Mirizzi syndrome type Vb with cholecystogastric fistula causing gastric outlet obstruction: A case report

Abstract

BACKGROUND

Mirizzi syndrome (MS) type Vb is an exceptionally rare and advanced form of gallstone disease characterized by the presence of a cholecystoenteric fistula associated with gastrointestinal obstruction. Its presentation as gastric outlet obstruction is uncommon and poses significant diagnostic and surgical challenges.

CASE SUMMARY

We report the case of a 36-year-old woman who presented with progressive vomiting, intolerance to solid food, and significant weight loss. Preoperative investigations revealed gastric outlet obstruction and features of chronic gallstone disease; however, the exact etiology remained unclear. Intraoperatively, a cholecystogastric fistula with migrated gallstones and severe cicatricial deformation of the pyloroduodenal region was identified, consistent with MS type Vb. The patient underwent distal gastrectomy with Billroth II reconstruction, cholecystectomy, exploration of the common bile duct, and intraoperative cholangiography. The postoperative course was uneventful, with complete resolution of symptoms.

CONCLUSION

MS type Vb should be considered a rare cause of gastric outlet obstruction in patients with long-standing gallstone disease. Definitive diagnosis is often established intraoperatively, and surgical management should be individualized based on the extent of inflammatory and structural changes to achieve favorable outcomes.

Key Words: Mirizzi syndrome; Cholecystogastric fistula; Gastric outlet obstruction; Gallstone disease; Biliary surgery; Case report

Core Tip: Mirizzi syndrome (MS) type Vb is an exceptionally rare and advanced form of gallstone disease characterized by a cholecystoenteric fistula. We report a unique case of MS type Vb complicated by a cholecystogastric fistula leading to fixed gastric outlet obstruction. Unlike typical gallstone migration, obstruction in this case was caused by irreversible inflammatory and cicatricial deformation of the pyloroduodenal region. This report highlights diagnostic challenges, the limitations of preoperative imaging, and the need for individualized surgical decision-making in advanced MS.

INTRODUCTION

Mirizzi syndrome (MS) is a rare but clinically significant complication of long-standing gallstone disease resulting from chronic inflammation of the gallbladder and its close anatomical relationship with the extrahepatic bile ducts. The condition is most commonly caused by an impacted gallstone in the cystic duct or Hartmann’s pouch, leading to progressive inflammatory changes, extrinsic compression of the common hepatic duct, and, in advanced stages, erosion of the bile duct wall with fistula formation[1,2]. Despite reported incidence rates ranging from 0.05% to 4% among patients undergoing cholecystectomy, MS remains uncommon and is frequently associated with increased operative complexity due to dense inflammatory distortion of the hepatoduodenal ligament[3].

Several classification systems have been proposed to describe the spectrum of MS and to guide surgical management. The most widely accepted is the Csendes classification, which was later expanded to include type V, reflecting the coexistence of MS with a cholecystoenteric fistula[4,5]. Within this extended classification, type Va denotes a cholecystoenteric fistula without gastrointestinal obstruction, whereas type Vb is defined by the presence of a cholecystoenteric fistula associated with gallstone-related obstruction of the gastrointestinal tract[5]. This modification emphasizes the shared inflammatory and fistulizing pathogenesis between advanced MS and gallstone-induced intestinal obstruction.

MS type Vb represents the most advanced and complex form of the disease and poses substantial diagnostic and therapeutic challenges. Clinical presentation may be atypical and dominated by symptoms of upper gastrointestinal obstruction rather than classic biliary manifestations such as jaundice or biliary colic[6]. Cross-sectional imaging modalities, including computed tomography and magnetic resonance cholangiopancreatography (MRCP), may reveal inflammatory changes in the gallbladder neck, biliary dilatation, and indirect signs of fistula formation; however, precise anatomical characterization is often limited in the preoperative setting[6]. As a result, the full extent of the disease frequently becomes apparent only during surgical exploration[6].

Within this clinical spectrum, a related but distinct condition described in the literature is Bouveret syndrome, a rare variant of gallstone ileus characterized by gastric outlet obstruction caused by migration of a gallstone through a bilioenteric fistula into the stomach or duodenum[7]. Although Bouveret syndrome has traditionally been regarded as a separate clinical entity and is most commonly reported in elderly patients, both conditions share common pathophysiological mechanisms, including chronic calculous cholecystitis, pressure necrosis, fistula formation, and gallstone migration into the upper gastrointestinal tract[8,9]. Recent studies indicate that while endoscopic therapy may be attempted in selected cases of Bouveret syndrome, definitive surgical intervention is required in a substantial proportion of patients, particularly in the presence of large impacted stones, extensive inflammation, or complex fistulous anatomy[9,10].

Given the rarity of MS type Vb and its potential to present as gastric outlet obstruction, detailed case reports remain valuable for improving clinical awareness, refining differential diagnosis, and optimizing surgical decision-making. In this report, we present a case of MS type Vb complicated by a cholecystogastric fistula and gastric outlet obstruction, successfully managed with definitive surgical treatment.

CASE PRESENTATION

Chief complaints

The patient presented with persistent postprandial vomiting, intolerance to solid food, early satiety, and progressive weight loss over the preceding several months.

History of present illness

A 36-year-old woman presented with a six-month history of progressive gastrointestinal symptoms, including early satiety, intolerance to solid food, recurrent postprandial vomiting, generalized weakness, and unintentional weight loss of approximately 15 kg. She reported episodic epigastric and right upper quadrant pain that gradually increased in both frequency and intensity over time. There was no history of gastrointestinal bleeding or prior abdominal surgery.

History of past illness

The patient had a history of long-standing gallstone disease with recurrent episodes of biliary colic managed conservatively. There was no history of previous abdominal surgery, pancreatitis, peptic ulcer disease, or inflammatory bowel disease. No chronic medical conditions were reported.

Personal and family history

The patient reported no relevant family history of gastrointestinal or hepatobiliary diseases. She did not smoke or consume alcohol. There was no history of hereditary disorders or malignancies.

Physical examination

On physical examination, the patient appeared asthenic and malnourished. Vital signs were stable, and she was afebrile. The abdomen was soft and non-distended, with mild tenderness in the epigastric region. No signs of peritoneal irritation were observed. The sclerae and skin were of normal color, with no clinical evidence of jaundice.

Laboratory examinations

Overall, laboratory findings were consistent with a chronic disease course complicated by malnutrition and a moderate inflammatory response, without evidence of persistent biliary obstruction. A transient elevation of liver transaminases was observed with subsequent spontaneous normalization, suggesting reactive hepatocellular injury rather than cholestasis Total bilirubin levels remained within normal limits throughout the observation period, supporting preserved biliary outflow.

Mild normocytic anemia and hypoalbuminemia were present, consistent with prolonged nutritional deficiency secondary to gastric outlet obstruction (hemoglobin 92-104 g/L; albumin 34.6 g/L; total protein 52-55 g/L). Electrolyte disturbances, including episodic hypokalemia and mild hyponatremia, were likely related to recurrent vomiting and reduced oral intake and were corrected with supportive therapy (potassium nadir 2.8 mmol/L; sodium 132-135 mmol/L). Renal function and coagulation parameters remained preserved or normalized during hospitalization. Collectively, the laboratory profile reflected chronic gastric outlet obstruction with associated metabolic and inflammatory changes that improved following definitive surgical treatment. Dynamic changes in liver enzymes are summarized in Table 1.

Table 1 Dynamic changes in liver function tests.

Parameter1	Preoperative	POD 1	POD 3	POD 10 (discharge)
ALT (U/L)	131.0	80.0	53.2	34.4
AST (U/L)	97.2	37.9	22.1	18.3
Total bilirubin (μmol/L)	6.2	3.0	5.7	3.0
Direct bilirubin (μmol/L)	4.42	2.70	1.5	0.8
Albumin (g/L)	34.6	33.5	35.0	37.1
Total protein (g/L)	53.2	52.2	54.8	64.5
C-reactive protein (mg/L)	46.9	55.0	30.0	10.0

¹Values for intermediate postoperative time points are approximate and reflect the overall laboratory trend observed during hospitalization.

POD: Postoperative day; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase.

Imaging examinations

A contrast-enhanced upper gastrointestinal radiographic study was performed as the initial imaging modality. The examination demonstrated marked gastric dilatation with delayed evacuation of contrast material. Passage of contrast through the pyloroduodenal region was significantly impaired, with persistent narrowing at the level of the gastric outlet. These findings were consistent with a fixed stenosis of the pyloroduodenal region and confirmed the presence of gastric outlet obstruction.

Immediate fluoroscopic imaging after contrast administration demonstrated inflammatory changes of the gastric mucosa consistent with gastritis, with cicatricial deformation of the duodenal bulb and narrowing of the pyloroduodenal region. Delayed images obtained 2 hours after contrast administration showed persistent retention of contrast material within the stomach with minimal passage into the duodenum, indicating delayed gastric emptying. These findings were consistent with a subcompensated gastric outlet obstruction caused by chronic inflammatory and cicatricial changes in the pyloroduodenal region. The radiographic findings consistent with subcompensated gastric outlet obstruction are shown in Figure 1.

Figure 1 Immediate and 2-hour delayed fluoroscopic images showing delayed gastric emptying and subcompensated gastric outlet obstruction due to fixed narrowing of the pyloroduodenal region. A: Immediate fluoroscopic image showing contrast retention within the stomach; B: Two-hour delayed image demonstrating persistent contrast stasis, consistent with subcompensated gastric outlet obstruction due to impaired pyloroduodenal passage.

MRCP was performed preoperatively to further evaluate the biliary anatomy. MRCP demonstrated deformity and narrowing of the extrahepatic bile duct at the level of the gallbladder neck, with features suggestive of biliary obstruction. Dilatation of the common bile duct (choledochoectasia) was also noted and was considered likely secondary to a stricture of the major duodenal papilla. The intrahepatic bile ducts were not significantly dilated, and there was no evidence of intraductal choledocholithiasis. Overall, these imaging findings indicated chronic biliary outflow impairment and supported the suspicion of MS, although definitive characterization of the cholecystogastric fistula was limited. The described inflammatory and obstructive changes of the biliary system are illustrated in Figure 2.

Figure 2  Magnetic resonance imaging showing gallstone disease with biliary outflow impairment and deformity of the extrahepatic bile duct at the level of the gallbladder neck.

Based on the intraoperative findings, including a cholecystogastric fistula, severe inflammatory and cicatricial changes of the pyloroduodenal region, and irreversible gastric outlet obstruction, a definitive surgical procedure was deemed necessary. The operative management included distal gastrectomy with Billroth II reconstruction (Hofmeister-Finsterer modification), cholecystectomy, exploration of the common bile duct, intraoperative cholangiography, and abdominal drainage. Endoscopic retrograde cholangiopancreatography was not performed due to the absence of biochemical cholestasis and the high likelihood of surgically correctable pathology. The chronological sequence of clinical events is summarized in the timeline (Table 2).

Table 2 Timeline of clinical events.

Time	Event
6 months pre-admission	Onset of progressive vomiting, early satiety, and unintentional weight loss
Admission	Hospital admission with clinical confirmation of gastric outlet obstruction
Diagnostic workup	Magnetic resonance imaging and contrast upper gastrointestinal study
Surgery	Distal gastrectomy with Billroth II reconstruction and cholecystectomy
Postoperative day 10	Discharge in satisfactory condition
Follow-up	Complete resolution of symptoms and restoration of oral intake

MULTIDISCIPLINARY EXPERT CONSULTATION

A multidisciplinary consultation involving surgeons, radiologists, and anesthesiologists was conducted. Based on the clinical findings and imaging results, a consensus decision for surgical management was reached.

FINAL DIAGNOSIS

The final diagnosis was MS type Vb complicated by a cholecystogastric fistula with gallstone migration, resulting in gastric outlet obstruction.

TREATMENT

Key steps of the surgical procedure

During abdominal exploration, a dense inflammatory conglomerate of stony consistency was identified involving the gallbladder, hepatoduodenal ligament, and pyloroduodenal region. The inflammatory mass caused marked deformation of the duodenal bulb and gastric outlet, resulting in severe luminal narrowing and obstruction. The inflammatory conglomerate involving the gallbladder and pyloroduodenal region is shown in Figure 3. After careful blunt and sharp adhesiolysis, the duodenum was mobilized using the Kocher maneuver, and the stomach was subsequently mobilized along the greater and lesser curvatures, allowing adequate exposure and assessment of the extent and irreversibility of the gastric outlet stenosis (Figure 4). The key intraoperative steps of the procedure are demonstrated in Video.

Figure 3  Dense inflammatory conglomerate involving the gallbladder, hepatoduodenal ligament, and pyloroduodenal region identified during abdominal exploration, resulting in marked deformation of the gastric outlet (blue arrow).

Figure 4  Mobilization of the duodenum and stomach using the Kocher maneuver, allowing assessment of the extent and irreversibility of pyloroduodenal stenosis.

Cholecystectomy was performed using a fundus-first approach. A cholecystogastric fistula was identified intraoperatively, with migrated gallstones embedded within the submucosal layer of the pyloric stomach. The gallstones were removed, and the fistulous tract was eliminated. Exploration of the common bile duct was carried out, followed by intraoperative cholangiography, which confirmed bile duct patency and absence of residual choledocholithiasis (Figure 5).

Figure 5 Cholecystectomy and gallstone extraction. A: Cholecystectomy with removal of gallstones; B: Removal of migrated gallstones from the pyloric stomach through the cholecystogastric fistula.

Distal gastrectomy involving approximately two-thirds of the stomach was performed. Gastrointestinal continuity was restored by a Billroth II gastrojejunostomy using an end-to-side configuration (Hofmeister-Finsterer modification). The anastomosis was created using a 60-mm linear stapling device. Intraoperative assessment confirmed satisfactory patency of the gastrojejunostomy.

The gastrojejunostomy was fixed within the transverse mesocolon window. The duodenal stump was managed using a hand-sewn technique with placement of a purse-string suture reinforced by interrupted seromuscular sutures. The main steps of gastric resection and reconstruction are illustrated in Figure 6. Subsequently, a water-soluble contrast agent was injected into the common bile duct through the indwelling catheter, and intraoperative cholangiography was performed. The follow-up image demonstrated no evidence of residual biliary calculi (Figure 7).

Figure 6 Distal gastrectomy and reconstruction. A: Distal gastrectomy involving approximately two-thirds of the stomach; B: Billroth II gastrojejunostomy (end-to-side, Hofmeister-Finsterer modification).

Figure 7  Intraoperative cholangiography demonstrating patency of the biliary tree and absence of residual choledocholithiasis.

The macroscopic specimen consisted of a resected segment of the distal stomach showing marked inflammatory and cicatricial changes of the wall with thickening and deformation of the pyloric region. The gastric mucosa appeared congested and edematous with an irregular surface, consistent with chronic inflammatory involvement. The pyloric area demonstrated pronounced fibrotic remodeling corresponding to long-standing obstruction. Separately, the gallbladder specimen and multiple gallstones were identified. The gallstones varied in size and shape and were firm in consistency, with a yellow-brown appearance. The macroscopic findings were consistent with chronic calculous cholecystitis complicated by gallstone migration and secondary stenotic changes of the gastric outlet (Figure 8).

Figure 8 Macroscopic pathological specimens. A: Macroscopic specimen of the resected distal stomach, gallbladder, and removed gallstones showing chronic inflammatory and cicatricial changes; B: Cross-sectional view of the stomach demonstrating fibrotic remodeling of the pyloric region.

OUTCOME AND FOLLOW-UP

The postoperative course was uneventful. Hemodynamic parameters remained stable, and postoperative pain was adequately controlled with standard analgesic therapy. Gastrointestinal function recovered in a timely manner, and enteral nutrition was gradually advanced. Surgical drains functioned appropriately and were removed as scheduled. Laboratory parameters showed progressive normalization.

Postoperative abdominal ultrasound demonstrated smooth liver contours. The intrahepatic bile ducts were not dilated. The portal vein measured 1.0 cm in diameter and was patent. No free fluid was detected in the abdominal cavity. Intestinal loops were not dilated, and peristalsis was preserved. These findings indicated adequate biliary drainage and an uncomplicated postoperative course.

Histopathological findings revealed pronounced chronic inflammatory and fibrotic changes consistent with long-standing obstructive biliary pathology. The gallbladder specimen demonstrated features of chronic cholecystitis, with marked fibrosis and chronic inflammatory infiltration of the wall, supporting the diagnosis of advanced MS. Gastric mucosal samples showed chronic active gastritis of moderate severity with minimal glandular atrophy. Overall, the histopathological findings supported the obstructive nature of the disease and were concordant with the clinical diagnosis of MS. The patient was discharged in satisfactory condition on postoperative day 10 with recommendations for outpatient follow-up.

DISCUSSION

MS remains an uncommon but clinically important complication of gallstone disease and continues to pose significant diagnostic and therapeutic challenges despite advances in hepatobiliary surgery. Contemporary literature published after 2020 confirms that prolonged gallstone impaction at the gallbladder neck or cystic duct leads to chronic inflammation, fibrosis, and progressive distortion of biliary anatomy, predisposing patients to extrinsic bile duct compression and, in advanced stages, fistula formation[11]. These pathological changes explain both the heterogeneity of clinical presentations and the increased risk of bile duct injury during surgical intervention.

Recent reviews emphasize that preoperative diagnosis of MS remains suboptimal, particularly in advanced disease forms. Although modern imaging modalities such as computed tomography, MRCP, and endoscopic retrograde cholangiopancreatography improve anatomical assessment, they frequently fail to delineate fistulous tracts and underestimate the extent of inflammatory-cicatricial involvement. Zhao et al[12], in a systematic review, demonstrated that a substantial proportion of MS cases, especially those with fistulas, are definitively diagnosed intraoperatively, highlighting persistent diagnostic limitations.

From a surgical standpoint, current evidence supports an expanding but selective role for minimally invasive approaches. Zhao et al[12] reported that laparoscopic management is feasible and safe in experienced hands, particularly for early-stage MS (Csendes types I-II), but remains technically demanding, with a conversion rate of approximately 30%-35%, reflecting dense fibrosis and altered anatomy. These findings underscore that laparoscopic intent does not guarantee minimally invasive completion in complex disease.

Comparative outcome studies published since 2020 further refine this perspective. Nag and Nekarakanti[13] demonstrated that laparoscopic surgery may achieve outcomes comparable to open surgery in carefully selected patients, with advantages such as reduced blood loss and shorter hospital stay. However, these benefits were largely confined to patients without extensive inflammatory changes or fistula formation, reinforcing the importance of patient selection.

More recent narrative reviews consolidate these findings and emphasize that open surgery continues to represent the most reliable approach for advanced MS, particularly in the presence of cholecystoenteric fistulas or severe anatomical distortion. Gulla and colleagues highlighted that although minimally invasive techniques are increasingly adopted, their applicability remains limited in advanced disease, where open or converted procedures are often required to ensure anatomical safety and definitive treatment[14]. Similarly, Nassar et al[15] reported that laparoscopic management can be successfully performed in specialized centers but stressed that open surgery remains necessary in complex or advanced cases.

With respect to outcomes, contemporary series indicate that perioperative mortality is low for both open and laparoscopic approaches when timely surgical intervention is performed. Nevertheless, procedure-related morbidity, including bile duct injury, bile leakage, and postoperative infectious complications, appears more frequently associated with laparoscopic attempts in advanced disease stages. Recurrence of biliary symptoms is uncommon following definitive open surgery with complete fistula elimination and adequate biliary exploration, whereas recurrence after laparoscopic treatment remains dependent on disease stage and procedural completeness[12-15].

The present case adds clinically relevant insights to the contemporary literature. Recent reports of MS type V with complex fistulas confirm the rarity and heterogeneity of advanced presentations and underscore the need for individualized surgical strategies[16]. Importantly, recent case reports have demonstrated that MS type Vb may present with gastric outlet obstruction, a presentation that overlaps with Bouveret-type pathology but involves distinct pathophysiological mechanisms[17].

In contrast to many previously reported cases, gastric outlet obstruction in the present patient was not solely caused by gallstone migration but was primarily driven by irreversible inflammatory-cicatricial deformation of the pyloroduodenal region. Such fixed obstruction limits the effectiveness of minimally invasive or limited surgical interventions and necessitates resectional and reconstructive procedures. Contemporary literature supports this concept, emphasizing that in advanced MS the surgical strategy should be guided not only by the presence of a fistula but also by the extent of irreversible structural damage to adjacent gastrointestinal segments[18].

In line with modern concepts of tailored or “on-demand” surgery, current evidence stresses that the final extent of surgical intervention should be determined intraoperatively based on anatomical distortion and tissue viability rather than on a predefined minimally invasive intent[19]. The operative strategy employed in the present case aligns with these recommendations and highlights the importance of prioritizing surgical safety and durable outcomes over access modality alone.

To further contextualize the present case within the published literature, a comparative overview of open vs laparoscopic surgical approaches, including diagnostic limitations, operative feasibility, morbidity, and recurrence, is summarized in Table 3, based on contemporary studies published since 2020[20]. This synthesis demonstrates that, despite advances in minimally invasive techniques, open surgery remains the cornerstone for managing advanced MS with complex fistulas and fixed gastric outlet obstruction, while laparoscopy plays an important but selective role in early and intermediate disease stages. Patient perspective: The patient reported significant improvement in symptoms, resolution of vomiting, and restoration of oral intake following surgery. She expressed satisfaction with the outcome and postoperative recovery.

Table 3 Comparison of open vs laparoscopic surgery in Mirizzi syndrome (literature-based).

Parameter	Open surgery	Laparoscopic surgery
Typical indication	Advanced Mirizzi syndrome (type III-V/Vb), cholecystoenteric fistula	Selected early-stage cases
Preoperative diagnosis	Often uncertain; diagnosis frequently established intraoperatively	Similar limitations
Technical feasibility	High due to direct anatomical control	Limited in advanced disease
Conversion rate	Not applicable	High in advanced stages
Perioperative mortality	Low	Low
Procedure-related morbidity	Acceptable; mainly related to disease severity	Higher in advanced disease
Risk of bile duct injury	Lower with controlled dissection	Increased in distorted anatomy
Recurrence of biliary symptoms	Low after definitive surgery	Variable
Long-term outcome	Generally favorable	Favorable only in selected cases

CONCLUSION

MS type Vb is an exceptionally rare and complex variant of gallstone disease that may present with atypical manifestations, including gastric outlet obstruction. Accurate preoperative diagnosis remains challenging, and definitive recognition is often achieved intraoperatively. Advanced forms of the disease require an individualized surgical approach, with the extent of intervention determined by intraoperative findings. In cases of irreversible pyloroduodenal deformation, combined resectional and reconstructive procedures may be necessary to achieve definitive resolution and favorable clinical outcomes.