Complication of peptic ulcer

Anatomy
 Anatomy
• Arterial blood supply
• Lymphatic drainage
• Nerve supply
Stomach blood supply
Stomach innervations
 Ulcer disease

• ulcer is a defect of gastric or duodenal mucosa which

interfere over lamina muscularis mucosae, submucosa or
penetrates across whole gastric or duodenal wall

• rise of ulcer is conditioned by presence of acid gastric

content

• frequent disease, men are affected 3-4x more than women

 Pathogenesis
• Due to imbalance in the normal interplay
between acid-pepsin aggressive and mucosal
defense mechanism
- Protective f.: saliva, food, alcalic duodenal fluid, mucus - mucine, fast
regeneration of gastric epithelial cells, well perfused gastric mucosa
- Aggressive f.: HCl, pepsin, bile acids (reflux), helicobacter pylori,
drugs (analgetics, aspirin, korticoids), nicotine, alcohol
Modified Johnson Classification
Type Location Acid
Hypersecretion
I Lesser curvature, incisura No

II Body of stomach, incisura, and Yes

duodenal ulcer (active or healed)
III Prepyloric Yes

IV High on lesser curve, near No

gastroesophageal junction
V Anywhere (medication induced) No
 Clinical features
Gastric ulcer disease:

Duodenal ulcer disease:

 epigastric pain after meal or  epigastric pain 2 hours after

during meal meal or on a empty stomach
or during night
 upper dyspeptic syndrome –
loss of appetite, nauzea,  pyrosis
vomiting, flatulence
 good nutrition
 vomiting brings relief
 obstipation
 reduced nutrition
 seasonal dependence
 loss of weight
(spring, autumn)
METHODS OF INVESTIGATION
Treatment
Surgical treatment

• Billroth I
• Billroth II
• Pyloroplasty
• Vagotomy
Billroth I
Modifications Billroth I
Billroth II
Modifications Billroth II
 COMPLICATION

• Dumping syndrome Crancle syndrome

• Ulcer in GJ anastomosis
Pyloroplasty Heineke-Mikulicz
Дренирующие операции 1 19
Pyloroplasty Finney
Pyloroplasty Jaboulay
Truncal vagotomy
 COMPLICATION
• Gastrostas
• Duodenostas
• Diarhea
• Gallstone disease
Selective vagotomy
Highly selective vagotomy
 Complication of peptic ulcer
• 1 perforation;
• 2 haemorrhage;
• 3 stenosis;
• 4 penetration;
• 5 malignisation.
 Perforated ulcer
it is complete destruction wall of the stomach or duodenum by ulcer, with

entering of contents of the stomach and duodenum into peritoneal cavity

Localization
 Classification
: cavity — 92 %);
1) Typical (in free abdominal
2) Atypical:
а) posterior wall of stomach (perforated into lesser
sac) and posterior wall of duodenum (perforated
into retroperitoneal space);
б) peptic ulcer after resection B II;
в) multiplex ulcer;
г) combination of perforated ulcer with bleeding;
3) Covered.
Stage of perforation

1. Shock (6h)
2. False improvement (6-12h)
3. Peritonitis (after 12h)
 Clinical features
Г. Мондор (1938)
Main :
(1) Knife-like pain
(2) ulcer anamnesis
(3) tense of abdominal muscles like wood

Side :
- functional,
- physical,
- general.
 SIGNS
• Elekera – irradiation pain from abdominal
cavity to clavicle
• Blumberg
• Gustena – cor tone in abdominal cavity
during auscultation, absent of peristalsis
• Kenigsberga - rigid breathness in upper part
of abdomen during auscultation
• Kulenkamfa – pain during digital
investigation of rectum (patch of Douglas)
• Spigarnova – absent of liver dullness
 Investigation
• X-ray investigation

• Gobera sign – free air in abdominal cavity

 Treatment

Method of operation depend of:

1)Time from start of perforation;
2)Localization;
3)Condition of patient.
Suture plication of perforated ulcer with omentum
 Peptic ulcer
complicated by bleeding

• Mortality rates for UGI bleeding 2 – 15 %

• Mortality for patients who develop bleeding after
admission to hospital for another reason is 20 – 30 %
 Stage of haemorrhage

I mild haemorrhage P 90-100 уд/мин, BP 100 мм Hg,

Ht – 35 %, Deficit of volume blood – 20 % (until 1000
ml).
II middle haemorrhage P 100 уд/мин, BP less 90 мм
Hg, Ht – 25–30 %, Deficit of volume blood – 30 % (until
1500 ml).
III severe haemorrhage P 130-140 уд/мин, BP less 70
мм Hg, Ht – low 25 %, Deficit of volume blood – 30-50
% (until 2500 ml).
 Clinical features
• Hematemesis ： vomitting of blood or
altered blood （ coffee grounds ） indicates
bleeding proximal to ligament of Treitz
• Melena ： Tarry stool. Altered （ black ）
blood per rectum （ >60ml ）
• General features of bleeding: weakness,
loss of consciousness, dizziness, decrease
BP, tachycardia
 Diagnostic program in patient
with gastrointestinal bleeding:
• (1)Determination source of bleeding;
• (2)Determination stage of bleeding;
• (3)Determination continuous of bleeding and
prognosis relapse of bleeding.
 I. Anamnesis morbi
II. Objective investigation
– Sign of Bergman — decrease of pain in abdominal
cavity after begin of bleeding.
– Sign of Taylor  increase the peristalsis of intestine
(when blood pass to intestine).
III. Laboratory investigation:
1)Clinical blood analysis;
2) coagulability; blood typing
3) determinate the deficit of volume blood
IV. Instrumental investigation:
1)endoscopy
 Modified Forrest and Finlayson's
classification
• Type I: Active bleeding:
Ia: Spurting hemorrhage
Ib: Oozing hemorrhage
• Type II: Stigmata of recent
hemorrhage:
IIa: Nonbleeding visible vessel
IIb: Adherent clot
IIc: Flat pigmentation
• Type III: Clean-base ulcers

no stigmata black base

 Endoscopic therapy
Modality Types
Thermal Argon laser
Electrocoagulation
Heater probe
Argon plasma coagulation

Injection Epinephrine
Hemospray Sclerosants
Alcohol
Thrombin
Fibrin glue
Mechanical Hemoclips
Band ligation
Endoloop
Suture
 Injection therapy
• The most convenient and least expensive method.
• The most commonly used solution is diluted adrenaline (1 in
10000) injected submucosally around the bleeding site in
aliquots of 1–2 mL to a total volume of 5–10 ml.
• Haemostasis is postulated to occur due to
– a combined effect of vasoconstriction
– tamponade of the bleeding vessel
• Other agents used are normal saline, 3% saline, distilled water
and 50% glucose in water.
• All these solutions have an effect similar to that of 1 in 10 000
epinephrine
 Thermal coagulation

 Contact:
Electrocoagulation
Heater Probe

 Non-contact:
APC
Laser

Monopolar Bipolar
 Hemoclips

Quickclip 2
(Olympus)

Resolution
(Boston)

Triclip
(Cook)
 Endoscopy hemostasis

Peptic ulcer hemoclips

 Endoscopy hemostasis

 Band ligation dilated varicose vein of esophagus

 Endovascular hemostasis

X-ray cardiovascular complex

 Эндоваскулярные методы
гемостаза
Roentgen endovascular cathetheral hemostasis of dilated variceus vein

Extravasation of contrast solution

 Conservative therapy include:
1. IV Fluid: crystalloid, colloid solution; blood preparations.
2. Parenteral haemostatic therapy: etamsilat, hemoksan
(tranecsam acid), solution of calcium chloride;
- PPI (omez, kontrolok);
- inhibitors of proteolysis (kontrical, acidum
aminocapronicum);
- protein preparations (fibrinogen, plasma).
3. Local therapy (gastric lavage with cold water, epinephrine,
antacid, thrombin).
4. Enema with Natrium Hydrocarbonatum (to prevent toxic
effect products of destruction RBC)
 Surgery treatment
Gastro and Duodenotomy
Ревизия брюшной полости 95

Рис. 3
PEPTIC ULCER COMPLICATED
BY PYLORIC STENOSIS
Pyloric stenosis
Compensation
Hypertrophy of stomach
Feeling of discomfort (fullness)
periodic vomiting
periodic abdominal pain
periodic gaseous eructation
Subcompensation
Hypotrophy of stomach
constant feeling of fullness
sistematic and high volume vomiting
bad-smelling eructation
Decompensation
Atrophy of stomach
constant vomiting
vomit mass with decay odor
Constant bad breath
Loss of weight
Dehydration
Hypoproteinemia
Hypokalemia
Hypocalcaemia
Azotemia
alkalosis
X-ray classification
Compensation
Normal size
Increased deep peristalsis
Evacuation < 6 hours
Subcompensation
Increased size
Decreased peristalsis
Evacuation < 24 hours
Decompensation
Dilatated stomach
Deformated stomach
Evacuation 24-48 hours
Endoscopic classification
Compensation
1,5 sm
Subcompensation
1,0 sm
Decompensation
0,5 sm

Urine output classification

Compensation
1,0-1,5 L
Subcompensation
1,0-0,5 L
Decompensation
0,5-0,3 L
Conservative treatment

• Correction of metabolic
disturbances

• Parenteral feeding

• Antiulcerogenic
treatment

• Sistemic nasogastric
operations
Surgical treatment

• Billroth I
• Billroth II
• Pyloroplasty
PENETRATED PEPTIC
ULCER
Penetration
• Pancreas
• Hepatogastric ligament
• Biliary tract
• Liver
• Greater omentum
• Mesocolon
• Colon
• Vascular structures
 Stages of penetration
1) chronic ulcer (intramural
penetration);
2) faulty union;
3) complete penetration.
Clinical features:
• Change of natural history:
– absence of cyclicity;
– unsuccessful conservative
treatment.
• Change of pain
characteristic:
– persistence;
– unrelated with meals;
– day-night cycling absence;
– more intense;
– typical irradiation.
• Vomit doesn’t relieve pain
• Local muscle rigidity
• mild leukocytosis
Diagnostic
• x-ray:
– deformation
– flexibility
– ventricular contractility
– fixation
– double, triple niche sign
• Endoscopy:
– deep ulcer
– edge rigidity
• ultrasonography, CT,
MRI
Treatment
Conservative
• antiulcerant
• antiinflamative
• Correction of metabolic
disturbances
• infusion therapy

Surgery
• Billroth I
• Billroth II
• Exteriorization
Gastric cancer
• High rate salt in food
• High quantity of
unrefined fats
• Low level of milk
products
• Smoking
• Alcohol abuse
• Hot food
• Irregular meals
 Classification
1. Polypoid.
(slow growing, late metastasis, 2,9% patients)
2. Excavated (Ulcerative)
(slow growing, late metastasis, 18% patients)
3. Ulcerative cancer with border infiltration
(infiltration 6-8 sm, 17% patients)
4. Linitis plastica
(ulceration, without defined borders, 62% patients)
 Clinical sings
• Stage 1 (Early)

• * Indigestion or a burning sensation (heartburn)

• * Loss of appetite, especially for meat
• * Abdominal discomfort or irritation

• Stage 2 (Middle)

• * Weakness and fatigue

• * Bloating of the stomach, usually after meals

• Stage 3 (Late)

• * Abdominal pain in the upper abdomen

• * Nausea and occasional vomiting
• * Diarrhea or constipation
• * Weight loss
• * Bleeding (vomiting blood or having blood in the stool) which will appear as black. This
can lead to anemia.
• * Dysphagia; this feature suggests a tumor in the cardia or extension of the gastric tumor in
to the esophagus.
 “Small sings” syndrome
(А.С. Савицкий,1951)
1) weakness, asthenia;
2) loss of appetite, hatred of meat;
3) stomach discomfort;
4) weight loss;
5) anaemia;
6) depression, apathy.

А. В. Мельников (1960) «cancer triade»

• loss of appetite
• weight loss
• stomach discomfort
Diagnosing
1. The medical interview
and the physical
examinations
2. Endoscopy
3. Endoscopic ultrasound
4. CT
5. MRI
6. PET
7. X-ray
8. Laparoscopy
 Metastasis
Virchow

sisters
Mary Joseph

Krukenberg

Schnitzler
Blumer
Diagnosing
1. The medical interview
and the physical
examinations
2. Endoscopy
3. Endoscopic ultrasound
4. CT
5. MRI
6. PET
7. X-ray
8. Laparoscopy
Diagnosing

1. The medical interview

and the physical
examinations
2. Endoscopy
3. Endoscopic ultrasound
4. CT
5. MRI
6. PET
7. X-ray
8. Laparoscopy
Surgery
Surgery
Thank you