1Temple University Hospital, Philadelphia 19140; 2The Pennsylvania State University, University Park 16802-1412; 4Thomas Jefferson University Hospital, Philadelphia, Pennsylvania 19107; and 3University of Minnesota, Minneapolis, Minnesota 55455
Submitted 13 January 2004 ; accepted in final form 15 June 2004
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ABSTRACT |
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esophageal varices; simultaneous ultrasound and manometry; variceal bleeding
No methods are presently available that can measure variceal pressures during a peristaltic contraction of the esophagus (13, 7, 12). Our hypothesis, based on the data generated in this study, states that variceal pressure and wall tension increase dramatically during esophageal peristalsis as a natural consequence of the anatomy and physiology of the esophagus and of the esophageal venous plexus.
The objective of this study was to estimate variceal pressure and wall tension and to characterize the mechanical and hemodynamic behavior of esophageal varices during peristaltic contractions. This was done through measurements on patients with esophageal varices and in a model varix system that simulates intravariceal pressure generated during peristalsis.
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MATERIALS AND METHODS |
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This study was approved by the internal review board at Temple University Hospital. Nine patients (8 men and 1 woman with a mean age of 53.1 ± 10.9 yr) with cirrhosis, portal hypertension, and esophageal varices documented on prior outside endoscopy were evaluated in this study. The etiology of the cirrhosis was hepatitis C in two patients, hepatitis B in two patients, alcohol in two patients, hepatitis B and C in one patient, alcohol and hepatitis C in one patient, and cryptogenic in one patient. None of the patients was treated with beta blockers during the study as per the referring physicians. None of the patients had bled from esophageal varices before the study.
Esophageal varices were imaged in cross section with high-frequency endoluminal sonography, using a 20-MHz ultrasonography transducer (Olympus, Tokyo, Japan or Microvasive, Boston Scientific, Boston, MA). The transducer produces a real-time 360° cross-sectional ultrasound image of the esophagus. Real-time images were recorded on Super VHS videotape using a Kayelemetrics swallowing workstation (Kayelemetrics, Lincoln Park, NJ).
A 3F angiography catheter was glued to the ultrasound catheter to measure pressure in the esophageal lumen. A 1-mm side port was made in the angiography catheter at the same level as the ultrasound transducer. The distal end of the catheter was closed with silicon glue, whereas the proximal end was attached to a water-perfused manometry system (Arndorfer, Milwaukee, WI). Water was perfused at a rate of 0.5 ml/min at a pressure of 15 lb./in.2. The manometry system was attached to a Kayelemetrics swallowing workstation, which was then used to synchronize the pressure tracings with the corresponding ultrasound images (Fig. 1).
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Still images were digitized and analyzed by using Image Pro Plus software (Media Cybernetics, Silver Spring, MD). Incomplete or inadequate tracings or images due to artifact were not used for evaluation. The maximum cross-sectional area of the varix at rest and at maximum distension was calculated by the Image Pro Plus software, from the outlined still images of the varix. The image of each varix was outlined at the border of the hyperechoic inner variceal wall and the hypoechoic blood within the varix. The readers of the images were blinded to the pressure data. Pressure measurements were read directly from the data stored and presented on the swallowing workstation.
Ultrasound imaging of the varices, during swallowing of water, showed that the varices initially increased in size, then decreased in size, and then flattened, closed, and opened sequentially. Variceal closure was defined as the first point, on the ultrasound image during the peristaltic contraction at which the hypoechoic blood within the varix was no longer visible in the image. Peak closing pressure was defined as the peak esophageal lumen pressure at which a particular varix closed. Variceal flattening was defined as the point at which the exposed (esophageal lumen) side of the varix flattened during the peristaltic contraction (Fig. 2). Because the videotape of the varices can be run in a forward or backward direction, variceal flattening was usually determined by finding the point of variceal closure and then backing the videotape up to the point of variceal flattening. Variceal opening was defined as the first point at which the hypoechoic blood in the variceal lumen was again visible after variceal closing. The points at which the varix closed, flattened, and opened were identified with the corresponding pressures on the esophageal lumen pressure curves. Variceal flattening, closing, and opening pressures were referenced to baseline esophageal pressure in the resting state. Varices were labeled on the ultrasound image to identify the same varix during multiple swallows. The amplitude of the peak esophageal lumen pressure during the peristaltic contraction was recorded and correlated with the variceal closing pressure to determine whether a relationship exists between the force of the peristaltic contraction and the intravariceal pressure.
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Patients were contacted every 6 mo after the initial study to determine whether they experienced any bleeding or were hospitalized for bleeding. If the patients were hospitalized for bleeding, their medical records were reviewed to determine the site of bleeding (variceal vs. nonvariceal) and the time of bleeding with respect to the original simultaneous ultrasound/manometry test. Peak closing pressures in patients that bled were compared with peak closing pressures in patients that did not bleed using an unpaired Students t-test.
Esophageal Variceal Swallowing Models
The varix model (Fig. 3) consisted of a thin narrow latex balloon, used to simulate a varix, placed inside a thicker and wider polyethylene tube, used to simulate the esophagus. The size, consistency, and material used for the model varix and model esophagus were chosen to simulate an actual esophageal varix and an actual esophagus as closely as possible. The latex balloon was attached to an open hydrostatic reservoir so that the balloon was filled with water at a constant pressure. The resting model varix pressure (pressure in the varix with the varix at rest) was chosen to simulate actual intravariceal resting pressures. A simultaneous ultrasound probe and manometry catheter was placed in the distal portion of the model varix and a pressure transducer was placed in the model esophagus at the same level 1 cm from a plastic electrical tie. The electrical tie was used to narrow the balloon to simulate the resistance due to the palisade vessels at the gastroesophageal junction.
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A second study was performed by using the same varix model to determine the effects of varying the resistance of the distal portion of the varix on the pressure and cross-sectional area of the varix during the simulated peristaltic contraction. The latex (varix) balloon was attached to the open hydrostatic reservoir so that the balloon was filled with water at a stable pressure of 10 mmHg. Four restrictions with electrical ties were used to decrease the cross-sectional area of the distal portion of the model varix (47, 67, 77, and 87% of the cross-sectional surface area of the original latex balloon). An individual balloon model was set up for each restriction. Ten simulated swallows were performed for each restriction. Peak pressures and peak distensions were correlated to the percent restriction in the varix model using a Pearson correlation coefficient.
Statistical Analysis
Statistics are reported as means ± SD. Statistical significance is analyzed by using the paired Students t-test and Pearson correlation coefficient. P < 0.05 was considered significant.
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RESULTS |
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Forty varices and sixty-three swallows were evaluated in nine patients. The mean closing pressure (43.8 ± 23.8) and flattening pressure (40.1 ± 16.8) were significantly higher than the mean opening pressure (11.6 ± 25.6) (P < 0.0001). Flattening pressures >80 mmHg (relative to resting esophageal pressure) occurred in varices during peristaltic contractions in 15.5% of swallows. Flattening pressures >100 mmHg relative to the resting esophageal pressure occurred in 4.5% of swallows. The interobserver variability, between the two blinded readers, for the closing pressure was very low with a correlation coefficient value of r = 0.97.
There was a strong correlation between the peak esophageal lumen pressure and the variceal closing pressure in the seven varices in which three or more swallows could be evaluated (r between 0.78 and 0.99). There was no correlation between variceal closing or flattening pressure and the maximum distension of the varix during the peristaltic contraction (r = 0.10). The varices distended, with a mean peak increase in cross-sectional surface area of 41% (range 789%), from a baseline mean of 0.29 cm2 to an average maximum of 0.41 cm2 during the peristaltic contraction (an increase in average variceal radius of 64%; P < 0.0001; Fig. 4).
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Varix Model Results
Varix model to determine the flattening pressures (74% restriction). The mean intravariceal pressure at the point at which the varix wall flattened was 63.1 ± 15.4 and 63.1 ± 14.9 mmHg (Fig. 5). The mean esophageal pressure at the point at which the varix wall flattened was 63.4 ± 15.9 and 62.9 ± 14.9 mmHg. The mean percent difference between the actual varix model pressure and the esophageal lumen pressure at the point at which the varix wall flattened was 3.8 ± 2.8 and 4.5 ± 2.8%. The correlation between the model esophageal and model varix pressures at the point at which the varix wall flattened was r = 0.98 and r = 0.98. The correlation between the two readers was r = 0.99 for both the variceal and esophageal pressures. The model esophageal and model variceal pressures at the point at which the varix wall flattened were statistically identical (P = 0.98). The point at which the model variceal pressure equaled the model esophageal pressure (variceal flattening) was always on the upslope of the esophageal model pressure curve and always on the down slope of the variceal model pressure curve and was less then the mean peak variceal pressure by an average of 34% (Fig. 6).
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DISCUSSION |
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Force balance laws explain why, at the point of variceal flattening, the esophageal lumen pressure is equal to the intravariceal pressure. By using this method, the pressure within the varix at variceal flattening can be unambiguously inferred from the measured esophageal lumen pressure. The flattening pressures of the varices during peristalsis were found to be significantly higher than would be expected on the basis of previous invasive and noninvasive measurements of intravariceal pressure while the esophagus is at rest.
The variceal cross-sectional surface area was measured throughout the peristaltic contraction sequence and was found to increase significantly during the phase of lumen distension just before the rise in the esophageal lumen pressure.
The above observations may be explained by considering the anatomy and physiology of esophageal varices. Varices, which are tubular vascular structures, run longitudinally in the body of the esophagus. The anatomy of esophageal varices in the body of the esophagus differs dramatically from the anatomy of the varices at the gastroesophagaeal junction. The venous structure of esophageal varices in the body of the esophagus is truncal. Truncal anatomy consists of a few large columns of varices. The venous structure of esophageal varices at the gastroesophageal junction consists of palisade vessels. The palisade veins consist of numerous tiny vessels. The total cross-sectional area of the varices in the palisade area is 74% less than in the truncal zone of the esophagus as determined previously by Schiano et al. (15).
We suggest that during peristaltic contraction the blood flow in esophageal varices reverses direction. Blood in varices normally flows via the gastric varices through the palisade vessels at the gastroesophageal junction and into the truncal varices in the body of the esophagus in a caudal to oral direction (distal to proximal in the esophagus). During the peristaltic contraction, a wave of pressure is propagated in an oral to caudal direction (proximal to distal in the esophagus), pushing the blood from the proximal portion of the varix to the distal portion of the varix and effectively reversing the blood flow in the varix. This movement is analogous to fluid being pushed down the lumen of the esophagus toward the stomach during swallowing. The resistance to blood flow at the gastroesophageal junction, due to the relative decrease in vessel cross-sectional area, causes the pressure within the distal truncal varices to rise dramatically during the peristaltic contraction.
The varix model demonstrated excellent correlation between the flattening pressure as measured by the observers from the esophageal lumen pressure at the point of variceal flattening and the actual measured pressure within the model varix. In addition, there was excellent correlation between the observers.
The model varix study in which the distal resistance was varied demonstrated that a small change in the resistance at the distal portion of the varix can have a profound effect on the pressure generated within the varix during the peristaltic contraction. At a physiological resistance of 77% decrease in cross-sectional area [based on the Schiano study (15)], the pressures generated corresponded very closely to the closing and flattening pressures observed in actual varices.
Another observation demonstrated by the varix model system was that the peak intravariceal pressures during the peristaltic contraction were much higher (an average of 34% higher) than the variceal flattening pressures (Fig. 6). This suggests that the flattening pressures measured in the actual varices probably underestimated the maximum intravariceal pressures generated during the peristaltic contraction. In addition, the varix model demonstrated that the maximum transmural pressure difference occurred coincidently with the maximum variceal distension during the peristaltic contraction, thus maximizing the variceal wall tension.
Although the number of patients in this series was small, it was found that the mean peak closing pressures in patients that experienced future variceal bleeding were significantly higher than the mean peak closing pressures in patients that did not experience variceal bleeding (P < 0.04). Patients with a mean peak closing pressure >61 mmHg were found to be more likely to bleed. The accuracy of predicting future variceal bleeding in this small series, based on these criteria, was 100%.
In conclusion, taken together, the clinical findings and the findings of the varix model confirm the hypothesis that peristaltic contraction increases the pressure, cross-sectional area, and wall tension in the distal portion of esophageal varices and may have negative consequences in terms of variceal bleeding. It may be possible, in the future, to use this technique to measure variceal pressures during peristaltic contraction to predict future variceal bleeding.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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