Medical symptom checker- Swollen stomach causes- Cirrhosis symptoms and management
Cirrhosis is a chronic disease or end stage liver disease/damage.It is caused by liver cell injury which later leads to inflammation, necrosis and activation of stellate cells. The liver normal lobular and vascular architecture will be destroyed and the normal liver tissue will be replaced with fibrosis. The normal function of the liver is decreasing and the blood flow through the liver is progressively diminished. In later stage, this will result in hepatocellular carcinoma or liver failure.
In term of geriatric perspective ,encephalopathy and jaundice are common while in term of pediatric perspective , other causes such as inborn error of metabolism may lead to congenital liver failure which is treatable surgically and by diet.
In term of prevention , generally the patient is counsel on how to avoid and prevent any risk factors for developing chronic liver disease such as abusive alcohol intake.
In term of epidemiology, it is the 10th leading causes of death worldwide. It affect people of the ages of 40-50 years olds and male > female with more female get cirrhosis as a result of chronic alcohol misuse. Between the age of 45- 54, it is the 15th leading causes of death worldwide and 12th leading cause of death in the US.
The etiology of cirrhosis besides chronic alcohol abuse which is common in UK also includes viral infection. The virus infection / chronic viral infection hepatitis B or hepatitis C are common worldwide. Toxin or drug such as hepatotoxic drug or methotrexate are also one of the contributing factors. Bile status or chronic biliary disease such as biliary atresia , primary sclerosing cholangitis and primary biliary cirrhosis may also leads to cirrhosis . Vascular disorder such as hepatic venous congestion and Budd Chiari syndrome as well as cryptogenic , autoimmune disease and metabolic disease may leads to cirrhosis.
Inherited disorder such as hemochromatosis , alpha 1 antitrypsin deficiency , Wilson disease, galactosaemia and cystic fibrosis may also leads to cirrhosis. Non alcoholic steatohepatitis is common with diabetes, short bowel syndrome, TPN, obesity and drug such as amiodarone and tamoxifen.
In term of symptoms , patient appears to be asymptomatic or suffer from non specific symptoms such as weakness, fatigue, nausea, anorexia and weight loss. Symptoms will appear at the end stages of liver disease such as :
Portal hypertension - PR bleeding, melaena , hematemesis and abdominal swelling.
Reduction in liver synthetic function - ankle swelling, ankle edema, abdominal swelling and easy bruising.
Reduction i detoxification action - jaundice,amenorrhea, personality changes and abnormal sleep pattern.
The signs of liver disease includes signs manifested at the skin such as ecchymosis, excoriation, jaundice, scleral icterus, hyperpigmentation , xanthoma, spider angiomata, caput medusa and palmar erythema. Splenomegaly in case of portal hypertension and hepatomegaly in case of alcohol fatty liver or viral and cirrhotic liver that is hard and small. Other signs includes, asterixis, dupuytren contracture, central obesity, gynecomastia, body mass index > 30 , leukonychia, parotid enlargement,testicular atrophy, spider nevi and stretch marks.
While examining the patient , he/she may appear fatigue, weak and malaise. The patient also suffers from anorexia, weight loss or gain ( in case of edema and ascites ) , present with tenderness at the right upper quadrant, amenorrhea, erectile dysfunction, diminished libido, clay colored stools and tea colored urine, edema of the leg , abdominal bloating / swelling , bruise easily, abnormal bleeding, pruritus, hematemesis, melena and hematochezia and night blindness.
Patient needs to be ask about risk factors that causes liver disease such as history of alcohol abuse, viral hepatitis infection , history of liver disease, autoimmune disease and primary liver cancer.
In terms of pathology, there will be loss of normal liver architecture, periportal fibrosis and formation of nodule. Nodule either macronodular > 3mm or micronodular < 3mm in case by alcohol intake. Grade refers to degree of inflammation and stages refer to distortion of architecture from mild portal fibrosis to cirrhosis. The liver will appear pathologically enlarged or shrunken cirrhotic liver in late stages.
The investigation need includes , routine blood investigation such as full blood count that reveals reduction in hemoglobin level and platelet in case of hypersplenism. The liver function test indicates normal or increase in ALT and AST with AST > than ALT, increase in ALP, bilirubin gamma glutamyl transpetidase and reduction in albumin. These liver enzymes will normalizes as cirrhotic progress . Cholesterol and triglycerides level are elevated if fatty liver present. Clotting studies may reveals prolonged prothrombin time, prolonged partial thromboplastin time and prolonged INR.
Other investigation includes, viral serology ( identification of hepatitis B surface antigen, core antibody and surface antibody ) . Hepatitis B quantitative viral loads if sAg is positive, hepatitis C antibody ( hepatitis C quantitative RNA if viral load is positive. Alpha1 - anti trypsin level , iron studies ( total iron binding capacity , serum iron, serum ferritin ) for hemochromatosis, caeruloplasmin level for Wilson disease, anti mitochondrial antibody for primary biliary cirrhosis, ANA and SMA for autoimmune hepatitis and alpha fetoprotein for liver disease.
Ascitic tap is useful for microscopy, culture and sensitivity as well as cytology and biochemistry ( glucose, albumin, protein and amylase, ) Subacute bacterial peritonitis if neutrophil is > 250 mm3
Liver biopsy is performed if INR < 1.5 and no ascites. Otherwise transjugular biopsy is performed, Not required in case of obvious end stage liver disease. If the patient cannot be biopsied, lever - spleen scan is useful to diagnosis portal hypertension in cirrhotic patient . If the patient suffer from portal hypertension , endoscopy is performed to rule out any esophageal varices or portal hypertensive gastropathy.
Imaging involves CT scan , MRI scan and MRCP scan, Child Purgh Grading is a grading system that is useful to determine the prognosis, the need for liver transplantation and the strength of the treatment of required. Class A is 5- 6 scores, Class B is 7-9 scores and Class C is 10-15 scores. Class A one year survival is 100 % and two year survival is 85% , Class B one year survival is 81 % and two year survival is 57% and Class C one year survival is 45% and two year survival is 35%.
Generally, the treatment include outpatient treatment with exception on major gastrointestinal bleeding, renal failure, rapidly deteriorating hepatic decompensation, hepatic encephalopathy, sepsis and infection.
The general measures include treatment of underlying causes. Patient must be reminded to abstain from drugs and alcohol. Immunization is required if patient suffer from hepatitis A , B , influenza, or suffer from pneumococcal disease. Phlebotomy is performed until iron stores is depleted per ferritin decreasing. Controls of lipids and diabetes are important in non alcoholic fatty liver disease as well as exercise and weight reduction.
Review of dietary intake is important. Consider enteral supplement . Nasogatric feeding may be tried if indicated . Patient needs to avoid any drugs that affect the liver such as opiates, sedatives , NSAIDS. Patient requires daily multi vitamin , without iron, high fiber diet, protein 1- 1. 5g/kg of body weight and < 2g/d sodium if edema / ascites .
If the patient suffer from decompensated cirrhosis, branched chain amino acid supplement improves survival and quality of life. Regular conditioning avoid fatigue.
Silymarin or milk thistle is likely safe and make improve symptoms if taken based on the recommendation dose from manufacturer. However some preparation may contains substance that interfere with transaminase and INR.
Surgical approach may includes relieving portal hypertension with TIPS insertion in case of diuretic resistance ascites or recurrent variceal bleeds. Liver transplantation is the only curative measures. Endoscopic ligation and beta blocker for 4- 6 treatment or consider transjugular intrahepatic shunts. Transplantation either cadaveric or living donor .
Complication such as spontaneous bacterial peritonitis can be treated with antibiotic treatment such as metronidazole or cefuroxime. Prophylaxis antibiotics such as ciprofloxacin is useful with recurrent spontaneous bacterial peritonitis.
Encephalopathy treatment includes excluding GI bleeding, treat infection and avoiding sedation considering lactulose and phosphate. Ascites is treated with diuretic ( spironolactone and furosemide ), restriction of salt intake and therapeutic paracentesis with human albumin replacement IV every 2 weeks PRN. Caution if pedal edema absent.
The complication of cirrhosis include edema, encephalopathy, muscle wasting, coagulopathy such as esophageal varices, colopathy and gastropathy, ascites ( SBP, dyspnea ) , umbilical , ventral hernia, hepatocellular carcinoma, hepatorenal syndrome and fulminant hepatic failure.
Patient should be reffer for hepatologist or gastroenterologist consult. Liver enzyme, prothrombin time and platelet is monitor every 6- 12 months. Patients with reduction in prothrombin time suffer from hepatitis B and C are at increase risk of hepatocellular carcinoma. Patient required every 6 - 12 months screening with liver ultrasound and alpha fetoprotein . Endoscopy every 2 years to screen for any varices. Consider immunization against hepatitis A and B , influenza vaccine and pneumovax.
In term of prognosis except 5 - 20 years for asymptomatic case of cirrhosis. 5% will develop hepatocellular carcinoma annually. 50% cases of compensated cirrhosis will develop ascites in 10 years. 50% 5 year survival if ascites develop. 30% mortality in acute variceal bleeding. life expentacy is short. Except death within 5 years at the onset of complication. Without liver transplantation , 85% survive in 1 year with liver transplant. Death occur 5% per year.< 25% eligible patient for liver transplant are transplanted due to donor shortage.
Decompensated cirrhosis develop when complication occurs such as encephalopathy, ascites, GI bleeding and jaundice. It is precipitated by portal vein thrombosis, alcohol and drugs, increase in protein meals, tumor development, electrolytes imbalances, constipation , infection and GI bleeding.
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