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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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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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