Perforated Peptic Ulcer

Bambang Suprapto
SMF Bedah RSUD A. Wahab Sjahranie
Samarinda
Gastric Juice Secretion
Danger of Ulcer
 Peptic Ulcer
• Peptic Ulcer disease usually occurs in the
stomach & proximal duodenum
• The predominant causes are infection with
Helicobacter pylori and use of NSAID
• Mucosal damage secondary to pepsin and
gastric acid secretion
 Peptic Ulcer
25% have serious complication :
• Hemorrhage 15 – 20 %
• Perforation 2 –10 %
• Gastric outlet obstruction 5 – 8 %
 Ulcers in the elderly

• Gregory Lockrey (1999)

3-10 times higher in NSAID users
Gasric ulcers twice common prevalence of H.
Pylori infection increased with aged
(20-30 years-old : 18 %, aged over 70 : 53%)

• Stephen Behrman (2005)

Seropositive H.Pylori showed linear relation-ship
with age
 Ulcers in the elderly
H. Pylori with NSAID-induced ulcer disease :
50%
Elderly population is most at risk for HP infection
and NSAID complications

• JM Liou (2008)
PPI maintenance therapy is helpful in the
prevention ulcers recurrence
 Peptic Ulcer

• Surgery for peptic ulcer complications, such as

perforations has not changed, although the use
of powerful drugs.

• Subsequently the uncontrolled use of NSAIDs

have contributed to the incident of perforated
peptic ulcer

G. Bazet al, ActaChirBelg. 2008, 108; 424-7

 Perforated Peptic Ulcer

• Patient may come in sepsis – severe sepsis.

• Intensive post operative care

• Nutritional support is essential

• Early enteral nutrition can be via TF

• Combined EN – PN as necessary
Perforated Peptic Ulcer

• Chronic Gastritis
• Endoscopy : ulcer (+)
• NSAID
• Helicobacter pylori
 Helicobacter Pylori

• Urease; hydrolysis urea to ammonia and CO2

• Urease protecting bacteri from damaging of

gastric acid

• Produced proinflammatory factors: proteases

and phospolipase  breakdown glicoprotein-
lipid complex of the mucus gel layer
Non-Steroidal Antiinflamamatory drugs

• Inhibiting effect :
-endogenous prostaglandins
-mucosal bicarbonate
-mucus secretion

• Reduced mucosal blood flow

 Miscellaneous

• Stress : increased tonus of the vagus

nerve  stimulation gastric gland

• Smoking : inhibition pancreatic

bicarbonate secretion
 Symptom
• Suddenly abdominal pain

Natural History :
- Chemical peritonitis / contamination
- Intermediate stage (6-12 hours)
- Intra abdominal infection
 Sign
• Diffuse or localized peritoneal irritation
 Defance Muscular (+)
• Paralytic Ileus :
 Decrease in Bowel movement / peristaltic
 Decrease in Tonus Sphincter Ani
• Liver dullness (-)
• Fever / subfebril
• Dehydration / Hipovolemic Shock
• Free air  under diaphragm (2/3 patients)
 Treatment

• Operative  Emergency
• Non operative (Taylor’s approach)
 ‘late presenter’ / ‘extremely sick’
 History

• 1880 : Mikulics, introduced closure of perforation by suture

• 1929 : Cellan Jones, first used pedicle omental patch

• 1937 : Graham, described the use free graft omental patch

• 2000 : Sharma, mushroom omental plug (giant perforation)

• Recently : Laparoscopy (selective)

 Ulcer Classification (location)
• Type I :
Along the lesser curve of the stomach

• Type II :
Gastric ulcers either concurrently associated with duodenal ulcers or
a historical presence of duodenal ulceration

• Type III :
Located in the prepyloric position

• Type IV : (Csendes et. al)

Esophagogastric junction
• Type I and IV
Associated with malignacy

• Type II and III

More likely to be related to acid mediated
or NSAID-related ulcer
 Management

• Operative procedure :
-Simple closure with omental patch
( open or laparoscopic)
-Partial gastrectomy ?

• Antisecretory agent : PPI

• Antibiotics : H. Pylori (+)

 Management

• Duodenal ulcer : simple closure with omental patch

• Gastric ulcer (II,III) : simple closure with omental patch

• Gastric ulcer (I,IV) : biopsy to the edge ulcer (Frozen

section if possible), simple closure

• Malignant : partial gastrectomy immediately or electively

(depend on severity of illness)

• H. Pylori (+) : multiple drugs

Management