Case Report

A 51 Years Old Female Came to The Hospital with Chief Complaint The Enlargement of Abdominal Bulging became Worse since One Day before Admission.

By : Much. Apriyanto, S.Ked (04061001008) Khori Pretika, S.Ked (04061001111)

Advisor : Prof. Dr. H. Eddy Mart Salim, SpPD, K-AI, FINASIM

Internal Medicine Department Medical Faculty of Sriwijaya University

2010
1

CHAPTER I INTRODUCTION

Tuberculosis (TB) is still become one of the leading health problem in the world. Based in the data in 1955, Approximately there 9 million people infected Tuberculosis and 3 million of those case are end with death. Beside that the cause of death among women with Tb are greater than the death with delivery. It is expected that the number of people affected by cirrhosis will continue to increase in the near future. Beause of that, since 1993 WHO announce TB as a global emergency Indonesia still in the 3rd rank for the number of TB patient and it is 10% from all TB patient all over the world. it is expected that start from 2004 there will be 539.000 new case of TB appear in every years with the number of death for about 101.000 people. Tuberculosis is refer to a contagious disease that caused by Mycobacterium Tuberculosis bacteria, it oftenly effect lungs, but in come case there are also infection outside the lungs. Tuberculosis is a chronic disease that can increase morbidity and mortality if not managed professionally. Accurate diagnosis and appropriate treatment are needed for physician to the treatment of Tuberculosis. Therefore we raised the Tuberculosis for our case to understand about this disease, so that it can help improve the quality of life of patients with liver Tuberculosis.

CHAPTER II CASE REPORT

II.1 IDENTIFICATION

Name Age Sex Address Status Occupation Religion

: Mrs. MN : 66 years old : Female : ogan ilir : Married : Mother Household : Muslim

Hospitalized : September, 14th 2010 (15.00 p.m) Med Rec No :

II.2 ANAMNESIS Chief complaint : Cough that became worse since one day before admission. History of illness : Since 3 month before admission, Mrs.Mn started to get cough, in every cough there was a half of pleghm that colorless and with no blood streak. There was complaint neither shortness of breath nor chest pain. She also felt fever, with no shaking and sweating in night time. There were no nausea and vomit. Since her sickness, Mrs. Mn felt that se oftened lost her appetite but still no body weight loss. The defecation and urination just like usual. Since 1 week before admission, Mrs.Mn started to get cough, in every cough there was a half of pleghm that colorless and with no blood streak. Sometimes there were shortness of breath while the weather is too hot. Mrs. Mn went to the midwife, then she got 3 kinds of drugs, an expectorant, vitamin and one another drug that she didnt recognize. After eat drugs the symptom didnt relieve at all. About one day before admission in RSMH, Mrs.Mn felt her cough became worse, the frequency and the amount of pleghm are increased. Beside that the
3

colour of pleghm has turned yellow. There are still no shortness of breath, chest pain, nausea and vomit. Her body weigh has decreased. Then, she came again to the midwife, and got suggestion to go to RSMH. History of previous illness :

No history of taking drugs for 6 months or taking drugs that make her urine turn red. There is a history of living among people that oftenly get cough for a long period. No history of hypertension. No history of diabetes.

Familiy history : There is no family member that has the same symptom like her. History of Habitual. She never smoke

II.3 PHISYCAL EXAMINATION (September,14th 2010) General Condition

Sickness condition : moderately sick Consciousness Blood Pressure Pulse rate Temperature Weight Height : compos mentis : 100/60 mmHg : 88 times/minute times/minute

Respiration rate : 28 : 36,80 C : 25 kg : 150 cm

Specific Condition

Skin The color of the skin is black-brown, cyanosis (-), pale on palm of hands (+), pale on sole of feet (-), normal hair growth, skin turgor (+) and dry skin (+)

Lymph nodes There are no enlargment of the lymph nodes on submandibular, neck, axilaries, and inguinal.

Head Oval, symmetrical, alopecia (-), puffy face (-), deformity (-), malar rash (-). Eyes Exopthalmus (-), endopthalmus (-), edematous of superior palpebrae (-), pale of conjungtiva palpebrae (-/-), icteric sclera (-/-), pupils were isokor, Good light response on both of eyes, symmetrical eyes movements.

Nose Normal outside appearance, no epitaksis, no obstruction. Ear decreasing hearing ability (-). Mouth Enlagrement of tonsils (-), no papils atrophy, stomatitis (-), rhagaden (-), specific breaths smell (-).

Neck Jugular venous pressure (5-2) cmH2O, lymph nodes enlargment (-), thyroid gland enlargement (-), hypertrophy sternocleidomastoideus (-), stiffness (-).

Thorax : Normal shape, spider naevi (-), pressure pain (-), crepitation (-) Cor Inspection Palpation Percussion : Ictus cordis was not seen. : Ictus cordis was not palpable. : Upper heart margin at 2nd intercostal space, right margin at linea parasternalis, left margin at LMC sinistra. Auscultation : HR 88x/menit, murmur (-), gallop (-)

Pulmo Anterior Inspection : Static: both hemithoraxs were symmetric.

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dynamic: same movement, no retraction. Palpation Percussion : Stem fremitus in both hemithoraxs were equal deceased. : Sonorous in both of lungs, border of pulmo-liver at ICS V. and medial areas of lungs, wheezing (-). Pulmo Posterior : Inspection Palpation : Static: both hemithoraxs were symmetric. dynamic: same movement, no retraction. : Stemfremitus in both hemithoraxs were equal decreased Percussion : Sonorous in both of lungs,. Auscultation : Vesicular (+) normal in both of lungs, middle wet ronchi (+) at apical and medial areas of lungs wheezing (-).

Auscultation : Vesicular (+) normal in both of lungs, middle wet ronchi (+) at apical

Abdomen Inspection Palpation Percussion : flat. : supple, pressure pain(-), liver and spleen didnt palpable. : Percussion pain (-), shifting dullness (-), undulation (-)

Auscultation : Normal bowel sound

Genital

: Had not been examined

Extremities :

Upper extremity Paint on joint (-), pale on finger (-), erythema of palm (-), pitting edema (-/-). Lower extremity Pain on joint (-), varices (-), pale on sole of foot (-), pretibial edema (-/-)

II.4. SUPPORTIVE EXAMINATION Laboratory Finding

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Hb Leukosit Trombosit LED Ht DC GDS SGOT SGPT Protein total Albumin Globulin Ureum Kreatinin Kolesterol

Result : 11,1 g/dl : 13.000 : 270.000 : 62 : 37% :0/0/1/84/8/7 : 180 mg/dl : 39 : 16 : 6,3 : 2,1 : 4,2 : 58 : 1,0 : 120

Normal value P = 12 14 g/dl 5000 10000/uI 150.000 400.000/uI < 20 mm/jam 33 43% 0-1/1-3/2-6/50-70/20-40/2-8 < 200 mg/dl < 40 U/I < 41 U/I 6,0 7,8 g/dl 3,8 5,1g/dl 1,5 3 g/dl 15 39 mg/dl 0,9 1,3 mg/dl < 200 mg/dl > 65 mg/dl < 130 mg/dl < 150 mg/dl 135 155 mmol/l 3,5 5,5 mmol/l

HDL Kolesterol : 58 LDL Kolesterol : 49 Trygliserida Natrium Kalium Rontgen Thorax PA

-

: 67 : 131 : 4,7

infiltrat pada upper and middle area of lungs ( lung tuberculosis with large lesion)

Electrocardiography Sinus rhytm, Right Axis, HR: 90x/m, P peak wave, PR interval 0,12 sc, komplex QRS 0,06 sc, R/S V1> 1, SV1 + RV5V6 < 35 mm, T inverted at II, III, aVF, V1, V6. assasment : RVH + P. pulmonal+ iskemik ekstensive anterior

BTA Examination ( September, 20th 2010 ) BTA I : Negatif BTA II : Negatif

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BTA III : Negatif II.4 RESUME A 66 years old women admitted to hospital on September 14th, 2010 with chief complaint worse since one day before admission since one day before admission. 3 month before admission, Mrs.Mn started to get cough, in every cough there was a half of pleghm that colorless and with no blood streak. There was complaint neither shortness of breath nor chest pain. She also felt fever, with no shaking and sweating in night time. There were no nausea and vomit. Since her sickness, Mrs. Mn felt that se oftened lost her appetite but still no body weight loss. The defecation and urination just like usual. one week before admission, Mrs.Mn started to get cough, in every cough there was a half of pleghm that colorless and with no blood streak. Sometimes there were shortness of breath while the weather is too hot. Mrs. Mn went to the midwife, then she got 3 kinds of drugs, an expectorant, vitamin and one another drug that she didnt recognize. After eat drugs the symptom didnt relieve at all. one day before admission in RSMH, Mrs.Mn felt her cough became worse, the frequency and the amount of pleghm are increased. Beside that the colour of pleghm has turned yellow. There are still no shortness of breath, chest pain, nausea and vomit. Her body weigh has decreased. Then, she came again to the midwife, and got suggestion to go to RSMH. From physical examination we found: There are a d decreased of skin turgor and dry skin. Palpation Stem fremitus in both hemithoraxs were equal deceased. Auscultation Vesicular normal in both of lungs, middle wet ronchi at apical and medial areas of lungs. From laboratorium examination we found : Hb 11,1 g/dl, Leukosit 13.000/uI, DC (0/0/1/84/8/7), LED 62 mm/Hours, Albumin 2,1 gram/dl, Natrium 131mmol/l, Ureum 58 mg/dl. Rontgen photo shows infiltration on upper and middle area of lungs ( lung tuberculosis with large lesion). Electrocardiograph shows RVH , P. pulmonal wave and ischemic extensive anterior .From BTA Examination we got BTA I, II, and III are all in Negatif value. II.6 WORKING DIAGNOSIS New case findings of tuberculosa with negative BTA and Positive radiologist and malnutrition.
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II.7 DIFFERENTIAL DIAGNOSIS Upper respiratory tract infection with malnutrition. II.8 TREATMENT Non-pharmacology: Bed rest Diet high calories and protein Pharmacology:
IVFD RL : D5% = 2:1 gtt xx/m (micro)

Ceftriaxone Ambroxol 3x1 CI Albumin 500 cc/hari Vitamin B1, B6, B12
Planning for OAT

INH 1 x 150 mg Rifampisin 1 x 450 mg Pirazinamid 1 x 1000 mg Ethambutol 1 x 500 mg

II.9 PLANNING EXAMINATION

Lab examination / 24 hours to monitor improvement of Natrium, Kalium, Albumin.

Electrocardiography Lung function test Alergic test

BTA I, II, III

II.9 PROGNOSIS
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Quo ad vitam Quo ad functionam

: dubia ad bonam : dubia ad bonam

FOLLOW UP September , 28th 2010 S Abdominal pain General condition Conciousness : compos mentis

Blood preassure : 90/70 mmHg Pulse rate : 70x/minute Respiration rate : 22x/minute Temperature : 36,2C Body weight : 25 kg

Spesific condition Pale of conjunctiva palpebra (-/-), icteric sclera (-/-), Jugular venous pressure (5-2) cmH2O Thorax : Cor: HR 78 x/menit, murmur (-), gallop (-) Pulmo: Stem fremitus in both hemithoraxs were equal deceased Vesicular (+) normal in both of lungs, middle wet ronchi (+) at apical area of lungs, wheezing (-). Abdomen Inspection Palpation

: flat, : supple, borderline of pulmo-liver at ICS V, pressure pain (-), liver and spleen didnt palpable Percussion : shifting dulness (-) Auscultation : normal bowel sound Extremities : pretibial edema -/New case findings of tuberculosa with negative BTA and Positive radiologist and malnutrition.
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IVFD RL : D5% = 2:1 gtt xx/m (micro) Ceftriaxone Ambroxol 3x1 CI Albumin 500 cc/day Vitamin B1, B6, B12 Planning for OAT INH 1 x 150 mg Rifampisin 1 x 450 mg Pirazinamid 1 x 1000 mg Ethambutol 1 x 500 mg

September 29th 2010 S (-) General condition Conciousness : compos mentis

Blood preassure : 100/70 mmHg Pulse rate : 75x/minute Respiration rate : 22x/minute Temperature : 36,3C Body weight : 25 kg

Spesific condition Pale of conjunctiva palpebra (-/-), icteric sclera (-/-), Jugular venous pressure (5-2) cmH2O Thorax : Cor: HR 75 x/menit, murmur (-), gallop (-) Pulmo: Stem fremitus in both hemithoraxs were equal deceased Vesicular (+) normal in both of lungs, middle wet ronchi (+) at apical areas of lungs, wheezing (-). Abdomen Inspection : flat, Palpation : supple, borderline of pulmo-liver at ICS V, pressure pain (-), liver and spleen didnt palpable Percussion : shifting dulness (-) Auscultation : normal bowel sound Extremities : pretibial edema -/New case findings of tuberculosa with negative BTA and Positive radiologist and malnutrition.
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IVFD RL : D5% = 2:1 gtt xx/m (micro) Ceftriaxone Ambroxol 3x1 CI Albumin 500 cc/day Vitamin B1, B6, B12 Planning for OAT INH 1 x 150 mg Rifampisin 1 x 450 mg Pirazinamid 1 x 1000 mg Ethambutol 1 x 500 mg

CHAPTER III CASE ANALYSIS

Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. The progression of liver injury to cirrhosis may occur over weeks to years.1 Many forms of liver injury are marked by fibrosis. Fibrosis is defined as an excess deposition of the components of extracellular matrix (ie, collagens, glycoproteins, proteoglycans) within the liver. This response to liver injury potentially is reversible. In contrast, in most patients, cirrhosis is not a reversible process.2 III.1 Epidemiology2 Hepatic cirrhosis more often found within male to female with ratio 2,1 : 1, average 44 years old. highest incidence are from 13 88 years old with peak 40 55 years old. This patient is 51 years old. It means that her age is included in the higest incidence of hepatic chirrosis.

III.2 Hepatic Cirrhosis Classifications3 Based on the morphology of dividing Sherlock Cirrhosis of three types, namely:
1. Mikronodular 2. Makronodular 12

3. Mixture (which shows the picture of the micro-and makronodular)

In Functional Cirrhosis divided as follows:

1. Hepatic cirrhosis compensated

Often

referred

to

as

Latent

liver

cirrhosis.

In

this

stage

visible symptoms are not real. This stage is usually found at the time screening examination.
2. Hepatic cirrhosis Decompensated

Cirrhosis of the liver known as Active, and this stage usually have symptoms clear, for example, ascites, edema and jaundice. Status classification of cirrhosis based on Baveno IV :4 Stage 1 : no varices, no ascites Stage 2 : varices, no ascites Stage 3 : ascites with or without varices Stage 4 : bleeding with or without ascites In this case, the patients is diagnosed with hepatic cirrhosis decompensate since the patient shows spider neavi, ascites, collateral vein, edema and jaundice. Based on cirrhosis classification of Baveno IV, she is included in stage 3. III.3 Etiology5 Causes of Cirrhosis Hepatic 1. Infectious Diseases a. Capillariasis b. Brucellosis c. Echinococcosis d. Schistosomiasis e. Toxoplasmosis f. Viral hepatitis hepatitis B, C, D g. cytomegalovirus; Epstein-Barr virus
2. Inherited and Metabolic Disorders

a. Antitrypsin deficiency b. Alagilles syndrome

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c. Biliary atresia d. Familial intrahepatic cholestasis(FIC) e. Fanconis syndrome f. Galactosemia g. Gauchers disease h. Glycogen storage disease i. Hemochromatosis j. Hereditary fructose intolerance k. Hereditary tyrosinemia l. Wilsons disease 3. Drugs and Toxins a. Alcohol b. Amioradone c. Arsenicals d. Oral contraceptives e. Pyrrolidizine alkaloids and antineoplastic agents 4. Other Causes a. Biliary obstruction (chronic) b. Cystic fibrosis c. Graft-versus-host disease d. Jejunoileal bypass e. Nonalcoholic fatty liver disease f. Primary biliary cirrhosis g. Primary sclerosing cholangitis h. Sarcoidosis 5. Unknown Aetiology The Etiology of hepatic cirrhosis in this patient is viral hepatitis B because the result of HbsAg serologic test is positive and HCV is negative. Besides, from the anamnesis we have known that the patient was suffered jaundice 5 years ago and was hospitalized in RSMH, and her mother also ever got hematemesis and yellowish eyes. From her statement we have thought that its possible
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the patient ever got hepatitis. We can think that the viral maybe was transmitted from her mother because her mother had ever shown the symtomps that lead to hepatitis, too. Her deniel about consuming alcohol at least can eliminate the etiology of alcohol.

III.4 Signs and Symptoms6 The signs and symptoms of liver cirrhosis may be absent or non-specific at early stages. Early non-specific symptoms include fatigue and itching. As scar tissue replaces healthy tissue and liver function worsens, a variety of liver-related symptoms may develop. Actually, the patient with hepatic chirrosis came to physician with complain of fatigue, itching, edema/ascites, digestive tract bleeding,and jaundice. III.5 Physical Examination7 Physical examination findings depend on the stage of the disease. In the early stages, examination findings are normal. Physical examination specific for hepatic cirrosis are :

Hepatomegaly Hyperpigmentation Splenomegaly Jaundice spider naevi, palmar erythema, ascites, and peripheral edema This patient came to hospital with complaint of the enlargement of abdominal

bulging, jaundice, fatigue. From physical examination, we can found spider naevi, ascites, collateral vein, icteric and pripheral edema. Spleen and hepar is difficult to examined due to massif ascites. All of the signs and symptoms can lead to diagnosis of cirrhosis hepatic. The formation of ascites in cirrhosis depends on the presence of unfavorable starling forces within the hepatic sinusoid. The increased sinusoidal pressure that develops in portal hypertension increases the amount of fluid entering the space of Disse. When the increased hepatic lymph production observed in portal hypertension exceeds the ability of
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the cisterna chyli and thoracic duct to clear the lymph, fluid crosses into the liver interstitium. Fluid may then extravasate across the liver capsule into the peritoneal cavity. 1 Therefore, we thought that this patient has had portal hypertension that was showed by presence of ascites and collateral vein. The absence of melena or hematemesis, means that there was no bleeding of gastroesophageal varices yet in this patient. But, we should considered it in the therapy in order to prevent the bleeding.

III.6 Laboratory Findings Laboratory Findings Hepatic Cirrhosis is marked by laboratory findings abnormalities such as: 8

Elevation of SGOT and SGPT. If SGPT is normal, it doesnt mean the diagnosis of cirrhosis hepatic is eliminated. In viral hepatitis, the serum SGOT is usually disproportionately elevated relative to SGPT, i.e , SGOT/SGPT ratio > 2. 5

Elevation of Alkaline phosphates. Elevation of Bilirubin. Elevation of globulin, reduction of albumin. Elongated PT. Reduction of Sodium. Hematology abnormalities such as anemia, trombositopenia and leukopenia.

Laboratory findings show anemia (Hb: 5,2 g/dl, Hct : 18%, eritrosit: 2.140.000/mm3), trombositopenia (trombosit : 158.000 mm), elevated of total bilirubin, direct bilirubin and indirect bilirubin, elevated SGOT (85u/l), normal SGPT (25u/l), hypoalbuminemia, due to decrease function the liver. This laboratory finding can strenghtened the diagnosis of cirrhosis hepatic. Anemia in this patient was normochromic normocitic, it was showed by normal MCV and decreased or normal MCHC.9 Based on the criteria, we diagnosed the patient with anemia chronic disease. It means that the anemia was appeared since the chronic disease that she had, in this case is cirrhosis hepatic.
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The elevated of SGOT because of decrease function the liver, aventhough SGPT was still normal. The ratio of SGOT/SGPT >2 is occured in viral hepatitis. 5 In this case, the ratio SGOT/SGPT is 3,4. ( 85u/l / 25u/l = 3,4). So, it can strenghtened that the etiology cirrhosis in this patient is from viral hepatitis. The elevated of total bilirubin, direct bilirubin and indirect bilirubin was also caused of decrease function the liver. The elevated of bilirubin has caused the urobilinogen in urine increased, so that the patient had tea color urine. The inverse of ratio albumin/globulin was also happened in this patient. It was showed by decreased of albumin and elevated of globulin. The decreased of albumin because of decrease function the liver has made hypoalbuminemia in this patient. At last, the hypoalbuminemia has caused the ascites became increased and edema pretibial was appeared. The benzidine test has been also done, and the result is negative. It means that both melena microscopic and macroscopic is not occured in this patient. The ureum and creatinin were also elevated in this patient. Based on assessment of Creatinin Clearence : (140-age) body weight x 0,85 72 x creatinin serum = (140-51) 55 x 0,85 = 36, 18 ml/minute 72 x 1,6 The CCT in this patient is 36,18 ml/minute. Its included early renal insufficiency (GFR or CCT : 30-59 ml/minute), according to the K/DOQI CKD classification. 10

III.7 Diagnosis Current diagnosis is hepatic cirrhosis decompensate that was built from anamnesis, physical findings, laboratory findings and supporting examination (abdominal USG, endoscopy,and liver biopsy). 5 This patient abdominal USG gave result: small size, uneven surface, parenchymal rude, blunt edge, ascites (+), no spleenomegali. It can can strenghtened the diagnosis of cirrhosis hepatic. Endoscope examination hasnt been done, but it is needed to found
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esophageal varices. Cirrhosis is best determined by examining a sample of liver tissue under the microscope, a procedure which is called a liver biopsy. Liver biopsy is the gold standard to diagnose hepatic cirrhosis and differentiate the stadium. The diagnosis is precise when examination shows fibrosis and regeneration nodul inside hepatic cells. Therefore liver biopsy examination is also planned for this patient.
5

III. 8 Treatments Non-pharmacology: 11

1.

Bed rest It is shown to inhibit the neurohomural system (RAAS and SNS) activated chronically in upright position in cirrhotic patients that impairs renal blood perfusion and causes sodium retention. Bed rest reduces the plasma aldosterone level and improves the response to diuretic therapy in cirrhotic patients. However, bed rest is not recommended routinely as it is often unpractical and could cause decubitus ulcers and muscle atrophy in malnourished cirrhotic patients.

2.
3.

Restrict dietary with balance nutrition: enough calories, protein 1gr/kgBB/day and vitamin. A balanced diet promotes regeneration of healthy liver cells. Eating five or six small meals throughout the day should prevent the sick or bloated feeling patients with cirrhosis often have after eating.

Pharmacology: 1. Diuretics Diuretics should be considered the second line of therapy. The diuretic of choice is spironolactone (50 to 200 mg per day). It blocks
1

the aldosterone receptor at the distal tubule.

It was began in initial dose , then

the dose can be increased gradually. After 4 days, if there is not improvement in maximal dose, it can be combined with another drug such as furosemide. 3 Furosemide (Lasix) may be used as a solo agent or in combination with spironolactone. The drug blocks sodium reuptake in the loop of Henle. Low doses of furosemide (20 to 40 mg per day) may be added during the first few days to increase natriuresis, especially when peripheral edema is present.
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Furosemide should be used with caution because of the risk of excessive diuresis, which may lead to renal failure of prerenal origin. The recommended weight loss to prevent renal failure of prerenal origin is 300 to 500 g per day in patients without peripheral edema and 800 to 1000 g per day in those with peripheral edema. Patients infrequently need potassium repletion when furosemide is dosed in combination with spironolactone. 1 In this case, we used spironolactone with initial dose 2 x 25mg. The dose has been increased gradually until 3 x 100 mg. The improvement of ascites and edema has been seen since 3 days after admission. It was proved by decrease of abdominal circumference and body weight. From physical examination at 8th August 2010, we found the abdominal circumference was 88 cm and body weight was 55kg. In follow up at 9th August 2010, the abdominal circumference was 88 cm and body weight became 54 kg. At 10th August 2010, abdominal circumference was 86 cm and body weight became 53 kg. Because of that, we maintened the dose in 3 x 100 mg without combination with another drug. To correct the hypoalbuminemia, we can use intravenous infusion of albumin at 25 g twice per day, in addition to ongoing therapy with spironolactone. 1 Another choice is albumin 20%, 35-70 drips/minute. 12 In this case, we used albumin 20% to treat the hypoalbuminemia. 2. Propanolol (Beta blockers) It may be prescribed to control cirrhosis-induced portal hypertension. Because the diseased liver can no longer efficiently neutralize harmful substances, medications must be given with caution. Interferon medicines may be used by patients with chronic hepatitis B and hepatitis C to prevent post-hepatic cirrhosis. 11 This patient has been given propanolol tab 2 x 10 mg in order to control the portal hypertension and prevent the bleeding as the complication of it. 3. Treatment of hyponatremia in cirrhosis Treatment of hyponatremia in patients with cirrhosis includes sodium and fluid restriction and continued treatments with spironolactone and loop diuretics. However, care must be taken when administering diuretics as they can exacerbate the reduction in tissue perfusion that occurs in cirrhosis, further impairing the ability
19

to excrete free water. Bolus infusions of 3% NaCl are reserved for patients with profound hyponatremia and severe symptoms. 13 Fluid intake should be restricted (to approximately 1000 ml per day) only in patients with dilutional hyponatremia, a condition characterized by a serum sodium concentration of less than 130 mmol per liter in the presence of ascites, edema, or both. Dilutional hyponatremia results from impaired renal excretion of free water due to inappropriately high concentrations of antidiuretic hormone. 13 In this patient, we used IVFD NaCl 3% gtt x/m (micro) to improve the hyponatremia. Then, to correct the hypokalemia we used KCl tab 3 x 600 mg. 12 Other drugs that we used to improve the sign and symptom in this patient are :
Curcuma tab 2 x 200 mg to improve anorexia in this patient. 12 Omeprazol tab 1 x 20 mg to cure the nausea and prevent vomit reflex, so the patient

could feel comfort and eat properly. 12

Vit B1 B6 B12 (Neurodex) 3x1 tab as the supplement to her anemia beside of blood

transfussion. III.9 Complications6 Since the liver performs many complex metabolic functions, there are many complications that arise from cirrhosis. In addition, some complications arise more commonly in certain diseases that cause cirrhosis (for example, osteoporosis occurs more commonly in patients with liver diseases that predominantly affect the bile ducts). Below is a list of some of the most common complications of liver disease. 1. 2. 3. 4. spontaneous bacterial peritonitis. Bleeding from esophageal or gastric (stomach) varices hepatic encephalopathy Liver Cancer (Hepatocellular Carcinoma. In this patient, we havent found complication like above. So, we try to make the best treatment in order to prevent the complications that can be occured in this patient.

III.10 Prognosis
20

Prognosis of patients with cirrhosis depending on the presence or absence of complications of cirrhosis. Patient with cirrhosis compensated have a longer life expectancy if they do not develop into cirrhosis decompensated. An estimated ten-year life expectancy of patients with cirrhosis compensated approximately 47%. Conversely patient with cirrhosis decompensated have life expectancy is only 16% within five years. these patients leads to a poor prognosis. severe derangement. 14
Measure Bilirubin (total) Serum albumin INR Ascites Hepatic encephalopathy 1 point <34 (<2) >3,5 <1.7 None None 2 points 34-50 (2-3) 2,8-3,5 1.71-2.20 Mild (can be controled easy) Grade I-II (or suppressed with medication) 3 points >50 (>3) <2,8 > 2.20 Severe Grade III-IV (or refractory) units mol/l (mg/dl) g/dl no unit no unit no unit
2

Based on Child-Pugh score, the score employs five

clinical measures of liver disease. Each measure is scored 1-3, with 3 indicating most

Different textbooks and publications use different measures. Some older reference works substitute PT prolongation for INR.

Interpretation Chronic liver disease is classified into Child-Pugh class A to C, employing the added score from above. 14 Points 5-6 7-9 10-15 Class A B C One year survival 100% 81% 45% Two year survival 85% 57% 35%

From the assessment has been done, the prognosis of this patient is included in 3 rd category. It means that one year survival for this patient is approximately 45 % and two year survival is 35%. It can be said dubia ad malam.

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REFERENCES
Wolf, David, Cirrhosis, New York Medical College. New York. USA. 2010. Available from www.emedicine .com Sulaiman, Ali. Akbar, Nurul. Lesmana L. Buku Ajar Ilmu Penyakit Hati. Jaya Abadi. Jakarta. 2007.
1. Maryani, Sri. Sirosis Hepatis. USU

Digital Library. Sumatra Utara 2003. Available from library.usu.ac.id/download/fk/penydalam-srimaryani5.pdf

2. DAmico G. Esophageal varices: from appearance to rupture; natural history and prognostic indicators. In: Groszmann RJ, Bosch J, editors. Portal hypertension in the 21st century. Dordrecht: Kluwer; 2004. p. 147154.
3. Kasper, Dennis, et al. Harrison Principle Of Internal Medicine Sixteenth

Edition.Mc. Graw-Hill. New York. USA 2005

4. Sanchez, William. Jayant, A. Talwalkar, Liver Cirrhosis. The American College of

Gastroenterology, Bethesda, Available from www.acg.gi.org

5. Pyrsopoulos, Nikolaos, Primary Biliary Cirrhosis: Differential Diagnoses &

Workup. University of Central Florida College of Medicine. USA 2010. Available from http://emedicine.medscape.com/article/171117.
6. Noer S. Sirosis Hati. Buku Ajar Ilmu Penyakit Dalam. Jilid I. Jakarta: Pusat

Penerbitan Departemen Ilmu Penyakit Dalam. Edisi IV FKUI. 2006; 445-48. 7. Baldy CM. Gangguan Sel Darah Merah. In : Price SA, Wilson LM, editors. Patofisiologi Konsep Klinis Proses Penyakit. Ed 6. Jakarta: EGC; 2003.hlm.256257. 8. Levey AS, Eckardt KU, Tsukamoto Y et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2005; 67: 2089100.
9. Pere Gines et al. Management of Cirrhosis and Ascites. The New England Journal

of Medicine. Masschusetts Medical Society. 2004; 350: 1646-54 10. Bromilow, David, dkk. MIMS Indonesia. Vol 2. Number 1. Medi Media International Group. 2000.
11. Lindsay A.

Profound hyponatremia in cirrhosis: a case report ,Case Western Reserve University, School of Medicine, 10900 Euclid Ave, Cleveland, OH 44106, USA Cases Journal 2010, 3:77

12. Child CG, Turcotte JG. Surgery and portal hypertension. In: The liver and portal hypertension. Edited by CG Child. Philadelphia: Saunders 1964:50-64.
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RATIFICATION

The case report with the title : A 51 Years Old Female Came to The Hospital with Chief Complaint The Enlargement of Abdominal Bulging became Worse since One Day before Admission.

By : Much. Apriyanto, S.Ked (04061001008) Khori Pretika, S.Ked (04061001111)

has been accepted as one of the requirements in following the registrar of senior clinic in Internal Medicine Department Medical Faculty of Sriwijaya University

Palembang, August 2010 Advisor :

Prof. Dr. H. Eddy Mart Salim, SpPD, K-AI

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CONTENTS

COVER.....................................................................................................................i RATIFICATION......................................................................................................ii CONTENTS............................................................................................................iii CHAPTER I INTRODUCTION..............................................................................1 CHAPTER II CASE REPORT................................................................................2 CHAPTER III CASE ANALYSIS.........................................................................12 REFERENCES.......................................................................................................22

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