Malaise, exertional dyspnoea and abdominal pain in a 50-year-old man

Introduction

A 50-year-old man and active smoker presented with a 4-week history of general malaise, exertional dyspnoea, abdominal pain and weight loss. He had a medical history of epilepsy and excess alcohol consumption with recurrent falls resulting in injuries including an L3 end-plate fracture. He had been taking naproxen and paracetamol for his injuries. Abdominal and rectal examination revealed mild epigastric tenderness and normal bowel sounds. He was haemodynamically stable with no stigmata of chronic liver disease. Bloods showed a normocytic anaemia with a haemoglobin of 81 g/L, and his liver and renal functions were within normal range. There was evidence of active inflammation with a C reactive protein of 254 mg/L, leucocytosis of 15.6×10⁹ /L, platelets of 554×10⁹ /L and albumin of 27 g/L.

Erect chest X-ray performed for dyspnoea and epigastric pain was normal. Gastroscopy demonstrated an abnormal stomach with evidence of hypertrophic gastric folds with a large invasive mass taking up the entire distal stomach suspicious of malignancy (figures 1–3). There was evidence of extensive excoriation of the gastric mucosa and the mass was friable and oozing from multiple points. Biopsies of the lesion were taken for histology and a CT chest abdomen and pelvis was organised for staging.

Figure 1.

Gastroscopy image of proximal stomach with thickened gastric folds.

Figure 2.

Gastroscopy image of mid stomach.

Figure 3.

Gastroscopy image of large gastric mass.

Question

What is the clinical diagnosis?

Answer

CT showed gastric thickening with a contained perforation within the lesser sac (figures 4 and 5). No distant metastatic lesions were seen. Gastric biopsies consisted of a small amount of non-specialised gastric type mucosa with chronic inflammation together with tissue indicative of hepatocytes. No evidence of Helicobacter pylori infection, dysplasia or malignancy were seen. The patient had a large contained gastric perforation secondary to peptic ulcer disease likely secondary to a combination of naproxen use, excess alcohol consumption and smoking. There was a 5-day lag-time between admission and histological diagnosis before the patient was made nil-by-mouth. Surgeons opted for conservative management with intravenous antibiotics and proton-pump inhibitors. Parenteral nutrition was given for 4 weeks until oral feed was tolerated. Repeat CT demonstrated healing of the defect and he was discharged safely.

Figure 4.

Axial CT image of abdomen.

Figure 5.

Coronal CT image of abdomen.

Peptic ulcer perforation occurs in 3.8–14 per 100 000 population with a mortality rate up to 30%.¹ Early diagnosis within 6 hours of onset with surgical repair is often critical to improving survival to prevent adversities including bleeding, obstruction and septic shock.² Liver penetration is rare with only 15 cases reported to date.^{3 4} Abnormal liver function tests are seldom seen secondary to localised hepatic excoriation from gastric acid. While surgery is often required, contained gastric perforations can be managed conservatively if the patient remains haemodynamically stable with no evidence of gastric leakage.³

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Ethics approval

This study does not involve human participants.