ORIGINAL ARTICLE


https://doi.org/10.5005/jp-journals-10018-1451
Euroasian Journal of Hepato-Gastroenterology
Volume 14 | Issue 2 | Year 2024

Thick-walled Gallbladder: A Pragmatic Management Approach


Ishtiyaq Ahmad Ganaie1, Sadatul Manzoor2, Arshid Iqbal Qadri3 https://orcid.org/0000-0001-8126-8487, Gowhar Aziz Bhat4

1–3Department of General & Minimal Access Surgery, Government Medical College, Srinagar, Jammu and Kashmir, India

4Department of General and Minimal Invasive Surgery, Sher-I-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India

Corresponding Author:Arshid I Qadri, Department of General and Minimal Access Surgery, Government Medical College, Srinagar, Jammu and Kashmir, India, Phone: +91 9010998241, e-mail: arshidqadri@gmail.com

How to cite this article: Ganaie IA, Manzoor S, Qadri AI, et al. Thick-walled Gallbladder: A Pragmatic Management Approach. Euroasian J Hepato-Gastroenterol 2024;14(2):191–197.

Source of support: Nil

Conflict of interest: None

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

Received on: 08 September 2024; Accepted on: 10 October 2024; Published on: 27 December 2024

ABSTRACT

Introduction: Thick-walled gallbladder (TWGB) is a common yet non-specific radiological finding associated with a wide range of gallbladder pathologies, including acute and chronic inflammation, infection, and malignancy. Among the inflammatory causes, xanthogranulomatous cholecystitis (XGC) is a rare but significant condition that often mimics gallbladder carcinoma. This paper presents a pragmatic approach to the diagnosis and management of TWGB, focusing on the complexities posed by XGC. Detailed analysis of imaging techniques, surgical strategies, and histopathological findings is provided to guide clinical decision-making.

Objective: This paper presents a pragmatic approach to the diagnosis and management of TWGB, with a particular focus on the complexities posed by XGC mimicking a gallbladder mass in operated patients of TWGB in a tertiary care center over 2 years. Detailed analysis of imaging techniques, surgical strategies, and histopathological findings is provided to guide clinical decision-making.

Study design: We had 18 patients of TWGB, 14 males (77.7%) and 4 females (22.2%) who were a part of the prospective study. All cases underwent anticipatory extended cholecystectomy (AEC) with frozen section assessment during the period of 2 years. All these cases were evaluated with ultrasound, triple-phase CT followed by MR/MRCP, and CA 19-9 levels as outlined in the flowchart.

Results: In this study out of 18 patients who underwent AEC the frozen section of 15 cases of patients was reported as XGC, and 3 cases were reported as carcinoma GB with T1b stage and these 3 cases further underwent EC in the same setting. Out of 18 cases, 16 had an uneventful postop period and 2 cases developed complications Bile leak which was managed by pigtail drainage and bleeding managed by blood transfusions (Clavien-Dindo Classification-Grade III).

Conclusion: All TWGB are not carcinoma GB. Xanthogranulomatous cholecystitis is an important differential diagnosis for TWGB and, therefore, XGC should be considered in the differential diagnosis of TWGB.

Keywords: AEC—Anticipatory extended cholecystectomy, CC—Chronic cholecystitis, EC—Extended cholecystectomy, GBC/CA GB–Gallbladder cancer, TWGB-Thick-walled gall bladder, XGC—Xanthogranulomatous cholecystitis.

INTRODUCTION

Thick-walled gallbladder (TWGB) poses a massive therapeutic dilemma as it can be benign chronic cholecystitis (CC) or Xanthogranulomatous cholecystitis (XGC) or malignant [gall bladder carcinoma (GBC)].1 Focal, localized, non-uniform, abnormal thickening of GB wall should be dealt with as malignant. Diffuse, generalized, uniform, regular thickening of the GB wall is usually benign, i.e., CC or XGC but occasionally can be malignant.

Gallbladder wall thickening is a common radiological finding that may be observed in various pathological states. It is defined as a gallbladder wall thickness greater than 3 mm on ultrasound.2 However, gallbladder wall thickening is a non-specific finding that can be associated with a range of conditions, including benign and malignant diseases. Conditions such as acute and CC, XGC, adenomyomatosis, and GBC frequently present with TWGB, making accurate diagnosis crucial for appropriate management.3,4 Among these conditions, XGC is particularly challenging to diagnose preoperatively due to its similarities with gallbladder cancer. Xanthogranulomatous cholecystitis is a rare, severe form of chronic cholecystitis characterized by extensive inflammation, thickening of the gallbladder wall, and the presence of xanthogranulomas—collections of lipid-laden macrophages.5 This paper aims to outline a pragmatic approach to managing TWGB with an emphasis on XGC, focusing on pathophysiology, diagnosis, and treatment options.

All TWGBs (except those seen during acute cholecystitis) should be operated on because it is far more difficult to differentiate benign (CC or XGC) from malignant (GBC) TWGB even after imaging (USG, Triple phase CT, MRI/MRCP). While cholecystectomy is enough for CC or XGC, extended cholecystectomy will be required for GBC. If TWGB is presumed to be benign and simple cholecystectomy alone is performed, but if it turns out to be GBC (on histopathological examination) it will be an inappropriate operation. If TWGB is suspected to be malignant and extended cholecystectomy is performed, but if it turns out to be benign (on histopathological examination) it will be overkill. If there is a high suspicion of GBC on imaging, extended cholecystectomy should be performed—some patients will turn out to have a benign pathology but that is acceptable.

MATERIALS AND METHODS

All the patients who were part of the prospective database of patients operated for TWGB during a period of 2 years were analyzed. All patients were evaluated with Ultrasound, Triple phase CT and MR/MRCP, and CA 19-9 levels as outlined in a flowchart in Figure 1. The demographic details of the patients has been summarized in Table 1. The imaging (Ultrasonography and CECT Abdomen and pelvis and MRI or MRCP) and tumor marker (CA 19.9) findings are summarized in Table 2. Operative and postoperative details for patients with Histopathology details are shown in Table 3. Imaging (CECT Abdomen and pelvis and MRI or MRCP) and histopathology details for Cases 1, 2, and 3 are shown in Figures 2 to 4, respectively. Intraoperative images of the surgical procedure are illustrated in Figure 5.

Fig. 1: Flowchart outlining ultrasound, triple-phase CT and MR/MRCP, and CA 19-9 levels

Table 1: Demographic details
S. No Sex Age Presenting symptoms
1 M 53 RUQ pain
2 F 26 RUQ pain
Dyspepsia
Loss of appetite
3 M 57 RUQ pain
Decrease appetite
4 F 42 RUQ pain
Loss of appetite
Jaundice
5 M 76 RUQ pain
6 M 54 RUQ pain
Dyspepsia
7 F 45 RUQ pain
Fever
8 M 62 RUQ pain
9 F 55 RUQ Pain
Vomiting
Loss of weight
Jaundice
10 M 54 RUQ pain
11 M 65 RUQ pain
Vomiting
12 M 40 RUQ pain
Dyspepsia
Fever
13 M 70 RUQ pain
Dyspepsia
Loss of weight
Jaundice
14 M 53 RUQ pain
Dyspepsia
15 M 63 RUQ pain
Dyspepsia
16 M 70 RUQ pain
17 M 56 RUQ pain
18 M 60 RUQ pain
Table 2: Imaging details
S. No USG CT findings MR/MRCP CA 19.9 levels (IU/mL)
1 Gall stones Thickened GB wall GB wall thickening (6–12 mm) Pericholecystic fat stranding Few submetacentric periportal nodes are present GB shows 8 mm calculus at neck GB thick-walled at body and fundus with heterogenous content in lumen 25.30
2 GB sludge GB thick-walled with hypoechoic areas Gall stones, GB wall thickening at fundus (14 mm) Infiltration into hepatic flexure Pericholecystic and peri colonic L node enlarged Irregular thick enhancing GB wall infiltration into hepatic flexure 31
3 GB wall thickening at body and fundus Few subcentimetric nodes at periportal location Gall stones, GB wall thickening in body and fundus, Adenomyomatosis Large calculus in GB 3.5 cm GB wall in fundus and body region grossly thickened (20 mm) Pericholecystic fat stranding 16
4 GB distended with focal wall thickening Few subcentric RP nodes Focal GB wall thickening in fundus with few hypodense intraluminal pockets   1973
5 GB distended with e/o echogenic foci measuring 20 mm at body, 11 mm calculus at neck GB wall Thickening 4 mm, GB stone 26 mm within lumen with surrounding pericholecystic edema GB thick walled 4.2 mm with dependent sludge noted within GB 1100
6 GB stones largest 19 mm with thick walled GB Focal GB wall Thickening 9 mm in neck and fundus Cholelithiasis Focal thickening present in GB wall max thickness in neck region 8.5 mm Few subcentimentric lymph node enlargement 26
7 GB stones Heterogenous thickening seen arising from fundus infiltrating into adjacent liver parenchyma Cholelithiasis Focal GB wall thickening 12 mm with irregular peripherally enhancing collection Heterogenous thickening in GB wall max thickness 12.5 mm with intramural hyperintense cystic foci 110
8 GB wall thickened 8 mm with echogenic foci within shows comet tail artifact GB wall thickening (9 mm) Intra luminal cystic foci GB wall thickening with max thickness 10 mm Loss of interface with adjacent hepatic margins noted along GB fossa 24
9 GB distended with 1.5 cm calculus within e/o of hypoechoic area along post wall GB wall thickening 12 mm extending into neck Few subcentimentric nodes present   1125.2
10 GB showing multiple stones largest 11 mm Diffuse GB wall thickening seen GB wall thickening max thickness 7.6 mm with lost of fat planes with liver Irregular thick enhancing GB wall thickening e/o of fat stranding noted in adjacent parenchyma 143
11 GB thick walled with pericholecystic edema GB thick walled 9.5 mm with surrounding fat stranding with lost of planes with liver   65
12 GB distended with calculi in lumen Localized thick wall measuring 12 mm Hyperdense calculus foci impacted in GB neck Focal mural thickening in GB fundus with loss of fat planes with liver GB distended 5.5cm in transverse diameter, with an impacted stone in neck Focal mucosal discontinuity along ant wall Mild pericholecystic edema 26
13 GB—thick-walled lesion 46 × 36 mm with ill-defined fat planes Enhancing irregular GB wall thickening 11 mm with focal mucosa breech Ill-defined planes with liver Diffuse wall thickening with il-defined planes along hepatic surface in body and fundic region 82
14 GB—contracted and heterogenous thick walled with multiple calculi Enhancing mass lesion in GB wall with loss of fat planes with liver Diffusely thick walled GB max wall thickness of 10 mm with multiple intraluminal calculi 26
15 GB = thick-walled 4.7 mm Thick-walled GB 6 mm, with type 2 GB perforation with small collection Diffuse thick-walled GB with loss of flat planes 87
16 GB—Diffuse thick walled more in neck region with GB sludge Asymmetrical enhancing polyploidal thickening in GB body with ill-defined fat planes with D2 a/w inflammatory thickening of D2 GB—diffusely thickened 12 mm in body region with loss of fat planes with liver 1100
17 GB—focal hypoechoic area in GB wall at fundus area GB—distended, shows focal thickening at fundus, fat planes with liver maintained Focal irregular wall thickening seen along the posterior wall/hepatic surface of GB measuring 8 mm likely inflammatory 27
18 GB—contracted and diffuse circumferential thickening at body & fundus GB—shows diffuse circumferential enhancing mural thickening in body and fundus Significant pericholecystic fat stranding Few enlarged periportal and pericaval nodes are seen GB—diffuse mural thickening inv body and fundus with pericholecystic fat stranding Few enlarged periportal nodes 1.6
Table 3: Operative details
S. No Surgery Postop HPE
1 AEC Uneventful XGC
2 AEC with Enbloc resection of Hepatic flexure of colon Uneventful XGC
3 AEC Bile leak (managed by pigtail drainage) XGC
4 EC Uneventful CA GB (T1b stage)
5 AEC Uneventful XGC
6 AEC Bleeding (managed by blood transfusion) XGC
7 AEC Uneventful XGC
8 AEC Uneventful XGC
9 EC Uneventful CA GB (T1b stage)
10 AEC Uneventful XGC
11 AEC Uneventful XGC
12 AEC Uneventful XGC
13 EC Uneventful CA GB (Stage T1b)
14 AEC Uneventful XGC
15 AEC Uneventful XGC
16 AEC Uneventful XGC
17 AEC Uneventful XGC
18 AEC Uneventful XGC

Figs 2A to C: Imaging and histopathology findings of case 1

Figs 3A to C: Imaging and histopathology findings of case 2

Figs 4A to C: Imaging and histopathology findings of case 3

Fig. 5: Intraoperative images of the surgical procedure

IMAGINING AND HISTOPATHOLOGY DETAILS (FIGS2 TO 4)

INTRAOPERTIVE IMAGES

RESULTS

In this prospective study, out of 18 patients who underwent AEC, the frozen section of 15 patients was reported as XGC, and 3 were reported as Carcinoma GB with T1b stage, and these 3 cases further underwent EC in the same setting. One patient had TWGB with infiltration into hepatic flexure and underwent AEC with Enbloc resection of Hepatic flexure of the colon. Out of 16 cases, 16 had uneventful postop periods and 2 cases developed complications Bile leak which was managed by Pigtail drainage, and bleeding managed by blood transfusions (Clavien-Dindo Classification—Grade III). There was a male predominance with 12 out of 16 patients. The majority of patients had right upper quadrant pain as the main symptom (95%). One patient had a fever, and another had dyspepsia and loss of appetite as the main symptom; CA 19.9 levels were variable with 5 patients having levels more than 100 units. All patients underwent AEC with frozen section assessment.

DISCUSSION

Xanthogranulomatous cholecystitis is a rare variant of chronic cholecystitis and the term was first coined by the Armed Forces Institute of Pathology (AFIP) from the nomenclature of “fibroxanthogranulomatous irritation” by Christensen and Ishak.6,7 It is a giant cell-mediated inflammation characterized by infiltration of multinucleated giant cells and histiocytes. Xanthogranulomatous cholecystitis is a chronic inflammatory disease of the gallbladder that can mimic carcinoma due to its aggressive presentation. The exact pathogenesis of XGC is still not fully understood but the most widely accepted theory involves the rupture of the Rokitansky-Aschoff sinuses due to chronic inflammation, leading to bile extravasation into the gallbladder wall.8 This bile leakage initiates an intense inflammatory response, resulting in the recruitment of macrophages that engulf the leaked bile, leading to the formation of xanthogranulomas (lipid-laden macrophages).9 Histopathologically, XGC is characterized by thickened and fibrotic gallbladder walls, with granulomatous inflammation, foamy macrophages, and multinucleated giant cells.10 The inflammatory process often involves the entire gallbladder wall and can extend into the surrounding structures, causing dense adhesions that complicate surgical resection.11 The disease predominantly affects middle-aged to elderly patients, with a slight female predominance, and is strongly associated with gallstones.12 The chronic irritation caused by gallstones is believed to contribute to the development of XGC, although it has been reported in the absence of stones as well.13

Clinically, XGC often presents similarly to other forms of CC. Patients typically report symptoms of right upper quadrant pain, fever, nausea, and vomiting, which may be intermittent or persistent.14 However, unlike uncomplicated chronic cholecystitis, XGC can present with a more severe clinical course, and patients may develop complications such as abscess formation, bile duct obstruction, or perforation.15 Laboratory findings are usually nonspecific and may include elevated white blood cell counts, liver function abnormalities, and elevated C-reactive protein levels.16 The non-specific nature of the clinical and laboratory findings further complicates the preoperative diagnosis, making imaging studies a critical component of the workup. The primary diagnostic modality for evaluating gallbladder pathology is ultrasonography (USG), which can detect gallbladder wall thickening, the presence of gallstones, and pericholecystic fluid.17 In XGC, USG often reveals diffuse or focal thickening of the gallbladder wall, with intramural hypoechoic nodules and heterogeneity.18 However, these findings can be difficult to distinguish from gallbladder carcinoma, which also presents with similar ultrasonographic features.19 Computed tomography (CT) scans are helpful in further characterizing gallbladder wall thickening and can identify adjacent organ involvement, which is common in XGC.20 The typical CT appearance of XGC includes marked gallbladder wall thickening, intramural hypoattenuating nodules (representing xanthogranulomas), and sometimes a mass-like lesion that may resemble carcinoma.21 Magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) provide additional detail, particularly in evaluating the biliary tree and differentiating between benign and malignant lesions.22 Magnetic resonance imaging can detect the tissue characteristics of XGC, showing hypointense areas on T1-weighted images and hyperintense areas on T2-weighted images, corresponding to granulomatous inflammation.23

CONCLUSION

Xanthogranulomatous cholecystitis is a rare but significant cause of a TWGB that presents unique diagnostic and surgical challenges. A pragmatic approach that combines careful preoperative assessment with meticulous surgical technique is essential for optimal outcomes. Surgeons should be aware of the potential for severe inflammation and adhesions in XGC cases and should be prepared for complex dissections, with a low threshold for conversion to open surgery when necessary. Future research should focus on improving diagnostic accuracy and refining surgical strategies to minimize complications and improve patient outcomes.

ORCID

Arshid Iqbal Qadri https://orcid.org/0000-0001-8126-8487

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