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PubMed1982

Anatomical and immunological responses of rabbit gallbladders to bacterial infections.

To study the sequential morphological and immunological response of the rabbit gallbladder to bacterial infection and to compare the inflammatory responses with different pathogens, gallbladders were infected with Streptococcus faecalis and two strains of Escherichia coli, one of which produced enterotoxin. Gallbladder infection was produced either by intravenously injecting bacteria into rabbits with a small liver infarct or by injecting bacteria directly into the gallbladder of normal rabbits. The percentage of gallbladders infected intravenously with a nonenterotoxigenic E. coli strain was 86% at 1 week, 70% at 3 weeks, and 15% at 6 weeks. Epithelial necrosis and leukocyte infiltration were prominent 1 week after infection. At 3 and 6 weeks after infection, there was crypt distortion and increased mucus secretion in the epithelium as shown by periodic acid-Schiff staining. The lamina propria was infiltrated with mononuclear cells, many of which were plasma cells. Myofibroblasts (contractile fibroblasts) were also identified on transmission microscopy, In addition to these changes, toxigenic E. coli produced subepithelial capillary dilation in the villus core. Morphological changes (excluding toxin-associated changes) were related to the duration of infection rather than to the specific species of infecting bacteria. Infected gallbladders studied by immunofluorescence had a greater than 50-fold increase in plasma cells compared with control cells. In addition, the number increased with the duration of infection. Immunoglobulin A cells were the major cell type in gallbladders infected by intravesical injection, whereas immunoglobulin G cells predominated in gallbladders infected intravenously. The gallbladder appears to mount a local immune response to bacterial infection.

Animals↗

PubMed2000

Actions of histamine on muscle and ganglia of the guinea pig gallbladder.

Histamine is an inflammatory mediator present in mast cells, which are abundant in the wall of the gallbladder. We examined the electrical properties of gallbladder smooth muscle and nerve associated with histamine-induced changes in gallbladder tone. Recordings were made from gallbladder smooth muscle and neurons, and responses to histamine and receptor subtype-specific compounds were tested. Histamine application to intact smooth muscle produced a concentration-dependent membrane depolarization and increased excitability. In the presence of the H(2) antagonist ranitidine, the response to histamine was potentiated. Activation of H(2) receptors caused membrane hyperpolarization and elimination of spontaneous action potentials. The H(2) response was attenuated by the ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide in intact and isolated smooth muscle. Histamine had no effect on the resting membrane potential or excitability of gallbladder neurons. Furthermore, neither histamine nor the H(3) agonist R-alpha-methylhistamine altered the amplitude of the fast excitatory postsynaptic potential in gallbladder ganglia. The mast cell degranulator compound 48/80 caused a smooth muscle depolarization that was inhibited by the H(1) antagonist mepyramine, indicating that histamine released from mast cells can activate gallbladder smooth muscle. In conclusion, histamine released from mast cells can act on gallbladder smooth muscle, but not in ganglia. The depolarization and associated contraction of gallbladder smooth muscle represent the net effect of activation of both H(1) (excitatory) and H(2) (inhibitory) receptors, with the H(2) receptor-mediated response involving the activation of K(ATP) channels.

Adenosine Triphosphate↗

PubMed1993

Contraction and evacuation of the gallbladder studied simultaneously by ultrasonography and 99mTc-labeled diethyl-iminodiacetic acid scintigraphy.

Emptying of the gallbladder was studied by the simultaneous use of 99mTc-labeled diethyl-iminodiacetic acid [HIDA] scanning and real-time ultrasonography. In response to a liquid test meal the gallbladder volume was reduced for 80 min and then increased again, but the radionuclide evacuation continued and was more complete than could be explained by the reduction of gallbladder volume. In response to intravenous infusion of cholecystokinin, a maximal contraction of the gallbladder to 35% of the basal volume was obtained at 40 min, and 36% of the HIDA then remained in the gallbladder. In a separate series repeated intravenous injections of 99mTc-HIDA were given after the test meal, and the isotope was found to enter the gallbladder even when the gallbladder contracted. The results support the view that the gallbladder acts like a 'bellows' when contracting and that postprandial fluid secretion by the gallbladder mucosa may help to evacuate its contents.

Adult↗

PubMed1997

Gallbladder motility after duodenum-preserving resection of the head of the pancreas.

BACKGROUND: Duodenum-preserving resection of the head of the pancreas (DPRHP) is performed in patients with chronic pancreatitis (CP) localized in the head of the pancreas. It has been suggested that functional integrity of the upper digestive tract is preserved after DPRHP. We tested this hypothesis with regard to gallbladder motility. METHODS: Gallbladder motility and cholecystokinin (CCK) secretion were studied fasting, after cephalic vagal stimulation with sham feeding, and after regular feeding in 9 patients after DPRHP, in 6 unoperated patients with CP, and 9 healthy control subjects. RESULTS: Mean fasting gallbladder volume in patients after DPRHP (49 +/- 10 cm3) and patients with CP (53 +/- 10 cm3) was larger than in controls (33 +/- 3 cm3). Sham-feeding gallbladder contraction did not differ between patients after DPRHP, patients with CP, and controls. Both postprandial CCK secretion and gallbladder contraction in patients after DPRHP (78 +/- 16 pM. 120 min; 47% +/- 6%) and patients with CP (72 +/- 18 pM.120 min; 40% +/- 7%) were significantly reduced (P < 0.05) compared with controls (151 +/- 13 pM.120 min; 74% +/- 4%). Fasting gallbladder volume, sham feeding, and regular-feeding-induced gallbladder contraction and postprandial CCK secretion did not differ between operated and unoperated patients with CP. CONCLUSIONS: Gallbladder motility and CCK secretion are reduced in patients with pancreatic insufficiency. A DPRHP procedure does not further influence these results. These findings support the concept that gallbladder motor function is preserved after DPRHP.

Adult↗

PubMedDate not supplied

Effect of omeprazole on gallbladder contraction in humans.

BACKGROUND/AIMS: Omeprazole causes hypergastrinemia because of the effects of prolonged complete suppression of acid secretion and also gastrin has an excitatory effect on gallbladder contraction. Therefore, we investigated the meal-induced gallbladder emptying in healthy subjects receiving omeprazole and compared them to controls. METHODOLOGY: Twenty healthy volunteers participated in this study. Gallbladder volume was measured by ultrasonography. After basal measurement, the volunteers received saline intravenously (i.v.) 2 cc (no:10) or omeprazole 20 mg i.v. (no:10). After 15 min the gallbladder volume was scanned at 15 min intervals for 60 min for each of the subjects. At the end of the period, all the subjects received a standard test meal (ensure 250 cal/250 mL), after 1 hour the gallbladder volumes were rescanned at 15 min periods for 60 min. RESULTS: Mean gallbladder volume in the omeprazole group was not significantly different during a 45 min period as compared to the baseline value. The residual gallbladder volume at the end of the 15th minute (43.9 +/- 5.6 mL), 30th minute (45.4 +/- 5.9 mL), 45th minute (40.5 +/- 6.1 mL) and 60th minute (40.5 +/- 6.1 mL) showed no significant differences in both the omeprazole group and the controls. Mean gallbladder volumes of both groups after meal intake were significantly lower during the 1-hour period as compared to the baseline value (P < 0.05). The mean volumes did not show any significant differences between the omeprazole group and the control subjects. CONCLUSIONS: Omeprazole did not change the gallbladder volume during fasting and the postprandial period as compared to the control group.

Adult↗

PubMed2002

Hepatic bile entry into and transit pattern within the gallbladder lumen: a new quantitative cholescintigraphic technique for measurement of its concentration function.

UNLABELLED: The aim of the project was to study hepatic bile entry into and the transit pattern within the gallbladder lumen during fasting and to introduce a new quantitative scintigraphic test for measurement of its concentration function. METHODS: Each of 10 control subjects and 10 chronic acalculous cholecystitis (CAC) patients received 111-185 MBq 99mTc-mebrofenin as a hepatic bile marker. Gamma-camera image data were collected in the anterior view on a 128 x 128 x 16 computer matrix at 1 frame per minute for 60 min for the hepatic phase and 30 min for the gallbladder phase. The radiolabeled hepatic bile area within the gallbladder lumen was traced, and the net transit area and transit time were noted. The hepatic bile transit rate was calculated (as mm2/min) and normalized to 1,000 mm2 of the anterior gallbladder area. The cholecystokinin-8-induced ejection fraction was calculated nongeometrically using counts. RESULTS: Hepatic bile entered the gallbladder continuously during fasting with a mean +/- SD of 71% +/- 20% in control subjects and 59% +/- 27% in CAC patients, which were not significantly different (P > 0.05). The maximum frontal gallbladder area was 1,699 mm2 in control subjects and 1,610 mm2 in CAC patients (P > 0.05). Radiolabeled hepatic bile entered the gallbladder first along its central long axis in both groups, at a mean of 15 min and 16 min, respectively, and traveled toward the periphery in a lamellar fashion at a normalized mean rate of 38 mm2/min and 40 mm2/min in control subjects and CAC patients, respectively. The mean ejection fraction of 17% in CAC patients was significantly lower than the mean value of 56% in control patients (P < 0.00001). CONCLUSION: Hepatic bile enters the gallbladder continuously during fasting. In patients with CAC, the gallbladder maintains the normal concentration function but the contraction and emptying are reduced significantly. This new cholescintigraphic technique enables measurement of both functions sequentially with a single dose of 99mTc-mebrofenin.

Adult↗

PubMed2002

Interdigestive contractions of the gallbladder in rabbits: the real time ultrasonographical studies.

There are no reports concerning the ultrasonographical examination of gallbladder contractility in rabbits. Thus, the aim of this study was to assess the dynamics of gallbladder contractions in 7 rabbits. Animals were fasted 24 h before the experiments lasting 3-5 h. Ultrasonographical examinations were performed every 10 min using USG 220 SLC machine. The sectorial ultrasound 3.5 MHz was placed in the right subcostal region. The maximal longitudinal gallbladder scans were obtained and the gallbladder volume was estimated using 3 methods. The highest values were obtained with the method approximating the gallbladder shape to ellipsoid. The second method approximating gallbladder shape to the barrel provided intermediate results and the lowest results were obtained with the sum-of-cylinders method. The overall mean of interdigestive gallbladder volume using the latter method was 1.34 +/- 0.10 ml. Peak and interpeak values were 2.23 +/- 0.33 and 0.99 +/- 0.18 ml, respectively, p < 0.01. The mean peak distance was 69.6 +/- 7.4 min approximately remaining in concert with the reported MMC intervals in rabbits. It is concluded that the rabbit model for gallbladder ultrasonography may be useful for the study of gallbladder dynamics.

Animals↗

PubMed2003

A MEK inhibitor (U0126) prolongs survival in nude mice bearing human gallbladder cancer cells with K-ras mutation: analysis in a novel orthotopic inoculation model.

Most cases of gallbladder cancer are found at an advanced stage accompanied by invasion to the liver, metastases to the lymph nodes and distant organs, and peritoneal dissemination. Then, the treatment for advanced gallbladder cancer is often ineffective, and the prognosis of this disease is poor. The specific aim of this study was to establish a model system for developing new therapeutic strategies, such as molecular target therapy, for human advanced gallbladder cancer. We used a human gallbladder cancer cell line, NOZ with K-ras mutation in this experiment. Then, we established a novel orthotopic inoculation model for gallbladder cancer by using NOZ cells in nude mice. Mitogen-activated protein kinase (MAPK) in NOZ cells was constitutively activated, and the activation of MAPK provided autonomous proliferation of NOZ cells. All of the mice orthotopically inoculated by NOZ cells developed tumors at the gallbladder. Direct invasion into the liver, and bloody ascites were observed. Metastases to the mediastinal lymph nodes were also recognized in all of the mice examined. Moreover, most of the mice showed lung metastases. Survival duration was 29-50 days after inoculation. Nude mice with NOZ tumor at gallbladder were treated by an intraperitoneal injection of a MAPK kinase inhibitor U0126 (25 micro mole/kg) twice a week. U0126 (p=0.0110, one-way ANOVA) significantly prolonged the survival duration of the mice with NOZ gallbladder tumor. Our orthotopic inoculation model is useful for developing new therapeutic strategies, such as molecular target therapy for advanced gallbladder cancer.

Animals↗

PubMed2004

Diagnosis and treatment of polypoid lesions of the gallbladder: report of 194 cases.

BACKGROUND: With the wide use of B-ultrasonography in recent years, the polypoid lesion of the gallbladder (PLG) has been one of the most common diseases detected in biliary surgery. This study was to investigate the diagnostic method and operative indications of PLG. METHODS: The clinical and pathological data of 194 patients with PLG who had received operation at our hospital from January 1994 to September 2002 were analyzed retrospectively. Categorized data were analyzed by the chi-square test. RESULTS: All the patients received preoperative B-ultrasonography. 185 of the 194 PLG patients were diagnosed as having cholecystic polyp, and 9 adenomas. Among the 42 patients who received CT, 6 showed early gallbladder cancer. Pathologically, cholesterol polyps were mostly multiple lesions (64.7%) with a mean diameter of 3.86+/-2.2 mm in 136 patients. Of 16 patients with adenomas, 10 had a tumor diameter of more than 10 mm (62.5%). In 11 patients with gallbladder carcinoma, 7 were accompanied with gallbladder stone (63.6%). In addition, inflammatory polyps and adenomyomas were found in 25 and 6 patients respectively. CONCLUSIONS: B-ultrasonography is the most effective diagnostic method for detecting PLG. When large or irregular lesions are found, CT should be performed in order to avoid missing of gallbladder carcinoma. Operative indications for PLG include: a maximal tumor diameter of more than 10 mm; an over 50-year-old patient with a widebase and a single polyp lesion; a wide-base lesion or a lesion showing a tendency to enlargement; co-existing gallbladder stone or cholecystitis; a patient without other diseases but obvious clinical features and failure of general management; big or long pedicels or polyps at the neck of the gallbladder for preventing the empty of the gallbladder and a history of biliary colic; and PLG with irregularly thickened local gallbladder wall.

Adult↗

PubMed1995

Inhibition of gallbladder emptying decreases cholesterol saturation in bile in the Richardson ground squirrel.

Impaired gallbladder emptying is frequent in cholesterol gallstone disease as well as in predisposing conditions like pregnancy and obesity. Gallbladder hypomotility is considered a pathogenic factor for gallstone formation, providing the residence time for cholesterol crystal nucleation, but any effect on the enterohepatic circulation of bile acids and subsequently on biliary lipid composition is unknown. Therefore, we studied the effect of prolonged suppression of gallbladder emptying with a cholecystokinin (CCK-A) receptor antagonist on bile formation in Richardson ground squirrels fed a trace versus a 1% cholesterol diet. Biliary lipid secretion was measured directly and bile acid pool size assessed by isotope dilution ([14C]-cholic acid). Gallbladder contraction was determined in vitro in response to CCK. The CCK-antagonist (MK-329) greatly inhibited gallbladder contraction in vitro and increased gallbladder fasting volume and bile acid pool size in vivo. It significantly lowered the cholesterol saturation index by 35% and 46% in hepatic bile and by 18% and 28% in gallbladder bile in the trace and cholesterol diet groups, respectively. Bile acid secretion and bile flow doubled with the CCK-receptor antagonist. Chronic CCK receptor antagonist-induced inhibition of gallbladder emptying increases bile acid secretion and thereby decreases cholesterol saturation in bile. Extensive biliary hypomotility thus leads to a more rapid cycling of bile acids by depriving the gallbladder of its function in the enterohepatic circulation.

Animals↗

PubMed1996

Pathology and cellular kinetics of gallbladder with an anomalous junction of the pancreaticobiliary duct.

OBJECTIVES: Anomalous junction of the pancreaticobiliary duct (AJPBD) is thought to be an important risk factor for gallbladder carcinoma in Japan. In this report, we examine histopathology and cellular kinetics of gallbladder mucosae of patients with AJPBD and the possible risk of gallbladder carcinoma. METHODS: We examined 62 gallbladders from patients with AJPBD (group A), 16 gallbladder carcinomas from patients with AJPBD (group B), 60 gallbladder carcinomas from patients without AJPBD (group C), and six normal gallbladders from patients without AJPBD (group D). Histopathology, mucosal heights, and proliferative cell nuclear antigen-labeling index were obtained from routinely processed tissue specimens. RESULTS: The incidence of hyperplastic changes in group A and in the noncancerous regions (NCRs) of group B was greater than in the NCRs of group C (p < 0.05). The incidence of dysplastic changes in the NCRs of group B was greater than in the NCRs of group C (p < 0.05). The mucosal heights in group A and in the NCRs of group B were higher than in the NCRs of group C (p < 0.05). A high proliferative cell nuclear antigen-labeling index was observed in group A and in the NCRs of group B, where hyperplastic changes were frequently observed. CONCLUSIONS: These results suggest that a sequence of hyperplastic changes with a corresponding increase in cellular kinetics with progression through dysplasia to carcinoma may be important in carcinogenesis in gallbladders of patients with AJPBD. AJPBD itself may be a possible risk for gallbladder carcinoma.

Adolescent↗

PubMed2000

Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III).

BACKGROUND: Ascorbic acid-deficient guinea pigs frequently develop gallstones, and ascorbic acid status may also affect the risk of gallbladder disease in humans. To examine the relationship of ascorbic acid, an antioxidant nutrient involved in cholesterol catabolism, to gallbladder disease, we analyzed data collected from a probability sample of US adults. METHODS: Analyses of data from 7042 women and 6088 men enrolled in the Third National Health and Nutrition Examination Survey, 1988-1994, were performed. Multiple logistic regression models stratified by sex were examined, controlling for the effects of age, race, diet, body mass index, and other potential confounders. RESULTS: A total of 761 women (11%) and 235 men (4%) reported a history of clinical gallbladder disease (symptomatic gallstones or cholecystectomy). Of the 9650 participants without a history of clinical gallbladder disease or abdominal pain consistent with gallbladder disease, and with valid abdominal ultrasonography, 408 (8%) of 4863 women and 274 (6%) of 4787 men had asymptomatic gallstones. Serum ascorbic acid level was inversely related to prevalence of clinical and asymptomatic gallbladder disease among women, but not among men. Among women, each SD (27 micromol/L) increase in serum ascorbic acid level was independently associated with a 13% lower prevalence of clinical gallbladder disease (P = .006) and asymptomatic gallstones (P = .048). CONCLUSION: Ascorbic acid, which affects the catabolism of cholesterol to bile acids and, in turn, the development of gallbladder disease in experimental animals, may affect the risk of gallbladder disease among women.

Adult↗

PubMedDate not supplied

Estrogen and progesterone receptors in human gallbladder.

Gallbladder disease is more prevalent in women than men. Estrogen therapy has been associated with an increased incidence of gallbladder disease in both sexes. Further, increased progesterone levels have been implicated in impairment of gallbladder motility in pregnancy. Because sex hormones often exert their action through specific receptors, we investigated whether human gallbladder contains receptors for estrogen and progesterone. Binding of radiolabeled hormones in cytosol and nuclei prepared from human gallbladder of both sexes is indicative of the presence of receptors for both estrogen and progesterone. The binding is saturable, of high affinity and highly specific for its particular type of hormone but not other steroids. Fractionation of sodium molybdate-stabilized gallbladder cytosol on Sephadex G-100 demonstrates that the labeled hormones are not bound to defined proteins such as sex steroid binding globulin or albumin. These studies indicate that human gallbladder contains both estrogen and progesterone receptors, that the presence of these receptors may explain the sensitivity of gallbladder tissue to these hormones and that certain aspects of gallbladder function may be mediated by the interaction of steroid hormones with these receptors.

Adult↗

PubMed1990

Role of cholecystokinin and the cholinergic system in intestinal stimulation of gallbladder contraction in man.

To determine the role of cholecystokinin and the cholinergic system in intestinal stimulation of gallbladder contraction, we studied the effects of atropine on plasma cholecystokinin and gallbladder contraction in six healthy volunteers (four men and two women aged 20 to 27 yr). Effects were noted after intraduodenal fat instillation and after dosage with exogenous cholecystokinin inducing plasma cholecystokinin concentrations similar to those after intraduodenal fat instillation. At regular intervals before and after administration of each stimulus, plasma cholecystokinin concentrations and gallbladder volumes were measured by radioimmunoassay and real-time ultrasonography, respectively. Intraduodenal infusion of 250 ml 20% Intralipid induced a peak plasma cholecystokinin increment of 10.2 +/- 1.6 pmol/L compared with 10.7 +/- 0.7 pmol/L during infusion of 1 Ivy dog unit per kilogram per hour of cholecystokinin. The increases in plasma cholecystokinin after fat and exogenous cholecystokinin administration were accompanied by similar decreases in gallbladder volume. Integrated gallbladder contraction after fat instillation was 3,939% +/- 288%.min compared with 3,301% +/- 359%.min during cholecystokinin infusion (NS). Atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg/hr) did not change plasma cholecystokinin concentrations but induced similar inhibition of gallbladder contraction to 2,296% +/- 511%.min (p less than 0.05) after intraduodenal fat instillation and to 1,756% +/- 456%.min (p less than 0.05) during cholecystokinin infusion. We conclude that cholecystokinin is of major importance in intestinal stimulation of gallbladder contraction. Atropine inhibits the gallbladder response to intraduodenal fat. This inhibition is not due to a reduction in cholecystokinin secretion but to a diminished gallbladder response to cholecystokinin.

Adult↗

PubMed1997

Cystic fibrosis transmembrane conductance regulator mediates the cyclic adenosine monophosphate-induced fluid secretion but not the inhibition of resorption in mouse gallbladder epithelium.

We have studied the physiological role of the cystic fibrosis (CF) gene product (cystic fibrosis transmembrane conductance regulator [CFTR]) in gallbladder epithelium using a knockout mouse model for CF. We found that normal mouse gallbladder epithelium expresses functional CFTR as shown by reverse-transcription polymerase chain reaction (RT-PCR) analysis and Ussing chamber experiments. Gallbladders from Cftr -/- mice were structurally intact as shown by microscopic and physiological parameters but lacked the cyclic adenosine monophosphate (cAMP)-induced chloride current observed in normal gallbladders. In fluid transport measurements, normal and Cftr -/- gallbladders were equally active in basal resorption. The addition of forskolin, which activates CFTR anion channel activity through the cAMP system, resulted in net fluid secretion in normal gallbladders. In contrast, Cftr -/- gallbladders were unable to secrete fluid while a complete inhibition of resorption by forskolin was observed. We conclude that, in normal mouse gallbladder epithelium, cAMP-induced fluid secretion involves simultaneous inhibition of apical sodium chloride resorption and activation of CFTR. Our data support the hypothesis that gallbladder disease in CF is at least in part caused by a deficient secretory response to the endogenous cAMP-linked hormones VIP and secretin.

Animals↗

PubMed2000

Association of diabetes, serum insulin, and C-peptide with gallbladder disease.

An inconsistent association has been found between gallbladder disease and diabetes mellitus. We hypothesized that insulin resistance rather than diabetes status may be a primary factor involved in gallstone formation. A total of 5,653 adult participants in the third United States National Health and Nutrition Examination Survey without known diabetes underwent gallbladder ultrasonography and phlebotomy after an overnight fast for measurement of serum insulin, C-peptide, and glucose. Gallbladder disease was defined as ultrasound-documented gallstones or evidence of cholecystectomy. Subjects were characterized as having normal fasting glucose (<110 mg/dL), impaired fasting glucose (110 to <126 mg/dL), or undiagnosed diabetes (>/=126 mg/dL). After controlling for other known gallbladder disease risk factors, among women, undiagnosed diabetes was associated with increased risk of gallbladder disease (prevalence ratio [PR] = 1.91, 95% confidence interval [CI] = 1.29-2. 83); whereas impaired fasting glucose was unassociated. Gallbladder disease risk in women increased with levels of fasting insulin (PR = 1.63, 95% CI = 1.11-2.40) and C-peptide (PR = 2.07, 95% CI = 1.32-3. 25) comparing highest to lowest quintiles. However, the association of gallbladder disease with undiagnosed diabetes was not diminished when the model included fasting insulin (PR = 1.85, 95% CI = 1.24-2. 77). In men, there was a statistically nonsignificant association with undiagnosed diabetes (PR = 2.11, 95% CI = 0.76-5.85), but no association of gallbladder disease with insulin or C-peptide. Among women higher fasting serum insulin levels increased the risk of gallbladder disease, but did not account for the increased risk in persons with diabetes.

Adult↗

PubMed2002

Role of sonography in the diagnosis of gallbladder perforation.

PURPOSE: Gallbladder perforation is a dreaded complication of acute cholecystitis that is associated with a high mortality rate. Early detection of gallbladder perforation reduces the associated mortality and morbidity rates. The purpose of this study was to highlight the role of sonography in the diagnosis of gallbladder perforation and to compare the diagnostic accuracy of sonography with that of CT. METHODS: We retrospectively evaluated the sonographic and CT findings in surgically proven cases of gallbladder perforation. RESULTS: In 18 of 23 cases, both sonography and CT had been performed; in the other 5 cases, only sonography had been performed. Sonography helped to diagnose the defect in the gallbladder wall and gallbladder perforation in 16 (70%) of 23 patients. In the 18 cases in which both sonography and CT had been performed, sonography showed the wall defect in 11 cases (61%), whereas CT was diagnostic in 14 cases (78%). The difference between sonography and CT in the ability to visualize a defect in the gallbladder wall was not statistically significant. CONCLUSIONS: Sonography is useful for diagnosing gallbladder perforation and detecting the defect in the gallbladder wall. We believe that sonography should be the first-line imaging modality for evaluating the patients in these cases.

Acute Disease↗

PubMed2001

Endoscopic sonography in the diagnosis of gallbladder wall lesions in patients with gallstones.

PURPOSE: The purpose of this study was to evaluate the diagnostic accuracy of endoscopic sonography (EUS) in the detection of gallbladder wall lesions in patients with and without gallstones. METHODS: We retrospectively reviewed the medical records, sonograms, and sonographic reports of 62 patients who underwent cholecystectomy for gallbladder wall lesions evaluated by EUS. We assessed the accuracy of EUS in diagnosing gallbladder wall lesions in the presence or absence of gallstones and on the basis of the size and number of stones and the size of the gallbladder wall lesions. We also evaluated the effect of acoustic shadowing. The EUS results were compared with the histopathologic results. RESULTS: EUS correctly diagnosed the gallbladder wall lesions in 17 (71%) of 24 patients with gallstones and in 34 (89%) of 38 patients without gallstones. The diagnostic accuracy of EUS was 86% in patients with gallbladder wall lesions smaller than 20 mm and 79% in patients with gallbladder wall lesions 20 mm or larger. The diagnostic accuracy was 75% in patients with gallstones smaller than 5 mm and 67% in patients with stones 5 mm or larger. The accuracy was 67% in patients with 1-5 stones and 83% in patients with 6 or more stones. None of these differences was statistically significant. Acoustic shadowing did not affect the diagnostic accuracy of EUS. CONCLUSIONS: The diagnostic accuracy of EUS for gallbladder wall lesions is not affected by the presence of gallstones. However, better diagnostic criteria must be established based on larger studies, and technical refinements of the equipment are needed to increase the accuracy of EUS in the diagnosis of gallbladder wall lesions.

Cholelithiasis↗