First published online October 1, 2007
British Journal of Radiology (2007) 80, 898-901
© 2007 British Institute of Radiology
doi: 10.1259/bjr/28510614
The CT appearances of gallbladder perforation
B S Morris, MD
P R Balpande, DNB
A C Morani, MD
R K Chaudhary, MD
M Maheshwari, MD
and
A A Raut, MD
Department of Radiology, K.E.M Hospital, Acharya Dhonde Marg, Parel, Mumbai-400012, India
Correspondence: Dr Ajay Morani, Department of Radiology, K.E.M Hospital, Acharya Dhonde Marg, Parel, Mumbai-400012, India. E-mail: ajaycmorani{at}yahoo.com
 |
Abstract
|
|---|
Perforation of the gallbladder is an uncommon complication of acute cholecystitis that is associated with relatively high mortality. Symptoms and clinical signs can be indistinguishable from those of uncomplicated acute cholecystitis, leading to delayed diagnosis. We reviewed the clinical and imaging findings in 17 patients with gallbladder perforation confirmed at surgery.
|
Introduction
|
|---|
Although an uncommon complication, it is essential to consider the possibility of perforation of the gallbladder in cases of acute cholecystitis, as this condition is associated with a relatively high morality rate. The semblance that clinical findings of a perforated gallbladder bear to those of uncomplicated acute cholecystitis explains the delay in recognition of perforation, often with catastrophic results. This paper highlights the imaging features on CT of 17 patients with gallbladder perforation who presented with an acute abdomen. As CT was the preliminary radiological investigation in most of these patients, it was not found practicable to perform an ultrasonographic examination in all, as several of the patients were taken up for exploratory laparotomy soon after the diagnosis was established on CT.
|
Methods and materials
|
|---|
CT of 17 patients with gallbladder perforation was performed on a Somatom Volume Zoom (4-slice multidetector CT; Siemens, Germany). The protocol was as follows: 10 mm slice thickness and a collimation of 5 mm for the pre-contrast scans, and a slice thickness of 5 mm and a collimation of 2.5 mm for the contrast scans; 120 kVp; 165 mAs; rotation time 0.5 s with feed/rotation, and 25 mm and 12.5 mm for the pre-contrast and contrast scans, respectively. 750 ml water-soluble iodinated contrast diluted to 1% was used as oral contrast. 2 ml kg–1 of intravenous iodinated contrast was injected at 2 ml s–1 over a period of approximately 30–40 s. The contrast scan was performed in the portal venous phase of enhancement approximately 55 s after the start of intravenous infusion of contrast. The scans were reviewed on the basis of the following criteria: the site and multiplicity of perforation, the presence of gallstones and pericholecystic collections, and the presence of gas within the gallbladder/abscesses. Extension of the inflammatory process into adjacent hepatic parenchyma and pathology in the pancreas and the lung bases were also noted. As CT was the preliminary radiological investigation in most of these patients, it was not practicable to perform ultrasonography as several of the patients were taken for exploratory laparotomy soon after the diagnosis was established on CT.
|
Results
|
|---|
17 patients were reviewed over a period of 9 months, with a range of 17 years to 76 years (mean age of 48 years). There were 10 females and 7 males. 16 patients (94.2%) had Type 2 perforation (subacute, localized) and only one had Type 1 (acute, generalized peritonitis) perforation. Surgical confirmation of gallbladder perforation was obtained for all patients. In two patients (11.8%), the perforation was not detected on CT. Seven patients (41.2%) were either known to be diabetic or, on investigation, found to have elevated blood glucose. The most common presenting symptom was upper abdominal pain; only two patients were febrile at presentation.
In the 15 patients (88.2%) in whom a perforation was identified at CT, 12 (70.5%) were solitary. Multiple perforations were identified in only three cases (17.6%). The fundus (40%) was found to be the most common site of perforation. The mean identifiable diameter defect was 14 mm, with a range of 8 mm to 32 mm. Ultrasound was performed in 11 patients and gallbladder perforation was either misinterpreted or not identified in six. Eight patients (47%) had biliary calculi, three of which were in the gallbladder (
Figures 1–7); one was in the common hepatic and four were in the cystic duct . A calculus in one patient was missed on CT because of its low attenuation value, which rendered it isodense with gallbladder contents. Pockets of air within collections in the liver were seen in three out of five patients in whom perforation had led to the formation of an intrahepatic abscess (Figure 1). These were thought to have resulted from the presence of anaerobic organisms rather than from either enteric fistulation or incompetence of the sphincter of Oddi. The striking appearance of calculi within an intrahepatic collection was seen in only one case (Figure 1). In two patients, perforation occurred in the context of emphysematous cholecystitis.
View larger version (138K):
[in this window]
[in a new window]
|
Figure 1. The gallbladder is grossly distended with poor definition of its walls. A large encapsulated low-attenuation collection within adjacent hepatic parenchyma shows internal loculation and a few air pockets. Multiple calculi are seen within both the gallbladder and the intrahepatic abscess. A rent in the lateral wall of the gallbladder (arrow) is seen.
|
|
View larger version (138K):
[in this window]
[in a new window]
|
Figure 2. An axial image reveals a 7 mm wide defect (arrow) in the medial wall of a distended gallbladder.
|
|
View larger version (141K):
[in this window]
[in a new window]
|
Figure 3. Empyema of the gallbladder. Irregularity and wall thickening at the fundus(asterisk) suggests the probable site of perforation.
|
|
View larger version (141K):
[in this window]
[in a new window]
|
Figure 4. A contracted gallbladder communicates through a 17 mm wide defect (arrow) along its anterior wall, with an encapsulated collection that tracts between the liver and the parietal wall.
|
|
View larger version (151K):
[in this window]
[in a new window]
|
Figure 5. Pericholecystic stranding is seen near a large defect(arrow) at the fundus of a distended gallbladder.
|
|
View larger version (153K):
[in this window]
[in a new window]
|
Figure 6. Pericholecystic inflammation confers a"star-burst" appearance to the fundus of the gallbladder. The arrow highlights poor definition of the posterior margin of the wall of the gallbladder.
|
|
View larger version (143K):
[in this window]
[in a new window]
|
Figure 7. A 24x27 mm calculus is seen in the neck of an irregularly marginated gallbladder. A 10 mm rent (arrow) along the wall of the gallbladder results in extensive collections within the right lobe of the liver.
|
|
|
Discussion
|
|---|
Complications such as empyema, gangrenous cholecystitis and gallbladder perforation have been reported in 4–12% of all cases of acute cholecystitis [1–3]. Perforation can occur as early as 2 days after the onset of acute cholecystitis, or after several weeks [3, 4]. The sequence of events that leads to acute cholecystitis and subsequently to perforation is thought to result from occlusion of the cystic duct (most often by a calculus), resulting in retention of intraluminal secretions. Distension of the organ with a consequent rise in intraluminal pressure impedes venous and lymphatic drainage, leading to vascular compromise and ultimately to necrosis and perforation of the wall of the gallbladder [5, 6]. Because of its poor blood supply, the fundus of the gallbladder is the most common site of perforation [3]. Despite a propensity for perforation in acalculous cholecystitis, most cases of perforation are associated with a calculus because of the higher incidence of calculus cholecystitis [7]. Of our eight patients with biliary calculi, stones in the hepatic duct, gallbladder (
Figures 1–7) and the cystic duct were demonstrable in one, three and four patients, respectively. For perforation of a non-distended gallbladder (when infection is thought to be the cause), it has been suggested that enlarged Rokitansky–Aschoff sinuses have become infected, leading to necrosis and then rupture [5]. Apart from cholelithiasis and infection, factors that predispose to perforation are malignancy, trauma and drugs (e.g. corticosteroids). Systemic diseases such as diabetes mellitus and atherosclerotic heart disease are also thought to be contributory [3] and elderly patients are especially susceptible to gallbladder perforation [8]. Glenn and Moore et al in an early study reported an incidence of perforation of the gallbladder five times higher among those patients treated conservatively than among those who underwent cholecystectomy [5]. The incidence of perforation is known to increase fourfold with a delay in surgery of more than 2 days from the onset of abdominal symptoms [9]. At surgery, the site of perforation is most commonly found to be sealed off by omentum and the transverse colon with adhesions to the liver capsule [10, 11], as seen in our study.
In the early decades of the last century, Niemeier categorized perforation into three types [12]: Type 1 (acute — 33% to 37%), which manifests with generalized peritonitis; Type 2 (subacute — 43% to 53%), which denotes localization of fluid at the site of perforation with the formation of a pericholecystic abscess; and Type 3 (chronic — 10% to 19%), in which internal (bilio-biliary or bilio-enteric) or external fistulae occur [1]. In our study, a Type 1 perforation was detected in a single patient. This finding is in keeping with more recent reports in the medical literature that cite a higher incidence of subacute perforation [2].
The clinical presentation of gallbladder perforation may range from an acute generalized peritonitis to benign non-specific abdominal symptoms. Clinical differentiation between gallbladder perforation and uncomplicated cholecystitis can often be difficult because the bile leak from a ruptured gallbladder might be contained in the extra peritoneal gallbladder fossa, and hence might not produce symptoms of peritonitis immediately [13]
Gore et al [14] thought that perforation and abscess formation should be suspected clinically in those patients with acute cholecystitis who suddenly become toxic and whose clinical condition was found to deteriorate rapidly. A delay in diagnosing gallbladder perforation could be explained by the similarity of clinical manifestations to those of acute cholecystitis. The site of maximal pain in regions other than those associated with gallbladder pathologies could lead to a mistaken diagnosis of acute appendicitis or of a perforated duodenal ulcer [10]. If unattended, the mortality associated with this condition is as high as 24% [2] and is higher still in patients with immune deficiency and in cases of malignancy [3]. The mortality rate is 10 times greater in acute than in subacute perforation [2].
As calculi are often missed on CT, sonography followed by CT is preferred in suspected biliary pathology; however, ancillary findings such as pneumobilia are more likely to be detected on CT. The crumpled wall of a decompressed gallbladder floating within fluid of the gallbladder fossa has a distinctive appearance and can be seen in some cases of Type 1 perforation. Soiva et al in their study of nine cases of acute gallbladder perforation found that distension of the gallbladder and oedema of its walls may be the earliest signs of impending perforation [15]. They also observed that pericholecystic or free fluid in the peritoneal cavity was not found in uncomplicated acute calculus cholecystitis [15]. The presence of air within the wall of the gallbladder (emphysematous cholecystitis) prognosticates impending perforation [7].
Following perforation, CT and ultrasonography both show complex fluid collections surrounding the gallbladder. The wall of the gallbladder can appear focally disrupted and the gallbladder lumen may be seen within, or peripheral to, the pericholecystic abscess [14].
Most studies of perforation of the gallbladder deduce that the wall of the gallbladder following perforation appears distended, thickened, oedematous and on occasion fails to be identified [15, 16]. Our identification of the gallbladder on CT following perforation in each of the 17 cases reviewed is at variance with the common belief that the gallbladder might not be detected on CT in over a third of cases. Kim et al [11] in their comparative study of CT and ultrasonography on 13 patients with gallbladder perforation detected the site of perforation in 50% of patients on CT but in no patient on ultrasonography. However, they found both modalities equally effective in demonstrating pericholecystic fluid collections, gallbladder wall thickening and cholelithiasis. A study of 23 patients with gallbladder perforation by Sood et al [17] in 2001 showed a marginally higher rate of detection of gallbladder wall defects on CT than with ultrasonography. In 11 of our patients who underwent ultrasonography, perforation was either misinterpreted or not detected in six. Ultrasonography in two cases missed small collections: an abscess in the liver on account of artefacts from an emphysematous gallbladder (Figure 5) and a perihepatic collection beneath the anterior chest wall remote from the gallbladder (Figure 6).
Ultrasonography is usually the initial mode of investigation in cases of suspected gallbladder perforation. As the sensitivity of CT in the detection of gallbladder perforation and biliary calculi was found to be 88% and 89%, respectively, we recommend that it be performed in all such cases.
Received for publication July 30, 2004.
Revision received June 3, 2006.
Accepted for publication November 10, 2006.
|
References
|
|---|
- Isch J, Finneran JC, Nahrwold DL. Perforation of the gall-bladder. Am J Gastroenterol 1971;55:451–8.[Medline]
- Bennet GL, Balthazar EJ. Ultrasound and CT evaluation of emergent gallbladder pathology. Radiol Clin North Am 2003;41:1203–16.[CrossRef][Medline]
- Strohl EL, Diffenbaugh WG, Baker JH, Chemma MH. Collective reviews: gangrene and perforation of the gallbladder. Int Abstr Surg 1962;114:1–7.
- Cope Z. A sign of gallbladder disease. BMJ 1970;3:147–8.[Free Full Text]
- Glenn F, Moore SW. Gangrene and perforation of the wall of the gallbladder. Arch Surg 1942;44:677–86.[Abstract/Free Full Text]
- Madrazo BL, Francis I, Hricak H, Sandler MA, Hudak S, Gitschlag K. Sonographic findings in perforation of the gallbladder. AJR Am J Roentgenol 1982;139:491–6.[Abstract/Free Full Text]
- Meire H, Cosgrove D, Dewbury K, Wilde. Gallbladder pathology. In: Cosgrove D, Meire H, Dewbury K, editors. Abdominal and general ultrasound. Longman Group; 1993: 195–8
- Martin JD Jr, Stone HH. Perforations of the gallbladder; a report of three cases. Geriatrics 1957;12:476–80.[Medline]
- Harland C, Mayberry JF, Toghill PJ. Type 1 free perforation of the gallbladder. J R Soc Med 1985;78:725–78.[Abstract]
- Ong CL, Wong TH, Rauff A. Acute gallbladder perforation — a dilemma in early diagnosis. Gut 1991;32:956–8.[Abstract/Free Full Text]
- Kim PN, Lee KS, Kim IY, Bae WK, Lee BH. Gallbladder perforation: comparison of US findings with CT. Abdom Imaging 1994;19:239–42.[CrossRef][Medline]
- Smith R, Rosen JM, Alderson PO. Gallbladder perforation: diagnostic utility of cholescintigraphy in suggested subacute or chronic cases. Radiology 1986;158:63–6.[Abstract/Free Full Text]
- Sood B, Jain M, Khandelwal N, Singh P, Suri S. MRI of perforated gallbladder. Australas Radiol 2002;46:438–40.[CrossRef][Medline]
- Gore RM, Yaghmai V, Newmark GM, Berlin JW, Miller FH. Imaging benign and malignant disease of the gallbladder. Radiol Clin North Am 2002;40:1307–23.[Medline]
- Soiva M, Pamilo M, Päivänsalo M, Taavitsainen M, Suramo I. Ultrasonography in acute gallbladder perforation. Acta Radiol 1988;29:41–4.[Medline]
- Johnson LB. The importance of early diagnosis of acute acalculus cholecystitis. Surg Gynecol Obstet 1987;164:197–203.[Medline]
- Sood BP, Kalra N, Gupta S, Sidhu R, Gulati M, Khandelwal N, Suri S. Role of sonography in gall bladder perforation. J Clin Ultrasound 2002;30:270–4.[CrossRef][Medline]
This article has been cited by other articles:
Top
Abstract
Introduction
