Variceal Pressure Research Articles

Noninvasive endoscopic determination of intravariceal pressure in patients with portal hypertension: clinical experience with a new balloon technique.

Recently, details of a noninvasive balloon manometry technique for endoscopic measurement of variceal pressure (VP) have been published. However, to date, only few data exist on its feasibility and virtually none on its relation to endoscopic or clinical variables of portal hypertension. We investigated a total of 64 patients with esophageal varices using a scaled transparent balloon and a calibrated pressure manometer. Averaged from both fivefold balloon insufflation (variceal collapse) or desufflation (variceal appearance), we took measurements of the VP (mmHg) using the two techniques. These measurements were correlated between two investigators as well as to both clinical and endoscopic signs of portal hypertension. Furthermore, pressures were assessed prospectively before and during propranolol application. Measurements were successful in > 95% of all sessions without side effects. The intraobserver variance was 11.0 +/- 13.1%. Measurements correlated significantly between two observers (r = 0.80, insufflation technique, p < 0.01/r = 0.81, desufflation technique, p < 0.01). Pressures correlated positively to variceal sizes (p < 0.05). The presence of fundic varices was strongly associated with higher pressures (p < 0.02). In patients without medical decompressive therapy we found a significant relationship between VP and the presence of red colour signs or previous bleeding episodes. Clinical parameters did not correlate with VP (p > 0.05). As assessed by this technique, 8/11 patients receiving propranolol showed a decrease in VP (18.6 +/- 19.5% after 1.5 months and 33.3 +/- 11.9% after 3 months). This noninvasive balloon technique is a safe and practical method for estimating VP in patients with portal hypertension. As found by invasive methods, patients with large varices and concomitant fundic varices have higher VP. A drop in intravariceal pressure after propranolol therapy appears to be assessable.

Changes in variceal pressure determined non-invasively by endoscopic balloon manometry prior to and after portal decompression by tips-insertion

Changes in variceal pressure determined non-invasively by endoscopic balloon manometry prior to and after portal decompression by tips-insertion

Variceal pressure is a factor predicting the risk of a first variceal bleeding: a prospective cohort study in cirrhotic patients.

Predictive criteria for a first variceal hemorrhage lack substantial accuracy. Cross-sectional studies suggest a close relationship between variceal pressure (VP) and the occurrence of variceal bleeding. In the present prospective cohort study, the significance of VP measurement for prediction of a first variceal bleed was assessed. Eighty-seven patients with cirrhosis and large esophageal varices who had never developed variceal bleeding were followed for 12 months. The endpoint of the study was the presentation or not of a variceal hemorrhage. Thirty-four patients (39%) were in Child's class A, 37 in class B (43%), and 16 in class C (18%). The median interval between endoscopic diagnosis of varices and the beginning of the study was 15 months. Twenty-eight patients (32%) developed a variceal hemorrhage with a bleeding-related mortality of 18% (n=5). The 1-year mortality overall was 16% (n=14). Variables predictive of a first bleed identified by Cox proportional hazards regression model were: the level of VP, the North Italian Endoscopic Club (NIEC) score, and the interval between the diagnosis of varices and the start of the study. By adding VP to NIEC, a significant gain in prognostic accuracy was obtained (P = .003). In conclusion, the present study provides evidence that the level of VP is a major predictive factor for variceal hemorrhage, and that it provides further prognostic information in addition to the NIEC index.

Endoscopic assessment of variceal volume and wall tension in cirrhotic patients: Effects of pharmacological therapy

BACKGROUND & AIMS: Variceal rupture is believed to occur when variceal wall tension is excessive. The combined use of endosonography, allowing the objective measurement of variceal radius, and endoscopic measurement of transmural variceal pressure may enable assessment of this important parameter. The aim of this study was to assess the effects on variceal hemodynamics of drugs acting through different mechanisms: decreasing portocollateral blood flow (propranolol) or resistance (isosorbide-5-mononitrate [ISMN]).METHODS: Repeated measurements of variceal radius, volume (by endosonography), and transmural pressure (using endoscopic gauge) were performed in 27 cirrhotic patients at baseline and 40 minutes after double-blind administration of placebo (n = 9), propranolol (n = 9), or ISMN (n = 9).RESULTS: Placebo had no effect. Propranolol significantly reduced variceal volume (-32% +/- 26%; P = 0.01), radius (-12% +/- 9%; P < 0.005), and pressure (-26% +/- 10%; P < 0.0001). The resulting decrease in wall tension (-34% +/- 13%; P < 0.0005) exceeded that in transmural pressure (P < 0.01). ISMN reduced transmural variceal pressure (-26% +/- 21%; P < 0.005), but not radius (-3% +/-14%; NS) and volume (-9% +/- 31%; NS).CONCLUSIONS: The combination of endosonography and endoscopic measurement of transmural variceal pressure allows quantitative estimation of variceal wall tension. Propranolol and ISMN reduce similarly transmural variceal pressure. Propranolol, but not ISMN, reduces variceal volume and radius. Therefore, despite similar decreases in variceal wall tension, propranolol may offer a greater therapeutic effect than ISMN in portal hypertension.(Gastroenterology 1997 Nov;113(5):1640-6)

3 Natural history. Clinical-haemodynamic correlations. Prediction of the risk of bleeding

Promoting the development of oesophageal varices and ascites, portal hypertension dominates the clinical course of cirrhosis. Varices appear in patients with portal pressure gradient above 10 mmHg and enlarge in 10–20% within 1–2 years of their detection. Bleeding occurs in patients with portal pressure gradient above 12 mmHg when the wall tension causes the rupture of varices, with an incidence of about 10% per year. Indicators of bleeding risk are portal pressure gradient, variceal pressure, large varices and liver dysfunction. Mortality per bleeding episode is 30–50%. Among survivors 60% will rebleed and 30% will die in the following year. The risk of rebleeding decreases in patients with spontaneous or treatment induced reduction of portal pressure gradinent or variceal pressure. Ascites develops in almost all patients along the course of the disease. Median survival after its appearance is less than 2 years. Less than 5% of cirrhotic patients die without ascites or without a previous bleeding. Thus portal hypertension is a major determinant of survival in cirrhosis.

Total Volume Paracentesis Decreases Variceal Pressure, Size, and Variceal Wall Tension in Cirrhotic Patients

It has been suggested that ascites is a risk factor for variceal bleeding in cirrhotic patients. However, no data of total volume paracentesis (TVP) effects on variceal hemodynamics has yet been published. The aim of this study was to investigate the effects of TVP on variceal pressure, size, and tension in cirrhotic patients. Before sclerotherapy, 18 cirrhotic patients with grade II esophageal varices were studied. The following measurements were performed on 12 patients at basal condition and after TVP: inferior vena cava pressure, esophageal pressure (EP), and intravariceal pressure (IVP) by direct punction and variceal size at endoscopy. The same measurements were performed at basal condition and 1 hour later without TVP on the other 6 patients used as a control group. Variceal pressure gradient (VPG) and variceal wall tension (WT) were calculated. Paracentesis and intra– abdominal pressure were obtained with a direct punction. No demographic differences were observed between both groups. Paracentesis produced a significant reduction of IVP (from 25.6 ± 2.4 to 17.9 ± 2.1 mm Hg, means ± SEM, –30%, P &lt; .05), VPG (from 16.6 ± 2.4 to 10.8 ± 1.4 mm Hg, –35%, P &lt; .05). TVP also reduced variceal size (from 9 ± 0.3 to 5.6 + 0.4 mm, –38%, P &lt; .05) and WT (from 75.3 ± 11.6 to 30 ± 4.7 mm Hg. mm, –60%, P &lt; .05). Intra–abdominal pressure decreased from 18 ± 2.2 to 4 ± 0.9 mm Hg ( P &lt; .05), and IVC decreased from 15.5 ± 2.4 to 5.7 ± 1.5 mm Hg ( P &lt; .05). No significant differences were observed in mean arterial pressure and heart rate. The mean ascitic fluid removed was 8 ± 0.71 L. No significant difference between measurements was observed in the control group. Our results show that TVP significantly decreases variceal pressure and tension. These results suggest that ascites removal can be useful in the treatment of variceal bleeding in cirrhotic patients.

Total volume paracentesis decreases variceal pressure, size, and variceal wall tension in cirrhotic patients

It has been suggested that ascites is a risk factor for variceal bleeding in cirrhotic patients. However, no data of total volume paracentesis (TVP) effects on variceal hemodynamics has yet been published. The aim of this study was to investigate the effects of TVP on variceal pressure, size, and tension in cirrhotic patients. Before sclerotherapy, 18 cirrhotic patients with grade II esophageal varices were studied. The following measurements were performed on 12 patients at basal condition and after TVP: inferior vena cava pressure, esophageal pressure (EP), and intravariceal pressure (IVP) by direct punction and variceal size at endoscopy. The same measurements were performed at basal condition and 1 hour later without TVP on the other 6 patients used as a control group. Variceal pressure gradient (VPG) and variceal wall tension (WT) were calculated. Paracentesis and intra- abdominal pressure were obtained with a direct punction. No demographic differences were observed between both groups. Paracentesis produced a significant reduction of IVP (from 25.6 +/- 2.4 to 17.9 +/- 2.1 mm Hg, means +/- SEM, -30%, P < .05), VPG (from 16.6 +/- 2.4 to 10.8 +/- 1.4 mm Hg, -35%, P < .05). TVP also reduced variceal size (from 9 +/- 0.3 to 5.6 + 0.4 mm, -38%, P < .05) and WT (from 75.3 +/- 11.6 to 30 +/- 4.7 mm Hg. mm, -60%, P < .05). Intra-abdominal pressure decreased from 18 +/- 2.2 to 4 +/- 0.9 mm Hg (P < .05), and IVC decreased from 15.5 +/- 2.4 to 5.7 +/- 1.5 mm Hg (P < .05). No significant differences were observed in mean arterial pressure and heart rate. The mean ascitic fluid removed was 8 +/- 0.71 L. No significant difference between measurements was observed in the control group. Our results show that TVP significantly decreases variceal pressure and tension. These results suggest that ascites removal can be useful in the treatment of variceal bleeding in cirrhotic patients.(Hepatology 1997 Jan;25(1):59-62)

The significance of esophageal variceal pressure in patients with cirrhosis.

We measured the portal circulatory hemodynamic parameters in 10 cirrhotic patients with portal hypertension and esophageal varices to determine the significance of esophageal variceal pressure. In 4 patients (group I), the temporary portal vein occlusion produced significant elevations in both the esophageal variceal pressure and the portal venous pressure. The results of the portal circulatory hemodynamic assessment in this group were consistent with the predominance of the backward flow mechanism. In the remaining 6 patients (group II), however, portal vein clamping resulted in a slightly increased esophageal variceal pressure with an enormous increase in the portal pressure. The forward flow mechanism thus appeared to be predominant in group II. In other words, the results of the pressure measurements were consistent with the functional separation of the hemodynamics in the esophageal varices and portal trunk in group II and the functional hemodynamic continuity in group I. This functional separation between the esophageal varices and the portal trunk in group II might therefore have resulted from the increased blood flow in the lesser splanchnic region.

Use of high-resolution endoluminal sonography to measure the radius and wall thickness of esophageal varices

Background: Measurement of variceal wall tension theoretically provides the most accurate method of predicting future variceal bleeding. Using high-resolution endoluminal sonography in 45 patients with known portal hypertension, we measured and correlated the two previously unmeasured variables involved in the calculation of variceal wall tension (radius and wall thickness) by the Laplace equation. Methods: A 20 MHz 6.2F ultrasound transducer was used to image esophageal varices during standard esophagoscopy. All images were captured on videotape and later reviewed by two blinded investigators. Outer and inner variceal wall circumferences were measured at a cross section of each varix. The radius of each varix and the variceal wall thickness were calculated. The radius of each varix was then correlated with its wall thickness. The interobserver and intraobserver variabilities were measured. Results: The mean variceal radius was .86 ± .34 cm for the inner radius and 1.48 ± .41 cm for the outer radius; mean variceal wall thickness was .099 ± 0.037 cm. Intraobserver and interobserver correlation for the radius was r = .98 and r = .97, respectively. The intraobserver and interobserver correlations for the wall thickness were r = .92 and r = .91, respectively. Variceal radius did not correlate with the wall thickness of the varix. Conclusions: High-resolution endoluminal sonography provides a method for the accurate measurement of esophageal variceal radius and wall thickness. Variceal radius does not correlate with variceal wall thickness, implying that variceal wall tension cannot be accurately estimated by measurement of variceal size alone. Combining these data with measurements of variceal pressure should allow for the direct determination of wall tension and, subsequently, identification of patients at risk for variceal bleeding. (Gastrointest Endosc 1996;44:425-8.)

The effect of long-term treatment with spironolactone on variceal pressure in patients with portal hypertension without ascites

The effect of spironolactone on esophageal variceal pressure (VP) in patients without ascites was investigated. VP was assessed using a noninvasive endoscopic gauge. Spironolactone was administered during a 6-week period at a dosage of 100 mg/d. This treatment decreased VP from 16.8 +/- 1.9 (SD) to 14.1 +/- 2.7 mm Hg (P < .001) in a group of 12 patients and from 18.6 +/- 2.1 to 13.7 +/- 4.1 mm Hg (P < .01) in another group of 8 patients who still had high VP despite chronic intake of propranolol. In both groups, placebo administration to 12 and 8 comparable patients did not significantly alter VP. Spironolactone induced a significant reduction of plasma volume (42.1 +/- 5.5 to 36.1 +/- 6.6 mL/kg body weight, P < .01) and of the concentration of alpha-atrial natriuretic peptide (alpha-ANP) (39.8 +/- 22 to 27.7 +/- 20 pg/mL, P < .01); in addition, a pronounced increase in plasma renin activity (PRA) (1.1 +/- 0.9 to 7.5 +/- 3.4 ng/mL/h, P < .001) was induced by the treatment. No significant changes in systemic hemodynamics were observed during the studies. Severe side effects were not observed except for a high incidence (55%) of painful gynecomasty in the male patients. In conclusion, chronic spironolactone administration effectively lowers VP, even in patients under chronic propranolol therapy. The combination of propranolol and spironolactone deserves further study as a prophylactic therapy of variceal hemorrhage, but development of gynecomasty might be a problem. Finally, we confirmed the reproducibility of VP measurements with the noninvasive gauge in chronic conditions. (Hepatology 1996 May;23(5):1047-52)

The effect of long-term treatment with spironolactone on variceal pressure in patients with portal hypertension without ascites

The effect of spironolactone on esophageal variceal pressure (VP) in patients without ascites was investigated. VP was assessed using a noninvasive endoscopic gauge. Spironolactone was administered during a 6-week period at a dosage of 100 mg/d. This treatment decreased VP from 16.8 ± 1.9 (SD) to 14.1 ± 2.7 mm Hg (P &lt; .001) in a group of 12 patients and from 18.6 ± 2.1 to 13.7 ± 4.1 mm Hg (P &lt; .01) in another group of 8 patients who still had high VP despite chronic intake of propranolol. In both groups, placebo administration to 12 and 8 comparable patients did not significantly alter VP. Spironolactone induced a significant reduction of plasma volume (42.1 ± 5.5 to 36.1 ± 6.6 mL/kg body weight, P &lt; .01) and of the concentration of α-atrial natriuretic peptide (α-ANP) (39.8 ± 22 to 27.7 ± 20 pg/mL, P &lt; .01); in addition, a pronounced increase in plasma renin activity (PRA) (1.1 ± 0.9 to 7.5 ± 3.4 ng/mL/h, P &lt; .001) was induced by the treatment. No significant changes in systemic hemodynamics were observed during the studies. Severe side effects were not observed except for a high incidence (55%) of painful gynecomasty in the male patients. In conclusion, chronic spironolactone administration effectively lowers VP, even in patients under chronic propranolol therapy. The combination of propranolol and spironolactone deserves further study as a prophylactic therapy of variceal hemorrhage, but development of gynecomasty might be a problem. Finally, we confirmed the reproducibility of VP measurements with the noninvasive gauge in chronic conditions.

Effects of isosorbide-5-mononitrate on variceal pressure and systemic and splanchnic haemodynamics in patients with cirrhosis

Background: Isosorbide-5-mononitrate is a long-acting nitrovasodilator which was introduced for the treatment of portal hypertension because of its capacity to reduce portal pressure. In contrast to vasoconstrictors, isosorbide-5-mononitrate acts primarily by decreasing portal-collateral resistance without deleterious effects on liver function, although at high doses, a reflex splanchnic vasoconstriction elicited by the fall in arterial pressure may further decrease portal pressure. However, there is no information on the effects of isosorbide-5-mononitrate on variceal pressure, which is thought to be a major determinant of variceal haemorrhage. Methods: We investigated the effects of isosorbide-5-mononitrate (40 mg, orally; in=12) or placebo ( n=10) on variceal pressure (non-invasive endoscopic gauge) and hepatic haemodynamics in 22 patients with cirrhosis. Results: Placebo administration had no significant effects. In contrast, isosorbide-5-mononitrate significantly reduced variceal pressure (from 13.5±3.6 to 9.8±3.2 mmHg, p<0.005). This was associated with a fall in wedged hepatic venous pressure (from 28±5.8 to 25.9±6.2 mmHg, p<0.005), hepatic venous pressure gradient (from 20±4 to 18±4.7 mmHg, p<0.005) and azygos blood flow (from 668±197 to 597±160 ml/min, p<0.05), suggesting that the decrease in variceal pressure caused by isosorbide-5-mononitrate could be caused by both reductions in collateral resistance and collateral blood flow. Isosorbide-5-mononitrate moderately reduced mean arterial pressure (−13±16%; p<0.005), its fall being directly related to the fall in hepatic venous pressure gradient ( r=0.6, p<0.01). Conclusions: The results of this study show that isosorbide-5-mononitrate markedly and significantly reduces variceal pressure in patients with cirrhosis and provide further support for its clinical use in the pharmacological treatment of portal hypertension.

Assessment of variceal pressure by continuous non-invasive endoscopic registration: a placebo controlled evaluation of the effect of terlipressin and octreotide.

Octreotide has been proposed for the treatment of variceal bleeding. The effects on portal pressure, however, have been variable in published studies. As bleeding is more directly related to pressure in the varices, this study investigated the effect on variceal pressure of octreotide and terlipressin, a vasoactive drug with a well established effect. Variceal pressure was measured during four to eight minutes by a continuous non-invasive endoscopic registration method. Thirty patients in whom a stable variceal pressure recording had been obtained during at least one minute, were randomised to receive either 2 mg terlipressin, 50 micrograms octreotide or an identical volume of saline, as a single intravenous injection given over 60 seconds. For the final analysis three patients had to be excluded because of lack of a satisfactory recording. There were no significant clinical differences between the three groups of patients. Placebo administration did not induce significant changes, but a mean decrease in variceal pressure of -27% was noted with terlipressin, starting from two minutes onwards. Variceal pressure changes after injection of octreotide were variable and the mean change in pressure did not reach statistical significance. Seven of 10 patients showed a temporary increase in variceal pressure. In conclusion, terlipressin induces a significant and progressive decrease in variceal pressure but inconsistent variations of variceal pressure changes were seen after octreotide administration. This is probably related to its effect on central venous pressure. This study also shows that continuous variceal pressure recording with the non-invasive endoscopic registration technique detects in an accurate way the effect of vasoactive drugs on variceal pressure, because placebo injection did not produce significant changes.

Noninvasive variceal pressure measurement may be useful for predicting effect of sclerotherapy for esophageal varices.

This study assessed the relationship between variceal pressure and morphological findings and hemodynamics of esophageal varices as well as the effect of sclerotherapy. Esophageal variceal pressure was measured in 40 patients with portal hypertension, using a noninvasive method. Esophageal variceal pressures were significantly higher in moderate or large varices than they were in small varices. Variceal pressures were significantly higher in patients with red color signs on the varices than in those without. According to the percutaneous transhepatic portography, the structure of the esophageal varices was classified into two types: the bar type and the palisading type. The maximum variceal pressure was significantly higher in the bar type than in the palisading type. In patients who underwent more than five sessions of sclerotherapy, the variceal pressure was significantly higher than in those receiving less than four sessions. These results suggest that variceal pressure may well reflect the vascular pattern and be useful for predicting the effect of sclerotherapy.

Measurement of variceal pressure with an endoscopic pressure sensitive gauge: validation and effect of propranolol therapy in chronic conditions

Aim/Methods: Variceal pressure was measured at endoscopy in 98 patients with a non-invasive, pressure-sensitive gauge technique. Results: In nine patients undergoing sclerotherapy, the values obtained correlated closely with those determined by fine-needle puncture of the varices ( r=0.95, p<0.001). In 15 patients receiving placebo as part of a double-blind, placebo-controlled prospective evaluation of prophylactic treatment with propranolol, variceal pressure did not change significantly over a 1-year period: 16.5±3.2 mmHg at onset: 16.7±3.4 after 3 months and 15.9±3.5 after 12 months. In contrast, propranolol therapy given to 15 patients decreased the pressure from 16.2±3.0 mmHg before therapy to 13.5±2.0 after 3 months ( p<0.001) and to 13.1±4.1 after 12 months ( p<0.05). Patients with a recent bleeding episode had higher pressures than those who had not yet experienced any haemorrhage (19.3±3.5 mmHg, n=17 vs 13.9±3.3, n=62) ( p<0.001). This was confirmed in a prospective study: the last variceal pressure in bleeders and non-bleeders was respectively 17.2±1.7 mmHg ( n=4) and 14.8±4.1 mmHg ( n=26) ( p<0.01). Overall, variceal pressure measurements correlated with the size of varices, the presence of red colour signs and with the North Italian Endoscopic Club score. Conclusions: This study has shown that the non-invasive pressure gauge Varipress® represents a reproducible method to regularly assess variceal pressure, an important parameter related to the risk of bleeding,and to assess the effects of pharmacological therapy with propranolol.

Reduction of esophageal variceal pressure and tension after total volume paracentesis (TVP)

Reduction of esophageal variceal pressure and tension after total volume paracentesis (TVP)

The effect of long-term treatment with spironolactone on variceal pressure in patients with portal hypertension

The effect of long-term treatment with spironolactone on variceal pressure in patients with portal hypertension

Assessment of variceal pressure by continuous non-invasive endoscopic registration: a placebo-controlled evaluation of the effect of terlipressin and octreotide

Assessment of variceal pressure by continuous non-invasive endoscopic registration: a placebo-controlled evaluation of the effect of terlipressin and octreotide

Portal and gastric mucosal hemodynamics in cirrhotic patients with portal-hypertensive gastropathy.

Controversy exists as to the nature of gastric perfusion in portal-hypertensive gastropathy. To investigate portal hemodynamics and gastric mucosal perfusion in cirrhotic patients with and without portal-hypertensive gastropathy, we subjected 56 cirrhotic patients with portal hypertension to portal vein catheterization, pneumatic pressure sensor technique, duplex sonography and laser Doppler flowmetry. Thirteen patients had portal-hypertensive gastropathy: In 10 it was mild, and in 3 it was severe. The presence of portal-hypertensive gastropathy seemed to be independent of age, sex, cause of cirrhosis or grade of esophageal varices. Portal venous pressure, esophageal variceal pressure, portal venous flow and congestion index in patients with portal-hypertensive gastropathy were not significantly different from the values in those without portal-hypertensive gastropathy. However, portal-variceal pressure gradient (subtracting esophageal variceal pressure from portal venous pressure) (p < 0.01) and the incidence of palisading-type esophageal varices on portography (p < 0.05) was increased in patients with portal-hypertensive gastropathy significantly more than in those without portal-hypertensive gastropathy. In the fundus, gastric mucosal blood flow was significantly higher in patients with portal-hypertensive gastropathy than in those without portal-hypertensive gastropathy, whereas in the corpus and the antrum the values were not significantly different. We suggest that the mucosa of the upper stomach in patients with portal-hypertensive gastropathy is congestive and highly perfused. The pathogenesis of portal-hypertensive gastropathy may be related to both congestion and hyperemia in the upper stomach.

Short-term effect of octreotide on intraoesophageal variceal pressure

Short-term effect of octreotide on intraoesophageal variceal pressure