Size Of Varices Research Articles

INDICATION OF TREATMENT FOR ESOPHAGEAL VARICES: WHO AND WHEN?

Variceal bleeding is a major cause of death in patients with liver cirrhosis. However, indication (to whom) and timing (when) of the treatment for patients who have never had previous variceal bleeing is not completely established. Given the poor outcome associated with variceal bleeding, the identification of those at high risk and the prevention of a first bleeding episode are critical objectives. Clinical factors associated with an increased risk of a first variceal bleeding include continued alcohol use and poor liver function. Endoscopic predictive factors for the risk of bleeding are large size of varices and presence of red signs on the varices. Current recommendations for primary prophylaxis pertain only to cirrhotics with large varices. However, more patients with small varices will bleed than those with large ones. Non‐selective beta‐blockers are the prophylactic therapy of choice in patients with medium‐sized/large varices, irrespective of the severity of liver dysfunction. Beta‐blockers should be continued life long. Endoscopic variceal band ligation should be contemplated in high‐risk patients who have contraindications or side effects of beta‐blockers. It is salutary to remember that prophylactic sclerotherapy caused harm and its use was abandoned. The use of venodilators (nitrates) alone should be discouraged because there is as yet no proof of their efficacy and evidence suggests that they could worsen the already altered circulatory state of the cirrhotic patient. In patients with small varices, follow‐up endoscopy should be performed every 1–2 years because the risk of bleeding is so small.

Farbkodierte Dopplersonographie: ein verlässliches Verfahren zur Erkennung des Risikos von Ösophagusvarizen-Blutung bei Patienten mit Leberzirrhose

The aim of the study was to examine the role of Doppler ultrasonography of the portal vein in predicting esophageal variceal bleeding in patients with liver cirrhosis and portal hypertension by comparing the ultrasound data to the endoscopic findings. 99 patients with liver cirrhosis and esophageal varices underwent color Doppler ultrasonography and esophagogastroduodenoscopy. The following portal hemodynamic parameters were analyzed: diameter and cross-sectional area, mean blood flow velocity, blood flow volume, perfusion pressure gradient, congestion index, and platelet count-to-spleen diameter ratio. Variceal characteristics, the size and the presence of red signs, were determined by endoscopic examination. Patients with variceal red signs had significantly higher values of portal diameter (1.538 +/- 0.246 vs. 1.243 +/- 0.167), cross-sectional area (1.286 +/- 0.448 vs. 0.945 +/- 0.256), blood flow volume (965.520 +/- 432.728 vs. 625.117 +/- 320.999) and congestion index (0.165 +/- 0.068 vs. 0.126 +/- 0.051) than patients without red signs, while the perfusion pressure gradient (0.260 +/- 0.087 vs. 0.447 +/- 0.271) and the platelet-to-spleen ratio (522.424 +/- 222.823 vs. 708.921 +/- 230.769) were lower. The same pattern of differences between the ultrasound parameters was found in patients with large varices comparing ones with red signs to the ones without them (diameter, 1.567 +/- 0.234 vs. 1.258 +/- 0.175; cross-section, 1.313 +/- 0.455 vs. 1.061 +/- 0.264; flow volume, 988.195 +/- 443.353 vs. 739.423 +/- 414.281; congestion index, 0.171 +/- 0.067 vs. 0.130 +/- 0.058; perfusion pressure gradient 0.247 +/- 0.078 vs. 0.501 +/- 0.379 and platelet-to-spleen ratio 479.930 +/- 184.302 vs. 699.094 +/- 316.171). Differences in values of ultrasonographic parameters were less obvious among groups of patients with different variceal sizes: only the diameter, cross-sectional area and blood flow volume were significantly different. The mean blood flow velocity did not depend on the variceal size or on the presence of red signs. The sensitivities and specificities of the analyzed parameters were 60-80% and 48.6-78.4%, respectively. Results suggest that color Doppler ultrasonography is a useful noninvasive method for evaluating the risk of esophageal variceal bleeding in patients with liver cirrhosis.

Causes of portal venous thrombosis in cirrhotic patients: the role of genetic and acquired factors

We compared frequencies of three common prothrombotic mutations (factor V Leiden, the G20210A mutation of the prothrombin gene, and homozygosity for C677T methylenetetrahydrofolate reductase) in 219 cirrhotic patients, 43 with and 176 without portal vein thrombosis (PVT). The following variables were related to PVT: prothrombin levels, platelet count, Child-Pugh classification, previous abdominal surgery, number of decompensation events, size of varices, red markers on varices, and sclerotherapy. All patients were followed up for a mean period of 18 months (range 10-30). Prothrombotic mutations were detected in 64 of the 219 cirrhotic patients (29.2%), at equal frequency in patients with or without PVT. At univariate analysis, PVT was associated with Child-Pugh classes B and C, signs of liver decompensation, large varices with red markings, sclerotherapy, and abdominal surgery. At multivariate analysis, PVT was associated with sclerotherapy [odds ratio (OR) 4.9, 95% confidence interval (CI) 2.2-11] and previous surgery (OR 2.8, 95% CI 1.2-6.3). The combination of the two acquired factors increased the risk of PVT, whereas the combination of local with genetic defects did not. Only a single patient with genetic thrombophilia and without PVT at inclusion developed the complication during follow-up, concomitantly with the development of hepatocellular carcinoma. In cirrhotic patients prothrombotic mutations by themselves are not causative of PVT. Sclerotherapy and previous abdominal surgery favour the development of two-thirds of cases of PVT; in the remaining cases the pathogenesis remains elusive.

Primary prophylaxis of variceal bleeding in cirrhotics unable to take β‐blockers: a randomized trial of ligation

To compare endoscopic banding ligation vs. no treatment in cirrhotics with intolerance or contraindications to beta-blockers for prevention of first bleeding in portal hypertension. A sample size of 214 was planned with all sizes of varices. However, the trial was stopped due to increased bleeding in 52 patients in the ligation group. The baseline severity liver disease and endoscopic features were similar. Ligation group: 25 (M/F = 21/4, mean age: 60 +/- 9.37 years); 27 not-treated group: 27 (M/F = 17/10, mean age: 63 +/- 10.27). The mean follow-up period was 19.5 +/- 13.3 months: five bled in the ligation group (20%), three from varices (two after banding at 11 and 17 days; one during the procedure), and two from gastropathy; two bled in the not-treated group (7%- two both varices) (P = 0.24). There were seven deaths in the ligation group and 11 in the not-treated group (P = 0.39). Sixty per cent of the bleeding in the banding group was probably iatrogenic, requiring the study to be stopped. Endoscopic banding ligation was no better than no treatment. This study suggests that ligation may be harmful when used as primary prophylaxis, similar to prophylactic sclerotherapy in the past.

Evolving Consensus in Portal Hypertension Report of the Baveno IV Consensus Workshop on methodology of diagnosis and therapy in portal hypertension

Portal hypertension is associated with the most severe complications of cirrhosis, including ascites, hepatic encephalopathy, and bleeding from gastro-esophageal varices. Despite the progress achieved over the last decades, the 6-week mortality associated with variceal bleeding is still in the order of 10–20%. Awareness of the difficulty inherent to the evaluation of diagnostic tools and the design and conduct of good clinical trials for the treatment of portalhypertensionhas led to theorganization, since1986,of a series of consensus meetings. The first one was organized by Andrew Burroughs in Groningen, The Netherlands [1]. After Groningen, other meetings followed, in Baveno in 1990 (Baveno I) [2] and in 1995 (Baveno II) [3,4], in Milan in 1992 [5], in Reston, USA, in 1996 [6], in Stresa in 2000 (Baveno III) [7,8], again in Baveno in 2005 (Baveno IV) [9,10], and in Atlanta in 2007 [11]. The aims of these meetings were to develop definitions of key events in portal hypertension and variceal bleeding, to review the existing evidence on the natural history, the diagnosis and the therapeutic modalities of portal hypertension, and to issue evidence-based recommendations for the conduct of clinical trials and the management of patients. All these meetings were successful and produced consensus statements on some important points, although some issues remained unsettled. To continue the work of the previous meetings, a Baveno V workshop was held on May 21–22, 2010. The workshop was attended by many of the experts responsible for most of the major achievements of the last years in this field. Many of them had attended the previous meetings as well. The main fields of discussion of the Baveno V workshop were the same as in Baveno I–IV, i.e. the definitions of key events concerning the bleeding episode and the therapeutic options in patients with portal hypertension. For each of these topics, a series of consensus statements were discussed and agreed upon. As in Baveno IV, whenever applicable, the level of existing evidence was evaluated and the recommendations were ranked according to the Oxford System [12] (i.e.: level of evidence from 1 = highest

Congenital absence of the portal vein with splenomegaly in a young woman (Case Report)

Congenital Absence of the Portal Vein (CAPV) is a rare anomaly in which the intestinal and splenic venous drainage bypasses the liver and drains into the systemic veins through various venous shunts. We present a case of a 32-year-old woman with this malformation, the patient experienced hematemesis and melena repetitively and had splenomegaly and hypersplenism. The angiography demonstrated absence of portal vein. Splenectomy was performed to reduce the pressure of the veins around stomach and to correct the hypersplenism. In endoscopy examination six months after surgery, the esophageal varices had disappear and the size of gastric varices had decrease. (Med J Indones 2005; 14: 122-7) Keywords: Congenital absence of portal vein, splenomegaly, hypersplenism, hematemesis and melena

211 In patients with cirrhosis, liver stiffness measurement (LSM) predicts the presence and size of oesophageal varices (OV) more accurately than portal gradient (PG)

211 In patients with cirrhosis, liver stiffness measurement (LSM) predicts the presence and size of oesophageal varices (OV) more accurately than portal gradient (PG)

Hemodynamic analysis of esophageal varices in patients with liver cirrhosis using color Doppler ultrasound

To study the portal hemodynamics and their relationship with the size of esophageal varices seen at endoscopy and to evaluate whether these Doppler ultrasound parameters might predict variceal bleeding in patients with liver cirrhosis and portal hypertension. One hundred and twenty cirrhotic patients with esophageal varices but without any previous bleeding were enrolled in the prospective study. During a 2-year observation period, 52 patients who had at least one episode of acute esophageal variceal hemorrhage constituted the bleeding group, and the remaining 68 patients without any previous hemorrhage constituted the non-bleeding group. All patients underwent endoscopy before or after color Doppler-ultrasonic examination, and images were interpreted independently by two endoscopists. The control group consisted of 30 healthy subjects, matched to the patient group in age and gender. Measurements of diameter, flow direction and flow velocity in the left gastric vein (LGV) and the portal vein (PV) were done in all patients and controls using color Doppler unit. After baseline measurements, 30 min after oral administration of 75 g glucose in 225 mL, changes of the diameter, flow velocity and direction in the PV and LGV were examined in 60 patients with esophageal varices and 15 healthy controls. The PV and LGV were detected successfully in 115 (96%) and 105 (88%) of 120 cirrhotic patients, respectively, and in 27 (90%) and 21 (70%) of 30 healthy controls, respectively. Among the 120 cirrhotic patients, 37 had F1, 59 had F2, and 24 had F3 grade varices. Compared with the healthy controls, cirrhotic group had a significantly lower velocity in the PV, a significantly greater diameter of the PV and LGV, and a higher velocity in the LGV. In the cirrhotic group, no difference in portal flow velocity and diameter were observed between patients with or without esophageal variceal bleeding (EVB). However, the diameter and blood flow velocity of the LGV were significantly higher for EVB (+) group compared with EVB (-) group (P < 0.01). Diameter of the LGV increased with enlarged size of varices. There were differences between F1 and F2, F1 and F3 varices, but no differences between F2 and F3 varices (P = 0.125). However, variceal bleeding was more frequent in patients with a diameter of LGV >6 mm. The flow velocity in the LGV of healthy controls was 8.70+/-1.91 cm/s (n = 21). In patients with liver cirrhosis, it was 10.3+/-2.1 cm/s (n = 12) when the flow was hepatopetal and 13.5+/-2.3 cm/s (n = 87) when it was hepatofugal. As the size of varices enlarged, hepatofugal flow velocity increased (P < 0.01) and was significantly different between patients with F1 and F2 varices and between patients with F2 and F3 varices. Variceal bleeding was more frequent in patients with a hepatofugal flow velocity >15 cm/s (32 of 52 patients, 61.5%). Within the bleeding group, the mean LGV blood flow velocity was 16.6+/-2.62 cm/s. No correlation was observed between the portal blood flow velocity and EVB. In all healthy controls, the flow direction in the LGV was hepatopetal, toward the PV. In patients with F1 varices, flow direction was hepatopetal in 10 patients, to-and-fro state in 3 patients, and hepatofugal in the remaining 18. The flow was hepatofugal in 91% patients with F2 and all F3 varices. Changes in diameter of the PV and LGV were not significant before and after ingestion of glucose (PV: 1.41+/-1.5 cm before and 1.46+/-1.6 cm after; LGV: 0.57+/-1.7 cm before and 0.60+/-1.5 cm after). Flow direction in the LGV was hepatopetal and to-and-fro in 16 patients and hepatofugal in 44 patients before ingestion of glucose. Flow direction changed to hepatofugal in 9 of 16 patients with hepatopetal and to-and-fro blood flow after ingestion of glucose. In 44 patients with hepatofugal blood flow in the LGV, a significant increase in hepatofugal flow velocity was observed in 38 of 44 patients (86%) with esophageal varices. There was a relationship between the percentage changes in flow velocity and the size of varices. Patients who responded excessively to food ingestion might have a high risk for bleeding. The changes of blood flow velocity in the LGV were greater than those in the PV (LGV: 28.3+/-26.1%, PV: 7.2+/-13.2%, P < 0.01), whereas no significant changes in the LGV occurred before and after ingestion of glucose in the control subjects. Hemodynamics of the PV is unrelated to the degree of endoscopic abnormalities in patients with liver cirrhosis. The most important combinations are endoscopic findings followed by the LGV hemodynamics. Duplex-Doppler ultrasonography has no value in the identification of patients with cirrhosis at risk of variceal bleeding. Hemodynamics of the LGV appears to be superior to those of the PV in predicting bleeding.

Endoscopic diagnosis, grading and predictors of bleeding in esophageal and gastric varices

The majority of patients with cirrhosis will develop varices during their lifetime. At least a third of these patients will bleed from their varices and despite significant improvements in treatment and diagnosis of first variceal haemorrhage, the mortality still remains high (30%). Patients with a high risk of bleeding need to be identified, in order to define a group who will benefit from primary prophylaxis. The most important predictors of oesophageal variceal bleeding are variceal size, presence of red wale markings and severity of liver dysfunction as defined by Child-Pugh score. These and other factors have been combined in prognostic indices in an effort to predict those patients most at risk of variceal haemorrhage. In recent trials, variceal size was found to be the most important predictor of variceal bleeding and therefore is the variable used to decide whether a patient should receive primary prophylaxis. Variceal size, location (fundus), Child-Pugh score are all associated with a higher risk of bleeding from gastric varices.

FEASIBILITY AND ACCURACY OF “STRING” CAPSULE ENDOSCOPY (SCE) IN THE DIAGNOSIS OF ESOPHAGEAL VARICES

Purpose: To determine: 1) feasibility and accuracy of SCE for esophageal varices, 2) procedure-associated discomfort and, 3) patient's acceptability when compared to the gold standard EGD. Methods: SCE was swallowed with water, in the sitting position and no sedation. Once a 50 cm mark was reached, SCE was slowly pulled across the LES into the lower esophagus and up to the UES. The process was repeated 3 times. The SCE was retrieved from the patient's esophagus, the strings disposed and the capsule underwent high level disinfection (2% gluteraldehyde for 45 min) and re-used. An independent endoscopist unaware of the patient's diagnosis reviewed the pictures and determined whether esophageal varices were present or not and then graded their size as 1 = small, 2 = small-medium, 3 = medium, 4 = medium-large, and 5 = large. The corresponding EGD grading (I-IV) was defined as follows: I = 1 and 2; II = 3; III = 4 and IV = 5. The grading system kept in mind that grades III and IV on EGD definitively require therapeutic intervention (for primary or secondary prophylaxis). Patients graded their difficulty experienced during the procedure and were asked their preference between SCE and conventional EGD. Results: 30 cirrhotic patients (ETOH and/or HCV: 93.1%) underwent EGD and SCE. All were men, mean age = 54.4 years, mean Child-Pugh score = 6.2. Eleven patients were for screening and 19 for surveillance. No capsule was lost during any of the procedures. The agreement for the presence/absence of varices was 96.7% (1 patient had Grade I varices on EGD but no varices on SCE). Size of varices was in agreement in 16/21 (76%) patients with varices. In the remaining 6, 3 were undersized and 2 oversized by SCE. Twenty-five patients (86.2%) preferred SCE to EGD, 2 had no preference and 2 EGD to SCE. The mean recording time was 5.78 minutes. Patient's discomfort is shown in Table.Table: Percent of patients and discomfort scoreConclusions: (1) SCE was well tolerated, safe and easy to perform; 2) Agreement of SCE for presence/absence of esophageal varices was over 95% in patients with cirrhosis; 3) SCE is an alternative to EGD in the screening/surveillance of esophageal varices and may be more cost-effective than EGD.

OUTCOME OF ENDOSCOPIC THERAPY IN RECURRENT VARICEAL BLEEDING AFTER INITIAL ENDOSCOPIC VARICEAL LIGATION (EVL)

Purpose: Acute variceal upper gastrointestinal bleeding (UGIB) carries a high mortality in the absence of definitive management. We reviewed our data to determine the outcome of therapy of recurrent bleeding after successful EVL. Methods: All patients with recurrent variceal UGIB within 30 days of successful initial EVL were eligible. Recurrent bleeding was diagnosed if patients with successful hemostasis during the initial endoscopic procedure developed recurrent hematemesis or melena requiring repeat endoscopy for bleeding control. Inpatient charts were reviewed to confirm the source of recurrent UGIB and determine clinical outcome. Results: Over a 3-year period, 149 distinct episodes of acute variceal UGIB were treated with EVL in 131 patients. Recurrent bleeding occurred in 38 instances in 36 patients (29%), 82% during the initial hospital stay. Two patients died before further intervention. The study group consisted of 34 patients (age 56.0 ± 2.3 years, 11F/23M) who underwent endoscopy for 36 episodes of recurrent bleeding after a mean of 6.4 ± 0.8 days after EVL. On endoscopy, ulcers at band ligation sites were identified as the cause of recurrent bleeding in 9 instances (25%), managed conservatively without further recurrence. Further therapy consisted of repeat EVL in 13 of the remaining 27 instances (48%), sclerotherapy in 3 instances (11%), and transjugular intrahepatic portosystemic shunt (TIPS) placement in 11 instances (41%). A third EVL was performed in 2 instances. TIPS was performed in one instance each for failed EVL and failed sclerotherapy. EVL was overall successful in 73% (as compared to 81% for initial bleeds, p = ns), and comparable numbers were obtained for TIPS (Table). Overall mortality after recurrent bleeding was 33%, significantly higher compared to patients without rebleeding after initial EVL (12%, p = 0.009). Coagulopathy (INR > 1.7, platelets <75,000) demonstrated a trend (p = 0.08) for higher mortality in patients with recurrent bleeding on univariate analysis, while MELD score, CPT score and variceal size did not predict mortality.Table: Comparison of EVL and TIPS for recurrent variceal bleedingConclusions: Repeat EVL for recurrent bleeding results in bleeding control comparable to EVL for initial variceal bleeding. Rebleeding appears to be a marker for higher mortality, and since coagulopathy may predict higher mortality, aggressive measures to correct coagulopathy could be important in recurrent variceal bleeding.

Avaliação intra-operatória da pressão portal e resultados imediatos do tratamento cirúrgico da hipertensão portal em pacientes esquistossomóticos submetidos a desconexão ázigo-portal e esplenectomia

The main cause of portal hypertension in Brazil is the hepato-splenic form of mansonic schistosomiasis and the most employed technique for the surgical approach of this disease is the esophagogastric devascularization with splenectomy, generally associated to postoperative endoscopical esophageal varices sclerotherapy. The hemodynamic alterations after surgical treatment and its possible influence on the outcome are not well established. To evaluate the immediate impact of esophagogastric devascularization with splenectomy upon portal pressure as well as the results of the surgical treatment on digestive hemorrhage recurrence and on esophageal varices. Nineteen patients with mean age of 37.9 years and portal hypertension and previous episodes of digestive hemorrhage caused by esophageal varices rupture due to hepato-splenic schistosomiasis were studied. None of the patients had received any treatment prior to the surgery and underwent to elective esophagogastric devascularization with splenectomy. Portal pressure was assessed at the beginning and at the end of esophagogastric devascularization with splenectomy through portal vein catheterization with a polyethylene catheter introduced through a jejunal branch vein. All patients were submitted to digestive endoscopy before and after the surgery, in order to classify the size of esophageal varices after esophagogastric devascularization with splenectomy according to Palmer's classification. In all patients the portal pressure had diminished with a mean decrease of 31.3% after esophagogastric devascularization with splenectomy. In the postoperative endoscopic follow-up (1 month), the esophageal varices showed a statistically significant reduction in their size, when compared to the pre-surgical measurements. These results have demonstrated that the esophagogastric devascularization with splenectomy promotes immediate decrease in the portal pressure and a consequent reduction in the esophageal varices size. We also observed that the risk of mortality and severe complications related to this technique is not insignificant.

This month in Gastroenterology

This month in Gastroenterology

Splenic artery ligation and distal splenorenal shunt in schistosomiasis

Background A prospective study was carried out to evaluate the results of distal splenorenal shunt (DSRS) with or without splenic artery ligation (SAL) in patients with schistosomal portal hypertension. Materials and methods Thirty patients were divided into two groups: 15 were submitted to DSRS (Group I) and the other 15 were submitted to DSRS + SAL (Group II). They were observed for 24 months. Clinical and laboratory features were analyzed. Results There was neither mortality nor clinical manifestation of portosystemic encephalopathy in both groups. Recurrent hemorrhage and thrombosis incidence had no statistical difference. Although patients in Group II presented higher levels of postoperative pain and fever, spleen size reduction was higher than in Group I. White blood cells and platelets were increased in patients who underwent DSRS + SAL, even though there was no statistically significant difference between the groups. An increase in bilirubin was observed on the first postoperative day. Arterial blood ammonia and liver function were similar in both groups. Endoscopic control showed reduction in size of varices or their disappearance in 80 and 93% of patients from Groups I and II, respectively. Conclusions Although SAL associated with DSRS was responsible for increasing postoperative morbidity, it did not increase the incidence of shunt thrombosis and improved white blood cells and platelets count as well as reduced the spleen size. Therefore, the authors believe that SAL associated with DSRS is an effective treatment for schistosomal portal hypertension. Besides, it should be performed when a large spleen and hypersplenism are present.

Incidental esophageal varices

Incidental esophageal varices

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.

Balloon-occluded retrograde transvenous obliteration performed in a pediatric patient with isolated gastric fundal varices

Background For giant gastric varices in association with portal hypertension, endoscopic treatment often is difficult. Although balloon-occluded retrograde transvenous obliteration (B-RTO) has been performed successfully in adult cirrhotic patients, there has been no report in pediatric patients. Methods A 10-year-old girl with biliary atresia (BA) who had been free of jaundice after hepatic portoenterostomy was detected to have isolated gastric fundal varices by routine endoscopy. They gradually enlarged up to 4 cm in diameter, showing a tense appearance, so prophylactic treatment was conducted. Magnetic resonance angiography showed the blood flow of the varices mainly drained by a large gastrorenal shunt. A balloon catheter was introduced into the gastrorenal shunt via the femoral vein and was inflated to occlude the outflow of the varices. Five percent ethanolamine oleate was injected into the varices, and the outflow occlusion was kept for more than 30 minutes. Extensive thrombosis was achieved by an additional embolotherapy after 17 months. Throughout the course, the patient has been doing well without bleeding or worsening of the liver function tests. Conclusions B-RTO for isolated gastric fundal varices has been performed safely in a pediatric patient and seems effective in reducing the variceal size and tension.

Avaliação da anamastose espleno-renal distal, com e sem ligadura da artéria esplênica, para tratamento a hipertensão portal esquistossomática

OBJETIVO: Avaliar os resultados da derivação espleno-renal distal (DERD) com ligadura da artéria esplênica (LAE) em pacientes com hipertensão portal esquistossomótica e história de sangramento por varizes esôfago-gástricas. MÉTODO: Estudo prospectivo de trinta pacientes que foram divididos em dois grupos: 15 foram submetidos à DERD (Grupo I) e 15 foram submetidos à DERD associada à LAE (Grupo II). Os pacientes foram acompanhados por 24 meses, e estudados quanto à recorrência de hemorragia digestiva por ruptura de varizes, controle endoscópico das varizes e permeabilidade da anastomose através de ultra-sonografia e angiografia. RESULTADOS: Um paciente do Grupo I (6,67%) apresentou trombose da anastomose e recidiva hemorrágica em decorrência de varizes. No Grupo II, nenhum paciente, em dois anos de observação, desenvolveu trombose da anastomose e hemorragia digestiva. Não houve diferença estatisticamente significativa entre os grupos. Quanto à análise endoscópica após seis meses, houve redução do tamanho ou desaparecimento das varizes em 80% dos pacientes do Grupo I e em 93% daqueles do Grupo II. CONCLUSÕES: A derivação espleno-renal distal com ligadura da artéria esplênica não está associada a uma maior incidência de trombose da anastomose, de recidiva hemorrágica e nem modificou o tamanho das varizes esôfago-gástricas em comparação com a derivação espleno-renal distal isolada.

Inter-observer and intra-observer variability in hepatology.

A determination of the inter-observer variability is an important step before determining diagnostic accuracy and requires a specific methodology and statistical tests. The aim of this study was to report the results, characteristics and methodological quality of agreement studies performed in hepatology. A search of published studies yielded 42 that could be used in this evaluation: three were clinical studies, 11 were in the field of endoscopy, 12 in histopathology and 16 in radiology. The studies were described with a grid of 28 items and evaluated with a quality score (QUAS; maximum, 35) including 22 items. The following agreement level was noted: intra-observer > inter-observer > inter-centre. The following signs had good agreement. Endoscopy: size and red signs of oesophageal varices; histopathology: cirrhosis, fibrosis and steatosis; Doppler: mean portal vein and superior mesenteric artery velocities, hepatic artery area and perfusion indexes. Frequent methodological weaknesses were noted. The real agreement (such as the kappa index excluding chance), and the prevalence of signs and biases were rarely assessed. Standardized observations (67% of the studies), blind assessment (48%), simultaneous observations (7%), and the recording technique were not frequently used. The mean QUAS was 13 +/- 6 with 17 +/- 4 in histopathology versus 11 +/- 6 in radiology (P < 0.05). Using multiple regression, four variables independently predicted the QUAS with R2 = 0.77: adapted tests, multiple observations, intra-class correlation coefficient and agreement proportion. Methodology was often insufficient. Agreement is often measured under biased conditions. Some areas were not or were rarely studied, e.g., biology and ultrasound. The agreement and QUAS were often poor, suggesting the need for studies with improved observation and methodological quality of agreement.

Reply

We have clearly demonstrated the efficacy of TIPS in the prevention of both gastric (GVB) and esophageal variceal (EVB) rebleeding. We agree that there is a lack of long-term data regarding endoscopic treatment of gastric varices, but believe that although the available data are promising, randomized studies in this field are required. The potential for better survival in patients who present with GVB has been noted in a previous study by our unit (Aliment Pharmacol Ther 1997;11:171–176). The increased number of patients and extended follow-up has resulted in the difference now being significant, particularly in the long term as demonstrated by a 5-year mortality of 49.5% versus 74.9% in the GVB and EVB groups, respectively. This difference in mortality is not fully understood, but one possibility is that the portal pressure gradient (PPG) may be a direct predictor of mortality as we have shown that it is significantly lower in the GVB group. Studies indicate a detrimental effect on mortality following TIPS insertion in patients with higher portal pressures, particularly shortly after the variceal bleed (Hepatology 1986;6:116–117, Gastroenterology 1999;117:626–631, J Hepatol 1995;23:123–128). All of our patients had TIPS insertion using the same technique, although some patients with GVB were treated with thrombin injections. We have recently reported our experience using this endoscopic modality (Am J Gastroenterol 2002;97:1381–1385). Variceal hemorrhage particularly from gastric varices does occur frequently at PPG of ≤12 mm Hg, a finding we have reported in the past (Aliment Pharmacol Ther 1997;11:171–176, Am J Gastroenterol 1995;90:1994–1996) and reinforced by the present study. This may be caused by the development of gastro-renal portosystemic shunts (Gastroenterology 1988;95:434–440), or the large size of the varices resulting in increased variceal wall tension (Semin Liver Dis 1986;6:318–331). Most of the gastric varices in our study originated from the fundus or cardia and were of a large size. Other factors such as the presence of red spots, variceal size, and that of gastritis may be important, although it is noteworthy that the NIEC index only applies to esophageal varices (N Engl J Med 1988;319:983–989). Our findings highlight the need to reconsider the therapeutic targets for portal pressure reduction following TIPS. We suggest, particularly for patients with EVB, that a PPG post-TIPS of <7 mm Hg is desirable to minimize variceal rebleeding. Large multicenter trials comparing TIPS with other endoscopic and pharmacological treatment modalities would be highly informative. In our experience, thrombin seems to be safe and effective, and therefore should be investigated further. In the absence of cost-effective analysis, we would currently continue to recommend TIPS as first line treatment in patients with refractory GVB in the presence of a patent portal vein.