Perforated peptic ulcer case study
The case
Patient: 58‑year‑old male, Mr R, a taxi driver.
Presenting complaint: Sudden onset of severe epigastric pain for 6 hours.
History of present illness:
- Pain began abruptly while he was eating a large meal, described as “sharp, tearing” and radiating to the left shoulder (Kehr’s sign).
- The pain is constant, worsens when lying supine, and is partially relieved by sitting forward.
- He noticed a low‑grade fever (38.2 °C) and two episodes of non‑bloody vomiting.
- No prior similar episodes.
Past medical history:
- Known duodenal ulcer diagnosed 2 years ago, treated intermittently with proton‑pump inhibitors (PPIs).
- Hypertension for 8 years, on amlodipine 5 mg daily.
- No history of diabetes, coronary artery disease, or previous abdominal surgery.
Social history:
- Smokes 15 cigarettes/day for 30 years.
- Drinks alcohol socially (≈2 units/week).
- No illicit drug use.
Medications: Amlodipine 5 mg, omeprazole 20 mg (irregular adherence).
Allergies: None reported.
Examination:
| Parameter | Value |
|---|---|
| General | Patient appears distressed, diaphoretic |
| Vitals | BP 110/70 mm Hg, HR 112 bpm, RR 22 /min, Temp 38.4 °C, SpO₂ 96 % on room air |
| Abdomen | Distended, generalized tenderness, especially epigastric; guarding and rebound tenderness present. Rigid board‑like abdomen. No palpable masses. Bowel sounds absent. |
| Cardiovascular | Regular rhythm, no murmurs |
| Respiratory | Clear breath sounds bilaterally |
| Neurological | Alert, oriented ×3 |
Initial investigations:
| Test | Result |
|---|---|
| CBC | Hb 13.2 g/dL, WBC 16.8 ×10⁹/L (neutrophils 85 %), platelets 210 ×10⁹/L |
| Serum electrolytes | Na⁺ 138 mmol/L, K⁺ 3.9 mmol/L, Cl⁻ 102 mmol/L, HCO₃⁻ 22 mmol/L |
| Renal function | Urea 38 mg/dL, Creatinine 1.1 mg/dL |
| Liver function | AST 28 U/L, ALT 30 U/L, ALP 78 U/L, Bilirubin 0.8 mg/dL |
| Serum amylase | 78 U/L (normal) |
| CRP | 78 mg/L |
| ABG (room air) | pH 7.32, PaCO₂ 32 mm Hg, PaO₂ 78 mm Hg, HCO₃⁻ 16 mmol/L |
| Plain erect chest X‑ray | Free sub‑diaphragmatic air (Rigler’s sign) on the right side |
| Abdominal erect X‑ray | No obvious obstruction; gas pattern consistent with perforation |
| Ultrasound abdomen | Limited view due to gas; modest free fluid in Morrison’s pouch |
The clinical picture and radiographic evidence strongly suggest a perforated peptic ulcer (PPU).
Questions
- What is the most likely diagnosis and which clinical and radiological findings support it?
- List the immediate investigations required to confirm the diagnosis and assess the patient’s physiological status.
- Outline the initial resuscitation measures and pre‑operative management according to the latest (2023) NICE and ACG guidelines.
- Describe the definitive surgical options for a perforated duodenal ulcer, including indications for each technique.
- Discuss the early and late postoperative complications of PPU repair and the strategies to prevent them.
Answers
1. Diagnosis and supporting findings
Diagnosis: Perforated duodenal ulcer (a type of perforated peptic ulcer).
Supporting clinical findings
- Sudden, severe epigastric pain with radiation to the shoulder (Kehr’s sign) – classic for diaphragmatic irritation by free air.
- Rigid, board‑like abdomen with guarding and rebound tenderness – indicates peritonitis.
- Pain relief on sitting forward – typical of intra‑abdominal irritation.
- Low‑grade fever and leukocytosis (WBC 16.8 ×10⁹/L) – systemic inflammatory response.
Supporting radiological findings
- Free sub‑diaphragmatic air on erect chest X‑ray (Rigler’s sign) – pathognomonic for gastrointestinal perforation.
- Absence of pancreatic enzyme elevation (normal amylase) helps exclude pancreatitis.
Together, the acute abdomen, peritoneal signs, and free air confirm a perforated peptic ulcer, most likely duodenal given his prior ulcer history.
2. Immediate investigations
| Investigation | Rationale | Normal reference |
|---|---|---|
| CBC | Detect leukocytosis, anemia, thrombocytopenia; guide transfusion if needed. | WBC 4–11 ×10⁹/L |
| Serum electrolytes & renal panel | Assess dehydration, electrolyte loss, renal perfusion before fluids/contrast. | Na⁺ 135–145 mmol/L, K⁺ 3.5–5.0 mmol/L |
| ABG | Identify metabolic acidosis from hypoperfusion; guide oxygen/ventilation. | pH 7.35–7.45 |
| CRP | Marker of inflammation; useful for postoperative monitoring. | <5 mg/L |
| Chest & abdominal erect X‑ray | Detect free intraperitoneal air; quick bedside tool. | No free air |
| Focused abdominal ultrasound | Look for free fluid; assess for other pathology if X‑ray equivocal. | No free fluid |
| CT abdomen (contrast‑enhanced) – if diagnosis uncertain | Provides precise location of perforation, size, and any associated collections. | N/A |
| Blood grouping & cross‑match | Anticipate need for intra‑operative transfusion. | N/A |
| Serology for H. pylori (urea breath test or stool antigen) – post‑stabilisation | Guides eradication therapy after acute phase. | N/A |
These investigations confirm the diagnosis, quantify physiological derangement, and prepare for safe surgery.
3. Initial resuscitation and pre‑operative management (NICE 2023; ACG 2023)
Airway, Breathing, Circulation (ABC)
- Administer high‑flow oxygen to maintain SpO₂ ≥ 94 %.
- Secure airway only if GCS < 8 or impending respiratory failure.
Fluid resuscitation
- Isotonic crystalloids (0.9 % saline or Ringer’s lactate) 30 mL/kg bolus (≈2 L for a 70‑kg adult) over 30 min, then titrate to maintain MAP ≥ 65 mm Hg and urine output ≥ 0.5 mL/kg/h.
- If ongoing loss or shock persists, consider colloids (e.g., albumin 5 %) after 30 mL/kg crystalloid.
Broad‑spectrum antibiotics (within 1 hour of diagnosis) – per ACG 2023:
- Ceftriaxone 2 g IV q24h + Metronidazole 500 mg IV q8h or
- Piperacillin‑tazobactam 4.5 g IV q6h (if high risk of resistant organisms).
Nasogastric tube (NGT) – Insert to decompress stomach and reduce leakage risk; keep on low suction.
Analgesia – IV paracetamol 1 g q6h; opioids (e.g., morphine 2–4 mg IV) only if needed, avoiding NSAIDs.
Proton‑pump inhibitor – Omeprazole 80 mg IV bolus, then 8 mg/h infusion to suppress acid secretion and promote ulcer healing.
Risk stratification – Use American Society of Anesthesiologists (ASA) classification; patient is ASA III (stable chronic disease + acute abdomen).
Consent & pre‑operative optimisation – Discuss surgical options, risks, and need for possible ICU stay.
Timing of surgery – NICE 2023 recommends surgery within 6 hours of diagnosis for perforated ulcer to reduce morbidity and mortality.
4. Definitive surgical options
| Technique | Description | Indications / Contra‑indications |
|---|---|---|
| Omental (Graham) patch repair | Simple closure of perforation by suturing a pedicled omental patch over the defect (2–3 sutures of 2‑0 absorbable material). | First‑line for most perforated duodenal ulcers ≤ 2 cm, stable patients, no large contamination. |
| Primary closure with omental patch | Direct suturing of ulcer edges (if viable) plus omental reinforcement. | Small, clean edges; minimal tissue loss. |
| Laparoscopic Graham patch | Same principle as open, but performed via 3–4 ports; CO₂ insufflation 12 mm Hg. | Hemodynamically stable, experienced laparoscopic team, perforation ≤ 1 cm, no extensive peritonitis. |
| Definitive ulcer surgery (truncal vagotomy + pyloroplasty or antrectomy) | Addresses underlying acid hyper‑secretion; performed when ulcer is large (> 2 cm), recurrent, or when H. pylori eradication is not feasible. | Chronic ulcer disease, poor compliance, or when perforation is associated with gastric outlet obstruction. |
| Partial gastrectomy (Billroth II) | Resection of distal stomach with gastrojejunostomy; reserved for malignant ulcer suspicion or massive tissue loss. | Suspicion of malignancy, large necrotic area, or failed previous repairs. |
Choice for Mr R: Given a 2‑cm duodenal perforation, moderate peritonitis, and stable hemodynamics after resuscitation, an open Graham patch repair is appropriate. If laparoscopic expertise is available and intra‑operative assessment shows limited contamination, a laparoscopic Graham patch could be considered.
5. Post‑operative complications and prevention
| Complication | Early (≤ 30 days) | Late (> 30 days) | Prevention / Management |
|---|---|---|---|
| Surgical site infection (SSI) | Wound erythema, purulent discharge | N/A | Pre‑operative antibiotics (as above), meticulous aseptic technique, wound irrigation, postoperative wound care. |
| Intra‑abdominal abscess | Fever, persistent leukocytosis, localized pain | N/A | Adequate peritoneal lavage intra‑operatively, postoperative drainage if contaminated, early imaging if suspicion. |
| Leak from repair | Peritonitis, rising CRP, sepsis | N/A | Tension‑free omental patch, avoid excessive suturing, ensure viable tissue; postoperative NGT decompression, early enteral feeding when safe. |
| Pulmonary complications (atelectasis, pneumonia) | Dyspnea, hypoxia | N/A | Incentive spirometry, early ambulation, analgesia that allows deep breathing, prophylactic DVT/PE measures. |
| Deep vein thrombosis / pulmonary embolism | Leg swelling, chest pain | N/A | Pharmacologic prophylaxis (e.g., enoxaparin 40 mg SC daily) and mechanical compression devices. |
| Recurrent ulcer disease | Re‑bleeding, new perforation | Chronic dyspepsia, ulcer recurrence | Long‑term PPI (e.g., omeprazole 20 mg daily), H. pylori eradication (triple therapy: amoxicillin 1 g BID + clarithromycin 500 mg BID + PPI for 14 days), smoking cessation, NSAID avoidance. |
| Adhesive small‑bowel obstruction | Abdominal distension, vomiting | May present months later | Gentle tissue handling, minimize peritoneal trauma, use of adhesion barriers (e.g., hyaluronic acid‑carboxymethylcellulose) when indicated. |
| Mortality | Usually due to sepsis, multi‑organ failure | N/A | Prompt diagnosis, early surgery (< 6 h), aggressive resuscitation, appropriate antibiotics, ICU support if needed. |
Monitoring protocol (first 48 h):
- Vital signs q1h, urine output hourly, CBC & CRP q12h, ABG if respiratory compromise.
- NGT output monitored; remove when output < 200 mL/24 h and bowel sounds return.
- Early ambulation on postoperative day 1, chest physiotherapy.
Key learning points
- Perforated peptic ulcer presents with acute abdomen, peritoneal signs, and free sub‑diaphragmatic air on erect chest X‑ray.
- Prompt resuscitation (fluid bolus, antibiotics, PPI, NGT) and surgery within 6 hours dramatically reduce mortality.
- Graham omental patch is the cornerstone repair for most duodenal perforations; laparoscopic approach is feasible in selected stable patients.
- Pre‑operative risk assessment (ASA, hemodynamics) guides choice between open vs. laparoscopic repair.
- Post‑operative care focuses on preventing leak, infection, pulmonary complications, and ensuring H. pylori eradication plus lifestyle modification to avoid recurrence.
- Guideline updates (NICE 2023, ACG 2023) emphasize early antibiotics, PPI infusion, and early definitive surgery.
- Complication surveillance includes serial CRP, clinical exam, and imaging when indicated; early detection of leak or abscess improves outcomes.
Practice MCQs
1. Which of the following is the most reliable bedside radiographic sign for diagnosing a perforated peptic ulcer?
A. Double‑bubble sign
B. Rigler’s sign
C. Westermark sign
D. Kerley B lines
Answer: B — Rigler’s sign (presence of free air on both sides of the bowel wall on an erect chest X‑ray) is classic for gastrointestinal perforation.
2. According to the 2023 ACG guideline, the recommended initial antibiotic regimen for a patient with a perforated duodenal ulcer is:
A. Ciprofloxacin + Metronidazole
B. Ceftriaxone + Metronidazole
C. Amoxicillin + Clavulanate
D. Vancomycin + Gentamicin
Answer: B — Ceftriaxone 2 g IV daily plus Metronidazole 500 mg IV q8h provides coverage for gram‑negative and anaerobic organisms commonly implicated in intra‑abdominal sepsis.
3. A 60‑year‑old woman undergoes an open Graham patch repair for a perforated ulcer. Which postoperative measure is most important to prevent recurrence of ulcer disease?
A. Continuation of IV omeprazole for 48 h only
B. Initiation of H. pylori eradication therapy after discharge
C. Routine use of NSAIDs for analgesia
D. Early oral feeding within 6 h
Answer: B — Eradication of H. pylori (triple therapy) after the acute phase is essential to prevent ulcer recurrence; NSAIDs should be avoided, and PPIs are continued longer than 48 h.
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