A 57-year-old Man Came With Abdominal Enlargement Since 2 Weeks Before AdmissionFitri Nurrahmi*, Dimas Swarahanura*, Eddy M. Salim**ABSTRACTIt was reported that there was a case of abdominal enlargement with anemia presented with an asymptomatic reactive HBsAg. A man, 57 years old, was admitted to the hospital with abdominal enlargement. 2 weeks prior to admission, patient complained about abdominal enlargement getting bigger each day, shortnees of breath (+) particularly on activities.2 days prior to admission, patient complained abdominal is getting bigger, swelling on both legs, void frequencies and volume lesser than usual. Patient went to RSMH. From physical examination, this patient has pale of conjungtivae palpebrae, spider nevi (+), distended abdominal, shifting dullness (+), edematous of pretibial (+/+). From the laboratory findings, Hb 10,4 mg/dl, erythocyte 2,83x106 mg/dl, hematocrite 28% L, thrombocyte 78.000/uL, albumin serum 2,7 mg/dl, globuline serum 4,4 mg/dl, uric acid 11,5 mg/dl, ureum 70 mg/dl, creatinine 2,54 mg/dl, and reactive HBsAg. Patient was diagnosed with decompensated hepatic cirrhosis with hepatorenal syndrome and anemia chronic disease and was given furosemide tablet 40 mg, spironolactone tablet 100 mg, and propranolol tablet 10 mg.Keywords: hepatic cirrhosis, abdominal enlargement, hepatorenal syndrome * Medical Student of Sriwijaya University, Clerkship Program Moh. Hoesin General Hospital** Staff of Allergy-Immunology Division of Internal Medicine Department of Dr. Moh. Hoesin General HospitalINTRODUCTIONHepatic cirrhosis is a complication of many liver diseases characterized by abnormal structure and function of the liver. Histologically, this disease is defined as a diffuse hepatic pathologic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. Fibrosis is an excess deposition of the components of the extracellular matrix (such as collagens, glycoproteins and proteoglycans) within the liver. Cirrhosis represents the final common histologic pathway for a wide variety of chronic liver disease.1World Health Organization (WHO) estimated prevalence of hepatic cirrhosis in 2006 is up to 170 million cases. This report reflects that approximately 3% of human world population have hepatic cirrhosis.2 Hepatic cirrhosis affects an estimated 7 million individuals in Indonesia. The prevalence of this disease in Indonesia is approximately 1-2,4% in 2007. Cirrhosis predominantly occurs in man than woman, with a male-to-female ratio is 2-4:1.The prevalence of this disease is highest in aged 40-50 years.3 This disease is the seventh leading cause of death in the world and is responsible of 25.000 of all deaths per year. There are 20-40% cases of cirrhosis, due to any causes, increases the risk of primary liver cancer (hepatocellular carcinoma). Primary refers to the fact that thetumor originates in the liver.4In 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 the 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 calledportal hypertension.5Because 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 blood that by passes 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 manifestations of cirrhosis. This condition refers that the hepatic cirrhosis has fallen into the decompensated phase. And it can lead to increase the morbidity and mortality rate in patient with hepatic cirrhosis.6With this kind of data, we can conclude that hepatic cirrhosis is a disease that needs a special attention, because, this disease is a chronic progressive that may increase morbidity and mortality if we dont act in a professional manner. Appropriate theraphy can be done if the medical practitioner is familiar with the risk factors, etiology, pathogenesis, clinical signs and symptoms of hepatic cirrhosis. Therefore, we take this case as a case presentation with our expectations is as a medical practitioner, we can identify this disease and able to make a clinical diagnosis so this case can be managed appropriately. We hope it will help to reduce the incidence of morbidity and mortality caused by hepatic cirrhosis.CASE ILLUSTRATIONA man, 57 years of age, who lived in Alang-alang Lebar (Palembang, Sumatera Selatan), was admitted to Moh. Hoesin General Hospital on May 29th, 2015 with a chief complaint of abdominal enlargement. The patient suffered from abdominal enlargement and shortness of breath two weeks prior to admission. Shortness of breath was particularly felt on activities. There was no complaint of cough, fever, and abnormality in urination. Patient did not take any medications. There was no chest pain and difficulty in sleeping. Two days prior to admission patient realized that his abdomen is getting even bigger and there were swelling on both legs, void frequencies and volume lesser than usual. Patient went to Moh. Hoesin General Hospital.

The patients was fully conscious, his general condition was good, body weight 48 kg, and 165 cm body height, blood pressure 110/70 mmHg, with a 72x/minute regular pulse rate, 20x/minute regular respiration rate and 36,3OC body temperature.

Physical examination of the skin, head, nose and ear showed no abnormalities and physical examination of the eya showed pale of conjunctiva palpebrae and icteric sclerae. Jugular venous pressure was (5-2) cmH2O and lymph nodes was not enlarge and unpalpapble. The chest was symmetric with normal shape presenting spider naevi, ictus cordis was neither seen nor palpable, heart boundary was normal with the upper boundary on second ICS parasternal line, right boundary was on right sternalis line, and left boundary was on fifth ICS midclavicular line. On auscultation, neither murmur nor gallop were heard. Pulmonary physical examination was generally normal. Inspection of abdominal region shows a distended and enlarged abdomen. Liver and lien are not palpable with a positive shifting dullness and normal bowel sound on auscultation. On the upper extremities of the patient showed palmar erythema and lower extremities showed pretibial edema.Laboratory findings demonstrated that his haemoglobin was 10,3 g/dL, RBC 2,85 106/mm3, Ht 29%, thrombocyte 113.103/l, the WBC differential count 0/17/41/22/20, AST 154 U/L, ALT 112 U/L, Ureum 110 mg/dL, creatinine 2,42 mg/dL, calcium 8 mg/dL and sodium 135 mg/dL. Prothrombin time 18,6 s, INR 1,58, APTT 46,1 s. Total protein was 5,9 g/dL with albumin of 1,8 g/dL and globulin 4,1 g/dL. HBsAg was reactive and Anti HCV was negative. Urinalysis demonstrated no abnormalitites and Benzidine test on the patients faeces showed no abnormalities.Second laboratory examination was done and the result showed Hb was 6.8 g/dL, RBC 1,87.106/mm3, WBC 4000mm3 Ht was 19% with thrombocytes were 61000l. The differential count was 0/14/42/28/16. Abdominal USG showed a smaller liver size, inhomogen parenchyma with irregular surfaces and blunt edges. No abnormalities were showed for gall bladder, lien, kidney and pancreas.

Differential diagnoses of this patient were decopempensated hepatic cirrhosis with chronic kidney diseases with chronic disease anemia and decopempensated hepatic cirrhosis with hepatorenal syndrome and chronic disease anemia. Based on all the data above the working diagnosis of this patient was decopempensated hepatic cirrhosis with hepatorenal syndrome and chronic disease anemia.The patient and his family were educated and informed about his illness and therapy. The patient was given hepatic diet category III and fluid balances are maintained. Pharmacological therapy for this patient were spironolactone 100 mg tablet 3 times a day, furosemide 40 mg tablet once a day, and propranolol 10 mg tablet twice a day. For the anemia, we plan to treat the patient with vitamin B1, B6, and B12 twice a day, and folic acid three times each day. The hipoalbuminemia was corrected by intravenous albumin. The patient showed a bad functional prognosis but a good vital prognosis.Further examinations, such as endoscopy and liver biopsy, are needed to accurately predict the prognosis and outcome of the therapy.DISCUSSIONAscites is the accumulation of fluid in the abdominal cavity. Fluids occur due to various underlying chronic diseases. The most common chronic diseases causing ascites are congestive heart failure, nephrotic syndrome, peritonitis tuberculosis and metastases of cancer to the abdominal cavity. In this case,there is no history of swelling of entire body and swelling of the palpebrae. No anasarca edema was found in the physical examination. Therefore we can rule out nephrotic as the underlying diseases of ascites. This patient meet neither major nor minor criteria of Frangmingham, so we ruled out congestive heart failure as the underlying disease. Results from the patients history, physical examination and laboratory findings is showing decompensated hepatic cirrhosis. Addition of Soebandiri criteria for the diagnosis of liver cirrhosis is spider nevi, collateral vein, ascites, splenomegaly, albumin-globulin ratio is reversed, palmar erythema, hematemesis melena. In these patients it is obtained collateral vein, ascites, albumin globulin ratio is reversed, and spider nevi. 3,4Cirrhosis is caused by scar tissue that forms in your liver in response to damage occurring over many years. Each time your liver is injured, it tries to repair itself. In the process, scar tissue forms. As the scar tissue builds up, liver function worsens. In advanced cirrhosis, the liver no longer works very well. It's important to determine the cause of cirrhosis because treating that underlying cause can help prevent further liver damage. A wide range of diseases and conditions can damage the liver and lead to cirrhosis. Some of the causes of cirrhosis are inherited or thought to be inherited, such as iron buildup in the body (hemochromatosis), cystic fibrosis and copper accumulated in the liver (Wilson's disease). Others occur later in life: chronic alcohol abuse, hepatitis C, hepatitis B, fat accumulating in the liver (nonalcoholic fatty liver disease), destruction of the bile ducts (primary biliary cirrhosis and infection by a parasite common in developing countries (schistosomiasis). Some people may have more than one cause for cirrhosis, such as alcohol abuse and viral hepatitis.In this patient, we did not get the risk factors that may be suspected as a cause of liver cirrhosis. He did not consume alcohol and never had a history of jaundice which we suspect to be hepatitis. The result of HBsAg obtained is reactive, but never complain of fever and yellow body. This patient does not have a particular genetic disease. Thus, we conclude that the risk factors of liver cirrhosis is Hepatitis B as the result of HBsAg in the laboratory examination was reactive. The pathological hallmark of cirrhosis is the development of scar tissue that replaces normalparenchyma. This scar tissue blocks the portal flow of blood through the organ therefore disturbing normal function. Recent research shows the pivotal role of thestellate cell, a cell type that normally storesvitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma (due to inflammation) leads to activation of the stellate cell, which increases fibrosis (calledmyofibroblast) and obstructs blood flow in the circulation. In addition, it secretesTGF-1, which leads to a fibrotic response and proliferation ofconnective tissue. Furthermore, it secretesTIMP1 and 2, naturally occurring inhibitors ofmatrix metalloproteinases, which prevents them from breaking down fibrotic material in the extracellularmatrix. The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout.4The clinical manifestasion of cirrhosis such as ascites is about portal hypertension arising at the junction of the superior mesenteric vein. With the splenic pain, the hepatic portal vein carries the major venous drainage from the gastroinstenial tract, pancreas and spleen to the liver. It delivers two thirds of hepatic blood flow but account for less than half of the total oxygen supply. Portal hypertension is defined by eiher an absolute increase in portal venous pressure gradient between the portal vein and the hepatic vein of 5 mmHg or more. Portal hypertension in cirrohis hepatic occurs as intrahepatic portal hypertension. Even before fibrosis distorts sinusoidal architecture, active contraction of vascular smooth muscle and stellate cells intiates the resistance to the flow of blood into the liver from the portal vein. As fibrosis develops, sinusoids become increasingly disordered. Regenerative nodules in the cirrhotic liver impinge on the hepatic veins, thereby obstructing blood flow distal to the lobules. The small portal veins and venules are trapped, narrowed and often obliterated by scarring of the portal tracts. In this way, portal hypertension due to obstruction of blood flow distal to the sinusoid is augmented by increased arterial blood flow.2,4The laboratory findings show slight hyperchromic macrocytic anemia possibly due to chronic disease or low intake. Bleeding in this patient could be a reason for the anemia and the most common cause of bleeding in patients with cirrhosis is rupture of esophageal varicess. Therefore endoscopy is needed to confirm eosophageal varicess bleeding. Thrombocytopenia, hypoalbunemia, inverted ratio of albumin-globuline showed a malfunctioning liver as thrombocytes and albumin are produced in liver, and globulin are destroyed in liver. Hyperuricemia and increase of ureum and creatinine level are caused by low renal blood flow due to portal hypertension, this condition of liver diseases affecting the kidney is called hepatorenal syndrome.Another abnormal finding from the laboratory examination is eosinophilia. First laboratory differential count result upon admission was 0/17/41/22/20, another blood examination was done a week later and the result was 0/14/42/28/16 showing eosinohilia in 2 examination. Eosinophilia is a condition when the peripheral blood eosinophil count is greater than 350 per mm3. There are some possibilities that may cause this condition. For patients with cirrhosis, drug-induced eosinophilia might occur. Spironolactone is one of the drugs that is associated with eosinophilia. However, in this case the laboratory finding has shown an increase in eosinophil since admission, meaning that spironolactone has not been administered. Primary Biliary Cirrhosis (PBC) should be considered in the differential diagnosis of eosinophilia with an otherwise unknown origin. At the present time, the exact cause of PBC is unknown. PBC results from an abnormal reaction of the body's immune system possibly initiated by an infection. The immune system of PBC patients attacks the liver causing slow, progressive damage to the bile ducts.When the bile ducts are damaged, bile and other substances can not be eliminated and accumulate in the liver. The retained toxic substances and inflammation cause further damage.This eventually results in scarring of the liver (cirrhosis). Diagnosis is made with special blood tests including liver bichemistry. One such test detects the presence of Antimitochondrial Antibodies (AMA) in blood. Also,a liver biopsy may be performed. This is a procedure in which a small needle is inserted into the liver to take a sample of the tissue for analysis.Therapy in patients with cirrhosis of the liver consists of non-pharmacological and pharmacological therapy. Nonpharmacological therapy is education which means that medical staff should explain the hepatic cirrhosis disease to the patients, especially regarding its treatment process and prognosis. In addition, other non-pharmacological therapy is fluid balance and liver diet III.Liver damages from cirrhosis are irreversible and pharmacological therapy in patients with liver cirrhosis aims to prevent further damage of the liver. Diuretics in this case are used to reduce ascites that occurs in this patient. Spironolactone which is a potassium-sparring diuretic competitively inhibits aldosterone-induced sodium ion reabsorption and secretion of potassium ions in the distal renal tubular so it will reduce Na+ reabsorption. These drugs also bind to aldosterone receptors and may also reduce the formation of the active metabolite of aldosterone in the cell. These drugs can cause fluid in the interstitial cavity to be absorbed back into the intravascular. It can be combined with furosemide to further reduce ascites and leg edema. Propranolol was given in this case to reduce portal hypertension in liver cirrhosis. Human albumin infusion is also given to treat the hypoalbuminemia in patients with cirrhosis.8The prognosis of patients with liver cirrhosis depends on two things: the severity and the complications of cirrhosis. Prognostic score on cirrhosis is useful to estimate the likelihood of death in the specified time period, illustrates the quantitative estimation of residual liver function and able to survive with surgery or other aggressive interventional therapy. Cirrhosis prognosis varies, influenced by a number of factors including the etiology, severity of liver damage, complications and other accompanying diseases. Scoring prognosis in patients with hepatic cirrhosis using Child Pugh classification. There are five important variables in Child Pugh criteria. They are serum levels of bilirubin, albumin serum, ascites, prothrombin time, and presence or absence of encephalopathy. Furthermore, these criteria are divided into three groups: A, B and C.9,10Parameter123

Serum Bilirubin3

Serum Albumin>3,52,8-3,56>2,3

EnsefalopatiAbsentGrade I-IIGrade III-IV

Tabel 1. Child Score ParameterPointsClass1-Year-Survival-Rate2-Year-Survival-Rate

5-6A100%85%

7-9B81%57%

10-15C45%35%

Tabel 2. Child Score Interpretation

This patients Child Score is 8. Thus, the probability of this patient to survive for 1 year is 81%.CONCLUSIONWe have discussed a case of decompensated hepatic cirrhosis with anemia in a 57 year old male patient who also had asymptomatic Hepatitis B presented with ascites, anemia, and hipoalbuminemia.REFERENCES1. Wolf, David. 2014. Cirrhosis. eMedicineMedscape Reference.

2. Schuppan, D., Afdhal, N.H. 2008. Liver Cirrhosis. US National Library of Medicine National Institue of Health. 371 (9615):838-851.

3. Sutadi, S.M. 2003. Sirosis Hepatis. USU Digital Library.4. Gunter, J.A. 2014. Cirrhosis. eMedicine Health.

5. Lee, Dennis. 2014. Cirrhosis of The Liver. Medicine Net.

6. Amico, Gennaro. 2014. Natural History and Stages of Cirrhosis. Springer Science Media New York. Hal 23-30.7. DeLegge, MH. 2010. Nutrition in Gastrointestinal Diseases. In: Feldman M, Friedman LS, Brandt LJ, eds.Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 9th ed. Philadelphia, Pa: Saunders Elsevier. Hal 317-320.8. Katzung, B.G. 2010. Farmakologi Dasar dan Klinik (edisi 10). Jakarta: ECG. Hal 107-113.9. Nurdjanah, Siti. 2006. Sirosis Hati. In: Sudoyo, AW., B. Setiyohadi, I. Alwi, M. Simadibrata, S. Setiati (Editor). Buku Ajar Ilmu Penyakit Dalam Jilid I. Edisi V. Pusat Penerbitan Ilmu Penyakit Dalam FK UI, Jakarta, Indonesia. Hal 668-673.10. Cholongitas, E; Papatheodoridis, GV; Vangeli, M; Terreni, N; Patch, D; Burroughs, AK (Dec 2005)."Systematic review: The model for end-stage liver disease--should it replace Child-Pugh's classification for assessing prognosis in cirrhosis".Alimentary pharmacology & therapeutics22(11-12): 1079892