Acid peptic disease and intestinal perforation

1. Perforation
Peritonitis
Lt. Dhirendra

2. Case
• 60 yrs Female(1530hrs)
• c/o
– Pain abdomen
– Abdominal distension x2 days
• H/o
– Nausea and vomiting
– Not passing stool and flatus
– Loss of appetite

3. On Examination
• Afebrile
• P-104/min
• RR-20/min
• BP-114/72mmHg
• spO2-98%
• Pallor ++
• Tongue dry
• Pt.wt-44 kg

4. • Per Abdomen
– Distension +
– Gen. guarding and tenderness +
– Tympanic note on percussion
– Liver dullness obliterated
– Bowel sounds absent
– Organs not palpable
– PR: rectum empty
• CVS
• Chest NAD
• CNS

5. On Investigations (2130hrs)
• USG abdomen (civil)
– Free intraperitonial fluid with internal echoes
– ?Hollow viscous perforation
• CXR
– Free gas under diaphragm

6. • Haematology and Biochemistry
– Hb-13.6gm%
– TLC-16,300/cmm
– DLC – P85 L12 M1 E2
– Blood sugar(R)-84mg/dl
– B.Urea-64 mg/dl
– S.creatinine-2.0 mg/dl
– PT-15.5/16.5
– INR-1.11

7. Management
• Kept NPO
• Ryle’s tube
• Catheterization with Foley’s catheter
• Resuscitated with IV fluids
• IV antibiotics
• Pantoprazole
• Prepared for Exploratory Laparotomy

8. Exploratory Laparotomy (2330 hrs)
• Intra OP findings
– Bilious peritoneal collection-1800ml
– 5mm perforation ant. aspect of 1st part of
Duodenum
• Surgery
– Peritoneal wash
– Grahm’s patch closure using 2/0 silk
– Drain placed
– Haemostasis ensured

9. Post OP management
• NPO
• IV fluids
• IV antibiotics
• Pantoprazole
• Epidural top up(morphine)
Patient gradually improved, orally started on
4th PO day, discharged on 12th PO day in
satisfactory condition.

10. Discussion

11. Acute Abdomen
• Abdominal condition
– abrupt onset
– severe abdominal pain
• Causes
– Inflammation
– Obstruction
– Perforation
– Infarction
– Rupture of intra-abdominal organs

12. Peptic Ulcer Disease
• Focal defects
– gastric or duodenal mucosa
– extend into the submucosa or deeper
• Caused by an imbalance between mucosal
defences and acid/peptic injury

13. Causative Agents
• Helicobacter Pylori infection
• Drugs (all NSAIDs,cocaine,etc)
• Smoking
• Alcohol
• Dietary habits
• Psychological stress

14. Pathogenesis
• Helicobacter pylori is implicated in 70–92% of all PUD
• The second most common cause-ingestion of
NSAIDs.
• The least common cause is pathologic
hypersecretory states, such as Zollinger-Ellison
syndrome

15. Helicobacter Pylori
• H.pylori possesses the enzyme urease:
– converts urea into ammonia and bicarbonate
• The Bicarbonate buffers the acid secreted by the stomach.
• The ammonia is damaging to the SECs
• Inhibitory effect on antral D cells that secrete
somatostatin
– No inhibition of antral G-cell gastrin production
• Local alkalinisation of the antrum(antral
acidification is the most potent antagonist to
antral gastrin secretion)
• The end result is hypergastrinemia and acid hyper
secretion

16. NSAID-Induced Disease

17. COMPLICATIONS OF PEPTIC ULCER
DISEASE
• Bleeding
• Perforation
• Gastric Outlet Obstruction
• Intractable disease(Carcinoma)

18. Complications
• Upper GI bleeding-most common complication.
• Sudden large bleeding-life threatening.
• Occurs when the ulcer erodes blood
vessels(gastroduodenal artery).

19. Perforation
• Most often chronic
ulcer
• 50%: sealed off
• Location: most often
anterior juxtapyloric
• Mean diameter: 5mm
(>1cm=giant ulcer:
rare)
• 10%: perforated
gastric ulcer

20. Complications of Perforation
• Spillage of stomach or intestinal content into the abdominal
cavity.
• Acute peritonitis
– initially chemical
– later bacterial peritonitis(The first sign is sudden intense abdominal
pain)
• Posterior wall perforation
– Pancreatitis(pain radiates to the back)
– Perforation in the CBD- aerobilia, cholangitis

21. Signs and Symptoms
• Perforated Peptic ulcer
– Sudden-onset, severe, generalised abdominal pain
– Tachycardia
– Board-like rigidity
– Distension
– Obstipation
– Fever(not initially)
– Hypotension(later stage)

22. Diagnosis
• Perforated Peptic ulcer
– Erect plain chest radiograph
• free air can be seen in about 80% of cases
• CT imaging more accurate
– Amylase levels
• Rule out acute pancreatitis

23. Following resuscitation, the treatment
is principally surgical
• Laparotomy
• Laparoscopy
Component
– Thorough peritoneal toilet(remove fluid and food
debris)
– Closing the ulcer (omental patch can be placed)
– Vagotomy (recently highly selective vagotomy)
– Systemic antibiotics
– Gastric anti-secretory agents

24. Minimally
Invasive Techniques
• Thorough peritoneal toilet
• Perforation closure by intracorporeal suturing
• Nasogastric suction
• Gastric anti-secretory agents
• Systemic antibiotics

25. • Patients who have suffered one perforation
may suffer another one
– Eradication therapy for Helicobacter
– Lifelong treatment with proton pump inhibitors

27. Surgical
management of
peptic ulcer diseases
• Vagotomy
– Truncal vagotomy and
drainage
– highly selective vagotomy
– Truncal vagotomy and
antrectomy
• Antrectomy
– Gastroduodenostomy
(Billroth I)
– Gastrojejunostomy
(Billroth II)

28. In a nutshell
• Most peptic ulcers are caused by H. pylori or
NSAIDs
• Common complications-perforation, bleeding and
stenosis
• Diagnosis(perforation)-Erect plain chest
radiograph(free air under diaphragm)
• The treatment of the perforated peptic ulcer is
primarily surgical following resuscitation
• Gastric anti-secretory agents
• Systemic antibiotics

29. Discussion