Chicago Classification v4.0 (CCv4.0) is the updated classification scheme for esophageal motility disorders using metrics from high‐resolution manometry (HRM). Fifty‐two diverse international experts separated into seven working subgroups utilized formal validated methodologies over two‐years to develop CCv4.0. Key updates in CCv.4.0 consist of a more rigorous and expansive HRM protocol that incorporates supine and upright test positions as well as provocative testing, a refined definition of esophagogastric junction (EGJ) outflow obstruction (EGJOO), more stringent diagnostic criteria for ineffective esophageal motility and description of baseline EGJ metrics. Further, the CCv4.0 sought to define motility disorder diagnoses as conclusive and inconclusive based on associated symptoms, and findings on provocative testing as well as supportive testing with barium esophagram with tablet and/or functional lumen imaging probe. These changes attempt to minimize ambiguity in prior iterations of Chicago Classification and provide more standardized and rigorous criteria for patterns of disorders of peristalsis and obstruction at the EGJ.

OBJECTIVES: Altered small-bowel motility, lengthening of the orocecal transit time, and small-intestinal bacterial overgrowth have been described in patients with liver cirrhosis. These changes might be related to the progressive course and poor prognosis of the disease. We investigated the effect of a long-term treatment with cisapride and an antibiotic regimen on small-intestinal motor activity, orocecal transit time, bacterial overgrowth, and some parameters of liver function. METHODS:Thirty-four patients with liver cirrhosis of different etiology entered in the study. They were randomly allocated to receive cisapride (12), an alternating regimen of norfloxacin and neomycin (12), or placebo (10) during a period of 6 months. At entry and at 3 and 6 months, a stationary small-intestinal manometry was performed, and orocecal transit time and small-intestinal bacterial overgrowth were also investigated using the H 2 breath test. Liver function was estimated with clinical and laboratory measurements (Child-Pugh score). RESULTS:After 6 months, both cisapride and antibiotics significantly improved fasting cyclic activity, reduced the duration of orocecal transit time, and decreased small-intestinal bacterial overgrowth. Cisapride administration was followed also by an increase in the amplitude of contractions. No statistically significant variations in these parameters were observed with placebo. An improvement of liver function was observed at 3 and 6 months with both cisapride and antibiotics. CONCLUSIONS:Long-term treatment with cisapride or antibiotics reversed altered small-intestinal motility and bacterial overgrowth in patients with liver cirrhosis. These findings suggest a possible role for prokinetics and antibiotics as a modality of treatment in selected cases of decompensated cirrhosis. (Am J Gastroenterol 2001;96:1251-1255

Because altered intestinal motility could be involved in the pathogenesis of small intestine bacterial overgrowth observed in some patients with cirrhosis, we investigated fasting proximal small bowel motility in 16 cirrhotic patients and 8 healthy controls. In addition, the effects of oral tetracycline administration on duodenal motility were investigated in seven cirrhotic patients with evidence of bacterial overgrowth. The mean duration and characteristics of the migrating motor complex were analyzed. Cyclic activity was observed in all healthy controls. It was absent in two cirrhotic patients showing a prolonged phase 2-like pattern. The duration of cycles was significantly longer in the remaining 14 patients with cirrhosis (166 +/- 19 min) compared with controls (81 +/- 14 min; p < 0.02). This difference was caused by a prolonged phase 2 (138 +/- 19 min in patients with cirrhosis vs. 52 +/- 11 min in controls; p < 0.02). Marked changes in the contraction pattern during phase 2 were noted in cirrhotic patients. They were characterized by multiple clusters (frequency, 12 +/- 1/hr; duration, 38 +/- 3 sec) of contractions (frequency, 11 +/- 1 cpm) separated by quiescent periods (duration, 2.4 +/- 0.2 min). This motility profile filled up 58% +/- 8% of the total duration of phase 2, and it was observed in patients with and without bacterial overgrowth. Treatment with tetracycline was followed by only mild modifications, such as a reduction of the fraction of phase 2 occupied by multiple-clustered contractions. In conclusion, an altered proximal small bowel motility has been observed in patients with cirrhosis. These disturbances appear not to be dependent on the presence of bacterial overgrowth.

SIBO was a frequent finding in obese patients and was associated with an increased pattern of clustered contractions, which was not observed in absence of SIBO.

The Chicago Classification v4.0 (CCv4.0) is the updated classification scheme for esophageal motility disorders using metrics from high‐resolution manometry (HRM). A key feature of CCv.4.0 is the more rigorous and expansive protocol that incorporates single wet swallows acquired in different positions (supine, upright) and provocative testing, including multiple rapid swallows and rapid drink challenge. Additionally, solid bolus swallows, solid test meal, and/or pharmacologic provocation can be used to identify clinically relevant motility disorders and other conditions (eg, rumination) that occur during and after meals. The acquisition and analysis for performing these tests and the evidence supporting their inclusion in the Chicago Classification protocol is detailed in this technical review. Provocative tests are designed to increase the diagnostic sensitivity and specificity of HRM studies for disorders of esophageal motility. These changes attempt to minimize ambiguity in prior iterations of Chicago Classification, decrease the proportion of HRM studies that deliver inconclusive diagnoses and increase the number of patients with a clinically relevant diagnosis that can direct effective therapy. Another aim in establishing a standard manometry protocol for motility laboratories around the world is to facilitate procedural consistency, improve diagnostic reliability, and promote collaborative research.

Abnormal small bowel motility has been described in patients with liver cirrhosis but the mechanisms involved are unknown. The aim was to investigate a possible relationship between the severity of liver failure and the intensity of small intestinal abnormalities. Motility was studied during fasting, by means of perfused catheters and external transducers, on 33 cirrhotics with different etiologies; 8 were at Child-Pugh stage A, 12 stage B, and 13 stage C. Both abnormalities of MMC and increased clustered activity were recorded. Absence of cycling activity was most frequently observed in Child-Pugh stage C patients compared to Child-Pugh stage A cirrhotics. A significant increase in clustered contractions from 4.7 +/- 0.4/hr in stage A patients to 11.3 +/- 1.1 in stage C was recorded. The frequency and amplitude of contractions was also increased from Child-Pugh stage A to stage C. Our findings might be related to a delayed transit time observed in these patients and a higher prevalence of bacterial overgrowth in cirrhotics with more advanced liver disease.

Just as cyclic changes in motility and secretions occur during fasting, recent evidence demonstrates that duodenogastric reflux during fasting is also cyclic and related to the motility and secretory variations. We investigated the characteristics of the migrating motility complex and duodenogastric reflux in 17 patients with gastric ulcer and compared these characteristics to those of 16 healthy subjects. We found three abnormalities of the complex in patients with gastric ulcer: (1) the antral motility was significantly decreased during the phase II of the complex (P less than 0.05) when compared to controls; (2) in about two thirds of them, the phase III of the complex was initiated at the duodenum or more distally; and (3) the mean bile salt concentration in the gastric aspirate was significantly higher (P less than 0.05) than that of the controls. We observed no relationship between the ulcer activity, the location of the crater, and the motility or reflux abnormalities.

We studied the pancreatic secretory response to sham feeding alone or during secretin infusion with and without administration of atropine in 10 human subjects. The magnitude of the response to sham feeding was compared to the response to cholecystokinin octapeptide. Sham feeding alone did not significantly increase pancreatic bicarbonate or amylase secretion above basal values. During a background secretin infusion, there was a significant increase of bicarbonate and amylase output (p < 0.05) during sham feeding. The amylase response was approximately 50% of the maximal response to cholecystokinin octapeptide. In the tests with atropine and secretin, sham feeding still caused a significant increment in amylase and bicarbonate output. We conclude that (1) the pancreatic response to sham feeding is not clearly demonstrated without a background of secretin; (2) during secretin infusion sham feeding is a potent stimulant of pancreatic enzyme secretion, and (3) atropine had no significant effect on the pancreatic response to sham feeding under the conditions of this study.