Cirorhosis Hepatis (Indy File)

44
CIRRHOSIS OF THE LIVER Defenition Cirrhosis of the liver is a chronic diffuse process with fibrosis and nodule formation anatomically. It was followed hepatocelluler necrosis. Although the causes are many, the end result and two mayor event, failure of liver function and portal hypertension. Etiology 1. The caused was known : Hepatitis virus type B and C. Alcoholic Metabolic, inherited and drug related Imunologic disturbance. Malnutrition. Cardiac Biliary 2. Unknown Case Presentation 1

Transcript of Cirorhosis Hepatis (Indy File)

Page 1: Cirorhosis Hepatis (Indy File)

CIRRHOSIS OF THE LIVER

Defenition

Cirrhosis of the liver is a chronic diffuse process with fibrosis and

nodule formation anatomically. It was followed hepatocelluler necrosis.

Although the causes are many, the end result and two mayor event, failure

of liver function and portal hypertension.

Etiology

1. The caused was known :

Hepatitis virus type B and C.

Alcoholic

Metabolic, inherited and drug related

Imunologic disturbance.

Malnutrition.

Cardiac

Biliary

2. Unknown

Pathogenesis

The response of the liver to necrosisasstricly limited, the most

important are collapse of hepati lobules, formation of diffuse fibrous

septum and nodular regrowth of liver ell. Thus, irrespective of etiology, the

ultimate histological picture of the liver is similar.

Case Presentation1

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When the liver cell became necrotic, the reticulinframe workcollapsis with

approxiamation of portal and central zones. Some cell grow to from

nodules of various size. The nodules distort the hepatic tree so that portal

flow is impanden and portal hypertention results.

Sinusoid persist at periphery of the site of the portal central bridges.

Portal blood is diverted past functioning liver tissue leading to vasculer

insufficiency at the centre of the nodules. Basement membranes from in

the perisinosoidal from the sinusoids and the liver cells.

Clinical feature

In patient with cirrhosis of known etiology in whom there is progression

to a post necrotic stage. The clinical feature an extension of those

resulting from the initial desease process. Ussually clinical symptom are

related to portal hypertension and the sequale such as ascites,

splenomegally, hipersplenisme and bleeding esophageal varicess. The

hematology and hiperfunction abnormalities resemble those seen with

other types of cirrhosis hepatis

A. Compensated Cirrhosis

There is no complain from the patient, no specially complain such as

not healthy, exhausted powerlss, decreased in appatite, felt swollen,

weight loss and fatique. There is no defferences symptoms with chroni

hepatitis without cirrhosis depend on the liver necrosis.

B. Decompensated Cirrhosis

We can diagnosed the patient with the clinical examination,

laboratorium finding and another suggest examination. Esspecially appear

Case Presentation2

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liver failure and portal hypertension complain with manifestation like

palmar erytema, vascular spiders, colateral vein, jaundice, oedema of the

feet and ascites.

Examination

Liver enlargement at earlier cirrhosis. The consistence is elastic

firm, blunt edge, pain pressure.

Splein, the parameter to known the enlargement is with scuffner

line ( I-VII).

Collateral vessels and ascites.

Spider teleangiectacia and palmaris erythema.

Dullnes percussion is very late sign of fluid under tension.

Ascitic fluid and paracentesis abdominis. Diagnosis

paracentesis is always performed. The terapeutic paracentesis

is very rarely necessary unless the patients is in severe

discomfort. Protein consentration rarely excess 10-20 g/l

Urine, the urine volume is diminished and it is deeply

pegmented and of high osmolarity. The daily out put of sodium

is greatly reduced.

Diagnosis

Post necrotic cirrhosis hepatis must be suspected in patient with

sign and sympton of cirrhosis or portal hypertension. Needle or

operativeliver biopsy confirm the diagnosis, also non uniformity of

patologic process my result in sampling errors.

Case Presentation3

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Cirrhosis hepatic decompensated stage diagnosed by Suharyono

Subandri that 5 from 7 sign below can asume as it, the sign are:

Ascites

Splenomegaly

Varicess esophageal bleeding

Low albumin

Spider naevi

Palmaris Erytema

Collateral

Treatment

Management is ussually limited to treatment of the complication of

portal hypertension, including control of ascites, avoidence of drugs or

excessive protein intake that my include hepatic coma and prompt

treatment of infection, in patient in whom post necrotic cirrhosis hepatic

has developed as a result of treatable condition. Therapy directed at the

primary disorders may limit further progression.

Complication

Portal hypertension

Varicess esophageal

Ascites

Splenomegaly.

Case Presentation4

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CASE REPORT

A 40 years old man was admitted to Internal Medicine Department

of General Hospital Dr. Ahmad Moechtar Bukittinggi on August 15 th 2002

with :

Chief complain : Have a right stomachache since 3 days ago.

Present Illness History :

Have a right stomachache since 3 days ago.

The patient feel weakness since 20 days ago.

The patient feel discomfort in his abdoment since 20 days ago.

Urine was like a strong of tea since 7 days ago.

Diarrhea with mucous since 3 days ago.

Febris since 3 days ago.

Headache since 3 days ago.

Nausea (+), vomite (-).

Previous Illness History :

No history of yellow disease, hypertension, diabetes melitus.

Family Illness History :

None of the family members had suffered the disease like this

Habitually History :

Never drinks alcohol

Physical Examination :

Vital sign :

General appearance : moderately ill

Case Presentation5

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Consciousness : composmentis cooperatif

Blood pressure : 120/70 mmHg

Pulse rate : 92 x/min

Respiratory rate : 23 x /min

Body temperature : 37,50 C

Skin : icteric

Lymph node : no enlergment

Head : Eye : conjunctiva was anemic

Sclera was icteric

Ears, mouth and nose : normal

Neck :

JVP : 5 – 2 cm H2O

Regional lymph node : no enlargement

Thyroid gland : no enlargement

Chest : normochest, spider naevi (+)

Lung :

Inspection : simetric movement left and right

Palpation : fremitus was the same on the right and left side

Percusion : sonor both of lung

Auscultation : vesicular normal, ronchi (–), wheezing (–)

Heart :

Inspection : ictus was not visible

Palpation : ictus was palpable at 1 finger medial LMCS ICS V

Percusion : left border : 1 finger medial LMCS ICS V

Case Presentation6

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right border : right sternalis line

upper border : ICS II

Auscultation : pure, regular rhythm, M1 > M2, P2 < A 2, murmur (–)

Abdomen :

Inspection : swollen abdomen (+), collateral (+)

Palpation : liver was palpable at 3 fingers under arcus costae, 3

fingers under processus xipoideus, difus, elastic, dull

and pain pressure (+)

Spleen was palpable (Schuffner 1) .

Percusion : tympany, shifting dullness (+)

Auscultation : peristaltic sound was normal

Back : pressure pain (–), knock pain (–).

Extremities :Right Left

Physiological reflex + +

Pathological reflex – –

Smooth sensibility + +

Rough sensibility + +

Edem - -

Palmar erythema : (–)

Laboratory findings :

Blood :

Hb : 5,6 g% Leucocyte : 9300/mm3

DC : 0 / 2 / 2 / 61/ 29/ 6 BSR : 30 mm/hour

Eritrocyte : 2 million ul Reticulocyte : 15 %

Case Presentation7

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HbsAg :(+) Anti Hbs : (–)

SGOT :46 u/I SGPT :36 u/I

Protein total : 5,19 gr%

Albumin : 3,05 gr%

Globulin : 2,14 gr%

Total bilirubin: 1,2 gr%

Direct bilirubin: 0,28 gr%

Indirect bilirubin: 0,92 gr%

Ureum : 28

Creatinin : 0,7

Pheriperal Blood Appearance : Anisositosis, polikromasi, micrositic

hipochrom anemia.

Urin :

Bilirubin : (-) Protein : (–)

Urobilin : (+) Reduction : (–)

Sediment : eritrocyte : 0–1/ wf

Leucocyte : 1-2 / wf

Cylinder : (–)

Epitel : squamous (+)

Crystal : (–)

Feces :

Colour : Yellow Consistance : mole

Blood : (-) Bacterial : (-)

Ancylostoma sp: (+)

Case Presentation8

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Working diagnosis :

- Cirrhosis hepatis post necrotic decompensated stage

- Micrositic hypocrhome anemic ec Ancylostomiasis

Differential diagnosis :

- Hepatoma

- Hepatitis B

Treatment :

Unagen 2x1

Aspar K 3x1

Spironolacton 2x1

Miniseronal 3x1

Suggested examination :

USG abdominal

Liver physiologic

Endoscopy

Follow up

August 15th 2002

A : Stomachache (+), weakness of the body (+), Fever (+).

Urine was like a strong of tea

PE :

GA Consc BP PR RR TModerate cmc 120/70 82x/i 24x/i 36,50C

Eye : conjungtiva was anemic

Sclera was icteric

Case Presentation9

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Abdomen : same as before

WD/ : same as before

Treatment : continue

Follow up

August 16th 2002

A : Stomachache (-), weakness of the body (+), Fever (-).

Urine was like a light tea

PE :

GA Consc BP PR RR TModerate cmc 100/70 80x/i 20x/i 370C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : same as before

WD/ : same as before

Treatment : continue

Follow up

August 17th 2002

A : Stomachache (+), weakness of the body (+), Fever (-).

Urine was yellow

Bowel (-), appetite (+)

PE :

GA Consc BP PR RR TModerate cmc 110/70 85x/i 20x/i 370C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : same as before

WD/ : same as before

Treatment : continue

Case Presentation10

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Follow up

August 19th 2002

A : Stomachache (+), weakness of the body (+), Fever (-).

Urine was yellow and irreguler mixturation.

Bowel (+), appetite decreased

PE :

GA Consc BP PR RR TModerate cmc 110/70 83x/i 20x/i 370C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : same as before

WD/ : same as before

Treatment : continue + Spironolacton 3x1

Follow up

August 20th 2002

A : Distanded stomache (+), weakness of the body (+), Fever (-).

Urine was yellow and regular.

Bowel (+), appetite (+)

PE :

GA Consc BP PR RR TModerate cmc 110/70 83x/i 20x/i 370C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : same as before

WD/ : same as before

Treatment : continue + Furosemid 1x1+Mebendazol 1x500 mg

Follow up

August 22nd 2002

A : Distanded stomache (+), weakness of the body (+), Fever (-).

Case Presentation11

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Urine was yellow and regular.

Bowel (+), appetite (+)

PE :

GA Consc BP PR RR TModerate cmc 110/70 83x/i 20x/i 370C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : Ascites decreased

WD/ : same as before

Treatment : continue

Follow up

August 29th 2002

A : Stomachache (+), weakness of the body (+), Fever (-).

Urine was yellow and regular.

Bowel (+), appetite (+)

PE :

GA Consc BP PR RR TModerate cmc 110/70 68x/i 20x/i 360C

Eye : conjungtiva was anemic

Sclera was icteric

Abdomen : Ascites decreased

Lab : Hb : 8 mg%

WD/ : same as before

Treatment : continue + blood transfusion

Case Presentation12

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DISCUSSION

The diagnosis on this case made based on anamnesa, physical

examination, and laboratory finding. From anamnesis was found right

stomachache, discomfort of stomache, urine was like strong of tea.

From physical exemination found that conjunctiva was anemic,

sclera was icteric, spider naevi (+), liver was palpable 3 fingers under

arcus costae, 3 fingers under processus xipoideus, difus, elastic, dull and

pain pressure (+), spleen was palpable (Schuffner 1), collateral (+).

From laboratory finding we found Hb 5,6 g%, Pheriperal blood

appearance anisositosis, polikromation, micrositic hypocrhom anemic,

HbsAg (+), SGOT increased, SGPT increased, total protein decreased,

Case Presentation13

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Albumin decreased.Total bilirubin increased, indirect bilirubin

increased.From the feces : ancylostoma sp (+).

Based on these data we can diagnose this patient with cirrhosis

hepatis post necrotic decompensated stage and micrositic hypocrhom

anemic ec ancylostomiasis.

CASE REPORT

A 51 years old man was admitted to Internal Medicine Department

of General Hospital Dr. Ahmad Moechtar Bukittinggi on May 31 th 2002

with :

Chief complain : Vomitus wich contain stomach liquid with a black colour

of blood since 5 days ago.

Present Illness History :

Vomitus wich contain stomach liquid with a black colour of blood

since 5 days ago ± 6 times aday aproximately ± 1 glass.

Feeling weakness, fatique, tired since 6 months go.

Case Presentation14

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Loose of apatite since 6 months ago.

Have a not persistent febris since 2 months ago.

Icterics eye s followed by all of bodies since 1 month ago.

Pruritus was positif all of body since 1 month ago.

Miksi was like a tea colour since 1 month ago.

Get stomach pain and feel puffed up since 1 month ago.

Bowel was have black colour like an aspal since 15 days ago.

Oedem at both of foot since 5 days ago.

Previous Illness History :

No history of yellow disease

Family Illness History :

None of the family members had suffered the disease like this

Habitually History :

Never drinks alcohol

Physical Examination :

Vital sign :

General appearance : moderately ill

Consciousness : composmentis cooperatif

Blood pressure : 110/70 mmHg

Pulse rate : 84 x/min

Respiratory rate : 20 x /min

Body temperature : 360 C

Body height : 160 cm

Body weight : 45 Kg

Case Presentation15

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Skin : icteric (+)

Lymph node : no enlergment

Head : Eye : conjunctiva was anemic

Sclera was icteric

Ears, mouth and nose : normal

Neck :

JVP : 5 – 2 cm H2O

Regional lymph node : no enlargement

Thyroid gland : no enlargement

Chest : normochest

Lung :

Inspection : simetric movement left and right

Palpation : fremitus was the same on the right and left side

Percusion : sonor both of lung

Auscultation : vesicular normal, ronchi (–), wheezing (–)

Heart :

Inspection : ictus was not visible

Palpation : ictus was palpable at 1 finger medial LMCS ICS V

Percusion : left border : 1 finger medial LMCS ICS V

right border : right sternalis line

upper border : ICS II

Auscultation : pure, regular rhythm, M1 > M2, P2 < A 2, murmur (–)

Abdomen :

Case Presentation16

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Inspection : distended abdomen (+), collateral (–)

Palpation : liver was palpable at 2 fingers below of arcus costae,

difus, elastic, dull and pain pressure (+)

Spleen could not palpable.

Percusion : shifting dullness (+)

Auscultation : peristaltic sound was normal

Back : pressure pain (–), knock pain (–).

Extremities :Right Left

Physiological reflex + +

Pathological reflex – –

Smooth sensibility + +

Rough sensibility + +

Edem + +

Palmar erythema : (–)

Laboratory findings :

Blood :

Hb : 7 g% Ureum : 101,3 mg %

Leucocyte : 13600/mm3 Creatinin : 2,9 mg %

DC : 0 / 2 / 3 / 61/ 30/ 4 SGOT : 130 uL

BSR : 20 mm/hour SGPT : 100 uL

Eritrocyte : 2.3 million ul Total bilirubin : 10,9 mg %

Reticulocyte : 2,5 % Bilirubin indirect : 5,13 mg %

HbsAg : (–) Bilirubin direct : 4,96 mg %

Anti Hbs : (–) Protein total : 3,59 g %

Case Presentation17

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ALP : 361 Albumin : 1,87 g %

Globulin : 1,72 g %

Urin :

Bilirubin : (+) Protein : (–)

Urobilin : (+) Reduction : (–)

Sediment : eritrocyte : 0–1

Leucocyte : (+)

Cylinder : (–)

Epitel : squamous (–)

Crystal : (–)

Working diagnosis :

Cirrhosis hepatis billiary decompensated stage

Differential diagnosis :

Cirrhosis hepatis post necrotic decompensated stage

Treatment :

Bad rest untill icteric, acites, and febris was recovery.

Diet low protein and low salt ( DH I )

Furosemid 1x1 tab

KCL 1x1 tab

Tramadol 2x1 tab

Miniproterenol 3x1 tab

Case Presentation18

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Curcuma 3x1 tab

Suggested examination :

Routine blood, urine, feces test HbsAg USG

abdominal

Liver physiologic Endoscopy Liver biopsi

Cholangiography

Follow up

June 3th 2002

A : Fatique, weakness, lose of apatite,

Feces was brown, urine was like a tea

Stomach pain

PE :

GA Consc BP PR RR TModerate cmc 120/70 88x/i 20x/i 36,50C

Eye : conjungtiva was anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

WD/ : Cirrhosis hepatis billiary decompensated stage

Treatment : continue

June 5th 2002

A/ : frigoris

Nausea (+), vomitus (+).

Fatique

Stomach pain

PE:

Case Presentation19

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GA Consc BP PR RR TModerate cmc 120/70 88x/i 20x/i 36,50C

Eye : conjungtiva was anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Laboratory finding:

Hb : 13,1 gr %

Leucocyte : 16200/mm3

Treatment : continue

June 6th 2002

A : Frigoris, Fatique, Diarhoe

PE :

GA Consc BP PR RR TModerate cmc 120/70 70x/i 22x/i 36,50C

Eye : conjungtiva was not anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Treatment : continue

June 8th 2002

A : Fatique

Distended abdome

Nausea (+)

Feces was yellow 5–6 x/ day

PE :

GA Consc BP PR RR TModerate cmc 120/70 85x/i 19x/i 36,50C

Eye : conjungtiva was not anemic

Case Presentation20

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Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Treatment : continue

June 10th 2002

A : febris (+), burn stomach

Distended abdomenfeces was gray

Mixturiatio was like a tea

PE :

GA Consc BP PR RR TModerate cmc 120/70 80x/i 20x/i 38,10C

Eye : conjungtiva was not anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Laboratory finding:

HbsAg : (–) Total bilirubin : 10,9 mg %

Anti Hbs : (–) Bilirubin indirect: 5,13 mg %

SGOT : 130 uL Bilirubin direct: 4,96 mg %

SGPT : 100 uL

Treatment: continue

June 12th 2002

A : febris (+), burn stomach

Distended abdomenfeces was gray

Mixturiatio was like a tea

PE :

GA Consc BP PR RR TModerate cmc 120/70 84x/i 20x/i 37,50C

Case Presentation21

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Eye : conjungtiva was not anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Laboratory finding:

Feces : Macroscopic: yelow, solid

Urine : Eritrocyte : 1–2

Leucocyte : +

Bactery : +

Bilirubin : +

Urobilin : +

Treatment: continue

June 19th 2002

A : Fatique, weakness, lose of apatite,

Stomach pain

PE :

GA Consc BP PR RR TModerate cmc 120/70 82x/i 21x/i 36,70C

Eye : conjungtiva was not anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Laboratory finding:

Total bilirubin : 7,79 mg % SGOT : 77 uL

Bilirubin indirect: 4,84 mg % SGPT : 98 uL

Bilirubin direct: 2,95 mg %

Case Presentation22

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Treatment: continue

June 20th 2002

A : Fatique, weakness

Urine was like a tea

PE :

GA Consc BP PR RR TModerate cmc 120/70 85x/i 20x/i 36,50C

Eye : conjungtiva was anemic

Sclera was icteric

Skin : icteric

Extremity : Edema of foot : +/+

Treatment : continue

Case Presentation23

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DISCUSSION

The diagnosis on this case made based on anamnesa, physical

examination, and laboratory finding. From anamnesis was found stomach

swelling since five months ago, the patients felt his stomach quikly full if

eaten some food since five months ago, and the patient also had history

alcohol consumption when his young, not all the times.

From physical exemination found that liver was palpable 5 fingers

below processus xipoideus, and 3 finger below arcus costae, blunt edge,

hard, surface was not flat, pressure pain negative. Spleen was palpable

until S4 and kidney was not palpable. in percussion of the abdoment is

tympany, but on the mass is dullnes. On the extremitas we found that

palmaris eritema in the patient hand.

From laboratory finding we found SGOT/ SGPT was increase, ratio

albumin and globulin inverse which albumin is decrease and globulin is

increase. Alkali fosfatase is normal. Concentration of ureum, kreatinin, and

uric acid is normal. Based on this data we can diagnosed this patient with

hepatoma.

Case Presentation24

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CASE REPORT

A 52 years old man was admitted to Internal Medicine Department

of General Hospital Dr. Ahmad Moechtar Bukittinggi on August 30 th 2002

with :

Chief complain : Vomitus wich contain stomach liquid with a black colour

of blood since 1 day ago.

Present Illness History :

Vomitus wich contain stomach liquid with a black colour of blood

since 1 day ago, 1 x, aproximately ± 1 glass,nausea (-).

Febris since 1 day ago.

Headache since 1 day ago

Urine was like a tea colour since 3 days ago.

Bowel was have black colour since 3 days ago.

Edema (-)

Previous Illness History :

No history of yellow disease

Consumed traditional drug for rheumatic disease since three

years ago

Family Illness History :

None of the family members had suffered the disease like this

Case Presentation25

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Habitually History :

Consumed traditional drug for rheumatic disease since three years

ago

Never drinks alcohol

Physical Examination :

Vital sign :

General appearance : moderately ill

Consciousness : composmentis cooperatif

Blood pressure : 120/80 mmHg

Pulse rate : 80 x/min

Respiratory rate : 28 x /min

Body temperature : 360 C

Skin : no icteric

Lymph node : no enlergment

Head : Eye : conjunctiva was anemic

Sclera was not icteric

Ears, mouth and nose : normal

Neck :

JVP : 5 – 2 cm H2O

Regional lymph node : no enlargement

Thyroid gland : no enlargement

Chest : normochest, spider naevi (+)

Case Presentation26

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Lung :

Inspection : simetric movement left and right

Palpation : fremitus was the same on the right and left side

Percusion : sonor both of lung

Auscultation : vesicular normal, ronchi (–), wheezing (–)

Heart :

Inspection : ictus was not visible

Palpation : ictus was palpable at 1 finger medial LMCS ICS V

Percusion : left border : 1 finger medial LMCS ICS V

right border : right sternalis line

upper border : ICS II

Auscultation : pure, regular rhythm, M1 > M2, P2 < A 2, murmur (–)

Abdomen :

Inspection : distended abdomen (-), collateral (–)

Palpation : liver was palpable at 1 finger under arcus costae, 3

fingers under processus xipoideus, difus, elastic, dull

and pain pressure (-)

Spleen was palpable (Schuffner 1) .

Percusion : tympany, shifting dullness (-)

Auscultation : peristaltic sound was normal

Back : pressure pain (–), knock pain (–).

Extremities :Right Left

Physiological reflex + +

Case Presentation27

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Pathological reflex – –

Smooth sensibility + +

Rough sensibility + +

Edem - -

Palmar erythema : (–)

Laboratory findings :

Blood :

Hb : 4,6 g% Leucocyte : 5200/mm3

DC : 0 / 2 / 3 / 59/ 30/ 6 BSR : 8 mm/hour

Eritrocyte : 1,6 million ul Reticulocyte : 3,2 %

Anti Hbs : (–)

Pheriperal Blood Appearance : Anisositosis, polikromasi, micrositic

hipocrhom anemia.

Urin :

Bilirubin : (-) Protein : (–)

Urobilin : (+) Reduction : (–)

Sediment : eritrocyte : 0–1/ wf

Leucocyte : 2-3 / wf

Cylinder : (–)

Epitel : squamous (–)

Crystal : (–)

Feces :

Colour : Black Consistance : mole

Blood : (-) Bacterial : (-)

Case Presentation28

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Working diagnosis :

- Hematemesis Melena ec varices esophageal bleeding

ec Cirrhosis hepatis post necrotic decompensated stage

- Micrositic hypocrhome anemic ec bleeding

Differential diagnosis :

Hematemesis Melena ec varices esophageal bleeding ec Cirrhosis

hepatis decompensated stage ec traditional drug.

Treatment :

Bed rest, fast 24 – 48 hours after bleeding (-)

Diet low protein and low salt ( DH I )

NaCl inj 20 gtt/ minute

Transamin inj 3x1 amp

Vit K inj 3x1 amp

Suggested examination :

USG abdominal

Liver physiologic

Endoscopy

Follow up

August 31th 2002

A : Vomite (-), Fever (-), Headeache (-)

Feces was black, urine was like a tea

PE :

GA Consc BP PR RR T

Case Presentation29

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Moderate cmc 120/70 81x/i 26x/i 36,50C

Eye : conjungtiva was anemic

Sclera was not icteric

Abdomen : same as before

WD/ :

- Hematemesis Melena ec varices esophageal bleeding ec Cirrhosis

hepatis post necrotic decompensated stage

- Micrositic hypocrhome anemic ec bleeding

Treatment : continue

Case Presentation30

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DISCUSSION

The diagnosis on this case made based on anamnesa, physical

examination, and laboratory finding. From anamnesis was found Vomitus

wich contain stomach liquid with a black colour of blood, febris, headache,

urine was like a tea colour, bowel was have black colour, and the patient

also had history drug traditional for rheumatic consumption since three

years ago.

From physical exemination found that Conjunctiva was anemic,

spider naevi (+), liver was palpable 1 finger under arcus costae, 3 fingers

under processus xipoideus, difus, elastic, dull and pain pressure (-),

spleen was palpable (Schuffner 1) .

From laboratory finding we found Hb 4,6 g%, Pheriperal blood

appearance anisositosis, polikromation, micrositic hypocrhom anemic,

HbsAg (+),

From the feces : colour was black. Based on this data we can diagnosed

this patient with hematemesis melena ec varices esophageal bleeding

ec cirrhosis hepatis post necrotic decompensated stage and micrositic

hypocrhom anemic ec bleeding

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Page 32: Cirorhosis Hepatis (Indy File)

Case Presentation32