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

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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.

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CHAPTER II

CASE REPORT

II.1 IDENTIFICATION

Name : Mrs. MN

Age : 66 years old

Sex : Female

Address : ogan ilir

Status : Married

Occupation : Mother Household

Religion : 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.

2

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

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 : compos mentis

Blood Pressure : 100/60 mmHg

Pulse rate : 88 times/minute

Respiration rate : 28 times/minute

Temperature : 36,80 C

Weight : 25 kg

Height : 150 cm

3

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 papil’s atrophy, stomatitis (-), rhagaden (-), specific

breath’s 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 : Ictus cordis was not seen.

Palpation : Ictus cordis was not palpable.

Percussion : 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

4

Inspection : Static: both hemithoraxs were symmetric.

dynamic: same movement, no retraction.

Palpation : Stem fremitus in both hemithoraxs were equal deceased.

Percussion : Sonorous in both of lungs, border of pulmo-liver at ICS V.

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

and medial areas of lungs, wheezing (-).

• Pulmo Posterior :

Inspection : Static: both hemithoraxs were symmetric.

dynamic: same movement, no retraction.

Palpation : 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 (-).

• Abdomen

Inspection : flat.

Palpation : supple, pressure pain(-), liver and spleen didn’t palpable.

Percussion : 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

5

Laboratory Finding

Result Normal value

Hb : 11,1 g/dl

Leukosit : 13.000

Trombosit : 270.000

LED : 62

Ht : 37%

DC :0/0/1/84/8/7

GDS : 180 mg/dl

SGOT : 39

SGPT : 16

Protein total : 6,3

Albumin : 2,1

Globulin : 4,2

Ureum : 58

Kreatinin : 1,0

Kolesterol : 120

HDL Kolesterol : 58

LDL Kolesterol : 49

Trygliserida : 67

Natrium : 131

Kalium : 4,7

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

Rontgen Thorax PA

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

Ele c tro c ardiogra phy

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 , 20 th 2010 )

6

BTA I : Negatif

BTA II : Negatif

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.

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II.6 WORKING DIAGNOSIS

New case findings of tuberculosa with negative BTA and Positive radiologist and

malnutrition.

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

8

II.9 PROGNOSIS

Quo ad vitam : dubia ad bonam

Quo ad functionam : dubia ad bonam

FOLLOW UP

September , 28th 2010

S Abdominal pain

O

General condition• Conciousness : compos mentis• Blood preassure : 90/70 mmHg• Pulse rate : 70x/minute• Respiration rate : 22x/minute• Temperature : 36,2ºC• Body weight : 25 kg

Spesific conditionPale of conjunctiva palpebra (-/-), icteric sclera (-/-), Jugular venous pressure (5-2) cmH2OThorax : 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 : flat, Palpation : supple, borderline of pulmo-liver at ICS V, pressure pain (-), liver

and spleen didn’t palpablePercussion : shifting dulness (-)Auscultation : normal bowel sound

Extremities : pretibial edema -/-A New case findings of tuberculosa with negative BTA and Positive radiologist and

9

malnutrition.

P

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 2010S (-)

O

General condition• Conciousness : compos mentis• Blood preassure : 100/70 mmHg• Pulse rate : 75x/minute• Respiration rate : 22x/minute• Temperature : 36,3ºC• Body weight : 25 kg

Spesific conditionPale of conjunctiva palpebra (-/-), icteric sclera (-/-), Jugular venous pressure (5-2) cmH2OThorax :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 didn’t palpablePercussion : shifting dulness (-)Auscultation : normal bowel sound

Extremities : pretibial edema -/-A New case findings of tuberculosa with negative BTA and Positive radiologist and

10

malnutrition.

P

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

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2. Makronodular

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

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b. Alagille’s syndrome

c. Biliary atresia

d. Familial intrahepatic cholestasis(FIC)

e. Fanconi’s syndrome

f. Galactosemia

g. Gaucher’s disease

h. Glycogen storage disease

i. Hemochromatosis

j. Hereditary fructose intolerance

k. Hereditary tyrosinemia

l. Wilson’s 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

13

“hematemesis” and yellowish eyes. From her statement we have thought that it’s possible

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

14

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

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 doesn’t 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

15

with anemia chronic disease. It means that the anemia was appeared since the chronic

disease that she had, in this case is cirrhosis hepatic.

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/minute72 x 1,6

The CCT in this patient is 36,18 ml/minute. It’s 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

16

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 hasn’t been done, but it is needed to found

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. 5

Therefore liver biopsy examination is also planned for this patient.

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. Restrict dietary with balance nutrition: enough calories, protein 1gr/kgBB/day and

vitamin.

3. 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 the

aldosterone receptor at the distal tubule. 1 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

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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.

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 8 th 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.

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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

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. spontaneous bacterial peritonitis.

2. Bleeding from esophageal or gastric (stomach) varices

3. hepatic encephalopathy

4. Liver Cancer (Hepatocellular Carcinoma.

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In this patient, we haven’t 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

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. 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

severe derangement. 14

Measure 1 point 2 points 3 points units

Bilirubin (total) <34

(<2)

34-50

(2-3)

>50

(>3)

μmol/l

(mg/dl)

Serum albumin >3,5 2,8-3,5 <2,8 g/dl

INR <1.7 1.71-2.20 > 2.20 no unit

Ascites None Mild (can be controled easy) Severe no unit

Hepatic

encephalopathy

None Grade I-II (or suppressed

with medication)

Grade III-IV (or

refractory)

no unit

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 Class One year survival Two year survival

5-6 A 100% 85%

7-9 B 81% 57%20

10-15 C 45% 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.

REFERENCES

1. Wolf, David, Cirrhosis, New York Medical College. New York. USA. 2010. Available from www.emedicine .com

2. Sulaiman, Ali. Akbar, Nurul. Lesmana L. Buku Ajar Ilmu Penyakit Hati. Jaya Abadi. Jakarta. 2007.

3. Maryani, Sri. Sirosis Hepatis. USU Digital Library. Sumatra Utara 2003. Available from library.usu.ac.id/download/fk/penydalam-srimaryani5.pdf

4. D’Amico 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. 147–154.

5. Kasper, Dennis, et al. Harrison Principle Of Internal Medicine Sixteenth Edition.Mc. Graw-Hill. New York. USA 2005

6. Sanchez, William. Jayant, A. Talwalkar, Liver Cirrhosis. The American College of Gastroenterology, Bethesda, Available from www.acg.gi.org

7. 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.

8. Noer S. Sirosis Hati. Buku Ajar Ilmu Penyakit Dalam. Jilid I. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam. Edisi IV FKUI. 2006; 445-48.

9. Baldy CM. Gangguan Sel Darah Merah. In : Price SA, Wilson LM, editors. Patofisiologi Konsep Klinis Proses Penyakit. Ed 6. Jakarta: EGC; 2003.hlm.256-257.

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10. 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: 2089–100.

11. Pere Gines et al. Management of Cirrhosis and Ascites. The New England Journal of Medicine. Masschusetts Medical Society. 2004; 350: 1646-54

12. Bromilow, David, dkk. MIMS Indonesia. Vol 2. Number 1. Medi Media International Group. 2000.

13. 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

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

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

22

Palembang, August 2010

Advisor :

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

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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