Characterization of basal hepatic bile flow and the effects of intravenous cholecystokinin on the liver,sphincter, and gallbladder in patients with sphincter of Oddi spasm

The major objectives of this project were to establish the pattern of basal hepatic bile flow and the effects of intravenous administration of cholecystokinin on the liver, sphincter of Oddi, and gallbladder, and to identify reliable parameters for the diagnosis of sphincter of Oddi spasm (SOS). Eight women with clinically suspected sphincter of Oddi spasm (SOS group), ten control subjects (control group), and ten patients who had recently received an opioid (opioid group) were selected for quantitative cholescintigraphy with cholecystokinin. Each patient was studied with 111–185 MBq (3–5 mCi) technetium-99m mebrofenin after 6–8 h of fasting. Hepatic phase images were obtained for 60 min, followed by gallbladder phase images for 30 min. During the gallbladder phase, 10 ng/kg octapeptide of cholecystokinin (CCK-8) was infused over 3 min through an infusion pump. Hepatic extraction fraction, excretion half-time, basal hepatic bile flow into the gallbladder, gallbladder ejection fraction, and post-CCK-8 paradoxical filling (>30% of basal counts) were identified. Seven of the patients with SOS were treated with antispasmodics (calcium channel blockers), and one underwent endoscopic sphincterotomy. Mean (±SD) hepatic bile entry into the gallbladder (versus GI tract) was widely variable: it was lower in SOS patients (32%±31%) than in controls (61%±36%) and the opioid group (61%±25%), but the difference was not statistically significant. Hepatic extraction fraction, excretion half-time, and pattern of bile flow through both intrahepatic and extrahepatic ducts were normal in all three groups. Gallbladder mean ejection fraction was 9%±4% in the opioid group; this was significantly lower (P<0.0001) than the values in the control group (54%±18%) and the SOS group (48%±29%). Almost all of the bile emptied from the gallbladder refluxed into intrahepatic ducts; it reentered the gallbladder after cessation of CCK-8 infusion (paradoxical gallbladder filling) in all eight patients with SOS, but in none of the patients in the other two groups. Mean paradoxical filling was 204% (±193%) in the SOS group and less than 5% (P<0.05) in both the control and the opioid group. After treatment, six of the SOS patients had complete pain relief and one, partial pain relief. The basal tonus of the sphincter is variable in patients with SOS, and allows relatively more of the hepatic bile to enter the GI tract than the gallbladder. Due to simultaneous contraction of the sphincter and gallbladder in response to CCK-8, most of the bile emptied from the gallbladder refluxes into intrahepatic ducts, and reenters the gallbladder immediately after cessation of hormone infusion. The characteristic features of gallbladder filling, emptying, and paradoxical refilling with cholecystokinin provide objective parameters for noninvasive diagnosis of SOS by quantitative cholescintigraphy.     

Gallbladder response to a second dose of cholecystokinin during the same imaging study.

Patients on total parenteral nutrition or after prolonged fasting may require treatment with cholecystokinin (CCK) prior to hepatobiliary imaging. Some may also require evaluation of gallbladder (GB) contractility, and the need for a second dose of CCK may arise. It is not clear whether gallbladder function can be adequately evaluated with CCK when a previous CCK dose had already been administered. We studied ten normal subjects to evaluate GB response to a second CCK injection. The subjects received 20 micrograms/kg sincalide in a 3-min infusion prior to administration of technetium-99m disofenin. They then received an identical sincalide dose at 60 min postinjection, and imaging was continued for another 30 min to quantify GB contraction. Gallbladder ejection fraction (GBEF) values ranged from 42-98% (mean: 71.5 +/- 19%). Pretreatment with CCK does not preclude GB contraction evaluation with a second dose of CCK. Expected GBEF values are similar to those obtained with single CCK injections.     

Diagnostic accuracy of 99Tcm-HIDA with cholecystokinin and gallbladder ejection fraction in acalculous gallbladder disease

The diagnostic accuracy and clinical impact of 99Tcm hepatic iminodiacetic acid (HIDA) imaging with cholecystokinin (CCK) was investigated in a prospective study of 359 patients over an 11 year period. All patients presented with right upper quadrant biliary type pain and had a normal ultrasound investigation prior to imaging. CCK was administered as a 3 min infusion at peak gallbladder uptake of HIDA. A gallbladder ejection fraction (GBEF) was used to quantify the gallbladder response to CCK. Two hundred and forty-four of 359 (68%) patients had an abnormal GBEF (< or = 35%). One hundred and thirty-four of 141 (95%) patients who underwent cholecystectomy had abnormal surgical/histological findings and/or relief of symptoms on long-term (mean 5.7 years) follow-up. Clinical follow-up, mean of 5.9 years, of the patients with GBEF > 35% showed 73/79 (92%) of them with little evidence of gallbladder disease. For a total 261 patients with mean clinical follow-up of 5.7 years the sensitivity of GBEF measurement is 95%, specificity is 92% and overall accuracy is 94%. It is concluded that 99Tcm-HIDA imaging, with a 3 min infusion of CCK, is a highly accurate technique and valuable in the diagnostic management of patients with suspected acalculous gallbladder disease.     

Detection of acalculous gallbladder disease using Tc99m EHIDA imaging and cholecystokinin

The use of Tc^99m ethyl hepatic iminodiacetic acid (EHIDA) imaging with cholecystokinin (CCK) in a prospective study of 115 patients with right upper quadrant biliary-type pain is described. All patients had normal US, oral cholecystography and/or endoscopy investigations. A 2-min infusion of CCK was administered at peak gallbladder uptake of EHIDA. A gallbladder ejection fraction (CBEF) was used to quantify the gallbladder response to CCK. A total of 79 of 115 patients (69%) had an abnormal GBEF ( 35%). Of 43 patients who underwent cholecystectomy 42 (97%) had abnormal surgical/histological findings and/or complete long-term relief of symptoms. It was concluded that Tc^99m EHIDA imaging, with a 2-min infusion of CCK and a measured GBEF 35%, is highly predictive of acalculous gallbladder disease and a favourable outcome following cholecystectomy. Correspondence to: G. W. Middleton     

Comparison of gallbladder function obtained with regular CCK-8 and pharmacy-compounded CCK-8.

This study was undertaken to test whether the octapeptide of cholecystokinin (regular CCK-8) and pharmacy-compounded CCK-8 produce similar results with regard to gallbladder function. METHODS: Twenty patients with suspected gallbladder disease were enrolled into quantitative cholescintigraphy. Each patient was infused for 10 min with 3 ng/kg/min of regular CCK-8 and pharmacy-compounded CCK-8, sequentially, with a 30-min interval between the beginning of infusion. The gallbladder ejection fraction, latent period, ejection period, and ejection rate were measured with both agents. RESULTS: Both regular CCK-8 and pharmacy-compounded CCK-8 produce similar, but not identical, results with close correlation between them with reference to all of the measured functions of the gallbladder. There is neither potentiation nor inhibition of the first dose on the effects of the second dose of CCK-8. CONCLUSION: Pharmacy-compounded CCK-8 functions much similar to that of regular CCK-8 as long as an interval of at least 30 min is allowed between doses.     

Constancy and variability of gallbladder ejection fraction: impact on diagnosis and therapy.

The main objective of this study was to test the constancy and variability of gallbladder (GB) ejection fraction (EF) in long-term studies to (a) determine whether EF ever becomes normal once it is low, (b) determine how long it takes for the EF to become abnormal once it is found to be normal, (c) explore the cause of low EF, and (d) define objective parameters for biliary and nonbiliary abdominal pain. METHODS: Fifty-two patients (42 women, 10 men) who underwent quantitative cholescintigraphy twice (total studies, 104), over a mean period of 38.54 mo between studies, were chosen for retrospective analysis. They were divided into the following groups: control (n = 13; nonbiliary abdominal pain), chronic acalculous cholecystitis (CAC) (n = 27; biliary abdominal pain), chronic calculous cholecystitis (CCC) (n = 6; biliary abdominal pain), and opioid (n = 6; nonbiliary abdominal pain). The last group had received an opioid before cholecystokinin-8 (CCK-8) infusion in one study but not in the other study. A GBEF value of > or =35% was considered normal with a 3-min infusion and > or =50% as normal with a 10-min infusion of CCK-8. RESULTS: The mean GBEF value was reproducible between the 2 sequential studies in the control group (66.0% +/- 20.5% vs. 73.9% +/- 17.7%), CAC group (24.4% +/- 22.3% vs. 16.9% +/- 10.9%), and CCC group (20.8% +/- 20.9% vs. 27.5% +/- 34.5%) but not in the opioid group (14.8% +/- 14.6% vs. 56.5% +/- 31.7%). The severity of GBEF reduction in CAC increased with time: 7.2% +/- 8.1% within 12 mo, 16.1% +/- 14.9% in 13-47 mo, and 23.5% +/- 21.3% in 48-168 mo. None of the 27 patients with CAC developed a gallstone as detected by ultrasound during the study period. In 5 patients with CAC, a mean period of 52.6 +/- 28.9 mo was required for conversion from normal to a low EF. CCK-induced cystic duct spasm is the etiology for low EF in both CAC and CCC. CONCLUSION: Normal and low GBEF values are reproducible in long-term studies. Once the EF reaches a low value, it does not return to normal, and a normal value requires many years to become abnormal. CCK-induced cystic duct spasm is the cause of low GBEF in CAC and CCC, and the severity of EF reduction is similar for both. Exclusion of opioid intake immediately before the study is critical before attributing a low GBEF value to an irreversible GB motor dysfunction.     

Gallbladder response to a second dose of cholecystokinin during the same imaging study

Patients on total parenteral nutrition or after prolonged fasting may require treatment with cholecystokinin (CCK) prior to hepatobiliary imaging. Some may also require evaluation of gallbladder (GB) contractility, and the need for a second dose of CCK may arise. It is not clear whether gallbladder function can be adequately evaluated with CCK when a previous CCK dose had already been administered. We studied ten normal subjects to evaluate GB response to a second CCK injection. The subjects received 20 g/kg sincalide in a 3-min infusion prior to administration of technetium-99m disofenin. They then received an identical sincalide dose at 60 min postinjection, and imaging was continued for another 30 min to quantify GB contraction. Gallbladder ejection fraction (GBEF) values ranged from 42–98% (mean: 71.5±19%). Pretreatment with CCK does not preclude GB contraction evaluation with a second dose of CCK. Expected GBEF values are similar to those obtained with single CCK injections.     

Cholecystokinin cholescintigraphy: detection of abnormal gallbladder motor function in patients with chronic acalculous gallbladder disease

CCK cholescintigrams were performed in 374 patients with recurrent postprandial right upper quadrant pain, biliary colic, and a normal gallbladder sonogram and/or cholecystogram. The results of these examinations were correlated with the patients' final medical/surgical diagnoses. Twenty-seven patients recruited as control volunteers without objective clinical evidence of biliary disease also underwent CCK cholescintigraphy to determine if the degree of gallbladder contraction post-CCK differs in symptomatic versus asymptomatic subjects. Decreased gallbladder motor function was identified (maximal gallbladder ejection fraction response to CCK less than 35%) in 94% of patients with histopathologically confirmed chronic acalculous cholecystitis or the cystic duct syndrome and in 88% of patients clinically believed to have chronic acalculous biliary disease. Decreased gallbladder motor function does not distinguish symptomatic from asymptomatic gallbladder disease.     

The dilated common duct sign. A potential indicator of a sphincter of Oddi dyskinesia

The cholescintigraphic findings of a Sphincter of Oddi dyskinesia (SOD) in a 45-year-old woman with persistent right upper quadrant pain and biliary colic are reported. After an overnight fast, the patient was injected with 5 mCi of Tc-99 disofenin and .02 micrograms/kg of cholecystokinin (CCK) post maximal gallbladder filling. Pre and postcholescintiscans were obtained and gallbladder ejection fractions determined. The hepatobiliary scan was normal, except for a delay in biliary-bowel transit. The gallbladder responded normally to CCK, however, the Sphincter of Oddi responded abnormally, as there was a paradoxical response to CCK manifested by a marked dilatation of the common bile duct. We postulate that this dilatation (the dilated common duct sign) was due to an inappropriate response of the smooth muscle of the Sphincter of Oddi (contraction vs relaxation) to CCK and was the cause of this patient's biliary colic. The dilated common duct sign should alert the physician to the possibility of a Sphincter of Oddi dyskinesia.     

Corn oil emulsion: a simple cholecystagogue for diagnosis of chronic acalculous cholecystitis.

This study investigated the use of a corn oil emulsion as an inexpensive alternative to sincalide in the scintigraphic diagnosis of chronic acalculous cholecystitis (CAC). METHODS: Thirty patients with abdominal or right upper quadrant pain underwent (99m)Tc-disofenin hepatobiliary imaging for 60 min. After gallbladder filling, 30 mL of corn oil emulsion were administered orally to all patients followed by dynamic imaging for an additional 60 min in all patients and for 90 min in 26 patients. Gallbladder emptying kinetics were determined with gallbladder ejection fractions calculated at 30, 60, and 90 min. The results were compared with histopathologic or clinical follow-up data. RESULTS: Corn oil emulsion was found to be palatable and free of side effects in all patients. Seven of the 30 patients had histopathologic evidence of CAC, whereas the remaining 23 did not have evidence of gallbladder disease based on clinical follow-up. The 30-, 60-, and 90-min gallbladder ejection fractions were determined to be 25% +/- 22% (mean +/- SD), 47% +/- 28%, and 62% +/- 29%, respectively. Receiver-operating-characteristic analysis showed that the 60-min gallbladder ejection fraction best distinguished between CAC and non-gallbladder disease with an area under the curve of 0.963. A 60-min gallbladder ejection fraction of < or = 20% had 100% sensitivity, 96% specificity, 88% positive predictive value, 100% negative predictive value, and 97% overall accuracy for the diagnosis of CAC. CONCLUSION: Standardized corn oil emulsion appears to be an adequate and well-tolerated gallbladder stimulant. Based on receiver-operating-characteristic analysis, a 60-min gallbladder ejection fraction of < or = 20% using this simple cholecystagogue results in high diagnostic accuracy for CAC.     

The effects of Lipomul, CCK, and TRH on gallbladder emptying

Tc-99m IDA compounds have been used in the quantitative analysis of motor function of the gallbladder. However, stimuli to provoke emptying have been variable and frequently nonphysiologic. To determine the utility and dependability of provocative agents for gallbladder emptying, we studied the effects of Lipomul, CCK, and TRH after the intravenous administration of Tc-99m disofenin. Computer processing of region-of-interest over the gallbladder permitted time/activity analysis of each study and computation of the ejection fraction (EF). Results showed that Lipomul consistently produced an effect on gallbladder emptying (EF 16-42%). CCK, while more dramatic in response, was less predictable (EF 8-100%). TRH favored accumulation of activity and did not cause gallbladder emptying. The combination of CCK and TRH decreased the rate of gallbladder emptying produced by CCK alone. We conclude that the availability, low cost, and dependable effect on gallbladder emptying make Lipomul the gallbladder stimulant of choice for clinical use.     

Quantitative cholescintigraphy: selection of random dose for CCK-33 and reproducibility of abnormal results.

Dynamic cholescintigraphy (DCG) is a valid technique for evaluating gallbladder emptying. Cholecystokinin (CCK) as a slow infusion is recommended as a contraction stimulus. The normal ejection fraction (EF) has been shown to be reproducible, although the reproducibility of abnormal results has not been investigated. The aims of the present study were to standardize the CCK administration method (phase 1), obtain EF normality values (phase 2), and evaluate the reproducibility of abnormal results in patients with clinically suspected gallbladder dysfunction (phase 3). METHODS: Phase 1 included 40 healthy volunteers divided into 4 groups (n = 10) and subjected to intravenous CCK infusion according to 4 different regimens (0.25, 0.30, 0.40, and 0.60 Ivy dog units [IDU]/kg). Phase 2 comprised 33 healthy volunteers for determining DCG normality values, and phase 3 evaluated the reproducibility of abnormal results in 44 patients having clinical manifestations compatible with gallbladder dysfunction and showing an abnormal EF in a previous study. RESULTS: The most effective CCK infusion regimen was 0.40 IDU/kg (3.07 ng/kg) over 20 min, because it afforded the least variability and a high EF. When this regimen was applied to the healthy population, the EF was found to be 74.2% +/- 17.1% (mean +/- SD); the inferior normality limit was estimated to be 40%. Abnormal results were recorded in 77% (95% confidence interval, 62%-89%) of the patients. When the 2 DCG studies of phase 3 were compared, the EF correlation coefficient between them was 0.439 (P = 0.003). CONCLUSION: Slow CCK infusion is the best regimen for stimulating gallbladder contraction; an EF of less than 40% is estimated to represent abnormality. The abnormal results for the EF in patients with clinically suspected gallbladder dysfunction proved to be reproducible.     

Cholecystokinin cholescintigraphic findings in the cystic duct syndrome

Fourteen patients with a cystic duct syndrome (CDS) underwent cholecystokinin (CCK) cholescintigraphy. All patients presented with persistent postprandial right upper quadrant pain and biliary colic. None of the patients had an abnormal oral cholecystography, gallbladder (GB) ultrasound exam or upper GI series. Each patient (NPO after 12 a.m.) received 5 mCi of technetium-99m disofenin. When the GB maximally filled, 0.02 microgram/kg CCK was administered (3 min) intravenously. Background corrected gallbladder ejection fractions (GBEFs) were determined every 5 min X 4 by rationing the pre-CCK GB counts minus post-CCK GB counts to pre-CCK GB counts. GBEFs were: 12% (3 patients), 17% (2), 0%, 1.3%, 3%, 4%, 6%, 11%, 14%, 18.5%, and 22% (1 each). All patients underwent a surgical exploration and all had macro- or microscopically abnormal cystic ducts (five fibrotic, seven elongated and narrow, two kinked) with (12 patients) or without (2 patients) concomitant chronic cholecystitis. No patient with a partially occluded cystic duct with or without concomitant chronic cholecystitis had an ejection fraction that exceeded 22%. In an appropriate clinical setting, a low EF response to CCK should alert the physician to the presence of either chronic acalculous cholecystitis, CDS, or the combination of both.     

Tc-99m-IDA gallbladder kinetics and response to CCK in chronic cholecystitis

The cholecystographic pattern and the contractile response of the gallbladder (GB) to cholecystokinin (CCK) were studied in 101 consecutive patients with uncomplicated chronic cholecystitis confirmed by pathology. Sequential GB images were obtained after administration of 5 mCi 99mTc-Disofenin and the ejection fraction was determined following a 15 min infusion of CCK. Sixteen of 101 (16%) GB failed to visualize up to 4 h; of the remaining patients, 3/85 (4%) showed delayed visualization beyond 1 h, and 82/85 visualized within 1 h. The mean ejection fraction (EF) in 67 patients was 56.9% +/- 27.5% compared to 74.8% +/- 19.8% in a normal control group of 27 subjects (P less than 0.005). However, there was a large overlap as 76% of chronic cholecystitis patients had EF values falling within the full normal range. GB disease could be identified with confidence when the EF was less than 35%, i.e. below the 2 standard deviation range of normal. On the basis of radionuclide kinetic studies alone, the majority of patients with chronic cholecystitis cannot be distinguished from normal.     

Tc-99m-IDA gallbladder kinetics and response to CCK in chronic cholecystitis

The cholecystographic pattern and the contractile response of the gallbladder (GB) to cholecystokinin (CCK) were studied in 101 consecutive patients with uncomplicated chronic cholecystitis confirmed by pathology. Sequential GB images were obtained after administration of 5 mCi ^99mTc-Disofenin and the ejection fraction was determined following a 15 min infusion of CCK. Sixteen of 101 (16%) GB failed to visualize upto 4 h; of the remaining patients, 3/85 (4%) showed delayed visualization beyond 1 h, and 82/85 visualized within 1 h. The mean ejection fraction (EF) in 67 patients was 56.9%±27.5% compared to 74.8%±19.8% in a normal control group of 27 subjects (P0.005). However, there was a large overlap as 76% of chronic cholecystitis patients had EF values falling within the full normal range. GB disease could be identified with confidence when the EF was less than 35%, i.e. below the 2 standard deviation range of normal. On the basis of radionuclide kinetic studies alone, the majority of patients with chronic cholecystitis cannot be distinguished from normal.     

Quantitative cholescintigraphy and bile abnormalities in patients with acalculous biliary pain

Acalculous biliary pain has been related to gallbladder dysfunction that produces a gallbladder emptying defect—a condition which favours the development of lithiasis. It is therefore probable that microlithiasis is present in patients with gallbladder dysfunction. The aims of this study were to measure gallbladder emptying and investigate bile abnormalities in patients with acalculous biliary pain. In 92 consecutive patients, gallbladder emptying was assessed by quantitative cholescintigraphy (abnormal ejection fraction 40%). In 64 patients, a microscopic study was performed on duodenal bile, defining abnormality as the presence of cholesterol crystals in any amount and/or calcium bilirubinate granules and/or microspheroliths at a rate of >10 per slide. The ejection fraction was abnormal in 45 patients (49%) (median 25.1%, range 6.8–39.3%) and normal in the remaining 47 cases (median 71.3%, range 41.0–96.1%). Bile was abnormal in 32 of 64 patients (50%), the most frequent finding being calcium bilirubinate granules. In the patients with bile abnormalities, abnormal ejection fraction was more frequent (20 of 32) and the median ejection fraction was lower (30.9%, range 12.0–94.1%) than in the patients with normal bile (16 of 32 with an abnormal ejection fraction; median ejection fraction 50.7%, range 6.8–96.1%). Abnormal bile was frequent (55.5%) in patients with reduced ejection fraction, but was not uncommon in patients with normal ejection fraction (33.3%). Fewer patients showed no alteration (25%). It is concluded that in most patients, acalculous biliary pain coexists with gallbladder dysfunction or abnormal bile, the combination of both alterations being common.     

Role of cholecystokinetic agents in 99mTc-IDA cholescintigraphy

Cholecystokinin (CCK) and its C-terminal octapeptide analog, Sincalide, have been utilized in two separate roles for the evaluation of gallbladder disease. These are: (1) prior to cholescintigraphy to evacuate the gallbladder and optimized subsequent filling with radiotracers, and (2) to study contractile function of visualizing gallbladders on cholecystography and cholescintigraphy. As a preparation for 99mTc-IDA studies, it clearly facilitates earlier gallbladder filling in patients with chronic cholecystitis, thereby ruling out complete cystic duct obstruction. The problem lies in the fact that the use of CCK as a premedication markedly decreases the sensitivity of the study to detect chronic cholecystitis, since the findings become indistinguishable from patients with normal gallbladders. For this reason, the authors prefer to obtain delayed images, since chronic cholecystitis is frequently associated with gallbladder filling beyond the first hour. The role of CCK in detecting abnormal gallbladder function in the normally visualizing gallbladder also is controversial. Other studies as well as the author's experience suggests that as much as one-forth of positive cases may be associated with normal gallbladders at surgery and often even on microscopic examination. However, most importantly, the great majority of these patients are relieved of their symptoms following surgery. It appears reasonable that CCK or Sincalide cholecystography or cholescintigraphy may be detecting functional abnormalities before anatomic changes occur and can, therefore, serve as a useful examination in selecting symptomatic patients who may benefit from cholecystectomy.     

Delayed biliary-to-bowel transit in cholescintigraphy after cholecystokinin treatment

The authors assessed the influence of cholecystokinin (CCK), administered before cholescintigraphy, on the biliary-to-bowel transit time (BBTT) of technetium-99m disofenin. Fourteen healthy volunteers underwent two separate cholescintigraphic studies with and without CCK treatment. BBTT was less than 1 hour in all 14 studies of subjects not treated with CCK. In 14 subjects treated with CCK, there was no tracer activity in the bowel up to 2 hours in seven (50%) (P = .006). Eighty-three cholescintigrams obtained in patients with suspected acute cholecystitis were also retrospectively analyzed. In 53 of 83 patients in whom the gallbladder was visualized within 1 hour, significantly delayed BBTT was found in 14 of 29 (48%) who received CCK, compared with the BBTT in one of 24 patients (4%) who did not receive CCK (P less than .001). In the 30 patients in whom the gallbladder was never visualized (n = 28) or was visualized after 1 hour (n = 2), BBTT was less than 30 minutes, regardless of whether patients were treated with CCK. Results show that CCK treatment causes significantly delayed BBTT in many cases, and this finding should not be interpreted as abnormal.     

Gallbladder contractility in patients with spinal cord injuries: a sonographic investigation

Approximately 30% of all patients who have spinal cord injuries have gastrointestinal symptoms. One cause is gallstone disease; indeed the literature suggests that gallstones are more common in patients with spinal cord injuries because these patients have impaired contractility of the gallbladder with a reduced ejection fraction. To test this hypothesis, we obtained gallbladder sonograms in 30 patients with spinal cord injuries (16 quadriplegics and 14 paraplegics) and in 32 uninjured age-matched control subjects. Four patients and four asymptomatic control subjects had gallstones and were excluded. The remaining 26 patients and 28 control subjects fasted for 12 hr. Longitudinal and transverse sonograms of the gallbladder were made immediately before the ingestion of 25 g of fat, and at 10, 20, 30, 45, and 60 min thereafter. Gallbladder volumes were measured by using the ellipsoid method. Resting and residual volumes and the emptying times were determined and the ejection fractions were calculated. The ejection fractions were significantly lower (p = .003) in the patients than in the control subjects because the resting volumes were lower than in the control subjects (p = .013). However, the emptying times and residual volumes were the same in the two groups. We conclude that gallbladder contractility is normal in patients with spinal cord injuries and that the lower ejection fraction found in such patients is due to a smaller resting volume.     

Gallbladder function: methods for measuring filling and emptying

Cholescintigraphy with [99mTc] disofenin was used to determine the optimal dose and method of administration of the octapeptide of cholecystokinin, and to determine the kinetics of gallbladder filling and emptying in 22 patients without disease of the liver or gallbladder. The peak filling rate of the gallbladder occurred at 30 min after injection; filling was complete at 1 hr. A 45-min constant intravenous infusion of the octapeptide 20 ng/kg X hr resulted in progressive emptying of the normal gallbladder; the mean ejection fraction at 45 min was 77.2 +/- 4.9%. A 1-min injection of 20 ng/kg resulted in a rapid, short-lived emptying; the mean ejection fraction was 52.2 +/- 9.3%. Doubling or halving the infusion dose produced no greater response or a smaller response. We conclude that a constant 45-min infusion technique is superior to short injection times, because of more complete emptying, no side effects, and more consistent response.