Preliminary experience with balloon dilation of the pylorus.
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Biomedical subjects
Publications and source records attributed to S B Benjamin.
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The authors report 8 cases of erosion of an Angelchik anti-reflux prosthesis into the stomach. Erosion is detected by the appearance of the smooth contour of the device in the stomach. One device migrated distally.
Various complications have been reported recently for the Angelchik antireflux prosthesis, a silicone-gel prosthesis used in the treatment of gastroesophageal reflux and associated hiatal hernia. We have studied the cases of 11 patients with complications of this prosthesis and have reviewed the literature for others. Complications included 8 erosions of the device into the gastrointestinal tract, 1 migration, 1 improper placement, and 1 case believed to be surgical trauma. These complications represent those typical to reflux surgery and some unique to the Angelchik prosthesis (migration and erosion). The exact frequency is unknown, with the manufacturer estimating migration at 0.81% and erosion at 0.15%. Available data indicate that complications may occur up to several years after implantation, and physicians may not recognize the problems with the prosthesis if they are unaware of the complications.
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Symptomatic patients with abnormal esophageal manometry characterized by esophageal peristaltic waves of increased amplitude ("the nutcracker esophagus," NE) have been recognized with increasing frequency. Whether or not this represents a true functional abnormality is unresolved at this time. We have utilized radionuclide transit (RT), a true esophageal function test, to evaluate patients with NE. Eighteen consecutive symptomatic patients with the NE and ten clinically and manometrically normal subjects constituted this study group. RT in normals were 6.8 +/- 0.2 sec (means +/- SE) and 27.6 +/- 3.8 in patients with NE. RT was abnormal in 17/18 patients with NE. Chaotic bolus transit was seen in 11/18 patients with NE but not in normals. The defect was localized to the distal esophagus since transit through the proximal esophagus was not significantly different between the two groups. This defect in RT may be related to spontaneous simultaneous contractions seen in 50% of these patients. Further work will be necessary to determine if NE is a true functional abnormality or a marker for other motility abnormalities such as diffuse esophageal spasm.
The esophagus is thought to be the cause of a large proportion of noncardiac chest pain syndromes. Often this is established solely by exclusion of more serious cardiopulmonary and esophageal-structural diseases. Using currently available manometric technology, a standardized esophageal manometric study and carefully defined values for normal, esophageal motility disorders (EMD) can be clearly defined. The subsequent development of an appropriate and generally agreed on nosology of EMD should serve as a basis for the prospective evaluation of these disorders, hopefully leading to a clear understanding of their exact importance and natural history. If the scientific method is used, order can be brought to this confusing area of clinical medicine.
Thirty-four consecutive patients referred to a gastroenterology clinic with suspected esophageal motility abnormality as a cause of their chest pain or dysphagia, or both, were prospectively studied in an 18-mo period. Peristaltic response to 10 wet (5 ml H2O) swallows was recorded in all studies with a low-compliance infusion system. To provoke symptoms and motility abnormalities after baseline evaluation, all patients had acid infusions (0.1 N HCl) and administration of edrophonium (80 micrograms/kg i.v.), pentagastrin (6 micrograms/kg s.c.), and bethanechol (40 micrograms/kg s.c.). Tracings were coded, read, and interpreted blindly. Baseline tracings were abnormal in 23 of 34 patients (68%), including increased amplitude peristaltic contractions ("nutcracker esophagus") in 10 and nonspecific esophageal motor disorders in 13. Acid infusion produced substernal burning in 3 of 33 patients, in motility change in 1 patient. Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients. Pentagastrin produced chest pain with manometric change in 1 patient. Bethanechol produced chest pain with manometric change in 2 patients. One patient with low amplitude had elevation of esophageal baseline and multiple simultaneous contractions but no chest pain (subsequently developed achalasia). It was concluded that (a) abnormal motility is a common finding in a symptomatic group of patients with presumed esophageal motility disorder, (b) the "nutcracker" esophagus is the most frequent defect, and (c) attempted provocation of symptoms with acid or drugs is not generally effective; however, edrophonium is the best tolerated and most effective of currently available drugs.
It has been shown that the ACAP causes significant increases in the LES pressure of supine primates which are maximal when properly placed at the EGJ. This effect appears to be due to posterior padding of the EGJ in supine animals and can be reproduced by dowel rods or Maloney dilators. Further studies to evaluate the contribution of this effect to the prevention of acid reflux are underway.
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Twenty-one patients referred for evaluation with a diagnosis of questionable ascites were examined independently by three investigators who performed five different physical examination maneuvers. With ultrasonography as the reference standard, six patients had ascites. The sensitivity and specificity of the physical examination maneuvers ranged from 50% to 94% and 29% to 82%, respectively. The overall accuracy of the maneuvers was only 58%. The results of this study indicate that routine physical examination has definite limitations in the precise diagnosis of equivocal ascites. The only conclusion that can be made by a physical maneuver with over 90% accuracy is that ascites is absent if no flank dullness is elicited. Ultrasonography is recommended in questionable cases.
Two patients are presented having lymphomatous involvement of the central nervous system in whom dysphagia was the predominant symptom. All indicated studies failed to reveal evidence of direct esophageal involvement, and the dysphagia improved during treatment of the neural component. Esophageal manometric studies revealed abnormalities of the striated muscle portion of the esophagus. These two case histories suggest that invasion of the central nervous system with lymphoma may produce abnormalities of the neuromuscular control of esophageal function resulting in dysphagia.
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A pathogenetic relationship between hepatic manifestations of alpha 1-antitrypsin deficiency (AATD) and hepatocellular carcinoma has previously been suggested but not established. We encountered three patients with hepatocellular carcinoma (HCC) and nonneoplastic hepatocytes containing globules positive for alpha 1-antitrypsin by immunoperoxidase staining or immunofluorescence microscopy. The AATD was severe in one patient, mild in the second, and not evaluated in the third; any pathogenetic relationship between the deficiency and HCC must therefore remain speculative. Nonneoplastic hepatocytes of all three patients demonstrated copper storage and, in two patients who were not alcoholic, Mallory bodies. Simultaneous presence of copper storage and Mallory bodies has not been reported in liver disease associated with AATD. The pathogenetic mechanisms of these findings are unknown.
Manometric evaluation of pharyngeal contraction and upper esophageal sphincter relaxation was performed in a group of patients with Zenker's diverticulum using a specially designed low compliance manometric recording system. The results were compared with those in normal controls. In all cases, the upper esophageal sphincter showed complete relaxation during swallowing and no incoordination between pharyngeal contraction and upper esophageal sphincter relaxation could be demonstrated compared to time intervals found in the control group. Resting upper esophageal sphincter pressures were significantly lower in diverticulum patients than in controls. It is concluded that symptomatic patients with Zenker's diverticulum have normal pharyngeal-upper esophageal sphincter coordination, exhibit complete upper esophageal sphincter relaxation on swallowing, and have low resting upper esophageal sphincter pressures. These results seriously question the previous concept of abnormalities of pharyngeal-upper esophageal sphincter coordination in patients with Zenker's diverticulum.
We report a patient with a case of Hodgkin's disease, stage IIB, presenting as achalasia. Not only did careful evaluation fail to reveal tumor involvement of the esophagus, but therapy of the Hodgkin's disease failed to improve and, in fact, worsened the dysphagia. Pneumatic dilatation was required after completion of radiation therapy. We still need to evaluate dysphagia in patients with lymphoma by standard means, despite reports of "secondary" achalasia.
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