30 yr old male brought to casuality with H/O severe abdominal pain of 1 day duration and ingetion of NSAID for 3 weeks for low back pain. O/E there is abdominal guarding and board like rigidity i. what is the probable diagnosis (3 marks) ii. how will you investigate (3 marks) iii. mention briefly the treatment
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NSAID induced peptic ulcer perforation diagnosis abdominal guarding board-like rigidity
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perforated peptic ulcer investigations treatment management surgery
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Here is a comprehensive structured answer:
Perforated Peptic Ulcer (NSAID-Induced)
i. Probable Diagnosis (3 marks)
Perforated Peptic Ulcer — most likely a perforated duodenal ulcer secondary to NSAID use.
Reasoning:
- History: 3 weeks of NSAID use for low back pain — NSAIDs inhibit COX-1, reducing mucosal prostaglandin synthesis, impairing the gastric mucosal barrier and predisposing to ulceration and perforation.
- Presentation: Sudden-onset severe generalized abdominal pain — classic for chemical peritonitis from gastric acid leaking into the peritoneal cavity.
- Examination: Board-like rigidity and guarding are hallmarks of generalized peritonitis following perforation — the patient will be disinclined to move due to pain, and the abdomen will not move with respiration.
Bailey & Love's (p. 1185): "The abdomen exhibits a board-like rigidity... Patients with this form of presentation need an operation, without which the patient will deteriorate with a septic peritonitis."
ii. Investigations (3 marks)
| Investigation | Findings / Purpose |
|---|---|
| Erect Chest X-ray | Free gas under the diaphragm (pneumoperitoneum) — present in >50% of perforations; simple, first-line investigation |
| CT Abdomen (with contrast) | Most accurate; confirms perforation, identifies site, detects pneumoperitoneum even when CXR is negative; also differentiates from pancreatitis |
| Serum Amylase | Done to exclude acute pancreatitis — amylase may be mildly elevated in perforation but not as markedly as in pancreatitis |
| Blood investigations | CBC (leukocytosis), LFTs, RFTs (baseline before surgery), coagulation profile, blood grouping and cross-match |
| Serum electrolytes & ABG | Assess metabolic status, degree of physiological derangement |
| USG Abdomen | Free fluid in peritoneal cavity; useful bedside tool |
Bailey & Love's (p. 1186): "An erect chest radiograph will reveal free gas under the diaphragm in more than 50% of cases... CT imaging is now most commonly used and is more accurate."
iii. Treatment (Brief)
A. Immediate Resuscitation
- IV access — aggressive fluid resuscitation with crystalloids (Normal Saline / Ringer's Lactate)
- NPO (nil per oral) + Nasogastric tube insertion for gastric decompression
- Urinary catheter for urine output monitoring
- IV broad-spectrum antibiotics (e.g., Ceftriaxone + Metronidazole) for peritonitis
- IV Proton Pump Inhibitor (e.g., Pantoprazole/Omeprazole infusion)
- Adequate analgesia
B. Definitive Surgical Treatment
- Emergency laparotomy (or laparoscopic repair where available) is the treatment of choice.
- Omental patch repair (Graham patch) — the perforation is closed with an omental plug and sutures; most commonly performed.
- Thorough peritoneal lavage with warm saline to remove contamination.
- In selected stable patients with a small perforation (< 6 hours), conservative (non-operative) management (Taylor's method — NG suction, antibiotics, PPI) may be considered, but surgery is preferred.
C. Post-operative Management
- Continue IV PPI followed by oral PPI for 4–8 weeks
- Stop NSAIDs permanently; use alternative analgesics (e.g., paracetamol, physiotherapy for back pain)
- Test and treat for H. pylori (CLO test / biopsy during endoscopy) — eradication therapy if positive (Triple therapy: PPI + Amoxicillin + Clarithromycin × 14 days)
- Regular follow-up with upper GI endoscopy to confirm ulcer healing
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