CHAPTER III PROBLEM IDENTIFICATION AND CASE ANALYSE

III.1 PROBLEM IDENTIFICATION 1. A 37 y.o.man, with ascites became worse since 1 day before admission as the chief complaint. 2. 3 months before, ascites and sclera icteric. His urine volume was normal, his defecation less than usual. 3. 1 months before, ascites became larger, sclera icteric, abdominal fullness, nausea, loss of appetite, fatigue, shortness of breath, he felt better if he took a rest, cough with clear sputum. 4. His urine was tea color urine, his defecation was less than usual and feces was black. 5. 2 weeks before, abdomen became larger again, yellowish eyes, abdominal fullness, abdominal pain, nausea, loss of appetite, fatigue, and swelling in both of lower extremity, shortness of breath became so heavy, he felt no better if he took a rest. 6. 1 day before, enlargement of abdomen became worse and shortness of breath became so heavy. 7. History of having same disease 3 years ago and was hospitalized (2 times) in RS, consuming herbs 5 years ago, and consuming alcohol 7 years ago, exposed by insectisida 1 years ago. 8. BP 100/60 mmHg, PR 78 times/minute, reguler, RR 22 times/minute, T 36,90 C, IMT= 20,2%. Pale of conjunctiva palpebra, sclera icteric, spider nevi, ginecomastia. Cor examination, ictus cordis can be seen and palpable in ICS IV LMC sinistra, upper boundary of cor is ICS III, left boundary of cor is ICS IV LMC, and right boundary of cor is in linea parasternalis dextra. Lung and liver boundary is in ICS IV, there is no peranjakan of liver. Abdominal is distended, stiffness, venectation, hepar and lien arent

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palpable, undulation. Pitting edema in both lower extremity, erythema of palmar. 9. Lab: Hb: 10.4 g/dl, Ht: 31 vol%, leucocyte: 31.700/mm, trombocyte: 676.000/mm, total bilirubin: 3.49 mg/dl, direct bilirubin: 2.91 mg/dl, SGOT: 46 U/L, ALP: 209 mg/dl, protein total: 6.2 g/dl, albumin: 2.1 g/dl, globulin: 4.1 g/dl, BSS: 39 mg/dl. III.2 PROBLEM ANALYZE 1. What are the cause of cirrhosis liver? 2. What are mechanism and manifestation of cirrhosis liver? 3. How are the diagnosis of this patient? 4. How does treatment for this patient? 5. How are the prognosis for this patient? 6. What are the complication of cirrhosis liver? III.3 SYNTHESIS What are the cause of cirrhosis liver Cirrhosis liver is a condition in which the liver slowly deteriorates and malfunctions due to chronic injury. When something attacks and damages the liver, liver cells are killed and scar tissue is formed. This scarring process is called fibrosis. When the whole liver is scarred it shrinks and gets hard. Cirrhosis has various causes such (1) alcohol-related liver disease; heavy alcohol use over several years can cause chronic injury to the liver. (2) Chronic hepatitis C; this disease can cause inflammation and damage to the liver over time that can lead to cirrhosis. (3) Chronic hepatitis B; hepatitis B like hepatitis C causes inflammation and damage to the liver that can lead to cirrhosis. (4) Nonalcoholic fatty liver disease (NAFLD); fat builds up in the liver and eventually cause cirrhosis. This increasingly common liver disease is associated with obesity, diabetes, protein malnutrition, coronary artery disease, and corticosteroid medications. (5) Autoimmune hepatitis; this form of hepatitis is caused by the bodys immune system attacking liver cells and causing

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inflammation, damage, and eventually cirrhosis. (6) Disease that damage or destroy bile ducts; several diseases can damage the ducts that carry bile from the liver, causing bile to back up in the liver and leading to cirrhosis. (7) Inherited diseases; several inherited diseases that interfere with how the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly. (8) Drugs, toxins, and infections; such drug reactions, prolonged exposure to toxic chemicals, parasitic infections, and repeated bouts of heart failure with liver congestion. In the United States, heavy alcohol consumption and chronic hepatitis C have been the most common causes of cirrhosis. Obesisty is becoming a common cause of cirrhosis. Many people with cirrhosis have more than one cause of liver damage. In this case, consuming alcohol and herbs could be the risk factor that could stimulate inflammation process and damage the liver, this process happens little by little over many years to become cirrhosis. What are mechanism and manifestation of cirrhosis liver? Injury to the liver from many causes leads to inflammation which may be detected by abnormalities in liver-related blood tests. Over time, ongoing injury leads to the development of scar tissue in the liver, a process called fibrosis. Since the liver has a substantial amount of reserve function, mild to moderate amounts of fibrosis usually do not lead to symptoms. However,as the amount of fibrosis increases it can lead to disruptions in the normal shape and function of the liver. Liver becomes lumpy and stiff. Cirrhosis occurs when the normal structure of the liver is disrupted by bands of scar tissue. One of the normal functions of the liver is to filter blood returning to the heart from the digestive system. When cirrhosis is present, the presence of scar tissue causes increased resistance to blood flow through the liver. This results in high pressures developing in the veins that drain into the liver, a process called portal hypertension. Many of the complications of liver disease, such as varices or venectation is to relieve portal hypertension so the blood passes

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through other veins, splenomegaly because the high pressure in the portal vein backs up into another organ like spleen, which gets big and destroys more platelets than usual, hepatic cells damage cant make the substances like albumin and clotting factors, fluid retention because of lack of albumin to maintain blood volume and body compensate by equalizing the pressure by reducing the volume of blood and esophageal bleeding is caused by liver is forced into smaller veins (esophagus and stomach) and this veins will become stretched with increased pressure, these veins can rupture causing hemorrhage. Compensated cirrhosis is defined as liver that is heavily scarred but can still perform most of the important chemical functions that keep the body running smoothly. In fact, people may not even know that the liver is damaged because many people will have only a few or non-specific symptoms. For this reason, it is important for everyone with risk factors like having disease that can lead to cirrhosis to be monitored on a regular basis. Decompensated cirrhosis means that the liver is severely scarred and damaged. At this stage, sign and symptoms of cirrhosis more proven. The symptoms of decompensated cirrhosis can be serious and life-threatening, but many of them can be successfully managed. The most common conditions and symptoms include (in alphabetical order): Ascites and edema, bleeding varices, bruising and bleeding, gynecomastia, hepatic encephalotpathy, infections, itching, jaundice, kidneys (hepatorenal syndrome), liver cancer, malnutrition, menstrual irregularities, nail changes, portal hypertension, spider nevi, sepsis. Sign and symptoms of decompensated cirrhosis such (1) jaundice, (2) easy bruising or excessive bleeding, (3) ascites, (4) mental problems, (5) flapping, (6) severe itching, (7) severe weight loss. Laboratoty finding usually find in cirrhosis liver are increasing of liver enzyme like SGOT, SGPT, alkali phosphatase, gamma glutamil transpeptidase, increasing of bilirubin, inverted of albumin and globulin, anemia, trombositopenia, leukopenia, neutropenia that usually find because congective splenomegaly. In this case, patient has shown sign and symptoms of decompensated cirrhosis that caused by his bad habit. Alcohol and herbs induce inflammation process in the liver (fibrosis), this process take a long time until liver become

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disruptions of its structure and function. Ascites caused by portal hypertension leads to vasodilatation and increasing of intracapilar pressure make transudation to peritoneum space, activation of RAAS can make reabsorption of Na and water increase which contribute to make ascites more severe. Edema caused by hypoalbuminemia that make decreasing of oncotic pressure and most of fluid from intravascular move to tissue. Shortness of breath cause of the amount of fluid is large enough to restrict the normal expansion of the chest during breathing. Yellowish eyes and tea colour urine that sign of high level of bilirubin in serum, black feces is melena caused by rupture of enlarged veins (varices) inside the digestive system. Nausea, loss of appetite and fatigue caused by disturb of liver function to detoxification so toxic substances cant be discarded and come into circulation. Laboratory finding, anemia caused by hipersplenisme, low nutrition intake, GIT bleeding. Hiperbilirubinemia caused by liver unable to process bilirubin so bilirubin accumulate in the blood. SGOT increase and SGPT normal caused of chronic destruction of hepatocyte, ALP increase caused of obstruction in bile duct. Albumin decrease and globulin increase caused by dysfunction of liver to product albumin and intestinal antigen in porta system to limfoid tissue stimulate production of immunoglobulin.. How are the diagnosis of this patient? The diagnosis of cirrhosis is usually based on the presence of a risk factor for cirrhosis, such as alcohol use or obesity, and is confirmed by physical examination, blood tests, and imaging. Blood tests that may be helpful in evaluating the liver and increasing the suspicion of cirrhosis. To view the liver for signs of enlargement, reduced blood flow, or ascites, the doctor may order a computerized tomography (CT) scan, ultrasound, magnetic resonance imaging (MRI), or liver scan. Cirrhosis is best determined by examining a sample of liver tissue under the microscope, a procedure which is called a liver biopsy. In this relatively simple procedure a thin needle is inserted, under local anesthesia, into the liver and removes a small piece of liver tissue. Liver biopsy not only confirms the

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presence of cirrhosis, but can often provide information as to its cause. In many cases, a liver biopsy may not be necessary to identify cirrhosis In this case, diagnosis can build from anamnesis which his complain that refer to symptoms of cirrhosis, physical examination that was found sign of cirrhosis and portal hypertension, laboratory finding with additional examination can help to proven diagnosis of cirrhosis liver. How does treatment for this patient? Management of cirrhosis liver: Non pharmacology Nutritious diet; protein 1g/kgBW, sodium restricted if there is ascites. Avoiding alcohol and other substances Compensated cirrhosis: treat the causal such hepatitis. Decompensated cirrhosis: o Diuretics for edema and ascites; spironolactone 100-200mg once a day, if no response use furosemide 20-40mg/day, and paracentesis with albumin correction. o Antibiotics to prevent infection o Beta blocker can lower the pressure in the varices and reduces the risk of bleeding. o Lactulose for cleansing the bowel (ammonia) and decreasing of bacteria intestine that produce ammonia. o Liver transplant is considered when complictions cannot be controlled by treatment. In this case, diuretics that used are spironolactone and furosemide can reduce fluid retention. Propanolol is beta blocker to overcome varices, Laxadin syrup is a laxative agent to cleaning the bowel and helps get rid of ammonia. Kanamycin is antibiotic aminoglycoside bacteriocidal to depress growing of intestine bacterial that produce ammonia. Ranitidine is antihistamine H2 that inhibits stomach acid production.

Pharmacology

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How are the prognosis for this patient? Prognosis of cirrhosis hepatis is very varied, confluenced by etiology, level of liver damage, complication, and others disease that followed the patient. Child-Pugh classification is used to evaluate prognosis of cirrhosis. The variable involve bilirubin concentration, albumin, present of ascites and encephalopathy. This classification related to life expextancy of cirrhosis patient. Life expectancy in 1 year sequently for the patient with classification A, B, C are 100%, 80%, 45%. Child-Pugh classification 1 None None <2 >3,5 <1,7 Value 2 Minimal Minimal 2-3 2,8-3,5 1,7-2,3 3 Severe Massive >3 <2,8 >2,3

Encephalopathy Asites Bilirubin (mg/dl) Albumin (g/dl) PT Note: Child A = 5-6 Child B = 7-9 Child C = 10-15

In this patient, there is no encephalopathy, massive ascites, bilirubin > 3 mg/dl (3,49 mg/dl), albumin < 2,8 mg/dl (2,1 mg/dl), and PT not checked. So total is 9, this patient is in child C. What are the complication of cirrhosis liver? Complication of cirrhosis liver are ascites, varices, hepatic encephalopathy, liver cancer. In this case, patient had fall into complication of cirrhosis liver such ascites and varices.

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DAFTAR PUSTAKA
1. Sanchez W, Talwalker J. Liver cirrhosis. The American College of Gastroenterology. Bethesda. 2. Grattagliano I, Ubaldi E, Bonfrate L, et al. Management of liver cirrhosis between primary care and specialists. World journal of gastroenterology. 2011: 17(18); 2273-2282. 3. Hernomo K. Pengelolaan perdarahan massif varises esophagus pada sirosis hati. Thesis. Airlangga University Press, Surabaya,1983. 4. Nurdjanah S. Sirosis Hati. Buku Ajar Ilmu Penyakit Dalam Jilid I Edisi IV. Jakarta: FK UI. 2006; 443-446. 5. National digestive diseases information clearinghouse. Cirrhosis. U.S Department of health and human services. 2008: 09; 1-8. 6. Franciscus A. Symptoms and complications of cirrhosis. HCSP Fact Sheet. San Francisco. 2012. 7. Gunnarsdottir SA. Liver cirrhosis-Epidemiological and clinical aspects. Section of Gastroenterology and Hepatology Departement of Internal Medicine Sahlgrenska University Hospital Goteborg University. Sweden. 2008.