PERFORATED

PEPTIC ULCER
DISEASE
PGI ALTO, ARLEX
OBJECTIVE
S
• Discuss what is Peptic Ulcer Disease and its Etiology
• Describe the pathophysiology of peptic ulcer disease.
• Outline the presentation of a patient with a perforated
peptic ulcer.
• Summarize the treatment options for perforated peptic
ulcers.
 Peptic ulcer disease refers to an insult
to the mucosa of the upper digestive
tract resulting in ulceration that
extends beyond the mucosa and into
the submucosal layers.

PUD While the majority of peptic ulcers

are initially asymptomatic, clinical
manifestations range from mild
dyspepsia to complications including
gastrointestinal bleeding, perforation,
and gastric outlet obstruction.
 increased acid
dietary factors,
production,

ETIOLO stress.
Helicobacter pylori

GY
infection

and the use of

nonsteroidal anti-
inflammatory drugs
(NSAIDs) including low-
dose aspirin
 The next most common complication is perforation.

The annual incidence of upper GI bleeding secondary to a peptic

ulcer is estimated to be between 19 to 57 cases per 100,000
individuals.

Epidemiolog Ulcer perforation is expected to be 4 to 14 cases per 100,000

individuals.
y
Advanced age is a risk factor as 60% of patients with PUD are older
than 60.

Infections with Helicobacter pylori and the use of nonsteroidal

anti-inflammatory drugs (NSAIDs) are each identified as risk factors
for the development of bleeding ulcers and peptic ulcer
perforation
5 TYPES
OF PUD
5 TYPES
OF PUD
 • Typical workup includes labs and imaging
studies.
• complete blood count (CBC), chemistry
panel, liver function tests, coagulation
profile, and lipase levels (to rule out
Evaluatio pancreatitis).
• Blood type and screening

n • A set of blood cultures and lactic acid

should be done on patients meeting the
systemic inflammatory response syndrome
(SIRS) criteria
• Imaging studies should be obtained once
the patient is stabilized.
MEDICAL TREATMENT OF PUD
• Inhibition of acid secretion
• Smoking cessation
• Alcohol avoidance
• NSAID withdrawal
• Eradicate H pylori
• Repeat EGD and biopsy at 6-8 wks
PYLORI ERADICATION
• PPI triple therapy – First line therapy
o PPI bid
o Amoxicillin, 1G bid
o Clarithromycin, 500mg bid

• Quadruple therapy - Gold standard

O PPI bid
O Bismuth, 2 tablets qid
O Amoxicillin, 1G bid
O Clarithromycin, 500mg bid
Bleeding
• Most common complication
• Presentation: melena or hematemesis with or without shock
• Diagnosis: NGT and Early endoscopy
• Treatment:
o Non-operative: NPO, acid suppression, endoscopic treatment (epinephrine/cautery)
o Indications for Surgery
▪Persistent bleeding /rebleeding after endoscopic therapy
▪Significant hemorrhage (>4 units/24 hours)
▪Elderly patients with co-morbidities
▪Ulcers located at posterior duodenal bulb and ulcers located at the gastric lesser
curvature
▪High risk of rebleeding based on endoscopic findings (active pulsatile bleeding, visible
vessel
THE FORREST CLASSIFICATION FOR ENDOSCOPIC
FINDINGS AND REBLEEDING RISKS
Perforation
• Usually presents as acute abdomen with marked abdominal
guarding and rebound tenderness
• Upright chest radiograph: pneumoperitoneum in 80%
• Treatment: Non-operative only if sealed leak w/o signs of
peritonitis
SURGICAL TREATMENT OF PUD
Indication Duodenal Gastric
Bleeding 1. Oversew 1. Oversew and biopsy
2. Oversew, V + D 2. Oversew, biopsy, V + D
3. V+A 3. Distal Gastrectomy
Perforation 1. Patch 1. Biopsy and patch
2. Patch, HSV 2. Wedge excision, V + D
3. Patch, V + D 3. Distal Gastrectomy
POST-GASTRECTOMY PROBLEMS
• Dumping syndrome
• Diarrhea
• Gastric stasis
• Bile reflux gastritis
• Roux syndrome
• Gallstones
• Weight loss
• Anemia
• Bone disease
DUMPING SYNDROME
• Caused by destruction of the pyloric sphincter causing abrupt
• delivery of hyperosmolar load to the small intestines

• Early dumping (15-30 mins post-prandial)

o peripheral and splanchnic vasodilatation leads to shock-like symptoms
(sweating, light-headedness, tachycardia) that is relieved by saline or recumbency
diarrhea then follows

• Late dumping ( 2-3 hours post-prandial)

• due to hyperinsulinemia with reactive hypoglycemia
• relieved by glucose administration
ROUX STASIS SYNDROME
• Results from functional obstruction due to disruption of normal
propagation of pacesetter potentials in the Roux limb from the
proximal duodenum, as well as altered motility in gastric
remnant
• Characterized by chronic abdominal pain, nausea, and vomiting
that is aggravated by eating
ROUX STASIS SYNDROME
• Upper GI series confirms these findings and may show delayed gastric
emptying
• Endoscopy may show retained food or bezoars, dilation of the gastric
remnant, and/or dilation of the Roux limb
• GI motility testing shows abnormal motility in the Roux limb, with
propulsive activity toward, rather than away from, the Stomach

• Management
• o Nonoperative: use of pro-motility agents
• o Surgery: Near-total or Total gastrectomy to remove the atonic stomach