Peptic duodenal ulcer
History (1)
Diocles
of Carystos (350 b.c.) - melancholic gassy
illness originating in the stomach (Yamada et al.)
Marcello
Donati first gastric ulcer (1586)
1975
China - 60 year old man with prepiloric
perforated ulcer (167 b.c.)
1688 - Muralto first ulcer description
1727 C. Rawlison first gastric perforation
1746
G. Hamberger - first duodenal perforation
History (2)
1881
Rydigier first gastric resection for
ulcer
1884
Mikulicz first attempt of suturing a
peptic ulcer perforation
1912
Bircher vagotomy in ulcer
surgery
1943
- L. Dragsted and H. Owens
troncular vagotomy
Definition
A breach,
mostly circumscribed of the
gastric or duodenal wall beyond
muscularis mucosae.
Erosion
mucosa
a breach limited only to the
Classification
Gastric
Duodenal:
Bulbar
Postbulbar
Anastomotic
Stress
ulcer (Curling or Cushing ulcers, in
sepsis)
Endocrine
ulcer (Zollinger-Ellison)
Classification
Histology
Acute
Chronic
Classification of benign gastric
ulcers (after Johnson, 1957)
Acute superficial:
Single or multiple ('erosions')
Chronic:
Type I, usually lesser curve
Type II, combined with duodenal ulcer
Type III, prepyloric
Type IV, proximal stomach <2 cm from oesophageal junction
Epidemiology 1
5-10%
in western world (300.000 new
cases in USA)
The 1-year point prevalence of active
gastric and duodenal ulcer in the United
States is approximately 1.8%
In 1998, it was estimated that there were
6.8 million cases of PUD in the United
States, representing a prevalence rate of
2490 cases per 100,000 persons.
Epidemiology 2
Duodenal/gastric
ulcer ratio is variable
Male:Female ratio=2-1 (clasically 4(6)-1)
More than 75% of patients with PUD are
of working age (18 to 65 years)
Stomach, gross and histology
From http://www.training.seer.cancer.gov
Anatomy
Vascularization
Nyhus et al.
Vagus nerve
into the
abdomen Testut
Inervation
Nyhus et al.
Lymphatics
Nyhus et al.
Gastric secretion
Gastric secretion regulation
Gastric secretion regulation
Nyhus et al.
Ohne magensaft kein peptisches geschwr K. Schwartz, 1911
Pathogenesis (1)
Gastric
secretion changes in peptic ulcer
patients
Increased BAO (normal: 0-10 mmol/hr)
Nocturnal increase of gastric output
Increased PCM
Exagerated response to stimuli (hystamine),
hypoglicemia, mechanical stimuli
Hypervagotony
Anomalous gastric secretion inhibition (secretin)
Pathogenesis (2)
Gastric
secretion regulation changes:
High output of gastrin as a response to
different stimuli
Anomalous negative feed-back of gastric
secretion gastrin-mediated
Somatostatin secretion inhibition
Pathogenesis (3)
Duodenal
mucosa changes in peptic ulcer
patients:
Prostaglandins deficit
Bicarbonate deficit
Diminished duodenal mucus
Helicobacter pylori (metaplasia)
Pathogenesis (4)
Genetics
Environment
NSAID
Smoking
Stress
Drugs (cocaine, crack)
Helicobacter pylori
Alimentary (alcohol etc.)
Helicobacter pylori
1975 - Howard Steer
1989 - J. R. Warren, B. J. Marshall
In 40-60% of western population
100% in tropics and the third world
More frequent in urban aria
Helicobacter pylori
Coco-bacil
Gram negative with multiple
enzymes
50%
are producing Vac A
cag A
higher virulence
Helicobacter pylori - genome
S SUERBAUM, M.D.,P MICHETTI, M.D. - N Engl J Med, Vol. 347, No. 15,2002
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Second level
Third level
Fourth level
Fifth level
H. pylori
interaction
S SUERBAUM, M.D.,P
MICHETTI, M.D. - N Engl J
Med, Vol. 347, No. 15,2002
Helicobacter pylori
Cliodna A M McNulty, Judith I Wyatt - Helicobacter pylori J Clin Pathol 1999;52:338-344
Helicobacter pylori
Helicobacter pylori
Produces
hypergastrinemia and
hyperacidity (hypotheses):
Inhibitory protein synthesis acting on gastrin
releasing cells
Direct inhibition of somatostatin
Helicobacter pylori
Direct disruption of mucosa and influencing
cytokines or of the phospholipase
Activating the macrophages, TNF (Tumor
Necrosis Factor), IL1 synthesis, and oxygen
free radicals;
Autoantibodies production
Ulcer equation
NS AID
Ge ne tic
fac to rs
H. pylo ri
S tre s s
Cirrho s is
S mo king
S mo king
Mucus
MEN
Epithelium
Clorhidro-peptic
secretion
Bicarbonate secretion
Vascularization
ulcer
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Second level
Third level
Fourth level
Fifth level
H. pylori infection natural history - S SUERBAUM, M.D.,P MICHETTI, M.D. - N Engl J
Med, Vol. 347,No. 15,2002
Morfopatholoy
Microscopy
(Askanazy) 4 strata
Exudative - detritus, fibrin, germs or even
yeasts
Necrosis (fibrinoid) with inflammatory
infiltrate (active region)
Granulation strata
Fibrosis
Pathology (1)
Pathology (2)
Clinical signs
Pain
Periodicity
Aching
(with meals and seasonal)
pain
Vomiting
Habitus
Essentials of diagnosis
Epigastric
pain relieved by food or antacids.
Epigastric
tenderness.
Normal
or increased gastric acid secretion.
Signs
of ulcer disease on upper
gastrointestinal x-rays or endoscopy.
Evidence
of Helicobacter pylori infection.
Lab&explorations
Laboratory
Gastrin in serum (normal < 100 pg/mL) over
200 pg/mL in Zollinger-Ellison syndrome
Secretory tests (no longer in use)
Lab&explorations
Endoscopy
is the principal method of
diagnosis, as it enables biopsies to be
taken to exclude malignancy in gastric
ulcers, and to do a rapid urease test or
histological examination for Helicobacter.
Endoscopy
On open-access endoscopy for 'dyspepsia',
about 12% per cent of patients have
duodenal ulcer and 3% gastric ulcer, but the
numbers and ratios vary with age.
Every gastric ulcer should be suspected of
being malignant until proved benign by
multiple biopsies and complete endoscopic
healing.
Radiology
Radiographic studies
Deformities
and an ulcer niche.
Inflammatory
swelling and scarring may
lead to distortion of the duodenal bulb,
eccentricity of the pyloric channel, or
pseudodiverticulum formation.
The
ulcer itself may be seen either in
profile or, more commonly, en face.
Helicobacter pylori testing
Noninvasive
14C breath test
Serology
Stool antigen determination
Endoscopy
Direct examination and test
Cultures
Cliodna A M McNulty, Judith I Wyatt
- Helicobacter pylori J Clin Pathol
1999;52:338-344
Cliodna A M McNulty, Judith I Wyatt - Helicobacter pylori J Clin Pathol
1999;52:338-344
Cliodna A M McNulty, Judith I Wyatt - Helicobacter pylori J Clin Pathol
1999;52:338-344
Detection and Treatment of Helicobacter pylori
Infection in Adult Patients
Peptic ulcer evolution
Recurrence
Complications
Hemorrhage
Perforation
Penetration
Stenosis
Malignancy (only for gastric ulcers)
Zollinger-Elison syndrome
Zollinger
and Ellison defined the syndrome that
now bears their names 1955
Triad
of
severe ulcer disease,
gastric acid hypersecretion, and
non-beta islet cell tumors of the pancreas
0.1
to 1% of patients with peptic ulcer disease
Gastrinomas: Origin and
Classification
One
third (15% to 77% in different studies) of patients
with gastrinomas have multiple endocrine neoplasia
type 1 (MEN-1)
MEN-1
is an autosomal dominant genetic disorder
associated with a high degree of penetrance
Patients
with MEN-1 may have involvement of all three
organs (parathyroids, pancreatic islets, and pituitary)
Zollinger-Elison syndrome
The
tumor may be single or multiple and
can range in size for less than 1 cm to
more than 3 cm.
When
associated with MEN-1, studies
suggest that gastrinomas are usually
multiple and commonly found within the
duodenum and pancreas
Diagnostic
Difficult
to find
Serum gastrin over 200 pg/ml
Secretin provocative test
US
CT-scan
EUS
Angiography with sampling
MRI
Portal venous sampling for serum levels of gastrin
IOUS
Treatment
Medical
PPI large doses
BAO measuring
Surgical
Tumor excision, or
Total gastrectomy, and
Metastazis treatment
Upper digestive hemorrhage
Definition
Hematemesis vomiting blood
Melena the passage of black, tarry stools composed
largely of blood that has been acted on by gastric juices,
indicative of bleeding in the upper digestive tract.
Hemochezia red blood in stools
Rebleeding - hematemesis and/or melena with shock
(pulse>100b/min, CVP drop of 5 mm Hg or drop in HGB
level with 2g. Confirmation needs endoscopic
reevaluation
Upper digestive hemorrhage
Diagnostic
Ulcer
35-50
Erosions (ulcerations)
8-15
Esophagitis
5-15
Varices (gastroesophageal)
Mallory-Weiss syndrome
5-15
15
Malignancy
Vascular malformation
Rare
65
After British Society of Gastroenterology Gut 2002;51(suppl.
IV):iv1-iv6
Bleeding risk (endoscopic
assessment)
Sign
% of rebleed
Arterial bleeding
90
Visible vessel
50
Fresh clot in ulcer crater
25
Small bleeding without vessel
<20
Dark spot, red spot
<10
Freeman ML The current endoscopic diagnosis and intensive care unit management of
severe ulcer and non-variceal upper gastrointestinal hemorrhage Gastrintest Endosc Clin
North Am 1991, 1:229
66
Hemorrhagic ulcer
Forrest tip IIb
Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.
Hemorrhagic ulcer
Ulcer perforation (1)
Brutal
debut
Severe
generalized abdominal pain
Shock
Loss
of bowel sounds
Board-like
rigidity of the abdominal wall
Feldman: Sleisenger & Fordtran's
Gastrointestinal and Liver Disease, 8th ed.
Ulcer perforation (2)
Diagnostic
(Mondor triad)
Pain (specific characteristics)
History for ulcer or dispepsia
Guarding or, more frequently abdominal wall
rigidity
Ulcer perforation (3)
Radiology (pneumoperitoneum) in 50-75% of
cases
Administration of oral soluble radiographic
contrast may demonstrate a leak.
Barium studies should be avoided when
perforation is suspected.
Endoscopy should not be performed.
In rare cases, urgent laparotomy is required to
make the diagnosis.
Pneumoperitoneum
Ecografie evideniind pneumoperitoneu
Stenosis (gastric outlet syndrome)
Gastric
outlet obstruction is the least common
complication of peptic (pyloric channel or duodenal)
ulcer disease (classically 1-3%).
Two
stages:
Functional (edema and inflammation surrounding an acute
ulcer, especially in the antrum or pyloric channel)
Organic (scarring with fibrosis and outlet narrowing)
Sistolic phase
Asistolic phase
Gastric outlet syndrome
Postprandial
epigastric fullness, early satiety,
and vomiting of materials ingested hours to
days previously.
Vomiting
may be worse toward the end of
the day.
If
gastric outlet obstruction is chronic,
patients may develop hypochloremic
alkalosis, tetany, weight loss, and, rarely,
aspiration pneumonia.
Gastric outlet syndrome
A succussion
splash may be audible on
physical examination.
The
diagnosis may be confirmed using
radiographic (barium), endoscopic, or
scintigraphic (gastric-emptying) studies
Gastric outlet syndrome treatment
Nasogastric
tube to fully evacuate the
stomach
Intravenous
replacement of fluid and
electrolytes is imperative
Intensive
antisecretory therapy with
intravenous H2RAs or proton-pump
inhibitors should be given to reduce
nasogastric fluid losses and to promote ulcer
healing
Gastric outlet syndrome treatment
Patients
with chronic obstruction and signs of malnutrition
should be given parenteral nutrition.
Upper
GI study using water-soluble contrast - after 72 hours
of gastric decompression.
About one-half to two-thirds of patients fail to improve after
5-7 days of gastric aspiration.
Up
to 90% of cases of gastric outlet obstruction will come to
either surgical or endoscopic dilatation within 1 year.
Treatment
Drugs
Antiacids
Cytoprotective agents - Sucralfate is a complex sucrose salt in
which the hydroxyl groups have been substituted by aluminum
hydroxide and sulfate. This compound is insoluble in water and
becomes a viscous paste within the stomach and duodenum,
binding primarily to sites of active ulceration.
Adverse effects - chronic renal insufficiency to prevent aluminum-
induced neurotoxicity. Hypophosphatemia and gastric bezoar
formation have also been rarely reported. (1 g four times per day)
Anticholinergics
Designed to inhibit activation of the muscarinic
receptor in parietal cells, met with limited
success due to their relatively weak acidinhibiting effect and significant side effects (dry
eyes, dry mouth, urinary retention).
Bismuth-containing compounds
Colloidal
bismuth subcitrate (CBS) and
bismuth subsalicylate (BSS, PeptoBismol)
Long-term
usage with high doses,
especially with the avidly absorbed CBS,
may lead to neurotoxicity. These
compounds are commonly used as one of
the agents in an anti-H. pylori regimen
Prostaglandin analogues
Prostaglandin
analogues enhance mucous
bicarbonate secretion, stimulate mucosal
blood flow, and decrease mucosal cell
turnover.
Misoprostol
is contraindicated in women who
may be pregnant, and women of
childbearing age must be made clearly
aware of this potential drug toxicity. (200 ug
four times per day)
H2 receptor antagonist
Four
of these agents are presently
available (cimetidine, ranitidine,
famotidine, and nizatidine), and their
structures share homology with histamine.
Presently,
this class of drug is often used
for treatment of active ulcers (4 to 6
weeks) in combination with antibiotics
directed at eradicating H. pylori
Proton pomp inhibitors
Omeprazole,
esomeprazole,
lansoprazole, rabeprazole, and
pantoprazole are substituted
benzimidazole derivatives that covalently
bind and irreversibly inhibit H+,K+ATPase.
Treatment
Goal
- relief of symptoms (pain or
dyspepsia), promote ulcer healing, and
ultimately prevent ulcer recurrence and
complications.
PPI, proton pump
inhibitor; RBC,
ranitidine bismuth
citrate;
R, metronidazole 400
mg, used adequately
in many countries - P.
MALFERTHEINER et
al. consensus
Maastricht 2 i 3
2000 i 2005
Hemorrhagic ulcer therapy
Vasopressors
Endoscopy
Surgery
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Second level
Third level
Fourth level
Fifth level
Surgery
Absolute
indications
Major hemorrhage
Perforation
Stenosis
Treatment
Relative indications
Repeated hemorrhage
Penetration
Arterial hypertension in hemorrhagic ulcer patients
Portal hypertension
Postbulbar ulcer
Multiple ulcers
Zollinger-Ellison syndrome
Professional risk patients
Surgery - goals
Excision
of the lesion
Lowering
pH (obtain an hypoacid
stomach)
Redo
the continuity of the digestive tract
Vagotomia- variante
Vagus nerves anatomy and
vagotomy types
VP posterior vagus, VA
anterior vagus, R. H-B hepatobiliary r., R. C. celiac r., N.A.M.C.
Lesser curvature anterior nerve
(Latarjet),
N.P.M.C. great curvature
anterior nerve, VT troncular
vagotomy, VS selective
vagotomy, VSS parietal cell
vagotomy (limit - 5-7 cm)
Posterior troncular
vagotomy with
anterior seromiotomy
(Taylor)
Pyloroplasty
Nyhus et al.
Suturing a
perforated
duodenal ulcer
Nyhus et al.
Hemostasis in situ
Nyhus et al.
Gastric resection (R),
hemigastrectomy (H) and antrectomy
(A);
a. Gastroduodenoanstomy (PanBillroth I),
b. Gastrojejunostomy - Billroth II
Billroth II operation and some of its modifications. (From Soybel DI, Zinner MJ: Stomach and duodenum:
Operative procedures. In Zinner MJ, Schwartz SI, Ellis H [eds]: Maingot's Abdominal Operations, vol I, 10th
ed. Stamford, CT, Appleton & Lange, 1997.)
JA Myers, JW Millikan, TJ Saclarides - Common Surgical Diseases, Springer 2008
