Asisten Anatomi 2013

APPLIED ANATOMY OF UPPER GIT AND

HEPATOBILLIARY ORGANS
The Foregut

CASE 1

2/80
Esophagus
 Esophagus
• Merupakan tabung muskuler yang menghubungkan pharynx dengan gaster.
• Berawal dari lanjutan laryngopharynx pada junction pharyngo-esophageal setinggi batas inferior cartilage
cricoidea (VC6).
• Secara external, junction pharyngo-esophageal terlihat sebagai bagian paling sempit dari esophagus oleh
karena musculus constrictor pharyngeus inferior pars cricopharyngeus (m. spinchter esophageal superior).
• Esophagus normalnya mempunyai 3 penyempitan, yaitu:
– (VC 6) Penyempitan Superior (Spinchter esophageal superior) yang dikarenakan musculus cricopharyngeus.
– (VT 3) Penyempitan Media (thoracic/broncho-aortic) saat esophagus menyilangi arcus aorta, dan saat menyilangi bronchus
principalis sinistra.
– (VT 10) Penyempitan Inferior (diaphragmatic) saat melewati hiatus esophagealis, suatu lubang yang terbentuk pada
diafragma, yang secara fisiologis disebut spinchter esophageal inferior.
• Esophagus menempel pada hiatus esophagealis oleh ligament phrenicoesophagealis, yang merupakan
kelanjutan dari fascia diaphragmatica
• Bagian terpendek esophagus, pars abdominalis terletak mulai dari hiatus esophagealis pada crus dextra
diaphragm hingga ostium cardiacum di gaster
Gaster
 Gaster
• Terdapat empat bagian penting dari gaster, yaitu;
– Cardia: bagian disekitar ostium cardiacum.
– Fundus: pelebaran superior pada inferior crus sinistra diaphragm.
– Corpus: bagian terbesar dari gaster, antara fundus dan anthrum pyloricum.
– Pars Pylorica: regio berbentuk corong, pelebarannya disebut anthrum pyloricum, dan saluran sempitnya disebut canalis
pyloricus. Pylorus merupakan lapisan otot polos sirkuler yang menebal dan terletak paling distal, berfungsi mengatur penyaluran
makanan dari gaster menuju ke duodenum. Pada posisi supinasi, pars pyloric berada pada planum transpyloricum (antara
incisura jugularis dan crista pubicum).
• Gaster memiliki dua cekungan (kurvatura), yaitu:
– Kurvatura minor, membentuk cekungan pendek pada margo dextra gaster. Bagian paling inferiornya adalah incisura angularis
(batas antara corpus dan pars pyloric).
– Kurvatura major, membentuk cembungan panjang pada margo sinistra gaster.
• Saat berkontraksi, mukosa gaster membentuk pelipatan-pelipatan yang disebut rugae gastric, yang sangat
nampak pada pars pyloric dan sepanjang kurvatura major.
• Saat menelan, terbentuk saluran yang disebut canalis gastrica yang terbentuk pada plica longitudinalis gastric
sepanjang kurvatura minor.
Duodenum
 Duodenum
Duodenum dibagi menjadi 4 bagian, yaitu :
• Pars superior  intraperitoneal, setinggi VL1.
Bagian proximal melekat pada ligament hepatoduodenale (bagian dari omentum minor) pada
superior dan omentum major pada inferior.
• Pars descenden  retroperitoneal, setinggi VL1-VL3.
Ductus choledocus dan ductus pankreaticus major bermuara pada dinding posteromedial, keduanya
bergabung membentuk ampulla hepatopancreatica yang akan bermuara pada papilla duodeni major
• Pars inferior/horizontal  retroperitoneal, setinggi VL3.
• Pars ascenden  intraperitoneal, setinggi VL3 - VL2.
Pars ascenden duodenum berujung pada junction/flexura duodenojejunalis. Pada junction tersebut,
terdapa penggantung yaitu musculus suspensorium duodeni (ligament of Treitz ) yang tersusun dari
otot skelet diaphragm dan jaringan fibromuskuler dari otot polos duodenum pars horizontal dan
ascenden. Kontraksi otot ini akan melebarkan sudut flexura duodenojejunales, menyebabkan
makanan dapat bergerak kearah distal.
Vaskularisasi Gaster
 Vaskularisasi Gaster
 From coeliac trunk
 Curvatura minoràA. gastrica
dextra et sinistra
 Curvatura majorà
A. gastroepiploica dextra et
sinistra
 Fundus & corpus bagian
superioràA. gastrica posterior et
A. gastrica posterior
 V. gastrica sinistra et V. gastric dextra
àV. porta hepatis
 V. gastrica posterior et V.
gastroepiploica sinistraàV. lienalis
 V. gastroepiploica dextraàV.
mesenterica superior
 V. mesenterica inferioràV. lienalis
 V. lienalis + V. mesenterica superior =
V. portae hepatisàheparàV.
HepaticaàV. cava inferior
Inervasi Gaster
• Simpatis: Nn. Splanchnici
major (T6-T9) 
membentuk plexus
coeliacus
• Parasimpatis:
- Truncus vagalis
anterior (berasal dari N.
vagus sinistra)
- Truncus vagalis
posterior (berasal dari
N. vagus dextra)
 Embryology

of Gaster
• Fusiform dilatation forms in the foregut in week 4;
this gives rise to the primitive stomach.
• The dorsal part of the primitive stomach grows
faster than the ventral part, resulting in the
greater and lesser curvatures, respectively.
• The primitive stomach rotates 90° clockwise
around its longitudinal axis.
• The 90° rotation affects all foregut structures and is
responsible for the adult anatomic relationship of
foregut viscera.
• As a result of this clockwise rotation, the dorsal
mesentery is carried to the left and eventually
forms the greater omentum; the left vagus nerve
(CN X) innervates the ventral surface of the
stomach; and the right vagus nerve (CN X)
innervates the dorsal surface of the stomach.
Esophageal Atresia & Tracheoesophageal fistula
 Esophageal Atresia & Tracheoesophageal fistula
• Esophageal atresia is associated with tracheoesophageal fistula in more than 85% of cases.
• Esophageal atresia results from deviation of the tracheoesophageal septum in a posterior
direction; as a result, there is incomplete separation of the esophagus from the
laryngotracheal tube.
• The other etiology of esophageal atresia is failure of recanalization of the esophagus during
the eighth week of development.
• A fetus with esophageal atresia is unable to swallow  polyhydramnios
• Excessive drooling may be noted early on after birth, and the diagnosis of esophageal atresia
should be considered if the infant fails oral feeding with immediate regurgitation and
coughing.
• Inability to pass a catheter through the esophagus into the stomach strongly suggests
esophageal atresia.
• A radiographic examination demonstrates the anomaly by imaging the nasogastric tube
arrested in the proximal esophageal pouch
 Mallory-Weiss Tear
“Longitudinal mucosal lacerations at the
gastroesophageal junction or gastric cardia.”
Achalasia
“ A condition in which the muscles of
the lower part of the esophagus fail to
relax, preventing food from passing
into the stomach.”

Berdasarkan causa:
Primary: loss of smooth muscle
ganglion cells of plexus myentericus
Auerbach
Secondary: infiltrasi gastric
ca/inflamasi kronis
Tampakan khas pada pemeriksaan X-
Ray: Bird’s beak appearance (dilatasi
esophagus proximal dari stricture)
Achalasia
Treatment :

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

Surgical
Distal esophagomyotomi
Laparascopic esophagomyotomy
Zenker Diverticulum
The pathologic process in Zenker
diverticulum involves herniation of the
esophageal mucosa posteriorly
between the cricopharyngeus (CP)
muscle and the inferior pharyngeal
constrictor muscles.
Therefore, by strict definition, a Zenker
diverticulum is a false diverticulum.
The retention of food elements and
secretions within the lesion’s pouch
frequently leads to halitosis,
regurgitation, aspiration, and
dysphagia in patients
Heartburn (Pyrosis)
The most common type of esophageal
discomfort or substernal pain. This
burning sensation in the abdominal
part of the esophagus is usually the
result of GERD or hiatal hernia.

Pyrosis is commonly perceived as a

“chest” (vs. abdominal) sensation.
Gastroesophageal
Reflux Disease (GERD)
• Normal Anatomy of LES:
• Mekanisme sphincter terjadi krn 3 proses fisiologis
berikut:
• Otot polos di 1/3 distal esophagus normalnya berada pada
kondisi tonic contraction. Akan relax pada saat menelan
kemudian kembali ke kondisi semula
• Sling fibers of the cardiac gaster
• Diaphragm (terutama saat inspirasi > diameter AP
diafragma (++) > menekan esofagus > tekanan (++) )
• GERD disebabkan karena lemahnya lower esophageal
sphincter:
• kerusakan diafragma crural muscles (paling sering)
• sliding hiatal hernia
• GERD  inflamasi pada esophageal lining  Barret’s
esophagus  cancer
GERD
Treatment :

Non surgery :
Perubahan lifestyle

Medikasi
Antacide
H2 receptor blocker (ranitidine, cimetidine)
Proton pump inhibitor / PPI (omeprazole, dkk) 
the most effective

Surgery :
(Partial) Fundoplication
Vagotomy (lihat di PUD)
 Barrett’s Esophagus

“Replacement of the normal stratified squamous epithelium lining of the

esophagus by simple columnar epithelium (Metaplasia columner) as a serious
complication of GERD. Increasing risk of esophageal carcinoma.
 Hiatal Hernia
Protrusi bagian dari gaster ke mediastinum posterior melalui hiatus esophagus (VT10).
Berdasarkan bagian gaster yg mengalami protrusi:

Sliding/rolling/axial hernia (95% Paraesophageal/nonaxial Mix: cardia dan fundus

of hiatal hernias): appears as a hernia: usually involves the mengalami protrusi
bell-shaped protrusion gastric fundus
 Radiology of hiatal hernia

Tipe 1 Tipe 2 Tipe 3

Schatzki’s ring
A Schatzki ring or Schatzki–Gary
ring is a narrowing of the
lower esophagus that can cause
difficulty swallowing (dysphagia). The
narrowing is caused by a ring
of mucosal tissue (which lines the
esophagus) or muscular tissue.
Several pieces of evidence link GERD
to the development of Schatzki rings
 Congenital Diaphragmatic Hernia
Congenital diaphragmatic hernia (CDH) is a condition in which a
hole in the diaphragm allows abdominal organs to move into
the chest, which prevents the lungs from developing normally,
resulting in pulmonary hypoplasia.
 Gastritis
Gastritis adalah proses inflamasi/peradangan pada lapisan mukosa dan submukosa
lambung sebagai mekanisme proteksi mukosa apabila terdapat akumulasi bakteri atau
bahan iritan lain. Proses inflamasi dapat bersifat akut, kronis, difus, atau lokal
 Peptic Ulcer Disease
“A lesion in the lining • Duodenal ulcer 4x lebih
(mucosa) of the digestive sering dibandingkan
tract, typically in the dengan gastric ulcer.
stomach or duodenum, • Causa tersering:
caused by the digestive – H. Pylori (60% gastric &
action of pepsin and 90% duodenal ulcer)
stomach acid.” – NSAID (dominan pada
gastric ulcer)
•Berdasarkan lokasinya:
–Primary gastric ulcer
–Duodenal ulcer
–Prepyloric/channel ulcer
–Proximal gaster/cardiac
•Berdasarkan karakteristik sakitnya:
–Gastric ulcer: hunger-pain-food-pain
–Duodenal ulcer: hunger-pain-food-relief (nyeri baru terasa lagi 2-3 jam setelah makan)
• 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)
• Scarring / stricture (ulcer > mengubah struktur mukosa > muncul stricture > narrowing the lumen >
gastric outlet obstruction)
Treatment:
– 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
Gastroscopy
 Gastrectomy
• Distal gastrectomy: B-C
• Subtotal gastrectomy: A-C
(menyisakan fundus gastrica)
• Total gastrectomy
 Rekonstruksi

Billroth I: distal gastrectomy + Gastroduodenostomy Billroth II: distal gastrectomy +

gastrojejunostomy
Rekonstruksi
Vagotomy
Truncal
Menghilangkan inervasi parasimpatis
pada visceral organ abdomen lainnya
Selective gastric vagotomy
Total gastric vagotomy, hilang efek
parasimpatis pada gaster (preserved
pada organ lain)
Selective proximal vagotomy
Hanya menghilangkan inervasi pada
sel parietalis yang fungsinya produksi
HCl
Congenital Hypertrophic
Pyloric Stenosis
Thickening of the smooth muscle
(hypertrophy) in the pylorus.

In neonates with pyloric stenosis, the

elongated overgrown pylorus is hard
and the pyloric canal is narrow,
resisting gastric emptying.
Congenital HPS
Clinical manifestation:
Muntah proyektil
Bile free (bolus+gastric
juice)
Terpalpasi massa pada
daerah pylorus
Diagnosis dengan OMD/Plain
photo: single-bubble appearance
Treatment: pyloromyotomy
Duodenal Atresia/Stenosis
“Absence or complete closure
(atresia) of a portion of the
channel (lumen) within the first
part of the small intestine
(duodenum), or partial
obstruction due to narrowing
(stenosis) of the duodenum.”
• Lokasi tersering pada duodenum pars
horizontalis.
• Clinical manifestation: bilous
vomiting, and/or regurgitation.
• Diagnosis dengan OMD/plain photo:
double-bubble appearance
Paraduodenal Hernia
Paraduodenal recess: an occasional
recess in the peritoneum to the left of
the terminal portion of the duodenum
located posterior to a fold containing
the inferior mesenteric vein (plica
paraduodenalis).
The Pancreas

CASE 2

32/80
Pancreas
Vascularization of Pancreas
Pancreatic duct
 Embryology of Pancreas
• From dorsal and ventral pancreatic buds
• dorsal pancreatic bud (larger and slightly cranial to ventral bud,
between dorsal mesentery)  most part of pancreas and distal
pancreas
• ventral pancreatic bud develops near the entry of the bile duct
into the duodenum and grows between the layers of the ventral
mesentery  uncinate process, part of the head of the pancreas,
and proximal pancreatic duct
• The proximal part of the duct of the dorsal bud often persists as an
accessory pancreatic duct
Blockage of
Hepatopancreatic Ampulla
Caused by gallstone from bile duct to
the constricted distal end of the
ampulla, sometimes caused by
pancreatic carcinoma.

blockage of the hepatopancreatic

ampulla  bile pigmen that
abnormally reflux  enter pancreatic
duct  Pancreatitis

“grey turner sign”, “Cullen sign”

A similar reflux of bile sometimes
results from spasms of the
hepatopancreatic sphincter.
Annular pancreas
Common Congenital defect of
pancreas

bifid ventral pancreatic bud around the

duodenum  fuse with the dorsal
bud  pancreatic ring

Pancreas encircles the second part of

the duodenum  duodenal
obstruction  pancreatitis
Pancreatic Cancer
Fifth leading cause of cancer death in
US
Most of the cancers (60%) occur in the
head of pancreas  obstructive
jaundice

Adjacent organs close to the pancreas

can be involved e.g. : duodenum,
gaster, liver, colon, spleen

Pancreatic metastases via the

lymphatic network
Rupture of Pancreas
can result from sudden, severe,
forceful compression of the abdomen

tears its duct system  pancreatic

juice enter the parenchyma of the
gland and invade adjacent tissues 
digestion by pancreatic juice is very
painful.
Pancreatectomy
Removal of the pancreas, mostly
because chronic pancreatitis.

The part of pancreas medial to the

duodenum will not be removed to
preserve duodenal blood supply.

Contraindications to distal
pancreatosplenectomy and spleen-
preserving pancreatectomy: metastatic
disease, peritoneal carcinosis, vascular
invasion, and pancreatitis involving the
entire pancreas.
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
Standard procedure for the diagnosis of
both pancreatic and biliary disease.
Fiber optic endoscope is passed through
the mouth, esophagus, and stomach 
papilla duodeni major by a cannula
The Liver

CASE 3

45/80
Liver position
Hepar
Couinaud’s Segment

Cantlie line
Hepar’s impressio
 Perihepatic spaces
Bare area

Epiploic
foramen
Arterial blood supply of hepar
Hepatic bile duct
Hepatic Portal System
v. Mesenterica inferior  v. lienalis

v. Lienalis + v. mesenterica superior 

v. porta hepatica

v. Gastrica dextra et sinistra  vena

porta hepatica

v. Porta hepatica  right and left

divisions  vv. Hepatica  v. hepatica
dextra, media, sinistra  VCI
Anastomosis Portocava
Cardia gaster:
v. gastrica sinistra (P)
v. esophagealis (C)

Periumbilical:
v. paraumbilicalis (P)
v. epigastrica superficial (C)

Retroperitoneal:
[veins of secondary retroperitoneal organ vs veins of
posterior abdominal wall]
v. colica sinistra (P)
v. lumbalis ascendens (C)

Rectum
v. rectalis superior (P)
v. rectalis media et inferior (C)
Embryology of Liver and
Gallbladder
Arises from hepatic diverticulum (from
foregut), differentiate become liver
cords and gallbladder, then grows
inside ventral mesogastrium, divides it
into anterior part (falciform ligament)
and posterior part (omentum minus)
Hepatitis
Kondisi dimana terjadi inflamasi pada
hepar. Biasanya disebabkan oleh
infeksi virus HAV. HBV, HCV, dkk.

Gejala umum: Fatigue.

Nausea/vomiting, Abdominal pain or
discomfort di epigastrik/RUQ, low
grade fever, jaundice, dsb.

Nyeri pada hepatitis dibawa oleh

plexus hepaticus melalui sympathetic
visceral afferent fiber secara
retrograde yg berjalan bersama trias
porta menuju ke plexus coeliacus lalu
ke medulla spinalis segmen T6-T9.
Hepatomegaly
Yaitu terjadinya pembesaran
(enlargement) dari hepar, basanya
diakibatkan hepatitis, heart failure,
dengue fever, peningkatan CVP, tumor,
dsb.

Hepatomegaly peregangan pada

capsula glisson  abdominal RUQ
pain.
Hepatomegaly  terpalpasi di regio
lumbal dextra.
Metastatic tumor : 2 rute
• Hematogen, via sistem vena porta
• Limfogen, biasanya dari right
breast (venous drainage sebagian
ke diafragma  bare area of liver)
Hepatic Cirrhosis
Chronic Inflammation or liver damage
(alcohol etc)  hepatocytes damage
 scarring and nodule Sirosis
hepatis  portal system constriction
 portal hypertension

Nodulasi pada hepar  hobnail

appearance

Portal hypertension  many

manifestations
Portal Hypertension
Biasanya diakibatkan sirosis hepatis 
stasis blood flow to hepar 
vasodilatasi pre hepaticum  ascites,
manifest di anastomosis portocava:

Cardia gaster  Varices esophagus 

ruptur  blood stained vomiting

Periumbilical  superficial abdominal

wall vein dilatation  caput medusae

Rectal  stasis of blood flow 

hemorrhoid
Portosystemic shunt
Salah satu treatment hipertensi portal
adalah dengan membuat shunt untuk
mengurangi stasis darah prehepatik 
dialihkan langsung ke sistem caval

Ada 3 jenis: Side to side, end to side,

central splenorenal portosystemic
shunt
Subphrenic and
hepatorenal Abscess
Inflamasi organ viscera 
ruptur/perforasi  eksudat purulen di
cavitas peritoneum  peritonitis 
mengalir ke recessus hepatorenal 
mengalir ke recessus subphrenicus

Drainase biasanya dengan pungsi pada

SIC 12 sehingga tidak perlu menembus
cavitas pleura
 Hepatic Lobectomy and Segmentectomy
Right hepatic lobectomy Hepatic segmentectomy
The Billiary System

CASE 4

63/80
Location of Gallbladder
The Gallbladder
 Billiary system
collum
Ductus hepaticus
dextra et sinistra

corpus Ductus hepaticus communis

Ductus cysticus

Ductus
fundus choledocus

Ampula Vateri
Common variations of Billiary duct
Cholelithiasis
Presence of calculi or stones in the
gallbladder:
• Cholesterol stones
• Pigment stones
causing RUQ colicky pain
Dx triad : RUQ tenderness, Fever, Lekositosis
More common in females (4F+2)
Risk Factors:
• Female
• Fat
• Forty
• Fertile
• +Fatty food

Called cholelithiasis if the gallstone is in the

gallbladder or cystic duct, if present in the
common bile duct  choledocolithiasis
Cholecystitis
Inflammation of the gallbladder
Bile becomes an irritant causing
inflammatory change in the walls of
the gallbladder.

Usually caused by gallstones,

aggravated by eating fatty food

Operative Tx: cholecystectomy

No bile  no fat disgestion 

Steatorrhea

If the inflammation occur in the billiary

duct  cholangitis
 cholecystoenteric fistula
Cholecystitis
Komplikasi:
Inflamasi menyebabkan adhesi ke
struktur sekitar.
Fistulasi  Cholecystoenteric fistula,
Cholecystocholedochal fistula (Mirizzi
syndrome type 2)

Tx operative: pada calculous

cholecystitis  cholecystectomy, pada
choledocholithiasis 
choledocholithotomy (via ERCP)
Clinical Sign of
Cholecystitis
“Murphy sign”  dielisitasi dengan
mempalpasi RUQ saat pasien
melakukan inspirasi dalam. Positif bila
inspirasi pasien terhenti akibat
merasakan nyeri pada RUQ.

“Boas Sign”  Nyeri rujuk pada regio

scapular dan bahu kanan. Diakibatkan
karena inflamasi pada gallbladder yang
turut mengeksitasi n. phrenicus dexter
dan dirasakan di dermatom C3-C5
Atresia Bilier
Biliary atresia is characterized by
obliteration or discontinuity of the
extrahepatic biliary system, resulting in
obstruction to bile flow.

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.

Operative Tx: Kasai

hepatoportoenterostomy
The Spleen

CASE 5

72/80
Spleen
LUQ or left hypochondrium region

The relations of the spleen are:

Anteriorly, the stomach
Posteriorly, the left part of the
diaphragm, which separates it from
pleura, lung, and ribs 9-11
Inferiorly, the left colic flexure
Medially, the left kidney
Spleen

Margo acutus/superior
Margo obtusus/inferior
Polus anterior
Rupture of Spleen
Mechanism of injury:

Severe blows on the left side 

fracture one or more of the ribs 
sharp bone fragments  lacerate the
spleen

Blunt trauma to other regions of the

abdomen  intra-abdominal pressure
↑  fibrous capsule of the spleen
rupture  ruptured spleen  profuse
bleeding (intraperitoneal hemorrhage)
 shock

“Kehr sign”
Splenomegaly
Etiology: portal hypertension,
granulocytic leukemia,
hemolytic/granulocytic anemia Schuffner scale I-VIII
Schuffner IV is in umbilicus
If its lower edge can be detected when
palpating below the left costal margin
at the end of inspiration, it is enlarged
about three times its “normal” size.
“Castell sign”
 Splenectomy
Subtotal/partial splenectomy Total splenectomy
Autotransplantation implant lien
Dapat digunakan untuk mencapai partial immunocompetence pada pasien muda
Accessory Spleen(s)
Splenic Needle Biopsy and Splenoportography
Mortui Vivos Docent

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