# Delayed Caecal Perforation Following Endoscopic Retrograde Cholangiopancreatography (ERCP)-Induced Severe Acute Pancreatitis: A Rare Pancreatitis Complication

## TL;DR

A rare case of delayed caecal perforation following severe acute pancreatitis triggered by ERCP is reported, highlighting the potential for distant gastrointestinal complications.

## Contribution

This case report presents a rare delayed complication of ERCP-induced pancreatitis with caecal perforation.

## Key findings

- Delayed caecal perforation occurred fifteen days after severe post-ERCP pancreatitis in a 64-year-old woman.
- Histopathology showed ischaemic necrosis without mechanical or vascular pathology, suggesting an inflammatory mechanism.
- The case underscores the need for vigilance regarding secondary gastrointestinal complications in severe pancreatitis.

## Abstract

Severe acute pancreatitis represents a systemic inflammatory condition that may extend beyond the pancreas and result in significant extra-pancreatic morbidity. Although colonic involvement is a recognised complication of severe or necrotising pancreatitis, it is uncommon and most frequently affects bowel segments adjacent to the pancreatic bed, with distal colonic perforation remaining exceedingly rare. Endoscopic retrograde cholangiopancreatography (ERCP) is a recognised iatrogenic trigger of acute pancreatitis and, in rare cases, may precipitate severe disease. We report a unique case of delayed caecal perforation developing fifteen days after the onset of severe post-ERCP pancreatitis (PEP) in a 64-year-old woman. The initial presentation of PEP was complicated by haemodynamic instability and multiorgan failure requiring prolonged intensive care unit support. Despite an initial period of apparent stabilisation, the patient subsequently deteriorated with gastrointestinal bleeding and haemodynamic compromise. Cross-sectional imaging demonstrated pneumoperitoneum arising from the caecum, and emergency laparotomy confirmed caecal perforation, which was managed with extended right hemicolectomy and end ileostomy formation. Histopathological examination demonstrated acute transmural ischaemic necrosis with associated omental fat saponification, in the absence of mechanical or primary vascular pathology, supporting an inflammatory and ischaemic mechanism secondary to severe acute pancreatitis. After a prolonged hospital stay and clinical stabilisation, the patient was discharged. This case highlights a rare and delayed manifestation of pancreatitis-associated colonic injury at a remote anatomical site and underscores the importance of maintaining a high index of suspicion for secondary gastrointestinal complications in patients with severe pancreatitis and unexplained clinical deterioration.