COMPLICATION OF

PEPTIC ULCER
Department of surgery
S. S. Medical College Rewa and
associate GMH and SGMH Rewa
Presentor
Guided By- Co-guide Akhilesh Choudhary
Dr. A.P.S. Gaharwar Dr. L. M. Singh Brajesh Mourya
Professor & Head Asst. Beenish Bano
Dept. of Surgery professor Chandrakanta Kannoj
Objectives
 Definition of peptic ulcer
 Comparison of duodenal & gastric ulcers
 Aetiology
 Clinical presentation
 Management
 Complication
 Bleeding
 Perforation
 Gastric outlet obstruction
Peptic ulcer
 A break in superficial epithelial cells
penetrating down to muscularis mucosa of
stomach and deodenam
Definition
A circumscribed ulceration of
the gastrointestinal mucosa
occurring in areas exposed to
acid and pepsin and most often
caused by Helicobacter pylori
infection.
(Uphold & Graham, 2003)
 CLASSIFICATION

By Region/Location
- Stomach

- Duodenum

- Meckel’s Diverticulum containing gastric

mucosa
Modified Johnson Classification of
peptic ulcers

 Type I: Ulcer along the body of the stomach,

most often along the lesser curve at incisura
angularis along the locus minoris resistentiae.

 Type II: Ulcer in the body in combination with

duodenal ulcers. Associated with acid
oversecretion.
Modified Johnson Classification of
peptic ulcers

 Type III: In the pyloric channel within 3 cm of

pylorus. Associated with acid oversecretion.

 Type IV: Proximal gastroesophageal ulcer

 Type V: Can occur throughout the stomach.

Associated with chronic NSAID use .
Duodenal and Gastric Ulcers
1.Gastric 2.Dudodenal
Duodenal vs Gastric

DUODENAL GASTRIC
INCIDENCE More common Less common

ANATOMY First part of duodenum – antram

anterior wall
DURATION Acute or chronic Chronic

MALIGNANCY Rare Benign or malignant

Duodenal Ulcers
 duodenal sites are 4x as common as gastric sites
 most common in middle age
 peak 30-50 years
 Male to female ratio—4:1
 Genetic link: 3x more common in 1st degree
relatives
 more common in patients with blood group O
 associated with increased serum pepsinogen
 H. pylori infection common
 up to 95%
 smoking is twice as common
Gastric Ulcers
 common in late middle age
 incidence increases with age
 Male to female ratio—2:1
 More common in patients with blood group A
 Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer
 Less related to H. pylori than duodenal ulcers –
about 80%
 10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
Etiology
 A peptic ulcer is a mucosal break, 3 mm or greater,
that can involve the stomach or duodenum.
 The most important contributing factors are H pylori,
NSAIDs, acid, and pepsin.
 Additional aggressive factors include smoking,
ethanol, bile acids, aspirin, steroids, and stress.
 Important protective factors are mucus, bicarbonate,
mucosal blood flow, prostaglandins, hydrophobic
layer, and epithelial renewal.
 Increased risk when older than 50 d/t decrease protection
 When an imbalance occurs, PUD might develop.
H Pylori
 Urease producing, gram negative bacillus
 Developing countries
 Infection increases with age
 Infects mucosa of stomach > inflammatory
response > gastritis > increased gastrin
secretion > gastric metaplasia > damage to
mucosa > ulceration
 Increased risk of developing gastric
adenocarcinoma
Symptom
 Pain—“burning””gnawing”, “aching”,
 Duodenal ulcers: occurs 1-3 hours after a meal and may
awaken patient from sleep. Pain is relieved by food,
antacids, or vomiting.
 Gastric ulcers: food may exacerbate the pain while
vomiting relieves it.
 Nausea, vomiting, belching, dyspepsia, bloating,
chest discomfort, anorexia, hematemesis, &/or
melena may also occur.
 nausea, vomiting, & weight loss more common with Gastric
ulcers
Sign
 Epigastric tenderness
 Guaic-positive stool resulting from occult blood loss
 Succussion splash resulting from scaring or edema
due to partial or complete gastric outlet obstruction
 A succussion splash describes the sound obtained by
shaking an individual who has free fluid and air or gas in a
hollow organ or body cavity.
 Usually elicited to confirm intestinal or pyloric obstruction.
 Done by gently shaking the abdomen by holding either side
of the pelvis. A positive test occurs when a splashing noise
is heard, either with or without a stethoscope. It is not valid
if the pt has eaten or drunk fluid within the last three hours.
Differential Diagnosis
 Neoplasm of the stomach
 Pancreatitis
 Pancreatic cancer
 Diverticulitis
 Nonulcer dyspepsia (also called functional
dyspepsia)
 Cholecystitis
 Gastritis
 GERD
 MI—not to be missed if having chest pain, mostly in
women
Diagnostic Plan

 Flexible endoscopy is the gold standard test for

diagnosis of peptic ulcer
 Double contrast barium meal
 Method for diagnosis of H. pylori infection
 Invasive
 Rapid urease
 Histology
 Culture
 Noninvasive
 Serology
 Urea breath test
 Stool antigen
 Treatment plan
 Lifestyle Changes
 Discontinue NSAIDs and use Acetaminophen for pain
control if possible.
 Acid suppression--Antacids
 Smoking cessation
 No dietary restrictions unless certain foods are associated
with problems.
 Alcohol in moderation
 Men under 65: 2 drinks/day
 Men over 65 and all women: 1 drink/day
 Stress reduction
Treatment Plan: H. Pylori
 Medications: Triple therapy for 14 days is considered the
treatment of choice.
 Proton Pump Inhibitor + clarithromycin and amoxicillin
 Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
 Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN
 In the setting of an active ulcer, continue qd proton pump inhibitor
therapy for additional 2 weeks.
 Goal: complete elimination of H. Pylori. Once achieved
reinfection rates are low. Compliance!
Treatment Plan: Not H. Pylori
 Medications—treat with Proton Pump
Inhibitors or H2 receptor antagonists to assist
ulcer healing
 H2blockade : ranitidine, fometidine,nizatidine for
up to 8 weeks
 PPI: Pentaprazole, lansoprazole, esmoprazole,
rebeprazole and omeprazole for 4-8 weeks.
Prevention
 Consider prophylactic therapy for the following patients:
 Pts with NSAID-induced ulcers who require daily NSAID therapy
 Pts older than 60 years
 Pts with a history of PUD or a complication such as GI bleeding
 Pts taking steroids or anticoagulants or patients with significant
comorbid medical illnesses
 Prophylactic regimens that have been shown to dramatically
reduce the risk of NSAID-induced gastric and duodenal ulcers
include the use of a prostaglandin analogue or a proton pump
inhibitor.
 Misoprostol (Cytotec) 100-200 mcg PO 4 times per day
 Omeprazole (Prilosec) 20-40 mg PO every day
 Lansoprazole (Prevacid) 15-30 mg PO every day
Evaluation/Follow-up/Referrals
 H. Pylori Positive: retesting for tx efficacy
 Urea breath test—no sooner than 4 weeks after
therapy to avoid false negative results
 Stool antigen test—an 8 week interval must be
allowed after therapy.
 H. Pylori Negative: evaluate symptoms after
one month. Patients who are controlled
should cont. 2-4 more weeks.
 If symptoms persist then refer to specialist for
additional diagnostic testing.
Surgery
 People who do not respond to medication, or who
develop complications:
 Vagotomy - cutting the vagus nerve to interrupt messages
sent from the brain to the stomach to reducing acid
secretion.
 Antrectomy - remove the lower part of the stomach
(antrum), which produces a hormone that stimulates the
stomach to secrete digestive juices. A vagotomy is usually
done in conjunction with an antrectomy.
 Pyloroplasty - the opening into the duodenum and small
intestine (pylorus) are enlarged, enabling contents to pass
more freely from the stomach. May be performed along
with a vagotomy.
Complication of peptic ulcer
 Bleeding
 Perforation
 Gastric outlet obstruction
 Bleeding peptic ulcer
A complication of peptic ulcer disease
Bleeding peptic ulcer
 Upper GI Bleeding is MC complication of PUD
 19.4-57/1,00,000 in general population
 15% patient of PUD
 Peptic ulcer is most common cause of Upper GI
bleeding(60%)
 Predisposing factor
 Age above 60 year
 Use of NSAIDs and steroids
 30day mortality - 5-10%
 20% bleeding without warning sign
Clinical Presentation

 Hematemesis
 Melaena (14hr)

 Hematochelezia (massive bleeding)

 History of S&S of peptic ulcer disease

 S&S of blood loss

 Tachycardia, hypotension, tachypnea,

cold & clammy skin, pallor
Clinical Prognostic Factors

 Clinical markers that indicate severe bleeding

or a high risk of further hemorrhage include:
 Hemodynamic instability on
presentation,
 Bleeding manifested as repeated red
hematemesis or hematochezia,
 Failure of the gastric aspirate to clear
with lavage.
 Advance age
 Diagnostic Endoscopy

 The endoscopic
appearance of an ulcer may
provide the most helpful
prognostic information.
Initial management I
 Airway is clear
 Breathing – RR 30 breaths/min, Sats 91% OA
 Circulation – HR 130 beats/min, BP 80/40
mmHg
 Protect airway & keep NBM
 High flow oxygen
 Gain access – 2 large bore cannulae
 Bloods- CBC, U&Es, LFTs, glucose, clotting, cross
match 6 units
 Catheterise to monitor urine output
Initial management II
 If shocked prompt volume replacement
 Either colloid or crystalloid solutions
 Red cell transfusion should be considered after
loss of 30% of the circulating volume
 Correct any clotting abnormalities
 Gastric lavage with normal temprature saline
solution
 Urgent endoscopy after resuscitation because
further management is depend on
endoscopy
PPI therapy
 Indicated in active bleeding , visible vessel, or
adherent clot on endoscopy
 It include IV pentaprazole 80mg bolus +
8mg/hour continous infusion for 72 hour
Management depend on endoscopy
 Active bleeding or visible vessel
 IV PPI therapy + endoscopic therapy

 Adherent clot-
 IV PPI therapy + /- endoscopic therapy(contraversial)

 Flat, pigmented spot-

 No IV PPI or endoscopic therapy

 Clean base-
 No IV PPI or endoscopic therapy
Endoscopy treatment-
 It is first line treatment of bleeding PU with PPI infusion
therapy
 Indication-
 Active bleeding
 Visible vessel
 Adherent clot
 Procedure-
 Tissue adhesive(cynoacrylate)
 Injection therapy with 1:10,000 solution of epinephrine with or
without sclerosant
 Thermal device
 Contact: heater probe, electrocoagulation
 Noncontact: laser coagulation, argon plasma coagulation)
 Mechanical device- heamoclip
Surgical treatment
Emergency surgery Elective surgery

 Emrgency surgery
 Emergency Sx is directed to achieve heamostasis
 Indication
 Failure endoscopic haemostasis
 Visible vessel on endoscopy
 Elderly patient with rebleeding
 Patient require more than 6 unite of blood
Emrgency surgery- heamostasis
surgery
Deodenal ulcer Gastric ulcer
 Open pylorus  Gastrotomy
longitudinally  Visualise the vessel
 Visualise bleeding vessel  Place suture that under
 Placed suture that under run vessel
run the vessel  Close the gastrotomy
 Close mucosa over ulcer

 Close the pyeloroplasty

Elective surgery
 These surgery are directed to reduce acid
secretion
 Anatomy preserving surgery are preffered
 Indication:
 Failure of medical therapy
 Suscipicion of malignancy
 Sustained pyloric stenosis
 Previous complication
Elective surgery for DU

 Gatrectomy biliroth-I
 BI(Gastrectomy +
gastrodeodenostomy
 BII ( gastrectomy +
gastroenterestomy)
 Gastroentrestomy
alone biliroth-II
Elective surgery for DU
 Vagotomy (truncal or
selective) with
drainage
 Pyloroplasty
 Gastrodeodenostomy
 Highly selective
vagotomy
 Vagotomy with
antrectomy
Elective surgery for GU
 Biliroth1
 Ulcer excision with
vagotomy and
drainage
Summary of bleeding PU
 Perforation
A complication of peptic ulcer disease
 DEFINITION
 A perforated peptic ulcer is a mucosal defect
which penetrate the muscularis mucosa and
muscularis propria
 EPIDEMIOLOGY
 Despite the use of anti-ulcer agent &
eradication therapy the incidence of
perforated peptic ulcer have changed little
 Most patient are middle aged with the ratio
more in men then women
 SMOKING and NSAIDs appear to be
responsible for most of these perforation.
 ETIOLOGY
 Helicobactor pylori
 NSAIDs
 Gastrinoma(Zollinger-Ellison Syndrome)
 Hypercalcemia
 Genetic factor
 Smoking
 Stress
 Alcohol and diet
SITE OF PERFORATION
 Perforation occur most commonly when an
anteriorly placed duodenal ulcer erodes
through the full thickness of the wall of
duodenum.
 Perforated duodenal ulcer is almost situated
on anterior wall of first part of duodenum.

 PATHOLOGY
 STAGE I :- STAGE OF PERITONISM
At this stage acid peptic juice ,bile and
pancreatic juice leak through a perforated ulcer
and enter into the peritoneal cavity.
 STAGE :-II STAGE OF REACTION
Peritoneum react to this by secreting large
amount of fluid which dilute the gastric juice,bile
and pancreatic juice
 STAGE :-III STAGE OF PERITONITIS
At this stage invasion of bacteria occurs
 CLINICAL FEATURES
 Almost always the patient is a middle aged male
 Acute perforation sometime develop in apatient
who is taking steroids or NSAIDs for arthritis
 Soon after perforation there occur severe pain in
epigastrium
 On examination patient look pale and anxious
 Skin is cold and clammy
 Abdomen is distended and patient lies quietly in
the bed
 There is generalised tenderness with
passage of time
 There is board like rigidity on palpating
abdomen
 Liver dullness is masked
 There is rise in pulse rate, temperature &
gradual fall in the blood pressure due to
hypovolumic shock,secondary to the
third space fluid loss.
 INVESTIGATION
 Diagnosis is made mainly on the basis of
clinical examination , this is confirmed by,
X-Ray abdomen in erect posture, which
show gas under diaphragm in most of cases
 If the patient is too ill to stand or due to
some other reason cannot stand , a left
lateral X-Ray film is taken
 TREATMENT
 Whenever a perforated ulcer is suspected an
nasogastric tube is passed in the stomach
through nose and gastric content aspirated
 This reduces further contamination of the
peritoneal cavity
 After initial resuscitaion , immediate exploration
and repair of the perforation is the treatment in
almost all the cases
 OPERATIVE
PROCEDURE:(GRAHAM’S PATCH
REPAIR)
 The abdomen is open with an upper
paramedial or mid line incision
 All fluid , acid secretion ,bile and
pancreatic juice is sucked by suction
machine which is connected to a bottle
via tube
 Abdominal cavity is washed by a normal saline
solution
 Site of perforation is identified
 The perforation is closed with interrupted suture
along with an omental patch(Graham patch)
 In a case of gastric ulcer biopsy must be taken
,as there is always risk of malignancy
 Nowadays surgeon are repairing duodenal
perforation leproscopically
 H.PYLORI induced peptic ulcer is treated with
 Antibiotics

 Proton pump inhibitor

Omeprazole

Lansoprazole

Pantoprazole

Rabiprazole
 Histamine receptor blocker
Cimetidine

Ranitidine

Famotidine

Nizatidine

 Antacid
Gastric outlet obstruction
A complication of peptic ulcer disease
GASTRIC OUTLET
OBSTRUCTION
The two common causes of gastric outlet
obstruction are:
1-pyloric stenosis secondary to peptic
ulceration.
2- gastric cancer(prepyloric tumor)
 Metabolic effects
The vomiting of hydrochloric acid results in hypochloraemic
alkalosis but, initially, sodium and potassium levels may be
relatively normal. However, as dehydration progresses, more
profound metabolic abnormalities arise. Initially, the urine has
a low chloride and high bicarbonate content, reflecting the
primary metabolic abnormality. This bicarbonate is excreted
along with sodium and so, the patient becomes progressively
hyponatraemic and more dehydrated,a phase of sodium
retention follows and potassium and hydrogen are excreted in
preference. This results in the urine becoming paradoxically
acidic and hypokalaemia .Alkalosis leads to a lowering of the
circulating ionised calcium, and tetany can occur
 FLOW CHART OF GOO
 DUE TO CHRONIC ULCER

VOMITING LOSS OF ION,

HYPOCHLOREMIC METABOLIC ALKALOSIS,

LOSS OF HCL WITH Na,

HYPONATREMIA AND DEHYDRATION ,

HYPOKALEMIA , ACIDURIA
Clinical features
• There is usually a long history of peptic ulcer disease.
• pain: the pain may become unremitting but in other cases it
may largely disappear.
• Vomiting: The vomitus is totally lacking in bile(nonbilious).
Very often it is possible to recognise foods taken several
days previously.
• The patient commonly loses weight, and appears unwell
and dehydrated.
• On examination it may be possible to see the distended
stomach and a succussion splash may be audible on
shaking the patient’s abdomen.
Investigations
Investigations
 Biochemical

CO2 + H20 <= H2CO3 => HCO3- + H+

 Loss of
 H+, Cl-, Na+
 Hypokalaemic hypochloraemic alkalosis
Initial Management

 Decompress the stomach

 Correct biochemical abnormalities

 Address the nutrition

Management
• the patient should be rehydrated with intravenous isotonic saline
with potassium supplementation.
• If the patient is anaemic it should be corrected.
• The stomach should be emptied using a wide-bore gastric tube.
• This then allows investigation of the patient with endoscopy and
contrast radiology. Biopsy of the area around the pylorus is
essential to exclude malignancy. 5-The patient should also have
an anti-secretory agent.
• severe cases are treated surgically, usually with a
gastroenterostomy.
Endoscopic treatment with balloon dilatation has been practised and
may be most useful in early cases. However, this treatment is not
devoid of problems. Dilating the duodenal stenosis may result in
perforation, and the dilatation may have to be performed several
times and may not be successful in the long term.
Definitive management
• Conservative

• Surgical

– Resect

– Bypass

– Stent
Colonic Z-Stent

 Delivery diameter:
10mm (30F)
 Deployed diameter:
35/25mm
Complications of Enteral
Stents
 Tumor ingrowth/overgrowth
 Migration
 Perforation
immediate
delayed
 Impaction
 Bleeding
 Pain/Tenesmus