GASTROENTEROHEPATOLOGY SYSTEM

Centre of Gastroentero-Hepatology
Department of Internal Medicine
Wahidin Sudirohusodo General Hospital, Makassar
2010

Tingkat Kompetensi Dokter

Kemampuan 1 : mengenali & menjelaskan
(gambaran klinik, cara mendapat informasi lanjut
penyakit, rujukan yang tepat)
Kemampuan 2 : diagnosis & merujuk (buat
diagnosis, rujukan utk penanganan lanjut,
menindaklanjuti setelah kembali dari rujukan)
Kemampuan 3 : diagnosis, penatalaksanaan
awal, merujuk (A bukan gawat darurat, B gawat
darurat)
Kemampuan 4 : diagnosis, penatalaksanaan
mandiri & tuntas

ESOPHAGUS

Level of competent :
2

ACHALASIA
Lack of relaxation = failure of the LES to relax
Secondary features : aperistalsis of the body of
esophagus
DEFINITION :
primary motor disorder of esophageal smooth
muscle function with 3 diagnostic prerequisite
Relatively uncommon, prevalence 10/10.000;
incidence 0.5 cases/y/100.000 p.
Acquired disorders affecting any age group (30-60
y.o, uncommon before 25 yo); M=F

Prerequiste diagnostic
1. Complete absence of primary &
secondary peristalsis in the
smooth muscle, skeletal muscle
function normal.
2. LES doesnt relax completely with
swallow
3. Resting LES pressure usually high

Etiology
Remain a mystery
Associated with viral infection
(herpes), autoimmun disorders

Pathophysiology
Myenteric plexus :
loss of ganglion cells (inhibitory
function)
relative sparing of cholinergic
(stimulatory function)
persistent LES constriction

Clinical manifestation
Dysphagia solid & liquid (most solid food)
Regurgitation 60-90% with bending or
recumbent position,awekening with
previous nights supper in mouth
Heartburn : fermentation of food in the
aperistaltic esophagus
Weight loss
Chest pain

 Laboratory study : not helpful

Diagnostic study :
BARRIUM SWALLOW : atonic &
dilated esophageal body, narrowing
of GE junction birds beak

classical radiological features of

a dilated esophagus, retained
barium and an intralumenal
air fl uid level with smooth
tapering of the esophagogastric
junction.

Thoracic CT scan on a patient with

vigorous achalasia demonstrating
marked thickening of the distal
esophageal wall.
The esophageal lumen is not
dilated although it is filled with
contrast material.

MANOMETRY : absent distal peristaltis in

body (smooth muscle), incomplete LES
relaxation (residual > 8mmHg), high resting
LES (>45 mmHg)

The corresponding high-resolution manometry

depicts the same phenomena with bizarre
morphology of the esophageal contractile
activity apparent within the distal esophagus
and paucity of activity within the proximal
esophagus. An increased intrabolus pressure is
evident proximal to the nonrelaxing LES

Low (b) and high (c) power views of a myenteric ganglion showing
nitric oxide synthase (NOS)- immunoreactive neurons (*).
Numerous lymphocytes infi ltrate this region suggesting ongoing
chronic infl ammatory activity of the myenteric plexus. Such
inflammation may lead to the eventual destruction of the myenteric
neurons that characterizes the pathophysiology of achalasia.

 EsophagoGastroDuodenal
Endoscopic
(role out pseudoachalasia) :
observed retained food, esophageal
dilatation, feel apop at GE junction

Differential diagnosis
Secondary achalasia : associated
with various diseases (cancer,
chagas disease, amyloidosis, mixed
connective tissue
Pseudoachalasia : infiltrating cancer
at GE junction (older age, short
duration symptom & rapid weight
loss)

Pseudo-achalasia

Figure (a) Pseudo- or secondary achalasia. The

tapering in the
distal esophagus makes this barium esophagram difficult to
distinguish from idiopathic achalasia. Note the dilated
esophagus with intralumenal air fl uid level. (b) Abdominal
CT scan image in a patient with pseudo- or secondary
achalasia. This CT image demonstrates a stellate pulmonary
mass originating in the left lung invading the
gastroesophageal junction.

Esophageal spasm.
The
corkscrew
appearance results from
simultaneous
nonpropulsive
contractions
of
the
esophagus occurring at
multiple
levels.

Treatment
Palliative
Directed removing the functional
obstruction at the LES

PHARMACOLOGIC
Nitrates, CCB,
botox

ENDOSCOPIC
Pneumatic ballon
dilatation

SURGICAL
Heller myotomy

Complication
Esophageal cancer risk 2-7% : mean
interval 17yr, squamous cell type, 5y
survival <5%

Reff
Atlas of Gastroenterology (Wiley,
2009)
Primo Gastro (Lippincot, 2008)

Level of competent :
3B

CORROSIVE ESOPHAGUS
Injury of esophagus cause by a number of
caustic agent
Epidemiology
Appproximately 26.000 case/year, suicidal
gestsure most common & most injurious
compared to accidental ingestion
80% case accidentally in children < 5y.o
(consumed household cleaners)

Etiology
Severity of damage depends on
corrosive properties & the
consentration
Alkaline cleaning product = most
severe injury

class

Caustic agent

Product

Strong alkalis

Ammonia
Lye (sodium &
potasium hydroxide)

Cleaning product
Disc battery, drain
cleaners,
nonphosphate
detergent, paint
removers, washing
products

Strong acid

Hydrochloric acid

Muriatic acid,
soldering fluxes,
swimming poool
cleaners, toilet bowel
cleaners
Gun barrel cleaners
Antirust compounds
Toilet bowel cleaners
Battery acid, toilet
bowel cleaners

Nitric acid
Oxalic acid
Phosporic acid
Sulfuric acid

Miscellanous

Sodium hypochlorite

Liquid bleach

Pathopysiology
Alkali Esophagitis : liquefactive necrosis
(complete destruction of entire cell &
membranes)
Phase of Injury
Acute (day 1-4)

liquefactive necrosis ; sloughing or

ulcer not apparent <24hr, vascular
thrombosis, inflammation

Subacute (day 5-14)

Sloughing casts; esophageal wall

is thinnest, granulation,
fibroblast/collagen deposition

Cicatrization (day 15-3mon)

Fibroblast proliferate, further

collagen deposition, stricture
formation, epithelization

 intense pain: in
Acid esophagitis
the mouth and
anterior
coagulation
necrosis
with
chest
clumping
& opaficationof celluler
marked
salivation
cytoplasm,
retained
cell boundaries
inability to swallow and tachypnea.
Bloody vomitus containing pieces of
Clinical Manifestation
esophageal tissue signals severe damage
Early sign
&symptoms
not
realible and
Signs
of esophageal
perforation
indicator
of the severity
mediastinitis,
especially crepitation,
indicate
destruction
of the entire
A history
of chemical
ingestion
and
esophagus.
physical examination revealing
Inability to speak implies laryngeal
oropharyngeal burns (including white
damage.

membranes and edema of the soft palate

and uvula) usually confirm the diagnosis.

Laboratory study : not helpful

Diagnostic study :
Endoscopy (in the first 24 hours after
ingestion) delineates the extent and
location of the esophageal injury and
assesses the depth of the burn; (a week
after
ingestion)
to
assess
stricture
development.
Barium swallow (1 week after
ingestion and every 3 weeks
thereafter) may identify
segmental spasm or fistula
(no mucosal injury)

Classification of injury by
endoscopy
Endoscopic
findings

Hospital
stay

Risk of
strictur
e

Treatment

No injury

None

None

Discharge

Gastric only

Observe 2448 hrs

None

Liquid diet

Linear esophageal
injury

Observe 2448 hrs

Low

Liquid diet

Circumferential
injury

Observe at
least 48 hrs

High

NPO, NGT

Treatments
ABC, need for intubation?,
obvious sign of mediatinitis/
peritonitis requiring injury
Determine quantitiy & type ofcaustic
agent and time ingestion; is the container
available?
Emesis should not be induced (re-exposed
esophagus & larynx)
NG lavage is controversial, potential risk
include vomiting, perforation. If NG place,
aspirate before cold lavage

 If known acid & within minute injury :

large volume water/milk may dilute &
neutralize acid; otherwise NPO
Steroid : reduce potential for stricture to
high risk lesions, however no consensus
on their use.
- should only use in circumferential injury :
prednisone 1.5mg/kg/d & tapered over
2 months
- probably use in patients with airway
compromise & bronchospasm

 Antibiotics : role has never been

established (ampicillin)
In acute setting, get CXR or CT to role out
perforation before endoscopy
Prophylactic dilatation once acute injury
has resolved (3rd week)
Supportive treatment includes I.V. therapy
to replace fluids or total parenteral
nutrition while the patient cant swallow,
gradually progressing to clear liquids and a
soft diet.

Complication
Strictures

Esophageal cancer : 1000x fold risk,

begin endoscopy survailence 15
years after ingestion (every1-3
years)

Level of competent :
2

HIATUS HERNIA

GASTRITIS

Level of competent :
4

Level of competent :
2

Variceal GI bleeding

VARICES ESOPHAGUS
Prevalance : 50% of all cirrhotic (80% in
Child C, 20% in Child A)
Incidence : 10% per year in cirrhotic
Variceal bleeding :
- incidence :24% per 2 years w/ moderate
to large v.; 50% acute bleeding
- mortality : >20% w/1st bleed; 70% 5 y.
mortality; 40-50% will rebleed

Architectural disturbances

Increased hepatic vascular resistence

Garcia-Pagan JC, Grozmann RJ, Bosch J. In Clinical Gastroenterology and Hepatology. 2005; p.7

Pathophysiology
Portal hypertension : an increase in the portal
venous pressure gradient (PVPG) and is a
function of portal venous blood flow and
hepatic and portocollateral resistence
Hepatic venous wedge pressure gradient
(HVWPG) : represent the pressure difference
between the wedge hepatic vein (pv pressure)
& direct mesurement of abdominal IVC (free hv
pressure)
6 mmHg normally, > 10mmHg variceal
development, >12mmHg high risk bleeding

MAJOR SITE COLLATERAL

Risk factors for

rebleeding
-

Age > 60 y.o.

Large varices

Severe initial bleed

(Hb <8 g/dl on
admission)

- Renal failure
Only 50% of patients
with variceal
hemorrhage stop
bleeding
spontaneously & high
risk to recurrent
bleeding within 6
weeks

Opening of pre-existing
Vascular
communication

Increases in portal
pressure
and portal collateral blood
flow by meals, alcohol,
physical exercise,
increased
intraabdominal pressure

Garcia-Pagan JC, Grozmann RJ, Bosch J. In Clinical Gastroenterology and Hepatology.

2005; p.709.

COLLATERAL CIRCULATION
(VARICES)

 Clinical manifestation : upper GI bleeding

Laboratory study : Hb/Ht, PT/APTT
(bleeding)
Diagnostic study : screening UGIE
- no varices : repeat EGD 2-3y, no
prophylaxis necessary
- s. varices : repeat EGD 1-2y, consider bloker if Child C
- m to L.varices : 1st prevention EBL, bloker, etc

Fig. 4. Esophageal
varices.
a. Large variceal columns
b. Varix with cherry-red spot
c. Varix with red wale sign

Fig. Portal Hypertensive

Gastropathy (PHG)
a. Mild portal hypertensive
gastropathy
b. Severe PHG with active
oozing

Wu et al. Gastroenterological endoscopy 2002: 541-543

Treatment PHARMACOTHERAPY
VASOCONSTRICTORS
decrease in splanchnic blood flow & leads to
decrease in portal venous blood flow and portal
pressure (e.g vasopressin, somatostatin,
nonselective -bloker)
VASODILATORS
alter resistence by inducing changes in the
intrahepatic perivenular & perisinusoidal
myofibroblast as the smooth muscle component
of portocollateral vessels (e.g. nitroglycerine,
long acting nitrate, prazosine)

Acute Bleeding
Transfuse Hb to 8gm/dl (aggressive transfusion may
precipitate further portal hypertension & bleeding)
consider : platelets, FFP, lactulosa, endotracheal
intubation
Pharmacologic (start immediately, do not wait EGD
to perform)
- octreotide : 50mcg Iv bolus then 50mcg/hr
infusion, continue for 4-7 day
- PPI : IV drip until po can be taken
- Antibiotics : all variceal bleeding should get
against bacterial gut (3rd generation) during
hospitalization for 4-7 days

Table 2. Pharmacologic treatment of acute

variceal bleeding
Drug

route

administration

Dose

Vasopressin
Nitroglycerine

i.V
i.v

Continous infusion

0.1-0.4 U/min
40-400 g/min

Glypressin

i.V

Initial bolus
Subsequent bolus

2 mg/4 h
1-2 mg/4 h

Somatostatin

i.V

Initial bolus
Continous infusion

250-500 g
250-500 g/h

Octreotide

i.V

Initial bolus
Continous infusion

25-50 g
25-50 g/h

Terlipressin

i.v

Initial bolus
Subsequent bolus

2 mg/4-6h in 2d
1mg/4-6h

Treatment should be continued for 5 days

Prophylaxis of variceal bleeding in cirrhosis.

Preprimary prophylaxis is aimed at preventing esophagogastric
varices (EV) from developing. The goal of primary prophylaxis is
to prevent a first variceal bleeding episode once medium or
large varices have formed. Secondary prophylaxis is used to
prevent recurrent variceal bleeding.
Photo by: Lianne Friesen and Nicholas Woolridge

Table 1. Pharmacologic treatment for prevention

of variceal bleeding
Drug

Initial Dose

Therapeutic dose

Propanolol

40 mg bid

40-400 mg

Nadolol

40 mg qd

40-160 mg

Timolol

10 mg qd

5 mg qd-40mg

Isosorbide 5mononitrate

20 mg bid

20 mg tid-20 mg qd

Goal : 20% reduction in HVWPG or 25% heart

rate; decreased bleeding risk 50-90% (only 35%
patients achieve this goal)

Complication of Variceal bleeding

Syock hypovolemik death
Induce :
Hepatic encephalopathy
Hepatorenal syndrome
Worsening clotting profile

SA Jenkins, Somatostatin and ocreotide in gastroenterology,

Medimedia, 1996

Prognosis
Primary prevention
indicated : moderate-large v. >5mm in D
- nonselective BB nitrate (50%
bleeding)
- band ligation (more greater than BB in
bleeding)
Secondary prevention
indicated : patients who has previously
bleed; >80% will bleed againin 2 years
- band ligation nonselective BB with
nitrates

PLEASE READ
KONSENSUS NASIONAL PERKUMPULAN
GASTROENTEROLOGI INDONESIA (PGI) 2007
Panduan penatalaksanaan perdarahn varises
pada sirosis hati

 The key factor in the natural history of

esophageal varices is increased portal
pressure, which in cirrhosis is due to the
combination of increased hepatic vascular
resistance and increased portal collateral
blood flow. The maintenance and aggravation
of this situation leads to the progressive
dilation of the varices and thinning of the
variceal wall, until the tension exerted by the
variceal wall exceeds the elastic limit of the
vessel, leading to variceal hemorrhage