Hematemesis

Melena
SUZETTE D.C.DANIEL
Laporan
Teori
Kasus

Pembahas
an

2
Laporan Kasus

3
 IDENTITAS PASIEN

Umur
40

Jenis Kelamin
Laki-laki

Alamat
Tini

Tn C.B. Pekerjaan
Jual Beli Mobil bekas
 ANAMNESIS
(Autoanamnesis) 29/4/2020

Keluhan Utama

BAB hitam

Keluhan Penyerta

Nyeri Ulu Hati

Perut Panas
Mual
 Hari MRS (28/4)

Pasien mengatakan BAB hitam seperti kopi

1x sejak ± 4 jam SMRS, BAB hitam agak
encer sebanyak kira-kira <10 cc (< 2 sendok
makan).
Keluhan disertai dengan nyeri ulu hati,
perut terasa panas sampai ke dada dan
Riwayat
mual. Sebelumnya os melakukan perjalanan Penyakit
jauh PP Soe-Atb dan belum sempat istirahat.
Muntah darah (-) Demam (-), penurunan BB Sekarang
(-), BAK biasa
 Hari MRS

BAB darah campur air 7x kira-

kira 5 cc (1 sendok makan) tiap kali
BAB, muntah warna hitam 2x ±
20 menit setelah makan, berisi
cairan dan sisa makanan, muntah
kurang lebih 1 setengah ember
kecil . Setelah muntah badan terasa
lemas dan berkeringat serta nyeri
ulu hati dan rasa panas di perut
sehingga os tidak mau makan
Demam (-), Batuk(-)

Riwayat Penyakit
Riwayat Penyakit Dahulu

Hepatitis B Hematemesis
HbSAg +

2007 2018 2019

Sirosis Hepatis

Varises Esofagus grade II Anemia

Riwayat Penyakit Keluarga

Keluhan Serupa: -
Hepatitis B :-
HT :-
DM :-
Riwayat Pengobatan
2018
Tafnat
(Tenofovir) Pengobatan selama 1,5 tahun.
Sejak ± 6 bulan tidak minum obat.
Atevir Pasien tidak rutin minum obat
(Entecavir)
Propanol
ol

Furosemid

Riwayat Alergi (-)

10
 Riwayat Sosial-Ekonomi

• Pasien memiliki perkerjaan yaitu jual-beli mobil bekas sehingga sering

melakukan perjalanan jauh ke luar kota.
• Riwayat konsumsi alkohol sejak tahun 2002-2005, sejak sakit pasien
tidak pernah minum alkohol lagi.
• Merokok (-)
• Pasien mengatakan dulu sering makan di luar rumah karena tidak
sempat makan di rumah, namun terkadang juga makan makanan yang
dimasak di rumah. Makan sehari 3x

11
 PEMERIKSAAN FISIK

80 K
U Lemah
110/60
Compos Kes
98 Mentis .
GC 15
20 S

36 63 kg
B
B

12
 Status
Generalis

CA +/+
SI -/-

Ginekomasti (-) Simetris

Ves +/+, Rh -/-, Wh -/-
S1S2 tunggal reguler
Status Lokalis
Ikterik (-)
Palmar eritem (-)

Edem +/+
Akral hangat
Status Lokalis

Inspeksi
Distensi (+), spider nevi (-), caput
medusa (-), simetris, jejas (-), eritem
(-)
Auskultasi
Bising usus (+)

Pekak
Hepatomegali (-) Padat, licin, nyeri -

Timpani
Perkusi Shifting dullness Palpasi Nyeri -, massa -
(+),undulasi (-)
Nyeri tekan + kiri
Splenomegali (-)
atas (LUQ)
 PEMERIKSAAN
PENUNJANG
2018

Endoskopi
Laboratorium

HBV DNA
• Varises Esofagus Kuantitatif HBeAg (-)
Anti-Hbe (+)
Gr I-II 3,45 x 10^3
• Gastropathy Copies/ml
Kongestif
• Gastritis Erosiva Anti HCV (-) HBsAg (+)
• Varises Esofagus Gr I-II
• Gastropathy Kongestif
• Gastritis Erosiva
• Fundal Varises

16
28/4/2020

WBC 4500/µL GDS 135

RBC 2.760.000/µL Kreatinin 0,6
Hb 5,8 g/dL Ureum 12
MCV 70,3 fL SGOT 21
SGPT 19
MCH 21 pg
HBsAg +
MCHC 29 g/dL
Bilirubin Tot. 6,9 mg/dL
Hct 19,4 % Alb. 2,6 g/dL
PLT 64.000/µL

17
 DIAGNOSIS

Diagnosis Utama Diagnosa Banding

• Hematemesis Melena Ulkus Peptikum

e.c Susp. Ruptur
Varises Esofagus
• Sirosis Hepatis
Dekompensata
• Hep. B Kronis
• Anemia Gravis
 TATALAKSANA

IVFD RL 20 tpm Puasa 8 jam

Inj. Omepazole 2x40 mg Pasang NGT  Pasien
Inj. Kalnex 3x500 mg menolak
Inj. Ondansetron 3x4 mg Transfusi WB 1 kolf/hari
Inj. Vit K 3x1
Inj. Ceftriaxone 2x1 g
ISDN 2X5 mg PO
Lactulosa syr. 3xCI PO
Propanolol 2x40 mg PO
 PROGNOSIS

Ad Vitam : Dubia ad malam

Ad Fungsionam : Dubia ad Bonam
Ad Sanationam : Dubia ad Bonam
 FOLLOW UP
TGL S O A P
28 April Nyeri ulu hati, KU : Lemah Hematemesis IVF RL 20 tpm
2020 mual, muntah N : 98x/m Melena e.c IV OMZ 2X40 mg
campur darah, TD : 110/60 S.Ruptur varises IV ODR 3X4 mg
BAB darah 7x RR : 20x/m Sirosis Hepatis IV Kalnex 3X500 mg
S : 36,7 Dekompensata Puasa
Kepala : CA+/+, SI-/- , Hep B.Kronik Transfusi WB1 kolf/hari
Cor : S1 S2 regular , murmur (-) Anemia Gravis
Pulmo : Ves +/+ , Rh-/ Wh-/-
Abd: Distensi, NTE +,
Eks : Akral Hangat , CRT < 2detik,
Edema pada kedua kaki
Hb : 5,8 g/dL

29 April BAB hitam 1x, KU : Lemah Hematemesis IVF RL 20 tpm

2020 pusing N : 86x/m Melena e.c IV OMZ 2X40 mg
TD : 110/80 S.Ruptur varises IV ODR 3X4 mg
RR : 20x/m Sirosis Hepatis IV Kalnex 3X500 mg
S : 36,2 Dekompensata IV Vit K 3X1
Kepala : CA+/+, SI-/- , Hep B.Kronik IV Ceftriaxone 2X1 g
Cor : S1 S2 regular , murmur (-) Anemia Gravis PO Propranolol 2X1
Pulmo : Ves +/+ , Rh-/ Wh-/- PO ISDN 2X5 mg
Abd: Distensi, Shiifting dullness + PO Syr. Lactulosa 3XCI
Eks : Akral Hangat , CRT < 2detik, NGT Pasien menolak
Edema pada kedua kaki Puasa
Hb : 6,7 g/dL Transfusi WB1 kolf/hari
 TGL S O A P
4 Mei Nyeri Ulu hati (-) KU : Lemah Hematemesis VF RL 20 tpm
2020 BAB hitam (-) N : 92x/m Melena IV OMZ 2X40 mg
Mual (-) TD : 100/70 (Perbaikan) IV Ceftriaxone 2X1 g
RR : 20x/m Sirosis Hepatis PO Propranolol 2X1
S : 36,5 Dekompensata PO ISDN 2X5 mg
Kepala : CA-/-, SI-/- , Hep B.Kronik PO Syr. Lactulosa 3XCI
Cor : S1 S2 regular , murmur (-) Diet Bubur Saring
Pulmo : Ves +/+ , Rh-/ Wh-/-
Abd: Distensi, NTE -,
Eks : Akral Hangat , CRT < 2detik,
Edema pada kedua kaki

5 Mei Nyeri Ulu hati (-) KU : Lemah Hematemesis BPL

2020 BAB hitam (-) N : 98x/m Melena Obat Pulang :
Mual (-) TD : 110/70 (Perbaikan) Propranolol 2x40 mg PO
RR : 20x/m Sirosis Hepatis Cefixime 2x100 mg PO
S : 36,2 Dekompensata
Kepala : CA-/-, SI-/- ,
Cor : S1 S2 regular , murmur (-)
Pulmo : Ves +/+ , Rh-/ Wh-/-
Abd: Distensi, NTE -,
Eks : Akral Hangat , CRT < 2detik,
Edema pada kedua kaki
Hb : 8,28 g/dL
PLT : 40,5
Teori
 SIROSIS HEPATIS

Penyakit hati kronis yang bersifat

irreversible dan ditandai dengan fibrosis
serta regenerasi nodulus di hati yang
mengakibatkan meningkatnya hipertensi
portal dan gagal hati
 Viral/Infectious
• Hepatitis B, Hepatitis C
• Schistosomiasis

Metabolic
ETIOLOGI

• Alcohol
• Toxins, Medication
• Non Alcoholic steatohepatitis
• Insulin Resistance
Vascular
• Right Heart Failure
• Cystic fibrosis

Cholestatic
• Billiary Cirrhosis
• Scerosing Cholangitis
MANIFESTASI KLINIS

Kegagalan Fungsi Hati Hipertensi Portal

● Ikterus ● Varises esofagus/cardia

● Spider naevi ● Splenomegali
● Ginekomastia ● Pelebaran vena kolateral
● Hipoalbumin dan malnutrisi kalori ● Ascites
protein ● Hemoroid
● Ascites ● Caput medusa (pelebaran vena
● Eritema palmaris hipogastrica)
● White nails
Clinical Findings
 DERAJAT KEPARAHAN
(Klasifikasi Child-Turcotte-
Pugh)
Vasoactive drug therapy should be
initiated as soon as AVH is suspected.
The recommended dose of terlipressin is
2 mg/4 h during the first 48 h, followed
by 1 mg/4 h thereafter
Pembahasan
KASUS TEORI

Anamnesis

The most common clinical presentation of

acute UGIB is hematemesis (30% ) and/or
melena (20%). Around 50% of patients
present with both hematemesis and
Melena
melena, and up to 5% of patients present
Hematemesis
with hematochezia, which is suggestive of a
Heartburn
rapid and significant amount of blood loss.
Patients bleeding from esophagitis or
esophageal ulcers usually have a
heartburn symptoms

Riw. Hepatitis B Viral/infectious of Hepatitis B/C are the

most etiology of liver cirrhosis by the
inflammation damage process
 KASUS TEORI

Pemeriksaan Fisik

Ikterik (-) Common Physical Examination Findings

Distensi abdomen in Patients with Cirrhosis :
Shifting dullness  Ascites  Abdominal wall vascular collaterals
Hepatomegali (-) (caput medusa)
Splenomegali (-)  Ascites
 Gynecomastia
 Hepatomegaly in acute condition,
sometimes can be normal or smaller
for cirrhosis
 Jaundice
 Palmar erythema
 Splenomegaly
 KASUS TEORI

Pemeriksaan Penunjang

Endoskopi Liver biopsy is still considered the gold-

Varises esofagus grade I-II standard diagnostic method to identify the
typical features of cirrhosis
Viral load
HBsAg (+) Esophageal varices are the most frequent
HBV-DNA Kuantitatif 3,45 x 10^3 source of UGI hemorrhage when
Anti HBe (+) emergency endoscopy is performed in
patients with cirrhosis, gastric varices,
Kimia Darah dan DL peptic ulcers, are also common causes of
HBsAg : + acute UGI bleeding in cirrhotic patients
SGOT : 21
SGPT : 19
BiTot: 6,9
Albumin : 2,6
Hb : 5,8
PLT : 64.000

38
 KASUS TEORI

Pemeriksaan Penunjang
The presence of HBsAg establishes the
diagnosis of hepatitis B.
Endoskopi
Varises esofagus grade I-II The presence of HBsAg for at least 6
months establishes the chronicity of
Viral load infection. Long-term chronic liver
HBsAg (+) inflammation and ineffective immune-
HBV-DNA Kuantitatif 3,45 x 10^3 mediated viral clearance, contribute to the
Anti HBe (+) development of cirrhosis and liver cancer.

Kimia Darah dan DL Serum HBV DNA varies from undetectable to

HBsAg : + several billion IU/mL. Subdivided into HBeAg
SGOT : 21 positive and negative. HBV-DNA levels are
SGPT : 19 typically >20,000 IU/mL in HBeAg-positive
BiTot: 6,9 CHB, and lower values (2,000-20,000
Albumin : 2,6 IU/mL) are often seen in HBeAg-negative
Hb : 5,8 CHB
PLT : 64.000 In chronic Hep. B ALT and/or AST levels are
persistenly normal
 KASUS TEORI

Pemeriksaan Penunjang
HBV-associated liver failure is reasonably
Endoskopi defined as 1 of the following:
Varises esofagus grade I-II 1. Impaired synthetic function (total
bilirubin >3 mg/dL or international
Viral load normalized ratio >1.5).
HBsAg (+) 2. Ascites
HBV-DNA Kuantitatif 3,45 x 10^3 3. Encephalopathy, or
Anti HBe (+) 4. Death following HBV-associated liver
failure attributed to HBV reactivation.
Kimia Darah dan DL
HBsAg : + Chronic liver diseaseof any cause is
SGOT : 21 frequently associated with hematological
SGPT : 19 abnormalities.
BiTot: 6,9 Anemia of diverse etiology occurs in about
Albumin : 2,6 75% of patients with chronic liver disease
Hb : 5,8 Thrombocytopenia is a common
PLT : 64.000 complication in liver disease, and liver
disease-related thrombocytopenia is often
defined as a platelet count < 100 × 10 9/L. 
 KASUS
Diagnosis
Hematemesis-Melena e.c.
Ruptur Varises Esofagus
TEORI
Variceal bleeding typically presents as
massive gastrointestinal (GI) bleeding with
hematemesis, melena or hematochezia
Endoscopy is the gold standard procedure
used in the diagnosis of gastroesophageal
varices (GOVs)
In cirrhotic patients, variceal bleeding occurs
in about 60–65% of patients.
 KASUS
Tatalaksana
IVFD RL 20 tpm
Transfusi WB 1 kolf/hari
Inj. Ceftriaxone 2x1 g
ISDN 2X5 mg PO
Propranolol 2x40 mg PO
Inj. Omepazole 2x40 mg
Inj. Kalnex 3x500 mg
Inj. Ondansetron 3x4 mg
Inj. Vit K 3x1
Lactulosa syr. 3xCI PO
TEORI
For patients with acute UGIB and
hemodynamic instability, resuscitation
should be initiated with Crystalloid (RL,NS).
Blood transfusion at a hemoglobin threshold
of ≤7 g/dL with a target range after
transfusion of 7 to 9 g/dl
Intravenous (IV) ceftriaxone (1 g/24 hours)
for a maximum of 7 days is the first choice in
patients with advanced cirrhosis.
NSBB recommended as first-line therapy for
chronic haemorrhage from PHG. The
Combination of NSBB and Isosorbid
mononitrate has a synergistic portal
pressure – reducing effect. However a
study that compare this combination with
NSBB alone failed to show benefit
 KASUS TEORI

Tatalaksana
PPIs should be initiated in case of upper GI
hemorrhage because peptic ulcers are the
IVFD RL 20 tpm
cause of bleeding in one third of the cases.
Transfusi WB 1 kolf/hari
However, when portal hypertensive bleeding
Inj. Ceftriaxone 2x1 g
is confirmed, PPIs should be discontinued.
ISDN 2X5 mg PO
Propranolol 2x40 mg PO
Lactulose is effective in prevention of HE in
Inj. Omepazole 2x40 mg
patients with cirrhosis and acute variceal
Inj. Kalnex 3x500 mg
bleed.
Inj. Ondansetron 3x4 mg
Inj. Vit K 3x1
Lactulosa syr. 3xCI PO
 KASUS TEORI

Prognosis

Berdasarkan Derajat Keparahan menurut

kriteria Child-Pugh
Ad Vitam : Dubia ad malam
Ad Fungsionam : Dubia ad Bonam
Total Skor pada pasien 9-10
Ad Sanationam : Dubia ad Bonam
Termasuk dalam Child B/C yang
menunjukkan kerusakan hepar yang berat
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