primary Biliary Cirrhosis is a liver disease caused by abnormal immune system that is predominantly female. Abnormal immunity in PBC causes chronic inflammation and destruction of small bile ducts in the liver. The bile ducts are the passages in the liver, bile travels to the intestine. Bile is a liquid produced by the liver that contains substances necessary for digestion and absorption of fat in the intestine, and other compounds that are waste products such as bilirubin, a pigment. (Bilirubin is produced by the breakdown of hemoglobin in red blood cells.). Along with the gallbladder, bile ducts form the biliary tract. In the PBC, the destruction of small bile duct blocks the normal flow of bile into the intestine. As the inflammation continues to destroy more of the bile ducts, also extends to destroy liver cells nearby. That the destruction of hepatocytes of products, the scar tissue (fibrosis) forms and propagates in the areas of destruction. The combined effects of ongoing inflammation, scarring, and the toxic effects of waste accumulation leads to cirrhosis.

• Primary sclerosing cholangitis (PSC)

PSC, better known as Primary Sclerosing Cholangitis is a rare disease that occurs frequently in patients with ulcerative colitis. In the PSC, the large bile ducts outside the liver become inflamed, narrowed and blocked. Outflow obstruction of the bile duct in biliary tract infections and jaundice, and eventually causes cirrhosis. In some patients, bile duct injury (usually after surgery) can also cause obstruction and cirrhosis of the liver.

• Autoimmune hepatitis

Autoimmune hepatitis is a liver disease caused by abnormal immune system that occurs most often in women. The abnormal immune activity in autoimmune hepatitis resulting in inflammation and progressive destruction of liver cells (hepatocytes), which eventually leads to cirrhosis.

• Babies can be born without bile ducts (biliary atresia)

Biliary atresia, also known as infant can be born without bile ducts and eventually develop cirrhosis. Other babies are born without enzyme vital for control of sugar 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 lungs (alpha-1 antitrypsin deficiency).

• Other less common causes of cirrhosis include unusual reactions to certain drugs and exposure to toxins, and chronic heart failure (cardiac cirrhosis)

In some parts of the world (especially North Africa), infection of the liver parasites (schistosomiasis) is the most common cause of liver disease and cirrhosis.

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Signs and Symptoms of Hepatic Cirrhosis Complications

Patients with cirrhosis may have little or no liver disease symptoms and liver disease. Some cirrhosis symptoms may be nonspecific, i.e. not suggest that the liver is the cause. Among the most common symptoms and signs of cirrhosis, it’s include : itching, fatigue, loss of appetite, weakness, jaundice (yellowing of the skin) due to accumulation of bilirubin in the blood, and easy bruising of the decreased production of blood coagulation by the diseased liver.

Some cirrhosis patients also develop signs and symptoms of cirrhosis complications. The complications of cirrhosis such as edema and ascites, Spontaneous bacterial peritonitis (SBP), Bleeding esophageal varices described here, and Hepatic encephalopathy, Hepatorenal syndrome, Hepatopulmonaire Syndrome, Hypersplenism and Liver cancer (hepatocellular carcinoma) will be explained in part 2.

Edema and ascites

As liver cirrhosis is severe, the signals are sent to the kidneys retain salt and water in the body. The excess salt and water is first stored in the tissue under the skin of the ankles and legs due to gravity standing or sitting. This fluid buildup is called swelling or edema marks. (Fovea refers to the fact that the pressure of a finger firmly against the ankle or leg with edema causes bleeding in the skin that persists for some time after pressure release. In fact, any pressure, as the elastic of a sock, can be enough to cause pitting.) Swelling is often worse at the end of the day, after standing or sitting and may lower overnight due to the loss the effects of gravity on the position supine. As cirrhosis worsens and more salt and water is conserved, the fluid can also accumulate in the abdominal cavity between the abdominal wall and abdominal organs. This accumulation of fluid (called ascites) causes abdominal bloating, abdominal discomfort, and weight gain.

Spontaneous bacterial peritonitis (SBP)

Of fluid in the abdominal cavity (ascites) is the ideal place for bacteria to grow. Normally, the abdominal cavity contains a very small amount of liquid that is able to resist infection well, and bacteria that enter the abdomen (usually the intestine) are killed or find their place in the door and the liver vein, which killed. In cirrhosis, fluid accumulates in the abdomen can not normally resist infection. In addition, more bacteria find their way from the intestine into the ascites. Therefore, the infection within the abdomen and ascites, known as spontaneous bacterial peritonitis or SBP, is likely to happen. SBP is a potentially fatal complication. Some patients with PAS have no symptoms, while others may have fever, chills, abdominal pain, diarrhea, and worsening ascites.

Bleeding esophageal varices

In cirrhosis of the liver, scar tissue blocks the flow of blood to the heart of the intestines and increases the pressure in the portal vein (portal hypertension). When the pressure in the portal vein is large enough, which causes blood flow to the liver through the veins with less pressure to reach the heart. The most common veins through which blood passes through the liver are the veins along the lower esophagus and upper stomach.

Because of increased blood flow and thereby increasing the pressure, the veins of the lower esophagus, upper stomach and the expansion and then called esophageal and gastric varices, portal pressure, varicose veins more and more likely that a patient is bleeding from varices in the esophagus or stomach.

Bleeding varices are often severe and, without immediate treatment can be fatal. Symptoms of bleeding varices are vomiting blood (vomiting can be red blood mixed with clots or “coffee” in appearance, the latter due to the effect of acid in the blood), passage of stool that is black and tarry stools, due to changes in the blood that passes through the intestine mane () and dizziness or fainting hypotension (caused by a fall in blood pressure, especially when standing in the supine position).

It may also be bleeding from varices that form in other parts of the intestine, for example, the colon, but this is rare. For unknown reasons, patients hospitalized with active bleeding from esophageal varices are at high risk for spontaneous bacterial peritonitis.

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