Liver Cirrhosis is a complication of many liver diseases characterized by abnormal structure and function of the liver.

The diseases that lead to cirrhosis do so because they injure and kill liver cells, after which the inflammation and repair that is associated with the dying liver cells cause 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.

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.

Complications of Liver Cirrhosis include:

• Swelling of the abdomen (ascites) and/or in the hip, thigh, leg, ankle, and foot,
• Spontaneous bacterial peritonitis,
• Bleeding from varices,
• Hepatic encephalopathy,
• Hepatorenal syndrome,
• Hepatopulmonary syndrome,
• Hypersplenism,
• Liver cancer.

Treatment of cirrhosis is designed to prevent further damage to the liver, treat complications of cirrhosis, and prevent or detect liver cancer early.

Transplantation of the liver is an important option for treating patients with advanced cirrhosis.

In allopathy there is no cure for cirrhosis of the liver, and for some people the prognosis is poor. The life expectancy for advanced cirrhosis is 6 months to 2 years depending on complications of cirrhosis, and if no donor is available for liver transplantation The life expectancy for people with cirrhosis and acholic hepatitis can be as high as 50%. The life expectancy is more than 12 years for a person with cirrhosis and no major complications.

But fortunately, in Homeopathy there are few medicines having good results to treat cirrhosis.

Symptoms of Liver Cirrhosis

Individuals 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.

Individuals with cirrhosis also develop symptoms and signs from the complications of cirrhosis.

There are many causes of cirrhosis including chemicals (such as alcohol, fat, and certain medications of allopathic drugs), viruses, toxic metals, 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 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 close proximity to the blood because 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. 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, which 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 a 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 the 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 signs of cirrhosis.

A second reason for the problems caused by cirrhosis is the disturbing relationship between the liver cells and the channels through which bile flows. Bile is 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 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. All of the ducts combine into one duct that enters the small intestine which 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.

Common symptoms and signs of cirrhosis include jaundice, fatigue, weakness, loss of appetite, itching, and easy bruising.

Signs and symptoms of liver cirrhosis

Patients with cirrhosis may have few or no symptoms and signs of liver cirrhosis/disease. Some of the symptoms may be nonspecific and don’t suggest the liver is their cause. 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.

Stages of cirrhosis of the liver

Cirrhosis in itself is already a late stage of liver damage. In the early stages of liver disease, there will be inflammation of the liver. If this inflammation is not treated it can lead to scarring (fibrosis). At this stage, it is still possible for the liver to heal with treatment.

If fibrosis of the liver is not treated, it can result in cirrhosis. At this stage with allopathic drugs, the scar tissue cannot heal, but the progression of the scarring may be prevented or slowed; only Homeopathy promises some god results.

Patients with cirrhosis who have signs of complications may develop the end-stage liver disease (ESLD) and the only treatment at this stage is liver transplantation.

• Stage 1 cirrhosisinvolves some scarring of the liver, but few symptoms. This stage is considered compensated cirrhosis, where there are no complications.
• Stage 2 cirrhosisincludes worsening portal hypertension and the development of varices.
• Stage 3 cirrhosisinvolves the development of swelling in the abdomen and advanced liver scarring. This stage marks decompensated cirrhosis, with serious complications and possible liver failure.
• Stage 4 cirrhosiscan be life-threatening, and people have developed the end-stage liver disease (ESLD), which is fatal without a transplant.

Edema, ascites, and bacterial peritonitis complications of liver 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 accumulate 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 peripheral 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 the release of the pressure. Any type of pressure, such as from the elastic band of a sock, maybe enough to cause pitting).

The swelling often is worse at the end of a day after standing or sitting and may lessen overnight 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 (called ascites) causing 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 can 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. Infection within the abdomen and the ascites, called 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 a fever, chills, abdominal pain and tenderness, diarrhea, and worsening ascites.

Bleeding and spleen complications of liver cirrhosis

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 the 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 is severe and without immediate treatment can be fatal. Symptoms of bleeding from varices include vomiting blood (it may appear as red blood mixed with clots or “coffee grounds”), passing stool that is black and tarries 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 may rarely occur from varices that form elsewhere in the intestines, for example, the colon. Patients hospitalized because of actively bleeding esophageal varices have a high risk of developing spontaneous bacterial peritonitis, though the reasons for this are not yet understood.

Hypersplenism

The spleen normally acts as a filter to remove older red blood cells, white blood cells, and platelets (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,” accumulating in the spleen, and the spleen swells in size, a condition referred to as splenomegaly. Sometimes, the spleen is so enlarged it causes abdominal pain.

As the spleen enlarges (Hypersplenism), it filters out more and more of the blood cells and platelets until their numbers in the blood are reduced.

Hypersplenism associated with a low red blood cell count (anemia), low white blood cell count (leukopenia), and/or a low platelet count (thrombocytopenia). Anemia can cause weakness, leukopenia can lead to infections, and thrombocytopenia can impair the clotting of blood and result in prolonged bleeding.

Liver (cancer and hepatic) complications of liver cirrhosis

Liver cancer (hepatocellular carcinoma)

Liver 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. Secondary liver cancer is one that originate 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 (hepatomegaly), weight loss, and fever. In addition, liver cancers can produce and release a number of substances, including ones that cause an increase in red blood cell count (erythrocytosis), low blood sugar (hypoglycemia), and high blood calcium (hypercalcemia).

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 to then be absorbed into the body. Some of these substances, such as 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.

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 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 an early symptom of hepatic encephalopathy. Other symptoms include irritability, inability to concentrate or perform calculations, memory loss, 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 allopathic drugs may have to be reduced to avoid a toxic buildup in cirrhosis, particularly sedatives and drugs used to promote sleep. Alternatively, drugs may be used that do not need to be detoxified or eliminated from the body by the liver, such as drugs 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, meaning 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 while 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 again.

This suggests that the reduced function of the kidneys is the result of either the accumulation of toxic substances in the blood or abnormal liver function 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 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.

 Schistosomiasis

Common causes of cirrhosis of the liver include:

2. Nonalcoholic fatty liver disease.
3. Cryptogenic causes.
4. Chronic viral hepatitis (A, B, and C).
5. Autoimmune hepatitis.
6. Inherited (genetic) disorders. Schistosomiasis
7. Primary biliary cirrhosis (PCB).
8. Primary sclerosing cholangitis (PSC).
9. Infants born without bile ducts.

Less common causes of cirrhosis include:

1. Unusual reactions to some drugs
2. Prolonged exposure to toxins
3. 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.

Alcohol and nonalcoholic fatty liver disease

Alcohol

Alcohol is a very common cause of cirrhosis, particularly in the Europe, USA and Russia. 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, which include simple and uncomplicated fatty liver (steatosis), more serious fatty liver with inflammation (steatohepatitis or alcoholic hepatitis), and cirrhosis.

Nonalcoholic fatty liver disease (NAFLD)

Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases that, like alcoholic liver disease, range 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 metabolic syndrome and diabetes mellitus type 2. Obesity is the main cause of insulin resistance, metabolic syndrome, and type 2 diabetes.

The number of livers 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.

Hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis

Chronic viral hepatitis (Hep B and C)

Chronic viral hepatitis is a condition in which hepatitis B or hepatitis C virus infects the liver for years. Most patients with viral hepatitis will not develop chronic hepatitis and cirrhosis. 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.

Primary biliary cirrhosis (PBC)

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.

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 culminate in cirrhosis.

Primary sclerosing cholangitis (PSC)

Primary sclerosing cholangitis (PSC) is an uncommon disease frequently found in patients with Crohn’s disease and 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, eventually causing cirrhosis. In some patients, injury to the bile ducts (usually because of surgery) also can cause obstruction and cirrhosis of the liver.

Inherited disorders, cryptogenic cirrhosis, and biliary atresia in infants

Inherited (genetic) disorders

Inherited (genetic) disorders result in the accumulation of toxic substances in the liver, which leads to tissue damage and cirrhosis. For example, abnormal accumulation of iron (hemochromatosis) or copper (Wilson disease).

In hemochromatosis, patients inherit a tendency to absorb an excessive amount of iron from food. Over the 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 phlebotomy (removing blood).

In Wilson disease, there 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 disturbances, and other neurological difficulties occur if the condition will not treat early.

Treatment with oral medication, which increases the amount of copper that is eliminated from the body in the urine.

Cryptogenic cirrhosis

Cryptogenic cirrhosis (cirrhosis due to unidentified causes) is a common reason for liver transplantation. It is termed called cryptogenic cirrhosis because for many years doctors have been being 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 transplants 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 people in their sixties.

Biliary atresia

Infants can be born without bile ducts (biliary atresia) and ultimately develop cirrhosis. Other infants are born lacking vital enzymes for controlling sugars that lead 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.

Liver Cirrhosis diagnosis

The single best test for diagnosing cirrhosis is a biopsy of the liver. Liver biopsies carry a small risk for serious complications, and 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 history, physical examination, or routine testing may suggest the possibility of cirrhosis. If cirrhosis is present, other tests can be used to determine the severity of cirrhosis and the presence of complications. Tests also may be used to diagnose the underlying disease that is causing cirrhosis.

Examples of how a doctors will diagnose and evaluate cirrhosis are:

• The patient’s history. The doctor may uncover a history of excessive and prolonged intake of alcohol, a history of intravenous drug abuse, or a history of hepatitis. This can 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. However, these spider telangiectasias also can be seen in individuals without liver disease.
• Jaundice (yellowing of the skin and 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, although other diseases can cause them commonly, for example, congestive heart failure.
• Patients with abnormal copper deposits in their eyes or certain types of neurologic disease may have Wilson disease, a genetic disease in which there are abnormal handling and accumulation of copper throughout the body, including the liver, which can lead to cirrhosis.
• Esophageal varices may be found unexpectedly during upper endoscopy (EGD), 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, which 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. Reduced levels of albumin in the blood or abnormal bleeding suggest cirrhosis.
• An 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.
• Autoantibodies (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.
• Elevation of tumor markers such as alpha-fetoprotein suggests the presence of liver cancer.
• If there is an accumulation of fluid in the abdomen, a sample of the fluid can be removed using a long needle to be examined and tested. The results of testing may suggest the presence of cirrhosis as the cause of the fluid.

Allopathic treatment options for Liver Cirrhosis

Allopathic treatment of cirrhosis includes:

1. preventing further damage to the liver: balanced diet, Patients with PBC with impaired absorption of fat-soluble vitamins may need additional vitamins D and K. Avoid nonsteroidal anti-inflammatory drugs especially NSAIDS, avoid alcohol.
2. Treat the disease Homeopathically,
3. treating the complications of cirrhosis,
4. preventing liver cancer or detecting it early, and
5. liver transplantation (if required).

Treat patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA), also called ursodiol. 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 (Homeopathic – Colchicum Autumnale – Q) and methotrexate (Note: methotrexate have severe side effects on patient as well as on fetus, may have benefits in subsets of patients with PBC, diarrhea, mouth sores, cough, shortness of breath, upper stomach pain, dark urine, numbness or tingling, muscle weakness, confusion, seizure, or skin rash that spreads and causes blistering and peeling. Do not prescribe this medicine to treat psoriasis or rheumatoid arthritis if patient have low blood cell counts, a weak immune system, alcoholism or chronic liver disease, or if she is breastfeeding).

Immunize patients with cirrhosis against infection with hepatitis A and B to prevent a serious deterioration in the liver.

There are currently no allopathic vaccines available for immunizing against hepatitis C.

Allopathic treatment for edema, ascites, and hypersplenism complications

Edema and ascites

Retaining salt and water can lead to swelling of the ankles and legs (edema) or abdomen (ascites) in patients with cirrhosis.

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, salt and fluid restriction are not enough and diuretics have to be added.

Pink salt or Himalayan salt (especially from Chevra – Pakistan) should not be restricted, it’s good for liver and spleen health.

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 (Lasix) 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 are said to be refractory), catheter is used to draw out the ascetic fluid directly from the abdomen, a procedure called abdominal paracentesis.

Paracentesis is common to withdraw large amounts (liters) of fluid from the abdomen when the ascites is causing painful abdominal distension and/or difficulty breathing (limits the movement of the diaphragms).

Another treatment for refractory ascites is a procedure called trans jugular intravenous portosystemic shunting (TIPS).

Hypersplenism

The spleen normally acts as a filter to remove older red blood cells, white blood cells, and platelets (small particles 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,” accumulating in the spleen, and the spleen swells in size, a condition referred to as splenomegaly. Sometimes, the spleen is so enlarged 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 (leukopenia), and/or a low platelet count (thrombocytopenia). Anemia can cause weakness, leucopenia can lead to infections, and thrombocytopenia can impair the clotting of blood and result in prolonged bleeding.

Once varices have bled, they tend to re-bleed and the probability that a patient will die from each bleeding episode is high (30% to 35%). Treatment is necessary to prevent the first bleeding episode as well as rebleeding.

Allopathic treatment for bleeding from varices complications

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.

Treatment is necessary to prevent the first 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 the 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 lower portal pressure is nitrates, such as 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) sclerotherapy or band ligation can be performed to obliterate varices, stop active bleeding, and prevent rebleeding. Sclerotherapy is less commonly used due to a higher risk of complications as compared to band ligation. Band ligation involves applying rubber bands around the varices to obliterate them. (Band ligation of the varices is analogous to rubber banding of hemorrhoids.
• Trans jugular intrahepatic portosystemic shunt (TIPS) is a non-surgical, radiologic 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 or variceal 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 blocking (occlusion) of the stent, causing recurrence of portal hypertension and variceal bleeding and ascites. Fortunately, there are methods to open blocked 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 procedure is called distal splenorenal shunt (DSRS). A surgical shunt may be considered for patients with portal hypertension who have early cirrhosis. The risks of major shunt surgery in these patients are 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 is then shunted from the spleen around the liver, lowering the pressure in the portal vein and varices and preventing bleeding from the varices.

Hepatic encephalopathy usually should be treated with a low protein diet and oral lactulose. Antibiotics work by suppressing the bacteria that produce the toxic compounds in the colon.

Allopathic treatment for 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 toxic compounds that cause hepatic encephalopathy. Lactulose, which is a liquid, traps toxic compounds in the colon so they cannot be absorbed into the bloodstream, and thus cause encephalopathy. Lactulose is converted to lactic acid in the colon, and the acidic environment that results is believed to trap the toxic compounds produced by the bacteria. To be sure adequate lactulose is present in the colon at all times, the patient should adjust the dose to produce 2 to 3 semi formed bowel movements a day. Lactulose is a laxative, and the effectiveness of treatment can be judged by loosening or increasing the frequency of stools.

Rifaximin (Xifaxan) is an antibiotic taken orally that is not absorbed into the body but rather remains in the intestines. It is the preferred mode of treatment of hepatic encephalopathy.

Allopathic treatment for spontaneous bacterial peritonitis complications

Patients suspected of having spontaneous bacterial peritonitis usually will undergo paracentesis. The fluid that is removed is examined for white blood cells and cultured for bacteria.

Blood and urine samples also are often obtained for culturing because many patients with spontaneous bacterial peritonitis also will have infections in their blood and urine. Many doctors believe the infection may have begun in the blood and the urine and spread to the ascetic fluid to cause spontaneous bacterial peritonitis.

Most patients with spontaneous bacterial peritonitis are hospitalized and treated with intravenous antibiotics such as cefotaxime (Claforan). Patients usually treated with antibiotics include:

• Ascites fluid cultures that contain bacteria.
• Patients without bacteria in their blood, urine, and ascetic fluid but who have elevated numbers of white blood cells (neutrophils) in the ascetic fluid (greater than 250 neutrophils/cc). Elevated neutrophil numbers in ascetic fluid often mean there is a bacterial infection. Doctors believe 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 (norfloxacin [Noroxin] or sulfamethoxazole and trimethoprim [Bactrim]) 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 treat presumed spontaneous bacterial peritonitis.
• Patients with recurring episodes of spontaneous bacterial peritonitis.
• Patients with low protein levels in the ascetic fluid (ascetic fluid with low levels of protein is more likely to become infected).

Homeopathic Treatment of Liver Cirrhosis and its complications

Cardus Marianus

The action of Cardus Marianus is centered in the liver, and portal system, causing soreness, pain, jaundice. Has specific relation to the vascular system. Abuse of alcoholic beverages, especially beer. Varicose veins and ulcers. Diseases of miners, associated with asthma. Dropsical conditions depending on liver disease, and when due to pelvic congestion and hepatic disease. Disturbs sugar metabolism. Influenza when liver is affected. Debility. Hemorrhages, especially connected with hepatic disease, dropsical accumulation of water in abdomen (ascetic).

The next field is bleeding consequent to liver damage, liver pain and sensitiveness, feel fatigued or tired and have bouts of nausea and vomiting due to Liver Cirrhosis. Taste bitter. Aversion to salt meat. Appetite small; tongue furred; nausea; retching; vomiting of green, acid fluid. Stitches in left side of stomach, near spleen (Ceanoth). Gallstone disease with enlarged liver.

Pain in region of liver. Left lobe very sensitive. Fullness and soreness, with moist skin. Constipation; stools hard, difficult, knotty; alternates with diarrhea. Stools bright yellow. Swelling of gallbladder with painful tenderness. Hyperemia of liver, with jaundice. Cirrhosis, with dropsy.

Rectum: Hemorrhagic piles, prolapse or rectum, burning pain in anus and rectum, hard and knotting, clayey stools. Profuse diarrhea due to rectal cancer. 10 drops doses (Wapler).

Urine: Cloudy; golden-colored.

Skin: Itching on lying down at night. Varicose ulcers (Clematis vitalba). Eruption on lower part of sternum.

Extremities: Pain in hip-joint, spreading through buttocks and down thigh; worse from stooping. Difficult rising. Weakness felt in feet, especially after sitting.

Chelidonium Majus

A prominent liver remedy, covering many of the direct reflex symptoms of diseased conditions of that organ. The jaundiced skin, and especially the constant pain under inferior angle of right scapula, are certain indications. Paralytic drawing and lameness in single parts. The great general lethargy and indisposition to make any effort is also marked. Ailments brought on or renewed by change of weather. Serous effusions. Hydrocele. Bilious complication during gestation.

Tongue yellow, with imprint of teeth; large and flabby (Merc; Hyd). Taste bitter, pasty. Bad odor from mouth. Prefers hot food and drink. Nausea, vomiting; better, very hot water. Pain through stomach to back and right shoulder-blade. Gastralgia. Eating relieves temporarily, especially when accompanied with hepatic symptoms.

Abdomen: Jaundice due to hepatic and gall-bladder obstruction. Gall-colic. Distention. Fermentation and sluggish bowels. Constriction across, as by a string. Liver enlarged. Gallstones (Berberis).

Urine: Profuse, foaming, yellow urine, like beer (Chenop) dark, turbid.

Stool: Constipation; stools hard, round balls, like sheep’s dung, bright yellow, pasty; clay-colored, stools float in water; alternation of diarrhea and constipation. Burning and itching of anus.

Skin: Dry heat of skin; itches, yellow. Painful red pimples and pustules. Old, spreading, offensive ulcers. Wilted skin. Sallow, cold, clammy.

Pain in nape. Stiff neck, head drawn to left. Fixed pain under inner and lower angle of right scapula. Pain at lower angle of left scapula. Pain in arms, shoulders, hands, tips of fingers. Icy coldness of tips of fingers; wrists sore, tearing in metacarpal bones. Whole flesh sore to touch. Rheumatic pain in hips and thighs; intolerable pains in heels, as if pinched by too narrow shoe; worse, right. Feels paralyzed. Paresis of the lower limbs with rigidity of muscles.

Lycopodium

Corresponds to Grau ogle’s carbo-nitrogenous constitution, the non-eliminative lithaemic. Lycopodium is adapted more especially to ailments gradually developing, functional power weakening, with failures of the digestive powers, where the function of the liver is seriously disturbed. Atony. Malnutrition. Mild temperaments of lymphatic constitution, with catarrhal tendencies; older persons, where the skin shows yellowish spots, earthy complexion, uric acid diathesis, etc; also precocious, weakly children.

Dyspepsia due to farinaceous and fermentable food, cabbage, beans, etc. Excessive hunger. Aversion to bread, etc. Desire for sweet things. Food tastes sour. Sour eructation. Great weakness of digestion. Bulimia, with much bloating. After eating, pressure in stomach, with bitter taste in mouth. Eating ever so little creates fullness. Wakes at night feeling hungry. Hiccough. Incomplete burning eructation rise only to pharynx there burn for hours. Likes to take food and drink hot. Sinking sensation; worse night. kidney affections, red sand in urine, pain in renal region; worse before urination. Intolerant of cold drinks. Best adapted to persons intellectually keen, but of weak, muscular power.

Deep-seated, progressive, chronic diseases. Carcinoma. Emaciation. Debility in morning. Marked regulating influence upon the glandular (sebaceous) secretions. Pre-senility. Ascites lacks vital heat (immune system); has poor circulation, cold extremities. Pains come and go suddenly. Sensitive to noise and odors. Cirrhosis of Liver when the liver has atrophied due to long-standing Cirrhosis. Hepatitis may be predominantly present.

Abdomen is bloated, full. Constant sense of fermentation in abdomen, like yeast working; upper left side. Hernia, right side. Liver sensitive. Brown spots on abdomen. Dropsy, due to hepatic disease. Hepatitis, atrophic from of nutmeg liver.

Stool: Diarrhea. Inactive intestinal canal. Ineffectual urging. Stool hard, difficult, small, incomplete. Hemorrhoids; very painful to touch, aching.

Urine: Pain in back before urinating; ceases after flow; slow in coming, must strain. Retention. Polyuria during the night. Heavy red sediment.

Arsenic Album

A profoundly acting remedy on every organ and tissue. Its clear-cut characteristic symptoms and correspondence to many severe types of disease make its homeopathic employment constant and certain.

Liver Cirrhosis with fatigue as the main symptom. The patient feels totally exhausted from doing a little labor. Cannot bear the sight or smell of food. Great thirst; drinks much, but little at a time. Nausea, retching, vomiting, after eating or drinking. Anxiety in pit of stomach. Burning pain. Craves acids and coffee. Heartburn: gulping up of acid and bitter substances which seem to excoriate the throat. Long-lasting eructation. Vomiting of blood, bile, green mucus, or brown-black mixed with blood. Stomach extremely irritable; seems raw, as if torn. Gastralgia from slightest food or drink. Dyspepsia from vinegar, acids, ice-cream, ice-water, tobacco. Terrible fear and dyspnea, with gastralgia; also, faintness, icy coldness, great exhaustion. Malignant symptoms. Everything swallowed seems to lodge in the esophagus, which seems as if closed and nothing would pass. Ill effects of vegetable diet, melons, and watery fruits generally. Craves milk.

Gnawing, burning abdominal pains; relieved by heat. Liver and spleen enlarged and painful. Ascites and anasarca. Abdomen swollen and painful. Pain as from a wound in abdomen on coughing.

Rectum: Painful, spasmodic protrusion of rectum. Tenesmus. Burning pain and pressure in rectum and anus.

Stool: Small, offensive, dark, with much prostration. Worse at night, and after eating and drinking; from chilling stomach, alcoholic abuse, spoiled meat. Dysentery dark, bloody, very offensive. Cholera, with intense agony, prostration, and burning thirst. Body cold as ice (Verat). Hemorrhoids burn like fire, relieved by heat. Skin excoriated about anus.

Urine: Scanty, burning, involuntary. Bladder as if paralyzed. Albuminoids. Epithelial cells; cylindrical clots of fibrin and globules of pus and blood. After urinating, feeling of weakness in abdomen. Bright’s disease. Diabetes.

Nux Vomica

Nux Vomica is greatest of polychrest. Liver Cirrhosis who has a history of long-term alcoholic abuse, chronic acidity and constipation. Sour mouth taste, and nausea in the morning, after eating. Weight and pain in stomach; worse, eating, sometime after. Flatulence and pyrosis. Sour, bitter eructation. Nausea and vomiting, with much retching. Ravenous hunger, especially about a day before an attack of dyspepsia. Region of stomach very sensitive to pressure. Epigastrium bloated, with pressure s of a stone, loves fats and tolerates them well. Dyspepsia from strong tea and/or coffee. Difficult belching of gas. Wants to vomit but cannot. soreness or stitching pain in liver region.

Inclination to take highly spicy diet, stimulants (tea, coffee, alcoholic drinks and fat etc). Mentally anger some and irritable nature, being sensitive to external impressions like noise and odor and also, a sensitivity to cold air.

Bruised soreness of abdominal walls. Flatulent distension, with spasmodic colic. Colic from uncovering. Liver engorged, with stitches and soreness. Colic, with upward pressure, causing short breath, and desire for stool. Weakness of abdominal ring region. Strangulated hernia. Forcing in lower abdomen towards genitals. Umbilical hernia of infants.

Stool: Constipation, with frequent ineffectual urging, incomplete and unsatisfactory; feeling as if part remained un expelled. Constriction of rectum. Irregular, peristaltic action; hence frequent ineffectual desire, or passing but small quantities at each attempt. Absence of all desire for defecation is a contra-indication. Alternate constipation and diarrhea-after abuse of purgatives. Urging to stool felt throughout abdomen. Itching, blind hemorrhoids, with ineffectual urging to stool; very painful; after drastic drugs. Diarrhea after a debauch; worse, morning. Frequent small evacuations. Scanty stool, with much urging. Dysentery; stools relieve pains for a time. Constant uneasiness in rectum. Diarrhea, with jaundice.

Urine: Irritable bladder; from spasmodic sphincter. Frequent calls; little and often. Hematuria. Ineffectual urging, spasmodic and strangury. Renal colic extending to genitals, with dribbling urine. While urinating, itching in urethra and pain in neck of bladder.

Phosphorus

Phosphorus is a destructive metabolism. Causes yellow atrophy of the liver and sub-acute hepatitis, jaundice in patients with Cirrhosis of Liver, stool very offensive, vomiting of blood, desire for cold drinks, juices and ice creams.

Hunger soon after eating. Sour taste and sour eructation after every meal. Belching large quantities of wind, after eating. Throws up ingests by the mouthfuls. Vomiting: water is thrown up as soon as it gets warm in the stomach. Postoperative vomiting. Cardiac opening seems contracted, too narrow; the food scarcely swallowed, comes up again. Pain in stomach; relieved by cold food, ices. Region of stomach painful to touch, or on walking. Inflammation of stomach, with burning extending to throat and bowels. Bad effects of eating too much salt.

Abdomen feels cold. Sharp, cutting pains. A very weak, empty, gone sensation felt in whole abdominal cavity. Liver congested. Acute hepatitis. Fatty degeneration (Carbon tetrachloride; Ars. Chlorof). Jaundice. Pancreatic disease. Large, yellow spots on abdomen.

Stool: Very fetid stools and flatus. Long, narrow, hard, like a dog’s and difficult to expel. Desire for stool on lying especially on left side. Painless, copious debilitating diarrhea. Green mucus with grains like sago. Involuntary; seems as if anus remained open. Great weakness after stool. Discharge of blood from rectum, during stool. White, hard stools. Bleeding hemorrhoids.

Urine: Hematuria, especially in acute Bright’s disease. Turbid, brown, with red sediment.

Apocynum Cannabinum

Increases secretions of mucous and serous membranes and acts on cellular tissue, reducing edema and dropsy.

Nausea, with drowsiness. Thirst on walking. Excessive vomiting. Food or water is immediately ejected. Dull, heavy, sick feeling. Oppression in epigastrium and chest, impeding breathing (Lobelia infl). Sensation of sinking in stomach. Abdomen bloated. Ascites.

Stool: Watery, flatulent, with soreness in anus; worse after eating. Feeling as if sphincter were open and stools ran right out.

Urine: Bladder much distended. Turbid, hot urine, with thick mucus and burning in urethra, after urinating. Little expulsive power. Dribbling. Strangury. Renal Dropsy.

Quassia Amara

Acts on gastric organs as a tonic. Seems to possess marked action on eyes, producing amblyopia and cataract. Pain in right intercostal muscles above the liver. Pressure and stitches in liver, and sympathetically in spleen.

Stomach: Atonic dyspepsia, with gas and acidity. Heart-burn and gastralgia. Regurgitation of food. Abdomen feels empty and retracted. Dyspepsia after infectious diseases; especially grip, dysentery. Tongue dry or with brown sticky coating. Cirrhosis of liver with ascites.

Urinary: Excessive desire-impossible to retain urine; copious micturition day and night. As soon as the child wakes up the bed is drenched.

Inclination to yawn and stretch. Sensation of coldness over back. Prostration, with hunger. Cold extremities, with sensation of internal coldness.

P. S: This article is only for doctors having good knowledge about Homeopathy and allopathy, for learning purpose(s).

For proper consultation and treatment, please visit our clinic.

None of above-mentioned medicine(s) is/are the full/complete treatment, but just hints for treatment; every patient has his/her own constitutional medicine.

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Dr. Sayyad Qaisar Ahmed (MD {Ukraine}, DHMS), Abdominal Surgeries, Oncological surgeries, Gastroenterologist, Specialist Homeopathic Medicines.

  Senior research officer at Dnepropetrovsk state medical academy Ukraine.

Location:  Al-Haytham clinic, Umer Farooq Chowk Risalpur Sadder (0923631023, 03119884588), K.P.K, Pakistan.

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