EUS analysis of collateral veins inside and outside the esophageal wall in portal hypertension

Irisawa, Atsushi; Obara, Katsutoshi; Satô, Yukio; Saito, Ayako; Takiguchi, Fujio; Shishido, Hideo; Sakamoto, Hiroaki; Kasukawa, Reiji

doi:10.1053/ge.1999.v50.97777

Cited by 88 publications

(72 citation statements)

References 14 publications

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“…These submucous veins are, thus, the first sites of 'bloodlogging' and become varicose before those upon the outer surface of esophagus in portal hypertension (Figure 1). 13 In patients with oesophageal varices dilated deep intrinsic veins displace the superficial venous plexus, assume a subepithelial position and are easily seen on endoscopy as the red color sign on varices i.e. telangiectasiae, cherry red spots, hemocystic spots and red wale markings or as the varices themselves.…”

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 esophageal varice was divided into three groups: peri-EV, para-EV and perforating veins [14] . The factors associated with the rupture of esophageal varices included the extent and collateral circulation of peri-EV and para-EV [15,16] . Therefore, the acquisition of reliable images for the above mentioned factors will provide valuable information for further treatment implementation and prognosis of the patients.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of paraesophageal varices: A study with 64-row multidetector computed tomograghy portal venography

Zhao¹,

He²,

Chen³

2008

WJG

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AIM:To identify the characteristics of morphology, location and collateral circulation involved in paraesophageal varices (para-EV) of portal hypertension patients with 64-row multidetector computed tomography (MDCT). METHODS: Fifty-two of 501 patients with portal hypertensive cirrhosis accompanied with esophageal varices were selected for 64-row MDCT examination after the observation of para-EV. The CT protocol included unenhanced, arterial and portal phases with a slice thickness of 0.625 mm and a scanning field of 2 cm above the bifurcation to the lower edge of kidney. The CT portal venography (CTPV) was reformatted on AW4.3 workstation. The characteristics of origination, location, morphology and collateral circulation in para-EV were observed. RESULTS: Among the 52 cases of para-EV, 50 showed the originations from the posterior branch of left gastric vein, while the others from the anterior branch. Fifty cases demonstrated their locations close to the esophageal-gastric junction, and the other two cases were extended to the inferior bifurcation of the trachea. The circuitous pattern was observed in 16 cases, while reticulated pattern was seen in 36 cases. Collateral circulation identified 4 cases of single periesophageal varices (peri-EV) communication, 3 cases of single hemiazygous vein, one case of single inferior vena cava, 41 cases of mixed type (collateral communications of at least 2 of above mentioned types) and 3 cases of undetermined communications. Among all the cases, 43 patients showed the communications between para-EV and peri-EV, while hemiazygous vein (43 cases) and inferior vena cava (5 cases) were also involved. CONCLUSION: Sixty-four-row multidetector computed tomography portal venography could display the location, morphology, origin, and collateral types of para-EV, which provides important and referable information for clinical management and disease prognosis.

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“…Endoscopic ultrasonography can detect vascular channels both inside and outside the esophageal lumen. It can map vessels in the connective tissue layer just outside the esophageal wall (periesophageal varices), collateral veins in the mediastinum running longitudinally alone with the esophagus (para-esophageal varices), as well as the perforators that connect the submucosal and peripheral vascular channels [104,105]. Paraesophageal varices and perforating veins are reported in around 80% of patients with esophageal varices, and their presence has been associated with a poor response to endoscopic therapy and early recurrence of varices [30,[106][107][108][109].…”

Section: Application Of Endoscopic Ultrasonography In Variceal Hemorrmentioning

confidence: 99%

Update on Treatment of Variceal Hemorrhage

Sung²

2002

Dig Dis

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Variceal hemorrhage accounts for one third of all deaths related to cirrhosis. To date, many modalities of treating variceal bleeding have been devised, including pharmacological therapy. Treatment of variceal hemorrhage includes resuscitation, initial hemostasis, and prevention of complications and recurrent bleeding. Intravenous vasoactive agents such as terlipressin, somatostatin, octreotide, or vapreotide should be administered in patients with suspected variceal bleeding. Endoscopic treatment remains the mainstay of treatment. Endoscopic variceal ligation is safer and more efficacious than sclerotherapy as initial treatment of bleeding esophageal varices, whereas cyanoacrylate injection is the endoscopic treatment of choice for gastric varices. An adjuvant vasoactive agent is useful for the prevention of early rebleeding. Prophylactic antibiotics are increasingly used for prevention of infection, notably spontaneous bacterial peritonitis. Follow-up endoscopic treatment is necessary in order to obliterate residual varices. The combination of a beta blocker and nitrate is an essential component of secondary prophylaxis for recurrent variceal bleeding. Transjugular intrahepatic portosystemic shunt or surgery offers the best salvage therapy in patients with failed hemostasis or breakthrough recurrent bleeding despite medical and endoscopic therapy. Endoscopic ultrasonography is useful in the prediction of recurrence of varices and facilitates visualization and guidance of further treatment of gastric varices. Despite advances in the treatment of variceal bleeding, liver function remains the determining factor of patient survival. Liver transplantation is the only definitive treatment that can alter the course of the disease.

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EUS analysis of collateral veins inside and outside the esophageal wall in portal hypertension

Cited by 88 publications

References 14 publications

Collateral Pathways in Portal Hypertension

Collateral Pathways in Portal Hypertension

Characteristics of paraesophageal varices: A study with 64-row multidetector computed tomograghy portal venography

Update on Treatment of Variceal Hemorrhage

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