Clinical Anatomy of GI and Hepatobilier

Anatomy Session I
Block 3.3

Erwin Widi N.

Esophagus

Achalasia
GERD Barrets esophagus
Hiatal hernia
Congenital : - Diafragmatica Hernia
- Atresia esophagus & TE
fistula

Achalasia
Definisi : failure / lack of relaxation.
Motor disorder of esophageal smooth
muscle > LES doesnt relax normally
with swallowing ditambah kegagalan
fungsi peristaltik dr esophageal body.
Berdasar etiologi :
Primary achalasia: idiopathic (loss of
smooth muscle ganglion cells of plexus
myentericus Auerbach)
Secondary achalasia: often caused by
gastric carcinoma that infiltrates
esophagus

Temuan klinis :
1. Regurgitasi (bentuk persis makanan,
blm bercampur gastric juice: tdk terasa
asam)
2. Pulmonary aspiration
3. Retrosternal fullness
4. Dysphagia
Classic
5. Chest pain
triad :
6. Weight loss
1,4,6

Ciri penderita achalasia :

- makan lambat
- minum air banyak utk
membantu menelan
- twist the upper torso
- elevated the chin & extend
the neck
- berjalan setelah makan

 Patofisiologi & komplikasi:

Destruction of
smooth
muscle cells
of Plexus
Myentericus
Auerbach

Mucosal
irritation
(retention
esophagit
is)

Motoric
dysfuncti
on, LES
failed to
relax

Retensi
makanan
di
esofagus

Disfagia,
retrosternal fullness,
chest pain & other
symptoms
pneumoni
a

REGURGITATI
ON

Metaplasi
a>
esophage
al
carcinoma

Dx :

Chest X-Ray
Barium meal

PULMONA
RY
ASPIRATIO
N

bronchospa
sm

Lung
abscess
hemoptysi
s

 Treatment :
Non surgical
Anticholinergic drugs
Calcium channel
blocker (nifedipine
dkk)
Botulinum toxin
injection
(intrasphincteric via
esophagoscope)
Balloon dilatation

Surgical
Distal
esophagomyotomy
Laparascopic
esophagomyotomy

 Normal Anatomy of LES

Berbeda dgn UES (kerja m.cricopharyng), pada LES
tidak ada struktur anatomi khusus yg berperan sbg
sphincter.
Mekanisme sphincter terjadi krn 3 proses fisiologis
berikut, yg meningkatkan tekanan di
esophagogastric juntion:
1. Otot polos di 1/3 distal
esophagus normalnya
berada pada kondisi tonic
contraction. Akan relax
pada saat menelan
kemudian kembali ke
kondisi semula
2. Sling fibers of the cardiac
gaster
3. Diaphragm (terutama saat
inspirasi > diameter AP
diafragma (++) >

GERD
Berdasar etiologi :
Kelemahan / disfungsi LES (lihat lg penyusun LES)
Plg sering karena kerusakan diafragma crural muscles

Kecendurungan gastric content utk reflux :

1. Gastric volume increased

After meals (fisiologis)

Pyloric obstruction
Status hipersekresi asam lambung (misal: pasien gastritis)

2. Gastric content near the Gastroesophageal Junction

Berbaring atau membungkuk (fisiologis)

Hiatal hernia

3. Gastric pressure increased

Pregnancy (fisiologis)
Obesity
Ascites

 Sign & symptom :

Regurgitasi (makanan/bolus
+ gastric juice)
Pyrosis / heartburn (epigastric
/ retrosternal area)
Disfagia
Chest pain
Cough
Aspiration

Derajat keparahan bergantung pd :

Jumlah reflux material per episode
Frekuensi
Rate of clearance (gravity & peristaltik)
Kerja saliva utk menetralisir

Diagnosis approach :
1. Documentation of mucosal injury (barium meal, esophagoscopy, &
mucosal biopsy)
2. Documentation & quantitation of reflux (24h esophageal pH recording)
3. Cari penyebab (apakah disfungsi LES, atau keadaan lain yg meningkatkan
kecenderungan reflux lihat etiologi)

 Patofisiologi & komplikasi :

GERD

MILD
ESOPHAGI
TIS
Hasil
endoskopi
bisa
normal

Risiko
Adenocarcino
ma
Esophagus
meningkat

Gastric
juice
mendestru
ksi
mukosa
esophagus

REFLUX
ESOPHAGI
TIS

EROSIVE
ESOPHAGI
TIS

PEPTIC
STRICTUR
E

Hasil endoskopi
nampak
kerusakan
mukosa,
kemerahan,
bleeding, ulcer &
eksudat

Fibrosis
(akibat
prolonged
NGT & vomit)

Bleeding kmd heal

by intestinal
metaplasia
(squamous >
columnar cells /
Barrets esophagus)

Luminal
constrictio
n

Barrets
Esophagu
s

 Treatment :
Non surgery :
Perubahan lifestyle (pengurangan BB,
posisi tidur dgn kepala lbh tinggi, hindari
makan dengan banyak minum air, hindari
kopi alkohol & makanan berlemak, dll)
Medikasi
Terutama mengurangi sekresi asam lambung
(mencegah munculnya symptom dan
komplikasi):
Antacide
H2 receptor blocker (ranitidine, cimetidine)
Proton pump inhibitor / PPI (omeprazole,
dkk) > the most effective

Surgery :
(Partial) Fundoplication
Gastric fundus is wrapped around the
esophagus
Indikasi : tdk membaik dgn PPI, relapse meski
sudah diberi medikasi, & severe case (ulcer,
stricture, Barrets esophagus).

Vagotomy (lihat di PUD)

Hiatal Hernia
Protrusi sebagian gaster ke mediastinum (posterior)
lewat hiatus esophagus diafragma.
Penyebab :
Weakening of the muscular part
of the diaphragm
Widening of the esophagus hiatal

Tipe :
Tipe I / sliding hiatal hernia (most common):
esophagus pars abdominal, cardia &
sebagian fundus gaster slide superiorly.
Symptom : regurgitasi (gastric juice content)
akibat kelemahan clamping action dr diafragma.

 Tipe II / paraesophageal / rolling hiatal

hernia : cardia remains normal, seringkali
fundus gaster meluas lewat hiatus
esofagus ke anterior dr esofagus.
Symptom : no regurgitasi, normal cardiac
orrifice.
Tipe III / mixed type : gabungan kedua tipe
di atas.

Congenital Diaphragmatic Hernia (CDH)

/ Hernia Bochdalek
Sebab : defek luas pd posterolateral diafragma di
sekitar trigonum lumbocostal (lewat foramen
Bochdalek)
Akibat : herniasi sebagian gaster & intestine ke
cavitas pulmo. Biasa diikuti hypoplasia pulmo (yg
terdesak intestine) > mortality rate 76%
Almost always di posterolateral sinistra dari
diafragma (sbb keberadaan liver di dextra berfx
sbg barrier)

Atresia Esophageal & TE

Fistula

5 varian anatomis atresia esophagus :

A. Esophageal atresia without TE fistula (8%)
B. Proximal esophageal atresia with proximal TE fistula (1%)
C. Proximal esophageal atresia with distal TE fistula (85%)
D. Proximal esophageal atresia with double (proximal & distal) fistula
(2%)
E. H-type TE fistula without esophageal atresia (4%)

Gaster

Mallory-weiss tear
Peptic ulcer disease
About n.vagus
Vagotomy
Gastrectomy
Congenital : Hipertrofi pilorik stenosis

Mallory-Weiss Tear
Kontribusi 10% kasus dr Upper GI
bleeding.
Definisi : robekan pd proximal
mukosa gaster dekat dgn
esophagogastric junction
Etiologi : unclear, biasanya
disebabkan muntah & batuk yg
vigorous
>90% pasien sembuh spontan, 10%
membutuhkan terapi
Dx : endoscopy (robekan mukosa bs
dgn perdarahan maupun tdk)
Tx :
Non surgery : transfusi packed RBC &
endoscopic therapy (by injection or
thermal energy)
Surgery : laparotomy

Peptic Ulcer Disease

Ulcer : mucosal erosion > 0,5cm
Duodenal ulcer 4x lbh sering drpd gastric ulcer
Etiologi & patogenesis :
a) Infeksi H.pylori (60% gastric & 90% duodenal ulcer)
Stimulasi
sekresi
gastrin

Kolonisasi
H.pylori

Sekresi asam
lambung o/
parietal cell
(++)

Erosi
mukosa

Ulcer
formation

b) NSAID use (terutama gastric ulcer)

Prolong use
of NSAID
(aspirin &
ibuprofen)

Blockin
g COX1

Inhibisi
sekresi
Prostaglandi
n

Mucos
secretion
(--)

Proteksi
thd asam
berkurang

Klasifikasi berdasar lokasi & tipe:

)
)
)
)

Tipe
Tipe
Tipe
Tipe

1
2
3
4

:
:
:
:

primary gastric ulcer, di proximal anthrum di curvatura minor

duodenal ulcer (bs secondary akibat tipe 1)
prepyloric or channel ulcer
ulcer di proximal gaster / cardiac gaster

 Sign & symptom :

Epigastric pain
Abdominal fullness
Bloating (kembung)
Nausea & vomit
Pyrosis / heartburn
Hematemesis (bleeding directly from ulcer atau
krn kerusakan pd esofagus)
Melena

Karakteristik pain :
Lokasi ulcer bisa bervariasi
Nyeri dikarenakan ulcer, namun ber+ parah o/ asam lambung
Gastric ulcer (hunger-pain-food-pain/HPFP); Duodenal ulcer (hunger-painfood-relief/HPFR).
Nyeri pd gastric ulcer akan muncul & meningkat segera stlh makan krn
sekresi HCl akan meningkat seiring masuknya makanan dan oleh krn kerja
lambung yg berat.
Sedangkan pd Duodenal ulcer, segera stlh makan nyeri akan dirasa
berkurang sebab lambung sdg mendigesti makanan dan sphincter pylori
tertutup. Stlh kira-kira 2-3jam makanan di proses di lambung dan akan di
release ke duodenum baru terasa nyerinya.
Komplikasi :
GI bleeding (ulcer mengerosi vasa) > Dx bs dgn tanda2 bleeding & NGT
aspiration ataupun endoskopi
Perforasi (severe ulcer > perforate the wall > konten gaster / duodenum
tercecer ke cavum abdomen > chemical peritonitis > bacterial peritonitis)

 Dx :
Barium meal
Endoskopi (nampak ulcer, bs clean ulcer,
bekas perdarahan ataupun active
bleeding)

Dx adanya infeksi H.pylori :

Blood test (tanda infeksi & antibody
level)
Biopsi spesimen (via endoskopi)
Urea breath test

Tx :
Non surgery
Anti-sekretorik (antacide, H2 RA, PPI)
Endoskopi (bipolar elektrokoagulasi & heater
probe therapy)
Patient using NSAID : tambahkan Misoprostol
(atau analog PG lainnya)
Patient infected H.pylori :
2 choice of antibiotic : amoxicillin, metronidazole,
tetracyclin, etc
1 PPI : omeprazole, pantoprazole, etc

Surgery
Gastrectomy (distal, subtotal & total
gastrectomy) + rekonstruksi
Vagotomy

Vagus nerve (N. X)

Table: Summary of n.x

DIVISION / PARTS + course

BRANCHES

Cranial
Keluar dr sulcus postolivarius
setinggi medulla oblongata

- Meningeal branch
- Auricular branch

Cervical
Keluar dr cranium via foramen
jugular, msk ke carotid sheaths,
berlanjut ke root of neck

- Pharyngeal branch (motor)

- Cervical cardiac branches
- N.laryngeus sup (r.internus-sensor;
r.externus-motor)
- N.laryngeus reccurent dextra
(mixed)

Thoracic
Msk lewat apertura thoracis
superior, (LARP) left vagus > anterior
esophageal plexus, right > posterior

- N.laryngeus reccurent sinistra

(mixed)
- Pulmonal branches
- Thoracic cardiac branches
- Plexus esophageal

Abdominal
Truncus vagalis ant & post msk
abdomen via hiatus esophageal

- Esophageal branches
branches
- Hepatic branches
branches

- Splenic
- Renal

Modalitas :
Somatic (general) sensory: inferior pharynx & larynx)
Visceral sensory: organ thorax & abdomen
Taste sensation: taste bud in epiglottis
Somatic (branchial) motor: palatum molle
Visceral motor (parasimpatis): organ thorax & abdomen

Vagotomy
Macam:
Truncal vagotomy
memotong trunkus vagalis, krn
mengorbankan inervasi ke viscera
abdomen lain
Selective gastric vagotomy
memotong stomach branches,
cabang lain (pylorus, hepatic,
intestinal branches, dll) msh
berfungsi. Semua efek
parasimpatis ke gaster ditiadakan
Selective proximal vagotomy
memotong cabang dr stomach
branches yg spesifik ke sel
parietal, shg menekan sekresi
asam, namun fungsi parasimpatis
gaster yg lain msh dipertahankan

Gastrectomy + Rekonstruksi
A

Pilihan rekonstruksi pd
gaster :
1. Gastroduodenostomy
2. Gastrojejunostomy

Macam gastrectomy :
1. Distal gastrectomy
(anthrectomy)
Mengangkat bagian B-C /
anthrum gaster.
2. Subtotal gastrectomy
Mengangkat bagian A-C.
Semua bagian gaster
(corpus, anthrum & pylorus)
diambil, menyisakan fundus
gastrica.
3. Total gastrectomy
Semua bagian gaster
diangkat.

Hipertrofi Pilorik Stenosis

Hipertrofi > m.sphincter
pylorus
Stenosis > canalis pyloricus
Temuan klinis :
Muntah proyektil, bile free,
bolus+gastric juice
Palpable mass di daerah pylorus

Dx : (single bubble)
barium meal / OMD
Plain photo

Komplikasi : dehidrasi &

aspirasi
Tx :
Non surgery : resusitasi cairan
Surgery : pyloromyotomy

Duodenum
Hernia paraduodenal
Congenital : Atresia / stenosis
duodeni

Hernia Paraduodenal
A loop of intestine that enters
paraduodenal fold and fossa (lie to
the left of duodenum pars ascenden,
around flexura duodenojejunales)

Atresia / Stenosis Duodeni

Atresia: complete
obstruction; stenosis:
partial obstruction
Lokasi tersering di
duodenum pars
horizontal
Symptom: regurgitasi
& vomit (bilous vomit)
Dx : (double bubble)
Plain photo
Barium meal / OMD

Small Intestine - Appendix

Small bowel obstruction

Intususepsi
Congenital : Diverticulum Meckel
Acute appendicitis

Small Bowel Obstruction

Penyebab bisa diklasifikasikan menjadi: (a)
extrinsic to the intestinal wall; (b) intrinsic to the
intestinal wall; (c) obstruksi intraluminal /
obturator. Intrinsik
Ekstrinsik
Intralumi
nal
Adhesion

Congenital
Malrotasi, cyst,
dll

Hernia
eksternal
(inguinal,
femoral, dll)
internal
(diafragmatica,
paraduodenal,
dll)

Inflamasi
infeksi
IBD, diverticulitis,
dll
Neoplasma
Primary &
Metastatic

Neoplasma

Traumatic
Hematoma

ekstraintestinal

Miscellanous
Intususepsi

Gallstone

Enterolit
h
Bezoar

Common cause of
small bowel
obstruction (in
industrialized
countries) :
1. Adhesion (60%)
2. Neoplasma (20%)
3. Hernia (10%)

 Tipe :
Simple obstruction : intraluminal mechanical blockage
Strangulating obstruction : close-loop obstruction > vascular
compromise > risiko iskemia (++)
Classic sign of strangulation: tachycardia, fever, leukositosis &
constant, non-cramping abdominal pain

Temuan klinis (cardinal symptom) :

Colicky abdominal pain
Distended abdomen
Diare (early) then konstipasi > obstipasi
Nausea & vomit

Komplikasi :
3rd space syndrome > dehidrasi & hipovolemi
Intraabdominal pressure (++)
Venous return (--)
Elevasi diafragma > compromising ventilation
Strangulation (iskemi > perforasi > peritonitis)

Dx :
Berdasar temuan (cardinal symptom, tanda strangulasi & tanda
dehidrasi)
Berdasar lab (tanda strangulasi lihat atas & tanda dehidrasi: cek Hct
[biasanya meningkat/hemokonsentrasi], cek kadar elektrolit serum)
Radiologis (USG, MRI, CT-scan, plain radiograph & barium study)

Tx :
Non-surgery
IV resuscitation & antibiotik
Tube decompression (NG suction > reduce pulmonary aspiration)

Surgery

Patofisiologi & Komplikasi

SBO

Intususepsi
Kasus obstruksi intestine yg cukup srg terjadi terutama pd infant & early
childhood
50% kasus terjadi pd usia 3bulan 1 tahun
Etiologi : idiopatik, diperkirakan krn inflamasi pd usus (enteritis).
Penyebab bermacam2, spt: infeksi bakteri, virus, parasit maupun cacing.
Tipe :
Ileocaecal / ileocolic (most common type)
Jejunojejunal
Colocolic (< 5% kasus)

Sign & symptom :

Acute abdominal pain
Distended abdomen
Screaming & drawing up the legs
Vomit, diarhea
Blood in stool (occult / hematochezia)

Temuan klinis & lab:

RLQ feel empty
Palpable sausage-shaped mass (RUQ / midabdomen)
Intususepsi terpalpasi saat rectal exam
Febril & leukositosis

 Dx :
Plain radiograph
Barium enema
USG

Tx :
IV rescucitation
NGT insertion
Antibiotics
Hydrostatic barium enema

Ileo-colic
intussusception

Diverticulum Ilei (Meckel)

Most common congenital anomaly of small
intestine (2% populasi)
True diverticulum
Lokasi : ileum terminal (pd antimesenteric
border), 74% free & 26% melekat pd umbilicus
Etiologi : incomplete closure of ductus
omphaloentericus (vitelline duct)
Karena sel yg melapisi ductus omphaloentericus
adl sel pluripoten, dpt ditemukan berbagai variasi
mukosa dr diverticulum ini (ileal type > tersering,
gastric, jejunal, pancreatic, or colonic type)
Temuan klinis : (jika tjd inflamasi)
RLQ pain (mimicking appendicitis)

Komplikasi :
Ulcer > hemorrhage
Perforation > peritonitis

Tx : diverticulum excision

Acute Appendicitis
Etiologi : unclear, most common: hiperplasia folikel limfoid
(akibat viral infection, parasit cacing & tumor) & fecalith
Patogenesis :
Mucous
hiperplasi folikel
limfoid, fecalith,
other factors

obstruksi
lumen
appendix

Patofisiologi & komplikasi :

inflama
si

Stage :

Distension of
the lumen &
intraluminal
pressure (++)

Lymphatic &
venous
obstruction
(mulanya)
diikuti arterial
compromise /
iskemia

secretion
menump
uk
Bacterial
overgrow
th

Nekrosis,
diikuti
transloka
si
bakterial

INFLAMMATI
ON

Perforate
d (konten
intralumi
nal
terburai)

PERITONIT
IS

Simple suppurativa gangrenous rupture / perforated abscess

appendicitis

 Temuan Klinis & Lab :

Migrating pain : visceral colic pain
(T10 / periumbilical) > severe constant
pain (RLQ / Mc Burney point akibat
peradangan peritoneum lokal)
Anorexia (hampir pd semua pasien),
nausea & vomitus (50-60% kasus)
Temperatur normal / mildly elevated
37,2-380C
Leukositosis (10.000-18.000 cells/uL)

Tanda peritonitis (perforated

appendicitis) :
Muscle guarding
Rebound tenderness
Fever (> 38,30C)
Leukositosis (> 20.000 cells/uL)

 Px patognomonis :
Nyeri tekan/tenderness RLQ (Mc Burney)
Rovsing sign Psoas sign

Obtura
tor
sign

Px penunjang :
Blood tests (AL, differential WBC)
Radiologis
Ct-scan (melihat enlarged & thicked wall of appendix)
USG (exclude others disease: ovarian cyst, ectopic pregnancy, etc)
Appendicogram (foto dengan kontras)

Alvarado Score for Acute Appendicitis

SIGNS

POINTS

RLQ tenderness

Rebound tenderness

Elevated temperature (> 37,30C)

SYMPTOMS
Migrating pain to RLQ

Anorexia

Nausea or vomitus

LABORATORY VALUES
Leukocytosis (> 10.000 cells/uL)

Leukocyte left shift (> 75% neutrofil)

Intervention based on score (Mc Kay, 2007) :

I. >= 7 : surgery consultation
II. 4-6 : CT scan recommendation
III. <= 3 : unlikely appendicitis, observasi, rescoring

 Treatment :
Non surgery :
IV fluid rescucitation
Antibiotik profilaksis

Surgery :
Laparoscopic appendectomy
Open incision
Transveral incision (Davis-Rockey)
Oblique incision (Mc Arthur-Mc Burney)

Large Intestine

Volvulus
IBD
Diverticulosis & diverticulitis
Large bowel resection
Rekonstruksi
Congenital : Hirschprung disease

Volvulus
Berpotensi mjd volvulus : intraperitoneal organ
(caecal, colon transversum & colon sigmoid) >
karena mobile
Organ retroperitoneal: affixed to the back muscles
(tdk mobile)
Tipe tersering:
Cecal volvulus
Sigmoid volvulus

Risk factor : distensi colon, poor intake of fluids &

dietary fiber
Komplikasi: infarction, bs terjadi lwt 2 mekanisme
a) Torsi vessel yg mensuplai segmen volvulus tsb,
interrupting inflow & outflow.
b) Torsi intestine > close-loop obstruction > strangulasi.

Tanda iskemia intestinal :

)
)
)
)

Increasing abdominal pain

Rebound tenderness
Sepsis
Acidosis

Cecal Volvulus
Temuan klinis :
Sudden onset abdominal pain (mildmoderate)
Nyeri biasanya memburuk stlh tjd iskemia
Distensi abdomen
Palpable mass in LUQ or midabdomen

Dx :
Plain radiograph (dilated & displaced cecum,
biasanya di left abdomen)
Barium enema (dpt jg meringankan pain &
distensi pd volvulus, jika blm tjd iskemia)

Tx : Surgery
Cecopexy > viable cecum
tacking of the cecum to the right paracolic gutter
with suture

Cecectomy > non-viable cecum, diikuti

rekonstruksi (ileostomy sementara, atau lgs
ileocolostomy)

Sigmoid Volvulus
Risk factor : pd pasien konstipasi dan pemberian
laxative berlebih, shg tjd megakolon, dgn dilatasi
maksimal pd sigmoid
Karakteristik pasien dgn sigmoid volvulus : elderly,
debilitated/lemah & pny kondisi patologis lain
Temuan klinis (srg tdk spesifik, krn plg bny pd
elderly):
Konstipasi
Abdominal distention

Dx :
Plain radiograph
Barium enema
CT-scan

Kasus ini mirip dgn cecal volvulus, namun perlu

diingat bbrp hal berikut membedakan manajemen
kedua kasus di atas (faktor pasien elderly pd sigmoid
volvulus) :
Initial condition pasien sigmoid volvulus srg lebih buruk
Morbiditas & mortalitas lbh tinggi pd sigmoid volvulus

Tx : Surgery
Sigmoidectomy, diikuti rekonstruksi (Colostomy
sementara, atau lgs dibuat coloproctostomy)

IBD
Macam : UC & CD
Kesamaan:
Autoimmune disease > extra-intestinal disease,
seperti: arthritis, pyoderma gangrenosa,
eritema nodusum, iritis/uveitis, primary
sclerosing cholangitis, ankylosing spondylitis
Sign & symptom : abdominal pain, weight loss,
nausea, vomit, rectal bleeding, diarrhea,

Komplikasi :
Toxic megacolon
Bowel perforation > peritonitis
Increase risk of CRC

Treatment :
Mild: imunosupresan
Steroid : prednison
Methotrexate

Severe case: bowel resection (ileocecectomy,

colectomy, dkk tergantung lokasi) dgn
rekonstruksi (ileostomy, colostomy, dkk yg
sesuai)

SIGN

CROHNS
DISEASE

ULCERATIVE COLITIS

Karakteristik lokasi

Bisa manapun dari

GIT (mulut-anus)

Terbatas pada colon

dan rectum

Keterlibatan organ

Mayoritas di mulai
dari ileum terminal
ke arah distal.
Colon: usually
Rectum: seldom

Di mulai dari
colon/rectal,
penyebaran ke arah
proximal (disebut
extensive UC jika lewat
flexura lienalis)
Colon: always
Rectum: usually
Ileum terminal: seldom

Perianal disease

Common

Seldom

Keterlibatan bile duct /

Primary sclerosing
cholangitis

No increase rate

Higher rate

Disease distribution

Skip lesion

Continue lesion

Kedalaman
inflamasi
Transmural
Dangkal, mucosa layer
SYMPTOM
CROHNS DISEASE
ULCERATIVE
(dalam) COLITIS
Stenosis
Fever

Common

CommonIndicate severeSeldom
case

Weight loss

Often

More seldom

Defecation

Sering spt bubur,

kdg2 steatorrhea

Sering spt mukus

disertai darah

Tenesmus

Less common

More common

Fistule

Common

Seldom

Tabel
Perbedaan
Sign &
Symptom
UC dan CD

Diverticular Disease

Diverticula : herniasi mucosa colon

Acquired
diverticula
=
false
diverticula, krn bagian
yg
protrude hanyalah stratum mukosa
Etiologi : low intake of dietary fiber.
Akibatnya bulk stool berkurang, shg
stratum
muscular
colon
memberikan tekanan yg berlebih pd
lumen
menyebabkan
stratum
mukosa mendesak keluar (herniasi)

Lokasi : bs dimana saja dr

colon, tersering di sigmoid
Karakteristik :
asimptomatis, kecuali tjd
komplikasi (bleeding &
inflammation)
Dx : Barium Enema or
Colonoscopy

Diverticulitis
Temuan Klinis :

LLQ pain (pd colon descenden/sigmoid) dsb juga left-sided

appendicitis
Pd pasien diverticulitis dgn RLQ pain, 11/12 pasien dilakukan
laparotomi dgn dx awal appendicitis
Fever & chills
Small bowel adhered to colon > lumen kolaps > develop sign &
symptom SBO (nausea, vomit, distensi abdomen, & konstipasi)

DD : appendicitis, salpingitis, PID, colon cancer, IBD, etc.

Dx :

Acute diverticulitis > hindari BE & Colonoscopy

Gunakan CT-scan or USG

Komplikasi :

Bleeding
Perforation > abscess > diffuse peritonitis
Scar & stricture in colon lumen
Internal fistula (colovesical, colovaginal, dll)

Tx :

Non surgery (IV antibiotik > mayoritas membaik)

Surgery (Indikasi: tdk membaik dgn antibiotik, peritonitis &
close-loop obstruction)

Colectomy, tergantung letak lesi (plg sering sigmoidectomy)

Rekonstruksi
(contoh:
Hartmann
procedure
>
Kombinasi
sigmoidectomy dgn colostomy dan penutupan rectal stump. 8-12weeks
kmd
disambung,
coloproctostomy)

Large Bowel Resection

A-B : ileocecectomy
B : cecectomy
A-E : hemicolectomy dextra
A-F : extended hemicolectomy
dextra
D-G: transverse colectomy
F-H : hemicolectomy sinistra
E-H : extended hemicolectomy
sinistra
H-I : sigmoidectomy
I-J : proctectomy
H-J : proctosigmoidectomy
A-I : subtotal colectomy
A-J : total proctocolectomy

C
B

A
H
I
J

Rekonstruksi (-stomy)

Macam rekonstruksi pasca -ectomy:

a) Primer : langsung dibuat anastomosis.
b) Sekunder : dibuat stoma terlebih dahulu,
bagian proximal & distal dr usus yg diangkat
dijahit, bbrp saat kmd baru dianastomosis
(menunggu pemulihan).
Prinsip penamaan:
a)
Nama anastomosis sesuai organ yg
disambung (mis: ileocolostomy,
proctocolostomy, ileoproctostomy, IPAA, dll)
b)
Nama stoma sesuai organ yg dipakai
(ileostomy, colostomy, dll)
Prinsip/syarat pembuatan stoma (mis: ileostomy
& colostomy), agar fecal continence baik:
1. Menembus m.rectus abdominis (fx: sbg sphincter
mechanism)
2. Bukan pada struktur tulang
3. Bukan pada midline / melewati umbilicus

Misal nih ada soal, titik pembuatan stoma yg

terbaik adalah (lihat gambar kanan) : jawabannya
D ya!
Alasannya: A di luar m.rectus abdominis; B
mengenai tulang; C pada midline.

C
D

Hirschprung Disease
Kelainan kongenital akibat kegagalan
migrasi krista neuralis ke colon.
Tidak terbentuk sel ganglionik pd plexus
myentericus (Auerbach) dan plexus
submucosal (Meissner)
80% kasus melibatkan area rectosigmoid,
10% kasus meluas ke proximal flexura
lienalis, dan 10% di antaranya melibatkan
keseluruhan colon & ileum terminal.
Temuan Klinis :
Delayed meconium (>24h)
Abdominal distention
Bilous vomiting
Severe diarrhea alternating with constipation

Dx :
Barium enama
Rectal biopsy
Anorectal manometry

Anorectal
Hemorrhoid
Congenital : Malformatio Anorectal
Proctectomy (APR & LAR)

Hemorrhoid
Klasifikasi (berdasar linea dentata):
Hemorrhoid interna (lapisan luar: mukosa)
Hemorrhoid externa (lapisan luar: kutis)

Faktor risiko :
Tekanan intraabomen yg tinggi (obese,
pregnancy, konstipasi kronis, batuk kronis, dll)
Change in bowel habit
Diet rendah fiber
Sedentary life (duduk terlalu lama, exercise -)
Kebiasaan BAB dgn jamban duduk (terutama
yg durasinya lama)

Sign & symptom :

Kebanyakan asimptomatis
Hemorrhoid interna: hematochezia, itchy,
painless
(kecuali tjd thrombosis / nekrosis)
Hemorrhoid externa: painful

Dx :
Rectal Exam / Toucher
Endoscopy (Anoscopy & Proctoscopy)

 Degree of Hemorrhoid
interna :
Grade I : bleeding but no
prolapse
Grade II : prolapse,
spontaneus reduction
Grade III : prolapse, manual
reduction
Grade IV : prolapse, cant
be manually reduced (risiko
strangulasi)
*prolapse hemorrhoid =
hemorrhoid interna yg
meluas dan terdorong
keluar dr anus

 Tx:
Non Farmakologis
Changing lifestyle
(menghindari risk
factor)
Diet tinggi serat
Endoskopi (Rubber
band & Sclerotherapy)

Farmakologis
Fecal softener
Fiber supplement
NSAID

Surgery
Electrocautery &
Cryosurgery
Hemorrhoidectomy
(excision or stapled)

Malformasi Anorectal
Wingspread Classification of Anorectal
Anomalies
Level

Female

Male

High

Anorectal agenesis
Rectal atresia
Fistula rectovaginal
Fistula rectocloacal

Anorectal agenesis
Rectal atresia
Fistula rectourethral

Intermedia
te

Anal agenesis without

fistula
Fistula rectovaginal
Fistula rectovestibular

Anal agenesis without

fistula
Fistula rectourethral

Low

Anal stenosis
Imperforate anal
membrane
Fistula anocutan
Fistula anovestibular

Anal stenosis
Imperforate anal
membrane
Fistula anocutan

Proctectomy
Indikasi: tersering adalah rectal cancer
2 pilihan metode yg bisa digunakan:
APR (Abdominoperineal Resection) :
pengambilan rektum disertai anus dan
mekanisme sfingternya
LAR (Low Anterior Resection) :
pengambilan rektum menyisakan anus dan
mekanisme sfingternya

AP
R

Pemilihan metode di atas melihat bny

faktor (spt derajat persebaran cancer,
regresi o/ radioterapi, dll)
Metode yg msh srg dipakai yaitu rule
of the finger (melalui DRE dan dilihat
apakah tumor terjangkau o/ jari
pemeriksa)
Jika terjangkau/teraba tumor berarti
memakai APR
Jika tidak teraba berarti LAR

Komplikasi APR :
Neurogenic bladder
Sexual dysfunction

LA
R

HEPATOBILIER DISEASE

Portal Hypertension
Tekanan normal porta: 5-10mmHg. Disebut hipertensi porta jika
tekanan >15mmHg
Resistens
Muncul
Patofisiologi
:

i&
tekanan
portal (+
+)
Etiologi:

Penuruna
n aliran
darah ke
hati

kolateral
portosistemik sbg
kompensasi

Vasodilator (+
+), sensitivitas
vasokonstriktor
(--)

1. Pre-hepatik (mis: oklusi v.porta, trombosis v.lienalis, hipertensi portal

non sirotik)
2. Intra-hepatik (klasifikasi ada 2 macam: a) sirosis dan non sirosis; b)
pre-sinusoid, sinusoid, & post-sinusoid)
3. Post-hepatik (mis: pericarditis, venoocclusive disease)

Dx (melihat kemgknan adanya sirosis jg):

. Radiologis (CT scan, MRI)
. Pemeriksaan invasif (arterial&spleno-portography, transhepatic
venography)
. Biopsi hati
. HVPG (Hepatic Vein Pressure Gradient) > mengukur tekanan porta

Tx (tersering pasien dtg bila sudah komplikasi [perdarahan

varises], lihat bagian varises esophagogastric)
Komplikasi : yg tersering adalah dilatasi (varises) vena-vena
terdekat terlebih dahulu (spt: v.gastrica sinistra/v.coronary,
v.lienalis). Vena-vena pembentuk anastomosis portocaval juga
bisa menjadi manifestasi dari hipertensi porta.
Lihat gambar slide berikutnya...

Vasodilat
asi
splanchni
c&
sistemik

Hyperdyn
a-mic
circulatio
n

Anastomosis Portocaval
LETAK

PORTAL

CAVAL / SISTEMIK

CLINICAL
CONDITION

Esophagus

v.gastrica
sinistra
(r.esophageal)

v.azygos
(r.esophageal)

Varises esophagus

Anterior
abdominal wall
(paraumbilical)

v.paraumbilical

v.epigastrica
superficial

Caput medusae

Rectum

v.rectalis
superior

v.rectalis media et
inferior

Hemorrhoid

Retroperitoneal

v.colica

v.retroperitoneal

No name

Manifestasi klinis:
1. Varises esophagus
2. Caput medusa
3. Hemorrhoid (di dpn
udah yaa..)
4. Splenomegaly
5. Ascites

Varises Esophagus
90% pasien sirosis mengalami varises esophagus,
25-30%nya hemorrhage
Angka kematian setiap episode hemorrhage 25%,
dan rekurensi (rebleeding) tjd pd 70% pasien
Komplikasi:
Bleeding > hematemesis & melena masif, hematochezia
Death (responsible for 1/3 of all death in cirrhosis & portal
hypertension patient)

Biasanya ketahuan klo udah bleeding, Dx :

Endoskopi (cari sumber perdarahan)
Tx:
Resusitasi cairan & transfusi darah
Farmakologis:
Beta-blocker (liver blood flow (-) > tekanan porta (-) )
Vasopresin (vasokonstriksi splanchnic vessel)
Somatostatin analog (octreotide)

Non-farmakologis:
Baloon tamponade
Endoskopi (sclerotherapy or rubber band ligation)

Surgery :
Portosystemic shunt
TIPSS

Caput Medusa

Ascites
Definisi : akumulasi cairan secara abnormal di
cavum peritoneum
Paling sering dijumpai pd pasien sirosis hati &
severe liver disease
Temuan klinis: abdominal distention, gizi
kurang (umumnya), otot atrofi, dan tanda2
kelainan kronis hati lainnya
Dx:
Berdasar temuan klinis & lab (blood test)
Px fisik (shifting dullness, fluid wave, knee-chest
position & puddle sign)
Radiologis (USG)
Abdominal paracentesis

Tx:
Medis:
Bedrest & diet rendah garam
Diuretic agent
Abdominal paracentesis

Operatif:
Porto-caval shunt
Peritoneal-vein shunt

 Ruang potensial (akumulasi

ascitic fluid) :

recessus hepatorenal

recessus subphrenicus

Saat berdiri cairan bs turun

ke pelvic cavity via
paracolic gutter

Biliary Tract

Biliary Tract Disease

1. Gallstone disease (cholelithiasis)
2. Cholecystitis
3. Gallstone in CBD
(choledocholithiasis)
4. Cholangitis
5. Congenital : Atresia bilier

Gallstone Disease /
Cholelithiasis
Terbentuk di gallbladder. Bisa bermigrasi ke distal : ductus cysticus,
ductus choledocus, ductus pancreaticus atau Ampula vater.
Tipe :
80% cholesterol & mixed stone
20% pigmented stone

Cholesterol & mixed stone

Konten : kolesterol monohidrat, garam Ca,
bile pigment, protein & fatty acid
Mekanisme penting : increased biliary secretion of
cholesterol, biasa pada pasien obese atau
diet tinggi kolesterol

Pigmented stone
Konten : kalsium bilirubinat (dominan)
Biasa pd pasien chronic hemolytic disease
atau alcoholic cirrhosis

Dx :
Plain film > deteksi radiopaque kalsium (kasus: 10-15% kolesterol & 50%
pigmented stone)
USG

 Sign & symptom :

Seringkali asymptomatik (terutama di dlm gall bladder)
Symptomatis jika sudah menimbulkan inflamasi atau
obstruksi
Gejala plg spesifik & khas: biliary colic. Yaitu severe pain
(akibat biliary contraction, terutama stlh makan berlemak) pd
epigastrium atau RUQ yg sering radiasi ke daerah
interscapular, scapula dextra dan bahu dextra
Nausea & vomit sering menyertai biliary colic

Temuan Klinis :
Fever (biasanya sdh komplikasi / peradangan)
Serum bilirubin (++)
Alkaline phospatase (++)

Lokasi tersering terjadi sumbatan / inflamasi :

Ductus cysticus
Ductus choledocus / choledocholithiasis

Cholecystitis
Berdasar penyebab :
Calculous cholecystitis (90-95%) :
terutama akibat obstruksi gallstone pada
ductus cysticus
Acalculous cholecystitis (5-10%) :
jarang, penyebab bervariasi: trauma
adenocarcinoma gallbladder
torsi gallbladder dan DM.

Sign & symptom :

Biliary colic > memburuk secara progresif
Radiasi ke interscapular area, scapula & bahu dextra (tanda terjadi
iritasi pd diafragma sensasi nyeri o/ n.phrenicus > C3-C5 dextra)
Anorexia, nausea & vomit
Jaundice (uncommon)

 Patofisiologi :
Prinsipnya sama dgn di appendicitis (monggo
dibaca lg)

 Temuan Klinis :
Fever
Trias
Leukositosis (10.000-15.000 cells/uL)
diagno
sis
RUQ tenderness
Serum bilirubin (mildly elevated, no symptom)
Murphy Sign (+)

Dx :
Berdasar triad &
temuan klinis lain
USG (identifikasi thickening of gallbladder wall)
CT-scan

Komplikasi :
Gangren & perforasi > bs diikuti abscess jika ada
superinfeksi bakteri > bs generalized peritonitis
Fistulization : biliary-enteric fistula

 Treatment :
Non surgery :
Analgetik & antispasmodik
Nutrisi parenteral (hindari oral intake)
Antibiotik profilaksis (mencegah peritonitis &
cholangitis)
Bedrest

Surgery :
Laparoscopic cholecystectomy
Open cholecystectomy

Choledocholithiasis
10-15% pasien cholelithiasis
Penyebab :
Gallstone (pigmented stone)
Sering pada pasien dgn kronik
hemolytic disease

Sign & symptom :

Asymptomatic
Biliary colic
Obstructive jaundice

Px lab (mirip dgn cholelithiasis) :

Serum bilirubin (++)
Alkaline phospatase (almost always elevated in biliary
obstruction)

 Komplikasi :
Cholangitis
Terjadi akibat ascending infection dari bacteria di duodenum.
Bisa terjadi krn bile duct sudah terobstruksi oleh gallstone.
Medical emergency
Sign & symptom : jaundice, fever, malaise, rigor & abdominal
pain (severe : hypotension & confusion)
Gambaran duktus : dilated, sclerosed & strictured ducts
Initial Tx : IV fluid & antibiotik

Pancreatitis

Px penunjang :

cholang
itis

Cholangiography
ERCP & MRCP
USG

Tx :
Choledocholithotomy
ERCP (Modalitas intervensi: endoscopic sphincterotomy,
stone removal, insertion of stent, dilation of stricture)

ERCP

Alat Dx sekaligus
Tx
Pilihan Tx lihat slide
sebelumnya...

Biliary Atresia
Kelainan kongenital yg cukup
jarang (1 per 15.000 kelahiran),
tapi kejadian ini 25-30%
berhubungan dgn anomali lain
seperti stenosis/atresia duodeni,
pancreas annulare, dll.
80% pd bile duct di atas level porta
hepatis, 15% pada ductus
choledochus, dan 5% pada ductus
hepaticus communis.
Etiologi : intrauterine
inflammatory process caused by
fibrosis of both the intrahepatic &
extra hepatic biliary tree.
Tx : Kasai hepatoportoenterostomy

Reference :
Sabiston, Textbook of Surgery
Schwartz, Principles of Surgery
Harrison, Principles of Internal Medicine
Buku Ajar Ilmu Penyakit Dalam FKUI
Keith L. Moore, Clinically Oriented
Anatomy 6th edition
en.wikipedia.org :D
dan lain-lain

.the end.