When Pancreatitis Strikes the Colon: A Rare Case Report of Sigmoid Perforation

Abstract

Introduction

Acute pancreatitis is a potentially severe condition that can lead to both local and systemic complications. Colonic complications are uncommon but include fistula formation and perforation, both of which are associated with high morbidity and mortality. This is a case of colon perforation in an unusual location, following an episode of acute pancreatitis.

Case Presentation

We report the case of a 75-year-old man with a history of arterial hypertension, dyslipidemia, and atrial fibrillation on direct oral anticoagulation who presented with sudden upper abdominal pain and vomiting. Abdominal ultrasound showed no evidence of gallstones or biliary obstruction. The patient reported a daily alcohol intake of approximately 50 g, and laboratory tests revealed markedly elevated amylase and lipase levels. On admission, the patient was hemodynamically stable, with no evidence of organ failure. A diagnosis of mild acute pancreatitis with uncertain etiology was made. Initially stable, the patient developed new-onset abdominal pain and signs of peritonitis on the fifth day of hospitalization. CT revealed pneumoperitoneum and a retroperitoneal hematoma. Exploratory laparotomy confirmed sigmoid colon perforation, and a segmental colectomy with end colostomy was performed. Histopathological examination of the resected sigmoid colon excluded the presence of diverticula or neoplastic lesions and revealed inflammation of the subserosa and serosa adjacent to the perforation.

Case Discussion

Colonic perforation secondary to acute pancreatitis is exceedingly rare, and its pathophysiology is not fully understood. The leading hypothesis suggests the spread of activated pancreatic enzymes through the mesocolon, leading to pericolitis, ischemia, and transmural necrosis. Most reported cases involve the transverse or descending colon, but sigmoid involvement, as in this case, underscores the unpredictable nature of this complication.

Conclusion

This case highlights a rare but severe complication of acute pancreatitis. Clinicians should consider colonic involvement in patients with unexplained clinical deterioration. Early recognition and prompt surgical intervention remain key to favorable outcomes.

Introduction

Acute pancreatitis is an inflammatory condition of the pancreas that can range from a mild, self-limiting disease to a severe and potentially fatal disorder with systemic involvement. While the most common complications involve the peripancreatic tissues and nearby organs such as the duodenum and stomach, colonic complications remain rare. These may include ischemia, necrosis, fistula formation, and, in exceptional cases, perforation [1–6].

Colonic perforation during the course of acute pancreatitis was first described several decades ago and remains a clinical rarity [1]. The reported incidence is low, yet when it occurs, it portends a poor prognosis, often reflecting severe pancreatic inflammation and enzymatic destruction of adjacent tissues. The underlying mechanisms are not fully elucidated, but several hypotheses have been proposed: the direct spread of pancreatic enzymes through the mesocolon causing pericolitis and ischemic necrosis; compression of colonic vessels by inflammatory or hemorrhagic collections; and hypoperfusion related to systemic inflammatory response and third-space losses [1–3, 5].

Most cases in the literature describe involvement of the transverse and descending colon due to their anatomical proximity to the pancreas and relatively tenuous blood supply [2, 5, 6]. However, sigmoid colon perforation is exceedingly uncommon [4]. Here, we present a rare case of sigmoid colon perforation secondary to acute pancreatitis, discuss the possible pathophysiological mechanisms, and review relevant literature.

Case Presentation

A 75-year-old Caucasian man, self-employed, with a history of arterial hypertension, dyslipidemia, and atrial fibrillation on direct oral anticoagulation, presented to the emergency department with sudden-onset, belt-like abdominal pain radiating to the back, lasting 16 h, rated 8/10 in intensity. He reported partial relief with paracetamol. Pain was associated with biliary vomiting; bowel movements were preserved. He denied fever, jaundice, previous episodes, trauma, or recent use of new medications. Alcohol intake was approximately 50/day. There was no other substance use. On examination, the patient was alert, breathing comfortably and well perfused. Abdominal exam show a soft, mildly tender right upper quadrant and epigastrium, without guarding or rebound; no peripheral edema.

Laboratory tests showed normal blood counts and liver tests with markedly elevated amylase (1,391 U/L) and lipase (4,161 U/L). Abdominal ultrasound revealed a normal-sized liver with steatosis, normal gallbladder, pancreas, spleen, and no lymphadenopathy or peritoneal fluid.

A diagnosis of acute, non-biliary pancreatitis of uncertain etiology was made. The patient was started on intravenous fluids, prophylactic anticoagulation, analgesia, and kept nothing by mouth. He was admitted to the gastroenterology ward for monitoring.

A contrast-enhanced abdominal computed tomography (CT) at 48 h showed pancreatic swelling, peripancreatic fat stranding, mesenteric involvement, and free fluid in the abdomen. Other organs were unremarkable Figure 1.

Fig. 1.

Contrast-enhanced CT 48 h after admission showing pancreatic swelling (white arrow), interstitial edema, and peripancreatic fat stranding consistent with acute pancreatitis, displacing the stomach (white arrowhead) anteriorly.

Following clinical deterioration, arterial blood gas revealed type 1 respiratory failure (PaO₂ 60 mm Hg, SpO₂ 92%, lactate 1.3 mmol/L). Laboratory findings indicated a transient acute kidney injury, possibly due to contrast administration. Due to organ dysfunction, he was transferred to intermediate care. His diet was gradually advanced and adequate analgesia optimized before returning to the ward.

Three days later, he developed new left lower quadrant pain, refractory to multiple analgesics, associated with diaphoresis, chills, and tachycardia. Peripheral pulses were palpable and symmetric. Repeat CT (shown in Fig. 2) revealed a 12 × 7.5 cm retrocavitary hematoma extending to Morrison’s space, displacing the stomach and the ascending colon, compressing the superior mesenteric vein, with mild ascites and moderate bilateral pleural effusions. Findings suggested a complication of acute pancreatitis, including vascular rupture or gastrointestinal perforation, with pneumoperitoneum.

Fig. 2.

Abdominal CT on day 5 showing a large retrocavitary hematoma (red arrow) displacing the stomach and ascending colon, with associated pneumoperitoneum (white arrow) and compression of the superior mesenteric vein (white arrowhead), consistent with possible ischemic compromise of the sigmoid colon.

Surgical consultation led to an emergency exploratory laparotomy, which revealed a sigmoid colon perforation with limited fecaloid contamination. A hematopurulent hemoperitoneum was aspirated, with localized hemoperitoneum in the right hypochondrium and infra-diaphragmatic region, including an organized infradiaphragmatic hematoma, which was not removed due to its apparent association with acute pancreatitis and retroperitoneal hematoma. Lavage of the abdominal cavity was performed. A segmental resection of the sigmoid colon with end colostomy (Hartmann’s procedure) was performed and two drains placed. The patient required vasoactive support intraoperatively and received 2 units of plasma and 1 unit of red blood cells.

Retrospective analysis of the initial CT scan demonstrated a non-redundant sigmoid colon located distant from the pancreas in the upper abdomen. A colonoscopy performed five years earlier showed no polyps or diverticula.

Due to intraoperative vasopressor requirements, the patient was transferred to the intensive care unit, where he remained for 14 days. Due to abdominal sepsis, empirical intravenous antibiotics (ceftriaxone and metronidazole) were given for 7 days, with no pathogens isolated. The patient also developed grade III abdominal hypertension secondary to pancreatitis, managed conservatively with fluid optimization, reduced enteral nutrition, and laxatives.

During intensive care unit stay, he developed acute respiratory distress syndrome requiring invasive mechanical ventilation, prone positioning, and neuromuscular blockade. He was subsequently extubated without further complications. Once stable on spontaneous ventilation, he was transferred back to the intermediate care unit, hemodynamically stable, afebrile, and tolerating oral diet. He subsequently recovered sufficiently and was discharged from the hospital in stable condition. A timeline of events during his hospitalization is shown in Table 1.

Table 1.

Timeline of clinical events

Date	Events
Day 1	The patient presented to the emergency department with abdominal pain and was diagnosed with acute pancreatitis. He was admitted to the Gastroenterology ward
Day 3	Respiratory and renal failure onset motivating transfer to the intermediate care unit
Day 6	Worsening, refractory abdominal pain prompted a CT scan, which revealed a retroperitoneal hematoma and pneumoperitoneum. Consequently, a laparotomy was performed, revealing a sigmoid colon perforation with hematopurulent peritonitis, treated with a sigmoidectomy and Hartmann procedure. A transfer to the intensive care unit was made
Day 20	After 14 days of intravenous antibiotics, vasopressors and mechanical ventilation he was transferred to the intermediate care unit
Day 26	He remained in the intermediate care unit for 6 days, receiving rehabilitation and antibiotics for nosocomial pneumonia, and was then transferred to the Surgery ward
Day 40	Once stable, the patient was discharged home

Histopathological examination of the resected sigmoid colon revealed a 7 cm segment with two perforations approximately 1 cm each. The external surface exhibited areas of fibrinopurulent material. Areas of hemorrhagic mucosal and wall necrosis were observed adjacent to the perforation, with neutrophilic infiltration, debris, and fibrin deposition in the subserosa and serosa. The mucosa appeared reddened with obliterated folds. No diverticula or lymph nodes were identified in the peri-intestinal adipose tissue. Margins of excision preserved normal mucosal architecture, with fibrin and debris on the serosal surface. No neoplastic changes were observed.

The collection identified on imaging gradually decreased in size on subsequent follow-up scans and remained asymptomatic; therefore, no drainage was required. The patient subsequently underwent a second surgery for bowel transit reconstruction, and no further episodes of pancreatitis have occurred during 2 years of follow-up.

Discussion

Based on his history of daily alcohol consumption, without evidence of gallstones or biliary obstruction, the pancreatitis was considered alcohol-induced. Our patient developed sigmoid colon perforation in the setting of acute pancreatitis without evidence of gallstones or biliary obstruction. Although the initial presentation and imaging were consistent with moderately severe acute pancreatitis, the subsequent clinical deterioration was abrupt, with radiologic findings of pneumoperitoneum and a retroperitoneal hematoma.

The pathophysiology of colonic perforation in acute pancreatitis is multifactorial and remains incompletely understood. The most widely accepted mechanism involves the retroperitoneal spread of activated pancreatic enzymes through the mesocolon, which can induce pericolitis, ischemia, and transmural necrosis of the colonic wall. Cho et al. [1] proposed that these enzymes directly digest the colonic tissue, while Yoshikawa et al. [2] and Hozaka et al. [3] emphasized that ischemia secondary to local inflammation and perivascular compression is a major contributing factor. Additional systemic factors such as hypotension, third-space fluid losses, and microvascular thrombosis may exacerbate ischemic injury and predispose the colon to necrosis [1]. A summary of reported cases of acute pancreatitis complicated by colonic perforation, including perforation site, proposed mechanism, and patient outcomes, is presented in Table 2.

Table 2.

Reported cases of colonic perforation in acute pancreatitis

Author (year)	Site of colonic perforation	Proposed mechanism	Patient outcome
Cho et al. [1] (1996)	Colon (unspecified segment)	Extension of pancreatic inflammation and necrosis into the colonic wall leading to transmural necrosis and perforation	Surgical intervention; full recovery
Dhadlie and Ratnayake [6] (2019)	Ascending colon	Severe acute pancreatitis leading to colonic ischemia and necrosis with subsequent perforation	Right hemicolectomy with end ileostomy; prolonged recovery with survival
Hozaka et al. [3] (2018)	Transverse colon	Severe peripancreatic inflammation with enzymatic and ischemic injury to the adjacent colonic wall	Video-assisted retroperitoneal debridement; survival
Yoshikawa et al. [2] (2020)	Descending colon (retroperitoneal)	Retroperitoneal spread of pancreatic inflammation causing ischemic transmural injury and perforation (associated duodenal fistula also reported)	Loop ileostomy with drainage; prolonged hospitalization; survival
Saleh et al. [4] (2024)	Sigmoid colon	Extravasation of pancreatic enzymes causing inflammation, necrosis, and subsequent perforation	Surgical management; favorable outcome
Derkaoui et al. [5] (2025)	Mid-transverse colon	Necrotizing pancreatitis with enzymatic and ischemic injury causing colonic wall necrosis and perforation	Emergency extended hemicolectomy; postoperative recovery under intensive care

Interestingly, our patient’s perforation involved the sigmoid colon – although the CT scan showed compression of the superior mesenteric vein by the retrocavitary hematoma, this finding is unlikely to have contributed to the colonic injury in our case, as the sigmoid colon is primarily supplied by branches of the inferior mesenteric vessels. A more plausible mechanism is ischemia secondary to systemic hypovolemia, particularly given that this segment of the colon includes the Sudeck’s point – a watershed area between the inferior mesenteric artery and the iliac arteries – making it especially vulnerable to reduced perfusion. This anatomical susceptibility may, therefore, have played a central role in the development of sigmoid ischemia and subsequent perforation [2, 4].

Perforations in the ascending and descending colon likely occur because these segments are retroperitoneal and, thus, anatomically closer to the inflamed pancreas. The transverse colon is also in close proximity to the pancreas, which may explain its involvement in reported cases. In contrast, sigmoid colon perforation [4] is less likely to result from direct contiguity and more likely arises from ischemia and the spread of activated pancreatic enzymes across the peritoneal surfaces.

Mild reactive edema due to local pericolonic inflammation secondary to pancreatic enzyme exposure may have contributed, as suggested by the presence of fibrinopurulent material on the surface of the resected specimen. Ischemic colitis is unlikely, given the relatively preserved mucosal architecture, which is typically the most vulnerable layer and most affected in this condition due to its high oxygen demand. Inflammatory bowel disease also appears unlikely, as no significant architectural mucosal changes were identified in the margins of the resected specimen (excluding ulcerative colitis). While a perforation of a segmental Crohn’s lesion could theoretically occur, the inflammatory infiltrate in this case was primarily confined to the serosa and subserosa, with the mucosa relatively preserved, suggesting that the necrosis originated externally rather than from within the bowel wall. Moreover, Crohn’s disease rarely presents with isolated perforation in the absence of local fistulas, perianal disease, or bowel wall thickening on imaging. The coexistence of both conditions would also be highly unusual. Therefore, it is most likely that this perforation represents a direct complication of acute pancreatitis. Surgical management remains the cornerstone of treatment once perforation is confirmed. In our case, a segmental colectomy with end colostomy was performed, consistent with recommendations for hemodynamically stable patients.

Early recognition of this rare complication is critical [4, 5]. Clinicians should maintain a high index of suspicion in patients with acute pancreatitis who develop new-onset abdominal pain, peritoneal signs, fever, or laboratory evidence of sepsis. Prompt imaging, ideally contrast-enhanced CT, is essential to identify pneumoperitoneum, retroperitoneal hematoma, or other colonic complications. Even in initially mild cases, local complications can evolve unpredictably, emphasizing the need for close monitoring during hospitalization [3, 5].

Sigmoid colon perforation is an exceptionally rare but life-threatening complication of acute pancreatitis, and this case adds to the growing body of evidence highlighting its clinical importance. The underlying mechanisms may include direct enzymatic injury, ischemia, and inflammatory necrosis, and clinicians should be aware that even a structurally normal colon (e.g., without diverticulosis) remains vulnerable when exposed to severe local inflammation. Maintaining a high index of suspicion is essential when patients with pancreatitis develop new or unexplained abdominal symptoms. Early imaging, timely diagnosis, and prompt surgical intervention are critical to improving outcomes in this uncommon but severe complication.

Statement of Ethics

Written informed consent of the patient was obtained for publication of his medical case and accompanying images. Ethical Committee approval was not required for this case report as it involves the retrospective review of a single patient’s medical records and no experimental interventions were performed. We used the CARE reporting guideline [7] to draft this manuscript, and the CARE reporting checklist [8] when editing, included in online supplementary 1 (for all online suppl. material, see https://doi.org/10.1159/000552160).

Conflict of Interest Statement

The authors declare no conflicts of interest.

Funding Sources

This study was not supported by any sponsor or funder.

Author Contributions

Diogo Simas wrote the case report. André Gonçalves, Plácido Gomes, Pedro Russo, and Catarina Atalaia-Martins critically reviewed the manuscript. All the authors approved the final manuscript.

Funding Statement

This study was not supported by any sponsor or funder.

Data Availability Statement

All the details about this clinical case are included in this article. Further inquiries can be directed to the corresponding author.