Intraluminal Pressures Generated During Esophageal Bougienage

Transcription

1 GASTROENTEROLOGY 1981;81:833-7 Intraluminal Pressures Generated During Esophageal Bougienage RICHARD A. KOZAREK, JOHN E. PHELPS, EDWARD K. PARTYKA, and ROBERT A. SANOWSKI Department of Internal Medicine, Section of Gastroenterology, Veterans Administration Medical Center, Phoenix, Arizona Although esophageal bougienage is a widely used palliative procedure for both benign and malignant esophageal strictures, little is known about the pressure generated or applied to the esophageal wall during this procedure. Accordingly, water-perfused catheters were radially implanted into Maloney dilators to monitor esophageal wall pressure in 13 patients undergoing bougienage for reflux-induced lower esophageal strictures. Maximal pressure generated in this group ranged from a low of 25 to a high of 830 mmhg and was generally higher in individuals with newly dilated strictures and with use of larger bougies. In a control group of 11 patients, resting esophageal wall pressure during dilation was 5 mmhg, a value similar to that measured in stricture patients. Maximal pressure occurred in the area of the lower esophageal sphincter and was not statistically higher than sphincter pressure measured with standard rapid pull-through technique. These studies help to define esophageal wall response to bougienage and the pressures generated at the time of esophageal dilation. Esophageal bougienage is a widely used therapeutic modality for treating dysphagia secondary to benign and malignant strictures. While the procedure is generally safe, perforations have been reported (1 17) and presently, endoscopic or fluoroscopic controls are used to guide dilators through tight or complicated strictures (18). Because little is known about the esophageal wall pressure generated during bougienage, we devised a method to measure dilationinduced esophageal wall pressure by externalizing water-perfused polyethylene catheters in sequential Maloney dilators. In this study, we attempt to corre- Received February 3, Accepted June 15, Address requests for reprints to: Richard A. Kozarek, M.D., VA Medical Center, Gastroenterology Section, 7th Street and Indian School Road, Phoenix, Arizona by the American Gastroenterological Association /81/ $02.50 late bougienage-induced increments in esophageal wall pressure in patients with reflux-induced lower esophageal strictures with previously compiled data on experimental esophageal perforation. Such a correlation, in conjunction with additional data on esophageal wall strength in the setting of mucosal disease or intramural fibrosis, may ultimately have clinical efficacy in prevention of dilation-induced esophageal perforation. Material and Methods Three Maloney dilators (sizes: 40, 44, 48 F) were modified to record pressure manometrically. Initially, the mercury was removed and three 1.5-mm holes were drilled radially at the widest part of the tapered tip (Figure 1). Three 0.9-mm (ID) polyethylene catheters measuring 150 em in length were inserted into these openings and threaded through the dilator lumen. The catheters were then imbedded into the wall of the dilator with a cyanoacrylate adhesive. The mercury was subsequently replaced and each catheter brought out through a threeholed rubber stopper. These catheters were connected to an Arndorfer pneumohydraulic capillary infusion system in line with a Cannon strain gauge and Narco physiograph (Figure 2). The response time of this system was greater than 400 mmhg/s. Thirteen patients with reflux-induced strictures of the lower 1/3 of the esophagus, and ranging in age from 42 to 85 years, were subjected to dilation with the modified bougies after informed consent. Approval by the Human Research and Education Committee, Phoenix VA Medical Center, was obtained on January 15, All patients had previously undergone barium swallow and fiberoptic esophagoscopy to localize their strictures as well as standard esophageal manometry using the rapid pullthrough technique (19) to measure the lower esophageal sphincter. Nine of these patients had undergone chronic bougienage (dilator size F) for a period of 1-8 yr prior to this study. Recording with the modified bougie, baseline pressure was defined as atmospheric pressure taken externally at stricture level with the patient seated. After baseline pressure had been recorded, each patient was successively dilated to a level judged to be both therapeutic and safe. The speed of bougie passage was stan-

2 834 KOZAREK ET AL. GASTROENTEROLOGY Vol. 81, No.5 some cases, this necessitated a several second or even a several minute delay to acclimatize the patient to the dilation. Five patients required fluoroscopic documentation of bougie passage through the strictured area, whereas in the remaining 8, endoscopic stricture localization and a long history of previous bougienage, precluded its need. After informed consent, 11 patients with no history of esophageal disease, served as controls. These individuals underwent standard water-perfusion manometry (LES measurements determined by rapid pull-through technique) followed by fluoroscopically directed dilation with a modified 48 F bougie prior to scheduled endoscopy. Three passes of the dilator were undertaken in each control. Mean maximal esophageal pressure achieved with dilation as well as the area in which this pressure was generated was subsequently recorded. Figure 1. Modified mercury-filled dilators (40, 44, 48 French)with three internalized catheters; insert: catheter openings at distal end placed radially. dardized to approximately 1 crn/s and mean maximal esophageal pressures achieved with dilation were recorded in a fashion similar to the rapid pull-through technique of standard manometry (in this case, rapid "pushthrough"). Each patient was instructed not to swallow or Valsalva as the strictured area itself was being entered. In Results Table 1 represents pressure recordings for the 13 stricture patients. Mean LES pressure in this group was 9.8 ± 2 (SEM) mmhg and mean resting esophageal wall pressure with the dilator in the esophagus was 8 mmhg (range 0-26). Dilator size did not affect resting wall pressure. Dilation pressures generated by stricture bougienage ranged between 25 and 830 mmhg. These pressures were generally lower in patients undergoing chronic bougienage (patients 5-13), and were considerably higher in previously untreated individuals (patients 1-4). In general, mean maximal pressure increased with larger dilators. A subgroup of patients with tight strictures (patients 2, 3, 4, 11) developed a pressure curve consisting of a plateau effect, whereas the majority of patients had pressure curves consisting of a peak occurring in the area of tightest stricturing (Figures 3A and 3B). The plateau effect was related to a delay in dilator passage prior to entry into the stomach. With both types of curves, superimposed Pneumotwdraunc Capillary Infusion System SI,;c,u, Catheter Openings Figure 2. Pressure recording system. Dilations are done in sitting position with atmosphericpressure at sternum considered "0" level. RecordingPaper Narco Physiograph

3 November 1981 ESOPHAGEAL BOUGIENAGE 835 Table 1. Pressure Generated with Modified Bougies Dilation pressure (mean maximal mmhg) Patients 40 F 44F 48 F l u u N.D. 3 u u (44) (46) (50) (44) (44) (44) (38) N.D. 12 (42) (46) MeanmmHg (± SEM) 163 (40) 276 (61) 307 (72) c Newly diagnosed strictures; ND = not done; parentheses = previous dilation. Valsalva maneuver and peristaltic waves were sometimes seen (Figure 3B). Peristaltic waves were distinguishable by the configuration (slope, amplitude, duration) of the wave form. Valsalva maneuver also occurred in several patients during actual stricture dilation. This was recognizable clinically and manometrically, and the actual value of bougienage pressure with the peak-type curve was considered to be total pressure measured minus distal esophageal pressure immediately proximal to the stricture. Sequential dilations with the same dilator led to progressively lower mean maximal pressure at the level of the stricture. For this reason, only that pressure level measured with initial dilator passage has been recorded in the table. In the control group, mean resting esophageal wall pressure during bougienage was 6 mmhg, a value not statistically different than that found in the stricture group (p < 0.1). Mean maximal pressure occurred in the area of the LES as documented fluoroscopically and was not significantly higher (p < 0.05) than that recorded with standard manometry (27 vs. 21 mmhg). Despite failure to reach statistical significance, however, there was a trend for higher LES pressure measurements with the dilators when compared with standard manometric technique. Discussion Although esophageal bougienage is a widely used palliative procedure for esophageal stricture related to peptic esophagitis (1,5,12), little is known about the pressure that is generated or applied to the esophageal wall during this procedure. Because of this, we modified standard Maloney dilators by inserting polyethylene catheters and externalizing them in a radial fashion at the widest point of the tapered tip. When connected to a low compliance capillary infusion system and physiograph, use of these dilators allowed continuous esophageal pressure monitoring at the time of bougienage. To define whether passage of a dilator is associ- A Distance From Incisors (cml B Distance From Incisors (ern) Figure 3 A. Pressure (mmhg) generated in distal esophageal stricture plotted against location (em from incisors) with the modified 44 French dilator (peak-type curve). B. Plateau-type curve. Arrows delineate superimposed Valsalva response.

4 836 KOZAREK ET AL. GASTROENTEROLOGY Vol. 81, No.5 ated with significant esophageal wall pressure in nonstrictured individuals, 11 patients who were free of esophageal pathology underwent bougienage with the 48 F dilator prior to a scheduled endoscopy. In this setting, baseline esophageal pressure was slightly positive with respect to atmospheric pressure. This finding, present in both control and stricture patients, is felt to be related to either increased esophageal tone or, more likely, breath holding and a minor degree of Valsalva at the time of dilator passage. During dilation of the control population, individual pressure waves with an amplitude of mmhg, often initiated by swallowing and consistent with primary or secondary peristalsis, were seen. In addition, high-pressure waves ( mmhg) associated with gagging and Valsalva maneuver were delineated. Pressure consistently elevated over baseline, however, was found only in the area of the LES. This pressure, which did not statistically differ from rapid pull-through LES pressure obtained with standard manometry (27 vs. 21 mmhg, p > 0.05), proved reproducible with three dilator passages in each patient. Individuals undergoing esophageal bougienage for peptic stricture, on the other hand, had esophageal wall pressures at the time of stricture dilation ranging from 25 to 830 mmhg. In general, dilation pressures increased as bougie size increased and were higher in newly dilated strictures. These higher pressures correlated with the physician's feeling of stricture "tightness" during initial dilation therapy as well as consistently more patient discomfort when compared with the group of individuals undergoing chronic bougienage. Pressures generated during dilation in the stricture group tended to remain stable or to decrease after multiple dilations with the same bougie. This was felt to be related to stretching or fracture of the stricture itself. In addition to stricture pressures, transient primary or secondary peristaltic waves were delineated in the esophageal body as were high-pressure waves associated with Valsalva or gagging. Whereas swallow-induced contractions in the body of the esophagus were easily defined by the configuration (slope, amplitude, duration) of the peristaltic waves as was Valsalva maneuver, superimposed primary or secondary peristaltic waves may have played a role in the absolute value of dilation pressure measured. This could happen if a peristaltic wave arrived at the level of the stricture at a time simultaneous with its stretching. The slope and characteristics of the pressure wave form generated appear to make this unlikely to be confused with dilation-induced stricture pressure, particularly with the plateau-type curve. However, even if a 40-mmHg peristaltic wave occurred with every stricture dilation and was unable to be differentiated from bougienage pressure, a significant pressure increase still occurs and would have a mean ranging between 123 (163-40) and 267 (307-40) mmhg. Superimposed Valsalva maneuver at the time of stricture stretch may also increase the bougienage pressure and may account for some of the increased LES pressure measured in the control group when compared with standard manometry. Alternatively, this increase may simply be related to increased intragastric pressure (20). A sustained Valsalva maneuver was noted in patients 1, 3, 6, and 10 immediately before and after stricture dilation. Bougienage pressure was defined as maximal pressure minus distal esophageal pressure in patients 2, 6, and 10 (peak-type curve) and as maximal pressure minus the Valsalva peak in patient 3 (plateau-type curve). Clinical efficacy of these dilators remains to be seen. Because esophageal bougienage remains the most common cause of esophageal laceration when tears associated with endoscope passage are excluded (2,3), an attempt to delineate pressures at which the esophagus will lacerate and to compare these with bougienage pressures may be applicable. Such dilation-induced perforations range between 0.04% and 0.2% with flexible dilators such as the Hurst and Maloney (4,5), rising to 0.3% and 1.1% with metal olives and pneumatic dilators respectively (3). These perforations usually occur in the diseased segment (5) and appear related to direct fracture of the stricture or perforation of the esophageal wall by the dilator tip. Pressure data relating to esophageal wall perforation are sparse. Fifty years ago, Burt demonstrated that pneumatically induced rupture of the human cadaver esophagus occurred at a mean pressure of 258 mmhg and was further dependent upon the velocity at which air was insuffiated into the esophagus (21). This value is slightly lower than that currently advised for pneumatic dilation of an achalasia esophagus (approximately 500 mmhg bag pressure) (22), a level of pressure known to be associated with muscular tear. Our data demonstrate that in previously undilated strictures, bougienage pressures exceeding 500 mmhg are not uncommon. Assuming that neither the nature nor the speed of the pressure associated with flexible bougienage is radically different from that associated with pneumatic or bag dilation, pressure levels generated with Maloney dilators in a tightly strictured esophagus would be capable of through-and-through perforation in the nondiseased human cadaver esophagus. Goyal et al., using the rat as a model, has demon-

5 November 1981 ESOPHAGEAL BOUGIENAGE 837 strated that mucosal contribution to esophageal wall strength is minimal until its outer wall diameter is doubled by pneumatic dilation (23). These data suggest that small increments in intraluminal pressure are accommodated by the muscular layers alone and that mucosal strength contributes to esophageal integrity only at higher levels of intraluminal pressure. Mucosal inflammation, in addition to intramural fibrosis, may therefore be an important factor in iatrogenic esophageal rupture in patients undergoing dilation therapy. Although development of this pressure monitoring system adds a new dimension to esophageal bougienage, additional studies to determine the etiology of dilation-induced perforations and to determine the esophageal wall strength in the setting of mucosal disease or intramural fibrosis must be undertaken to establish whether this method has clinical applicability in improving the safety of esophageal bougienage. References 1. Lanza FL, Graham DY: Bougienage is effective therapy for most benign esophageal strictures. JAMA 1978;240: Loop FD, Groves LK: Collective rev iew: Esophageal perforations. Ann Thorac Surg 1970;10: Mandelstam P, Sugawa C, Silvis SE, et al: Complications associated with esophagogastroduodenoscopy and with esophageal dilation. Gastrointest Endosc 1976;23: Triggiani E, Bclsey R: Oesophageal trauma: incidence, diagnosis, and management. Thorax 1977;32: Boyce HW, Palmer ED: Techniques of clinical gastroenterology. Springfield, Illinois: Charles C. Thomas, 1975: Wychulis AR. Fontana RS, Payne WS: Instrumental perforation of th e esophagus. Dis Chest 1969;55: Briggs IN, Germann TO: Traumatic perforations of the esophagus. Surg Clin North Am 1968;48: Hardy JD, Tompkins WC, Ching EC, et al: Esophageal perforations and fistulas. Ann Surg 1973;177: Benedict EB: Peptic stenosis of the esophagus. Am J Dig Dis 1966;11: Jannsen CW [r: Perforation of the intrathoracic oesophagus: A report of 19 cases. Scand J Thorac Cardiovasc Surg 1976; 10: Herrera AF: Reflux esophagitis and esophageal ulcer. In: Bockus HL, ed. Gastroenterology. Philadelphia: WB Saunders, 1974: Williamson RCN: The management of peptic esophageal stricture. Br J Surg 1975;62: Palmer ED, Werts CW: Survey of gastroscopic and esophagoscopic accidents. JAMA 1957;164: Wells CA, Hughes JH, Edwards R. et al: Perforations following dilation of esophageal strictures: A report of three cases with recovery. Thorax 1949;4: Nealon TF, Templeton JY, Cuddy VD, et al: Instrumental perforation of the esophagus. J Thorac Cardiovasc Surg 1961; 41: Jones JD, Bozymski EM: Instrumental esophageal perforation: a possible complication of bougienage following Quinton-Rubin esophageal biopsy. Dig Dis Sci 1979;24: Bill AH [r, Mebust WK, Sauvage LR, et al: Evaluation of techniques of esophageal dilation in relation of the danger of perforation: A study of 441 dilations of benign strictures in children. J Thorac Cardiovasc Surg 1963;45: Pope CE: Gastroesophageal reflux disease. In: Sleisinger MH, Fordtran JS, eds. Gastrointestinal disease. Philadelphia: WB Saunders, 1978: Dodds WJ: Instrumentation and methods for intraluminal manometry. Arch Intern Med 1976;136: Harris LD: The regulation of lower esophageal sphincter strength. In: Gastrointestinal motility: International symposium on motility of the GI tract, Erlangen, July New York: Academic Press, 1971: Burt CA: Pneumatic rupture of the intestinal canal with experimental data showing mechanism of perforation and the pressure required. Arch Surg 1931;22: Vantrappen G, Hellern ans J: Tre atment of achalasia and related motor disorders. Gastroenterology 1980;79: Goyal RK, Biancani P, Phillips A, et al: Mechanical properties of the esophageal wall. J Clin Invest 1971;50: