Pyloric Pseudonecrosis Caused by Biliary Peritonitis: A Rare Intraoperative Pitfall

ABSTRACT

Biliary peritonitis can cause subserosal bile staining that mimics pyloric or duodenal necrosis. When endoscopy or ICG fluorescence is unavailable, pseudonecrosis remains an operative diagnosis of exclusion, supported by preserved serosal integrity, absence of visible perforation, careful inspection, and uneventful 1‐month follow‐up.

1. Introduction

Acute cholecystitis is a common emergency general surgery condition. Early laparoscopic cholecystectomy is recommended for suitable patients, whereas delayed treatment or clinical deterioration can lead to severe complications, including gallbladder gangrene, perforation, and biliary peritonitis [1, 2, 3].

Intraoperative decision‐making becomes especially challenging when adjacent gastrointestinal structures appear dark, thickened, or devitalized. In septic biliary peritonitis, such discoloration may raise concern for true ischemia of the stomach, pylorus, or duodenum, potentially prompting conversion to open surgery or extensive resection.

True gastric or pyloric necrosis remains exceptional because of the stomach's extensive collateral blood supply. Reported cases usually involve profound systemic hypoperfusion, acute gastric dilation, gastric outlet obstruction, volvulus, vascular compromise, or invasive infection [4, 5, 6, 7, 8, 9, 10]. These entities differ from bile‐induced serosal staining, yet they may appear similar during emergency laparoscopy.

The knowledge gap addressed by this report is the limited description of bile‐induced subserosal discoloration of the pylorus and duodenum as an intraoperative mimic of necrosis. This case is clinically relevant because pseudonecrosis should be considered only after excluding perforation, devascularization, transmural ischemia, and iatrogenic injury as far as the operative setting permits. We present this case to highlight both the surgical pitfall and the diagnostic limitations encountered when objective adjuncts are unavailable.

2. Case History/Examination

A 58‐year‐old woman with an 18‐year history of Type 2 diabetes mellitus complicated by chronic renal insufficiency and diabetic retinopathy presented to the emergency department with a 6‐h history of severe, progressive right upper quadrant abdominal pain radiating to the epigastrium and right flank. She was afebrile and initially hemodynamically stable.

Laboratory investigations revealed leukocytosis (white blood cell count: 18.9 × 10⁹/L) and elevated C‐reactive protein (10.9 mg/dL). Liver function tests and serum bilirubin were within normal limits.

Abdominal ultrasonography showed a markedly distended gallbladder measuring 160 × 60 mm, a positive sonographic Murphy sign, wall thickening of 5.5 mm, and pericholecystic fat stranding (Figure 1). There was no intrahepatic or extrahepatic bile duct dilatation, and no free intraperitoneal fluid was identified.

FIGURE 1.

Abdominal ultrasonography showing acute cholecystitis with a markedly distended gallbladder, wall thickening, positive sonographic Murphy sign, and pericholecystic inflammatory changes.

The patient was admitted, started on intravenous hydration and broad‐spectrum antibiotics, and scheduled for laparoscopic cholecystectomy the following day.

3. Differential Diagnosis, Investigations, and Treatment

While awaiting surgery, the patient developed septic shock and was transferred urgently to the operating room. Exploratory laparoscopy revealed a markedly distended and edematous gallbladder with necrotic patches, adherent to the duodenum and greater omentum. Moderate bilious fluid was present in the suprahepatic spaces, consistent with biliary peritonitis.

The source of biliary contamination was attributed intraoperatively to gangrenous cholecystitis, with presumed leakage through the necrotic gallbladder wall or a sealed microperforation. A discrete macroscopic perforation site was not identified in the operative field, and no intraoperative bile duct injury or duodenal injury was recognized.

The pylorus and adjacent duodenum appeared dark and thickened (Figure 2), with discoloration extending proximally toward the antrum and distally toward the duodenum. The differential diagnosis included true gastroduodenal ischemic necrosis secondary to septic shock, peptic ulcer perforation, spontaneous or iatrogenic duodenal injury, bile staining of the serosa, and inflammatory discoloration caused by local chemical peritonitis.

FIGURE 2.

Laparoscopic view of the pylorus and adjacent duodenum during biliary peritonitis. The dark discoloration and inflammatory thickening simulated necrosis. The figure shows operative context only; no calibrated scale was available. Interpretation should therefore rely on the operative description rather than size measurement alone.

Careful laparoscopic inspection suggested that the discoloration was caused by bilious fluid tracking beneath the visceral peritoneum from the duodenum toward the pylorus, producing a pseudonecrotic appearance rather than obvious transmural necrosis. The serosa appeared intact; no perforation was seen, and there was no visible segmental devascularization.

Intraoperative endoscopy, indocyanine green fluorescence imaging, and Doppler perfusion assessment were not available during the emergency intervention. Therefore, the decision not to perform gastroduodenal resection was based on the preserved serosal integrity, the pattern of bile tracking, absence of visible perforation or devascularization, and the need to avoid unnecessary resection in a septic patient.

Treatment consisted of laparoscopic cholecystectomy, extensive peritoneal lavage, placement of intra‐abdominal drainage, and postoperative resuscitation with intravenous fluids, vasopressors, and antibiotics. The procedure was completed laparoscopically without conversion.

4. Conclusion and Results (Outcome and Follow‐Up)

The patient improved rapidly after surgery, was weaned from vasopressors, and had an uneventful postoperative course.

At 1‐month postoperative outpatient follow‐up, she remained asymptomatic, tolerated oral intake normally, and had no clinical evidence of gastric outlet dysfunction, delayed perforation, recurrent peritonitis, or ischemic sequelae. In the absence of objective intraoperative perfusion testing, this favorable clinical evolution supports, but does not independently prove, the intraoperative diagnosis of pyloric pseudonecrosis.

Subserosal bile diffusion should be considered when dark pyloroduodenal discoloration is encountered during emergency surgery for biliary peritonitis, particularly when serosal integrity and vascular supply appear preserved. However, the diagnosis should remain cautious and should be supported by objective adjuncts when such tools are available.

5. Discussion

This case expands the differential diagnosis of apparent pyloroduodenal necrosis encountered during emergency biliary surgery. Its clinical importance lies not only in the rarity of the finding, but also in the consequences of misinterpretation: unnecessary conversion, gastroduodenal resection, prolonged operative time, and additional morbidity in a patient already compromised by sepsis.

The existing literature on dark or “black” gastric wall findings is dominated by true ischemic, infectious, and mechanical etiologies. Reported mechanisms include acute gastric distension, gastric outlet obstruction, systemic hypoperfusion, vascular compromise, and invasive fungal disease [4, 5, 6, 7, 8, 9, 10]. These reports support the principle that apparent gastric discoloration during acute illness must be taken seriously, while also emphasizing the need to distinguish true necrosis from mimics.

The presumed mechanism in the present case was chemical and anatomical rather than primarily vascular. Bilious fluid appeared to dissect beneath the visceral peritoneum and produced dark staining and inflammatory thickening over the duodenum and pylorus. This pattern explains why the laparoscopic appearance was alarming despite the absence of a visible full‐thickness defect or devascularized gastric segment.

Visual assessment of gastrointestinal viability has recognized limitations. Color, serosal sheen, peristalsis, bleeding, pulsation, and palpation are subjective and may be unreliable in shock, inflammation, vasopressor exposure, or chemical peritonitis [11]. In similar equivocal cases, additional modalities may improve diagnostic confidence before deciding between organ preservation and resection.

Modern intraoperative adjuncts include indocyanine green fluorescence angiography, which can provide real‐time assessment of tissue perfusion and has influenced intraoperative management in acute bowel ischemia cohorts [12]. Emergency surgery and endoscopic surgery consensus documents also discuss the role of fluorescence‐guided surgery in anatomical navigation and perfusion assessment [13, 14]. Intraoperative endoscopy may also help assess mucosal viability and exclude a luminal defect when the serosal appearance is ambiguous.

In the present intervention, endoscopy, indocyanine green fluorescence, and Doppler assessment were not available. This limitation has two implications. First, transmural ischemia could not be excluded by objective intraoperative testing. Second, pseudonecrosis should be interpreted as an operative diagnosis supported by clinical and laparoscopic findings plus 1‐month follow‐up, rather than as a histologically or perfusion‐imaging‐confirmed diagnosis.

The source of biliary peritonitis was also clarified cautiously. Operative findings supported gangrenous cholecystitis with presumed leakage through the necrotic gallbladder wall or sealed microperforation. However, because no discrete perforation site was identified, the exact leak point cannot be stated with absolute certainty. No iatrogenic bile duct or duodenal injury was recognized during the procedure.

This case reinforces two practical lessons. First, apparent pyloroduodenal necrosis during biliary peritonitis should prompt systematic assessment for ischemia, perforation, and ductal or duodenal injury. Second, when objective adjuncts are unavailable, the manuscript should clearly state that limitation and avoid claiming definitive exclusion of ischemia based on visual assessment alone.

Author Contributions

Christian Mouawad: writing – original draft, writing – review and editing. Dollen Eid: writing – original draft. Nehad Dager: validation.

Funding

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. The signed consent form has been uploaded separately through the journal's submission system for verification, in accordance with journal guidelines.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.