High-resolution endoluminal sonography assessment of the hematocystic spots of esophageal varices

Schiano, Thomas D.; Adrain, Alyn L.; Vega, Kenneth J.; Liu, Ji‐Bin; Black, Martin M.; Miller, Larry S.

doi:10.1016/s0016-5107(99)70037-4

Cited by 34 publications

(21 citation statements)

References 15 publications

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“…PSCV present in the periesophageal, peri-gastric and perirectal areas are easily seen by EUS. [14][15][16][17][18] Veins on the mucosal aspect can cause gastrointestinal luminal bleeding and those outside the wall may cause extraluminal i.e. pleural or peritoneal bleeding.…”

Section: Order Of Appearance Of Collateralmentioning

confidence: 99%

Collateral Pathways in Portal Hypertension

Sharma

Rameshbabu²

2012

Journal of Clinical and Experimental Hepatology

128

104

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Presence of portosystemic collateral veins (PSCV) is common in portal hypertension due to cirrhosis. Physiologically, normal portosystemic anastomoses exist which exhibit hepatofugal flow. With the development of portal hypertension, transmission of backpressure leads to increased flow in these patent normal portosystemic anastomoses. In extrahepatic portal vein obstruction collateral circulation develops in a hepatopetal direction and portoportal pathways are frequently found. The objective of this review is to illustrate the various PSCV and portoportal collateral vein pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. ( J CLIN EXP HEPATOL 2012;2:338-352) A lmost any vein in the abdomen may serve as a potential collateral channel to the systemic circulation. Presence of abnormal collateral vessels appears to be one of the most sensitive (70-83%) and specific sonographic signs for the diagnosis of portal hypertension. 1 When blood flow through a vessel or a vascular bed is obstructed due to occlusion, as in EHPVO, or distortion, as in liver cirrhosis, collateral pathways open up as blood bypasses the occlusion or obstruction, always flowing down a pressure gradient from a high pressure to a low-pressure vessel or bed. The formation of portosystemic pathways occurs due to reopening of collapsed embryonic channels or reversal of the flow within existing adult veins. 2,3 The number of collateral channels depends on the severity of portal hypertension i.e. the differential gradient driving the flow between the portal and the systemic circulations and the duration of portal hypertension. The more severe and more prolonged the portal hypertension, the higher are the number of portosystemic pathways. However, this traditional hypothesis has been challenged and it has been suggested that the formation of portosystemic collateral circulation may be due in part to angiogenesis driven by vascular endothelial growth factor. 4,5 Almost 50 years have passed since the first detailed description of portosystemic collateral veins (PSCV) in portal hypertension appeared. 6 Precise mapping of PSCV is essential to therapeutic decisions and multidetector computerized tomography (MDCT) is sometimes used for cartography of PSCV. 7 EUS is increasingly being used for evaluation of PSCV and additionally provides an option for performing therapeutic interventions. 8 In addition to PSCV, PPCV pathways are frequently found in extrahepatic portal vein obstruction (EHPVO). The objective of this review is to illustrate the various PSCV and PPCV pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. NORMAL PORTOSYSTEMIC ANASTOMOSESThe left gastric vein (LGV) anastomoses with the esophageal veins, which in turn drain into the azygos vein (AV). The superior rectal vein (SRV) anastomoses with the middle and inferior rectal veins (IRV), which are, respectively, tributaries of the internal iliac and the pudendal veins. The paraumbilical vein (PUV) anastomoses with subcutaneous veins in the anterior abdominal...

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Section: Order Of Appearance Of Collateralmentioning

confidence: 99%

Collateral Pathways in Portal Hypertension

Sharma

Rameshbabu²

2012

Journal of Clinical and Experimental Hepatology

128

104

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“…The simultaneous ultrasound and manometry device, used in this study to measure variceal pressure during peristaltic contraction, is based on prior work using high resolution endoluminal ultrasound (4,5,8,9,11,13,14) and simultaneous ultrasound and manometry to evaluate esophageal motility (6,10,15,16).…”

Section: Discussionmentioning

confidence: 99%

Mechanics and hemodynamics of esophageal varices during peristaltic contraction

Miller

Kim²,

Dai³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Our hypothesis states that variceal pressure and wall tension increase dramatically during esophageal peristaltic contractions. This increase in pressure and wall tension is a natural consequence of the anatomy and physiology of the esophagus and of the esophageal venous plexus. The purpose of this study was to evaluate variceal hemodynamics during peristaltic contraction. A simultaneous ultrasound probe and manometry catheter was placed in the distal esophagus in nine patients with esophageal varices. Simultaneous esophageal luminal pressure and ultrasound images of varices were recorded during peristaltic contraction. Maximum variceal cross-sectional area and esophageal luminal pressures at which the varix flattened, closed, and opened were measured. The esophageal lumen pressure equals the intravariceal pressure at variceal flattening due to force balance laws. The mean flattening pressures (40.11 Ϯ 16.77 mmHg) were significantly higher than the mean opening pressures (11.56 Ϯ 25.56 mmHg) (P Յ 0.0001). Flattening pressures Ͼ80 mmHg were generated during peristaltic contractions in 15.5% of the swallows. Variceal cross-sectional area increased a mean of 41% above baseline (range 7-89%, P Ͻ 0.0001) during swallowing. The peak closing pressures in patients that experience future variceal bleeding were significantly higher than the peak closing pressures in patients that did not experience variceal bleeding (P Ͻ 0.04). Patients with a mean peak closing pressure Ͼ61 mmHg were more likely to bleed. In this study, accuracy of predicting future variceal bleeding, based on these criteria, was 100%. Variceal models were developed, and it was demonstrated that during peristaltic contraction there was a significant increase in intravariceal pressure over baseline intravariceal pressure and that the peak intravariceal pressures were directly proportional to the resistance at the gastroesophageal junction. In conclusion, esophageal peristalsis in combination with high resistance to blood flow through the gastroesophageal junction leads to distension of the esophageal varices and an increase in intravariceal pressure and wall tension. esophageal varices; simultaneous ultrasound and manometry; variceal bleeding ESOPHAGEAL VARICEAL BLEEDING occurs when an expanding force within the varix exceeds the maximum wall tension. Wall tension is an inwardly directed force opposing an outwardly directed expanding force. Wall tension can be calculated by the Laplace equation. The Laplace equation (WT ϭ p v Ϫ p e ϫ r/w) states that the wall tension (WT) is equal to the transmural pressure difference (p v Ϫ p e ) (where p v is the intravariceal pressure and p e is the esophageal lumen pressure) times the radius of the varix (r) divided by the wall thickness (w). Thus this force is directly proportional to the transmural pressure difference and the radius of the varix and inversely proportional to the wall thickness of the varix.No methods are presently available that can measure variceal pressures during a peristaltic contraction of the e...

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“…High-resolution EUS clearly examinates the variceal wall and may demonstrate the haematocystic spots that are saccular aneurysms protruding on the variceal surface; they were assumed to be focal weaknesses of the variceal wall that favour the variceal rupture (87). …”

Section: Endoscopy and Endosonographymentioning

confidence: 99%

Invasive and non-invasive techniques for detecting portal hypertension and predicting variceal bleeding in cirrhosis: A review

et al. 2013

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Portal hypertension is a severe syndrome that may derive from pre-sinusoidal, sinusoidal and post-sinusoidal causes. As a consequence, several complications (i.e., ascites, oesophageal varices) may develop. In sinusoidal portal hypertension, hepatic venous pressure gradient (HVPG) is a reliable method for defining the grade of portal pressure, establishing the effectiveness of the treatment and predicting the occurrence of complications; however, some questions exist regarding its ability to discriminate bleeding from nonbleeding varices in cirrhotic patients. Other imaging techniques (transient elastography, endoscopy, endosonography and duplex Doppler sonography) for assessing causes and complications of portal hypertensive syndrome are available and may be valuable for the management of these patients. In this review, we evaluate invasive and non-invasive techniques currently employed to obtain a clinical prediction of deadly complications, such as variceal bleeding in patients affected by sinusoidal portal hypertension, in order to create a diagnostic algorithm to manage them. Again, HVPG appears to be the reference standard to evaluate portal hypertension and monitor the response to treatment, but its ability to predict several complications and support management decisions might be further improved through the diagnostic combination with other imaging techniques.

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High-resolution endoluminal sonography assessment of the hematocystic spots of esophageal varices

Cited by 34 publications

References 15 publications

Collateral Pathways in Portal Hypertension

Collateral Pathways in Portal Hypertension

Mechanics and hemodynamics of esophageal varices during peristaltic contraction

Invasive and non-invasive techniques for detecting portal hypertension and predicting variceal bleeding in cirrhosis: A review

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