PUD and its Complications

• Lecture for clinical year -1 students

BY : Tilahun Temesgen (M.D.)

Surgeon
April 08/2019 G.C.

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Contents
• Introduction
• Epidemiology
• Pathophysiology and Etiology
– H. pylori Infection, NSAIDs, Acid Secretion
• Clinical Manifestations
• Diagnosis
• Medical mx
• Complicated Ulcer Disease
• Ulcer operations
• Complication of ulcer operations

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Introduction

• Peptic ulcers are focal defects in the gastric or

duodenal mucosa that extend into the submucosa or
deeper

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Epidemiology

• 300,000 new cases per year

• Prevalence- 5 -10%; incidence – 0.1 – 0.3%
• 4 million pts receive some form of ulcer tx
• 15,000 operations for PUD per year
• 10,000 deaths from PUD complications
• Over last 20y:
– Increase in emergency operations
– Decrease in elective operations

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Pathophysiology and Etiology

• Peptic ulcers are caused by an imbalance b/n mucosal

defenses & acid/peptic injury
• majority of duodenal & gastric ulcers are caused by H. pylori
infection and/or NSAID use

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• Helicobacter pylori
– Helical ,flagelated, microaerophilic ,urease producting G-
ve
– Association: 90% duodenal; 75% gastric
– ? Mechanism
• Local mucosal injury by toxic products
• Induction of local immune response
• Increased acid secretion: increased gastrin (D cell
destruction)
– Inversely related to socioeconomic status
– Lifetime risk of PUD if +H.pylori: 15%

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• NSAIDS
– 2nd most cause of PUD
– 3 million on NSAIDS; 1 in 10 has active ulcer
– Risk of gastric complication: increased 2- 10x
– Risk is proportional to anti- inflam potency
– Ulcers are more frequent in the stomach

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• Factors that put patients at increased risk for NSAID-induced
GI complications:
– age >60, prior GI event, high NSAID dose, concurrent
steroid or anticoagulant intake

– ANY pt taking NSAIDs or aspirin who has one or more of

these risk factors should receive concomitant acid
suppressive medication

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• Acid secretion
– In DUs, overlap of acid levels b/n ulcer pts & normal subjects
– 70% of pts with DUs have normal range acid output
– Some patients with DU
• higher mean BAO & mean MAO
• produce more acid in response to acid secretory
stimulus
– GU pts

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 Types of gastric Ulcer

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 PUD …
• Clinical Presentation
–Symptoms—Pain, Anemia, wt loss
–20% asymptomatic
–15-20% gross bleeding
–5-10% perforation
–5% GOO
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Clinical Manifestations

• 90% pts complain ABDOMINAL PAIN

– duodenal ulcer
• experience pain 2 to 3 hours after a meal & at night
• 2/3 of pts complain pain that awakens them from sleep
– gastric ulcer
• older than DU pts
• Pain occurs with eating
• nausea, bloating, weight loss, stool positive for occult blood,
and anemia

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Diagnosis

• Contrast radiograph
– Less expensive
– 90% accurate (double- contrast)
– But
• 5% of “ benign” ” ulcers are actually malignant
• 50% of duodenal ulcers may be missed by single
contrast studies

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• Endoscopy
– Accuracy 97%; the most reliable method
– Ability to biopsy lesions and sample forH.pyloridx

– Indications
 Patients ˃ 45 yrs old with symptoms
 Any alarm symptoms
• Weight loss
• Recurrent vomiting
• Dysphagia
• Bleeding
• Anemia

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 Diagnosis …

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 Investigation
• H.Pylori test
1.Invasive (endoscopy)
-Culture biopsy
-Histology
-Rapid urease breath test
2.Non Invasive (non-endoscopy)
-Urea Breath test,C13,14
-fecal H.Pylori antigen test
-Serology

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• H. pylori testing
– Noninvasive
• Serology
– ELISA or others
– 90% sensitivity / specificity
– May be positive for ~ 1 year after eradication
• Carbon - labeled urea breath test
– 95% sensitivity / specificity
– Test of choice to document eradication
– Needs to be done ~ 4 weeks after tx because of
possible false negatives

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• Invasive
– Rapid urease test
• Method of choice for diagnosis with EGD (cheap)
• Mucosal biopsies are placed in a medium containing
urea & a pH indicator. If urease+, it will become alkaline
• Sensitivity 90%; specificity 98%
– Histology
• Direct visualization of H. pylori
• Gold standard of tests; Sensitivity 95%; specificity 99%
– Culture
• Sensitivity 80%; specificity 100%
• Requires 3- - 5 days

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 PUD …
Management
Medical Management
Life style modification
Pharmacologic therapy
(Antacids,H2 receptor antagonists, Proton pump inhibitors,
treatment of H.Pylori infection)
• Read on duration of treatment before
declaring failure, intractability ,relapse and
recurrence after medical treatment

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• „ Proton Pump Inhibitors
– Most potent class
– Irreversebly bind to proton pump
– More prolonged & complete inhibition than H2RAs
– More rapid healing of ulcers (85% 4w; 95% 8w)
– Require an acidic environment within the gastric lumen to
become activated

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• Eradication of H. pylori
– Duodenal ulcer recurrence: 75% with no maint tx, 25%
with maint tx, < 2% with H.pylori eradication
– All patients with ulcer + H. pylori should be treated

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 Surgical treatment for Peptic ulcer and its
Complications
• Indications for Surgery
–Intractability
–Hemorrhage
–Perforation
–Obstruction

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 Surgery for duodenal ulcer
(intractable)
• Truncal Vagotomy and drainage
• Highly selective/parietal cell/proximal
gastric vagotomy …recurrence rate 10-
15%
• Truncal vagotomy and antrectomy
Reconstruction… Billroth I or II
Recurrence rate 2%
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 Types of vagotomy

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 Types of Pyloroplasty

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 Antrectomy with
Billroth I or Billroth II anastomosis

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 Operations for Gastric Ulcer
(intractable)
• Vagotomy not routinely done
• Antrectomy inclusive of the ulcer
• Truncal vagotomy with drainage
procedure and biopsy of the ulcer
• Operations for complications of pud:-
bleeding,perforation,intractability,GOO

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 Complications of surgery for peptic ulcer
disease
• Postgastrectomy syndromes
– Dumping syndrome
GI/Vasomotor
– Postvagotomy diarrhea
– Afferent loop syndrome
– Efferent loop syndrome
– Alkaline reflux gastritis

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 Roux en Y Reconstruction
(bile reflux gastritis)

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Complicated Ulcer Disease

• Hemorrhage
– Most common cause of upper GI bleeding in pts admitted
to hospital (40%)
– ulcer bed(small vessels in the wall of ulcer crater) or from
erosion of named vessels
– melena and/or hematemesis, Shock, ±abd.pain
– 80–85% of bleeding ulcers stop bleeding spontaneously

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• Tx
• Endoscopic
– 85%–95% of peptic ulcer bleedings handled by endoscopic
treatment
– High risk pts or Forrest grade 1a, 1b, & 2a
– Methods
• epinephrine injection alone
• combined therapies with
– epinephrine injection + thermal coagulation or
– epinephrine injection + placement of a hemoclip

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• Surgical
– 5–10% of bleeding peptic ulcers need emergency operation
– mortality rate is around 20%
– Indications
• Hemodynamic instability despite vigorous resuscitation (transfusion of
>3 units)
• Failure of endoscopic techniques to arrest hemorrhage
• Recurrent hemorrhage that cannot be controlled endoscopically (after
2attempts)
• Shock associated with recurrent hemorrhage
• Continued slow bleeding with a transfusion requirement exceeding 3
U/day

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 – Options
• Dus
– Oversew
– Oversew, V + D
–V+A
• Gus
– Oversew and biopsy
– Oversew, biopsy, V + D
– Distal gastrectomy

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• Perforation
– 5–10% of patients with peptic ulcers suffer a perforation
– higher in men than in women
– 15% of patients die from ulcer perforation
– Two types
• Free perforation
• Contained perforation
– location of perforation:
• duodenal bulb (62%), pyloric region (20%), gastric body
(18%)

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• Clinical presentation
– Early (onset to 2 hours): abdominal pain begins abruptly;
exact time the pain started
– Intermediate (2 to 12 hours): improvement in pain;
increased pain with movement, the abdominal wall is rigid
– Late (after 12 hours): increased pain & fevers, signs of
hypovolemia, & abdominal distension; Vomiting is most
common at this stage

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 – Workup
• Upright chest X-ray: free air in 80% of pts

• upper GI study
• abdominal CT scan

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 – Tx
• Resuscitation + Antibiotics + analgesia
• Surgery
– DUs
Patch
Patch, HSV
Patch, V + D
– Gus
Biopsy and patch
Wedge excision, V + D
Distal gastrectomy

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• Gastric Outlet Obstruction
– ˂5% of pts develop GOO from PUD
– due to duodenal or prepyloric ulcer disease
– acute (from inflammatory swelling
& peristaltic dysfunction) or chronic (from cicatrix)

– nonbilious vomiting, hypokalemic hypochloremic

metabolic alkalosis, Pain or discomfort, Weight loss,
succussion splash

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 – Diagnosis
• Endoscopy
– Tx
– Nasogastric suction, rehydration, & IV antisecretory agents
– Endoscopic hydrostatic balloon dilatation
– Surgery
• DUs GUs
– HSV + GJ
–V+D Biopsy; HSV + GJ
–V+A Distal gastrectomy

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• „Truncal vagotomy
– Division of L+R vagal trunks after they emerge below the
diaphragm
– reduces acid secretion
– alters gastric motility
• receptive relaxation of the stomach
• loss of antral pump mechanism
• failure of pylorus to relax & allow emptying into the
duodenum
– Requires drainage procedure

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• Highly Selective Vagotomy
– parietal cell vagotomy or proximal gastric vagotomy
– Nerves of Latarjet are divided at the crow’s feet (5 cm on
esophagus proximal to GEJ to 7 cm proximal to the pylorus)
– same reduction in acid secretion that occurs after truncal
vagotomy
– No need for drainage procedures

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• Drainage Procedures
– truncal, selective, or supradiaphragmatic vagotomy
– 2 categories:
• Pyloroplasty ˃ gastrojejunostomy
• perpetuates the original anatomy, simple, & associated
with less bile reflux
• 90% of all drainage procedures performed today are
variations of pyloroplasty

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• Gastric Resection / antrectomy
– removes the gastrin stimulus to acid secretion
– GI continuity must be restored by some form of
reconstruction

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• Metabolic disturbances
– severity is proportional to extent of resection
– Anemia
• Iron
• Most common (30% of pts after gastrectomy)
• decrease iron intake, impaired absorption, chronic
subclinical blood loss at margins of stoma
• Oral supplements correct problem
• Vitamin B12
• when resection > 50% stomach; rare with antrectomy
• Megaloblastic anemia occurs 2nd to lack of IF
• Treatment: IM cyanocobalamin

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 – Osteoporosis and osteomalacia
• Calcium deficiency
• worsened by impaired absorption of fat (fatty acids bind
calcium)
• Bone disease usually starts 4-5 years after surgery
• Tx: calcium supplement + vitamin D

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 Thank you !

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