Portal Diameter in the Diagnosis of Esophageal Varices in 266 Cirrhotic Patients: Which Role?

Zardi, Enrico Maria; Uwechie, Valentina; Gentilucci, Umberto Vespasiani; Dobrina, Aldo; Petitti, Tommasangelo; Laghi, V.; Picardi, Antonio; Afeltra, Antonella

doi:10.1016/j.ultrasmedbio.2006.10.002

Cited by 16 publications

(19 citation statements)

References 20 publications

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“…Zardi et al [29] reported that the mean PVD slightly but not significantly increased in patients with portal hypertensive gastropathy; and that the oscillatory trend of PVD from control to large size esophageal variances (EV) might indicate that EV may unload portal pressure in the initial phases of portal hypertension; and concluded that PVD was not able to predict EV or large size EV in a large series of patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Correlation Between Sonographic Portal Vein Diameter and Flow Velocity With the Clinical Scoring Systems MELD and CTP in Cirrhotic Patients: Is There a Relationship?

Shateri

2012

Gastroenterology Research

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Section: Discussionmentioning

confidence: 99%

Correlation Between Sonographic Portal Vein Diameter and Flow Velocity With the Clinical Scoring Systems MELD and CTP in Cirrhotic Patients: Is There a Relationship?

Shateri

2012

Gastroenterology Research

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“…They found that the portal vein diameter in cirrhotic patients was larger in patients with PHG and no esophageal varices (13.0 ± 2.6 mm) than in patients with F1 esophageal varices (12.6 ± 2.3 mm) or F2 esophageal varices (12.9 ± 2.0 mm) (NS). They further supported this concept by finding that patients with portal vein diameter < 12 mm have a significantly higher prevalence of F1 and F2 esophageal varices than patients with a portal diameter between 12-13 mm, and argued that the absence of hepatofugal collateral circulation created by flow inversion, in patients without esophageal varices, left the entire pressure gradient over the portal vein [45] .…”

Section: Location Of Varicesmentioning

confidence: 92%

“…Primignani et al [34] confirmed the correlation of PHG with severity of portal hypertension, by correlating PHG with presence and size of esophageal varices. Sacchetti et al [24] Cirrhosis 142 38 (27%) 28 (20%) 10 (7%) D'Amico et al [25] Cirrhosis 212 130 (61%) 110 (52%) 20 (9%) Calès et al [26] Cirrhosis 100 98 (98%) 57 (57%) 41 (41%) Rabinovitz et al [27] Cirrhosis 510 (43%) Not reported Not reported Iwao et al [28] Cirrhosis 47 32 (68%) 15 (32%) 17 (36%) Taranto et al [29] Cirrhosis 394 317 (80.5%) Not reported Not reported Gupta et al [30] Cirrhosis 230 (61%) (52%) (9%) Iwao et al [31] Cirrhosis 476 254 (53%) 208 (43%) 46 (9%) Carpinelli et al [32] Cirrhosis 566 362 (64%) 192 (34%) 170 (30%) Zaman et al [33] Cirrhosis 120 74 (62%) 47 (39%) 27 (23%) Primignani et al [34] Cirrhosis 373 299 (80%) 127 (34%) 172 (46%) Chaves et al [35] Cirrhosis vs schistosomiasis 43 18 (81%) vs 7 (33%) Not reported Not reported Merkel et al [36] Cirrhosis 62 49 (79%) 29 (46%) 20 (32%) Merli et al [37] Cirrhosis, with mild portal hypertension 222 48 (21%) 43 (19%) 5 (2%) Ito et al [38] Cirrhosis 47 13 (27%) 10 (21%) 3 (6%) De Palma et al [39] Cirrhosis 37 23 (62%) Not reported Not reported Menchén et al [40] Cirrhosis 549 353 (64%) 275 (50%) 77 (14%) Yüksel et al [41] Cirrhosis 114 total 76 (66%) 38 (33%) 38 (33%) Fontana et al [42] Cirrhosis or bridging fibrosis from hepatitis C 1016 374 (37%) 345 (34%) 29 (3%) Bresci et al [43] Cirrhosis 85 36 (42%) Not reported Not reported Akatsu et al [44] End stage liver disease 29 19 (65.5%) 18 (62.1%) 1 (3.4%) Zardi et al [45] Cirrhosis 266 84 (31%) Not reported Not reported Barakat et al [46] Cirrhosis with portal hypertensive duodenopathy 105 105 (100%) 17 (16.2%) 88 (83.8%) Bellis et al [47] Cirrhosis 59 44 (76%) 16 (27%) 28 (47%) Gravante et al [48] Liver transplant candidates with cirrhosis 80 41 (51.2%) Not reported Not reported Canlas et al [49] [58] Cirrhosis 611 448 (73.3%) 37.3% 36% Abbasi et al [59] Cirrhosis 102 87 (85%) Not reported Not reported Ahmed et al …”

Section: (50%) Not Reported Not Reportedmentioning

confidence: 99%

“…Wu et al [68] reported that the rate of moderate or severe PHG was higher in patients with common collaterals [45] proposed that PHG is promoted by minimal collateral circulation because a significant collateral circulation would otherwise reduce portal pressure and gastric mucosal congestion. They found that the portal vein diameter in cirrhotic patients was larger in patients with PHG and no esophageal varices (13.0 ± 2.6 mm) than in patients with F1 esophageal varices (12.6 ± 2.3 mm) or F2 esophageal varices (12.9 ± 2.0 mm) (NS).…”

Section: Location Of Varicesmentioning

confidence: 99%

“…Duan et al [85] reported de novo PHG developed in 13 of 34 patients (38%) after percutaneous transhepatic variceal embolization for massive esophagogastric variceal hemorrhage. These phenomena are attributed to increased portal pressure and flow after eradication of esophageal varices because of redistribution of residual blood flow that had passed through the previously patent varices [5,41,45,81,[86][87][88][89][90] . Itha et al [11] concluded that the significant increase in Lo et al [81] 77 patients with bleeding from EV underwent variceal ligation and were randomized to receive propranolol (37/77) Pre vs post ligation, both groups; P < 0.05; frequency of PHG significantly higher in control group post ligation when compared to propranolol group; P = 0.002 de la Peña et al [82] 93 patients with history of variceal hemorrhage and cirrhosis, randomized to receive either EVS (46/88) frequency and severity of PHG after variceal eradication resulted from decreasing collateral blood flow through esophageal varices causing increasing PHG from gastric mucosal congestion.…”

Section: Esophageal Variceal Eradicationmentioning

confidence: 99%

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Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Portal venous hemodynamics as predictors for the development and grades of esophageal varices in Post‐HCV cirrhotic patients: An Egyptian center study

Salman

Saadawy

et al. 2020

Adv in Digestive Medicine

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There is no consensus regarding the precise predictive role of portal vein hemodynamics for the prediction of esophageal varices. We performed the current prospective work to assess the diagnostic ability of portal vein hemodynamics for the prediction and grading of esophageal varices. The present work is a prospective one performed in the period from April 2014 till September 2017. Two hundred patients with HCV-related cirrhosis with esophageal varices were enrolled in the present work as case group (group I). In addition, 100 cirrhotic cases, with no esophageal varices, were included in the work as control arm (group II). Doppler ultrasound (US) and upper endoscopy were performed to all patients. Case group were further subdivided according grades of esophageal varices into four grades. These grades were correlated to splenic size, portal vein velocity, portal vein caliber, and hepatic artery resistivity index. Cases in group I had significantly larger spleen & portal vein diameter and higher hepatic artery resistivity index than cases in group II (P < .001). The portal vein caliber had the highest diagnostic performance for the detection of esophageal varices with cut-off values of ≥12.5 mm (sensitivity = 99% and specificity = 94%). Patients with grade IV varices had significantly elevated values of splenic diameter, portal vein caliber, and hepatic artery resistivity index; and lower portal vein velocity than other patients with lower grades (P < .001). The same findings were observed with other esophageal varices grades. In conclusion, non-invasive portal hemodynamic parameters are good indicators for the prediction and severity of esophageal varices.

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Portal Diameter in the Diagnosis of Esophageal Varices in 266 Cirrhotic Patients: Which Role?

Cited by 16 publications

References 20 publications

Correlation Between Sonographic Portal Vein Diameter and Flow Velocity With the Clinical Scoring Systems MELD and CTP in Cirrhotic Patients: Is There a Relationship?

Correlation Between Sonographic Portal Vein Diameter and Flow Velocity With the Clinical Scoring Systems MELD and CTP in Cirrhotic Patients: Is There a Relationship?

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Portal venous hemodynamics as predictors for the development and grades of esophageal varices in Post‐HCV cirrhotic patients: An Egyptian center study

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