Perforation
- 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
- 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