Portal venous pressure in non-cirrhotic bilharzial patients undergoing elective splenectomy, can it affect mortality? A prospective study

Background and study aims: To evaluate the impact of intra- operatively measured portal vein pressure (PVP) on mortality in non-cirrhotic bilharzial patients undergoing splenectomy. Methods: The present study is a prospective study that was conducted in Egypt from April 2014 to April 2018. Adult patients with non-cirrhotic bilharziasis who were scheduled to undergo splenectomy were included. Studied cases were divided into a survival cohort and a non-survival cohort. The main objective was the correlation between the incidence of mortality and intraoperative PVP. Results: The present work comprised 130 cases with a mean age of 51.8 ± 6.4 years old. The in-hospital mortality rate was 22.3%, with sepsis as a major cause of death (37.9%). In term of the association between preoperative variables and mortality, survivors had statistically significant lower portal vein diameter (13.6 ± 1.8 versus 15.2 ± 1.8mm; p<0.001) and higher portal vein velocity (14.2 ± 1.8 versus 10.4 ± 2.3 cm/sec; p<0.001) than non- survivors. The survived patients had significantly lower PVP (13.9 ± 1.1 versus 17.7 ± 2.7; p <0.001). A cut-off value of ≥14.5 mmHg, the PVP yielded a sensitivity of 86.2% and a specificity of 69% for the prediction of mortality. The association analysis showed a statistically significant association between mortality and postoperative liver function parameters. Conclusions: High intraoperative PVP is linked to early postoperative death in non-cirrhotic cases undergoing splenectomy. Our study showed that PVP > 14.5mmHg was an independent predictor of death and showed good diagnostic performance for the detection of early postoperative mortality.

Two Birds with One Stone

Despite improved serological and imaging diagnostic methods, liver biopsy remains an essential tool in diagnosing, evaluating and managing liver diseases. Endoscopic ultrasound-guided liver biopsy (EUS-LB) has been demonstrated to be a safe, feasible and effective technique with at least comparable or even better samples than transjugular or percutaneous liver biopsies.1-3 EUS-LB has various advantages: better patient comfort, if needed portal vein pressure measurements can be conducted simultaneously and different regions in the liver can be easily sampled. Moreover, as demonstrated in this case, EUS-LB can be performed concomitantly with an upper, lower endoscopy or EUS.

IMbrave150: Exploratory efficacy and safety results of hepatocellular carcinoma (HCC) patients (pts) with main trunk and/or contralateral portal vein invasion (Vp4) treated with atezolizumab (atezo) + bevacizumab (bev) versus sorafenib (sor) in a global Ph III study.

4073 Background: Atezo + bev has been approved in >60 countries for pts with unresectable HCC who have not received prior systemic therapy, based on IMbrave150 (NCT03434379; Finn RS NEJM 2020). Due to their poor prognosis and the hemodynamic changes from increased portal vein pressure, pts with main portal vein tumor thrombus are often excluded from pivotal HCC trials. Here, we report exploratory efficacy and safety results of pts with Vp4 (presence of a tumor thrombus in the main trunk and/or contralateral portal vein) using updated IMbrave150 data (Finn RS ASCO GI 2021). Methods: Pts were randomized 2:1 to atezo 1200 mg IV q3w + bev 15 mg/kg IV q3w or sor 400 mg bid until unacceptable toxicity or loss of clinical benefit per investigator. IMbrave150 enrolled 501 systemic treatment (tx)–naive unresectable HCC pts, ≥1 measurable untreated lesion (RECIST 1.1), Child-Pugh class A liver function and ECOG PS 0/1, including 73 (15%) Vp4 pts. This post hoc exploratory analysis was conducted with a median follow-up of 15.6 mo in ITT pts. Results: Of the Vp4 pts, 48 received atezo + bev and 25 received sor. Median OS (mOS) was 7.6 vs 5.5 mo (HR, 0.62; 95% CI: 0.34, 1.11) and median PFS (mPFS) per independent review facility (IRF)–assessed RECIST 1.1 was 5.4 vs 2.8 mo (HR, 0.62; 95% CI: 0.35, 1.09) with atezo + bev and sor, respectively. ORR per IRF RECIST 1.1 was 23% (11/47) with atezo + bev (2 [4%] pts had CR) vs 13% (3/23) with sor (1 [4%] pt had CR). All-grade variceal bleeding was higher with atezo + bev in Vp4 (13.6%) vs rest of ITT pts (2.5%). See table for further efficacy and safety data. Conclusions: The benefits of atezo + bev over sor in Vp4 pts are consistent with those in ITT pts across all efficacy endpoints, despite the expected disease-intrinsic increase in variceal bleeding in Vp4 vs rest of ITT pts. The overall positive benefit-risk profile supports the use of atezo + bev in pts with Vp4. Clinical trial information: NCT03434379. [Table: see text]

Increase of Portal Vein Pressure Gradient After Hepatectomy Predicts Post-operative Liver Dysfunction

Background. Post-hepatectomy liver failure (PHLF) is an important cause of mortality and morbidity. Whether Child–Pugh A patients with varying degrees of cirrhosis are good candidates for hepatectomy is disputed. The purpose of this study was to analyze the impact of portal venous pressure gradient (PVPG) variation during surgery on PHLF. Methods. PVPG, the pressure gradient between the portal vein and central vein, was measured in consecutive patients before and after liver resection. The optimal cutoff of PVPG to predict PHLF was determined by receiver operating characteristic curve analysis. Risk factors for PHLF were subjected to univariate and multivariable analysis. Results. Sixty Child–Pugh A patients were recruited. The mean PVPG was increased from 5.17 ± 4.78 mm of mercury (mmHg) to 6.37 ± 4.44 mmHg after liver resection. The optimal cutoff value of PVPG increments to predict PHLF was 1.5 mmHg. Multivariable analysis showed prothrombin time (PT), post-hepatectomy PVPG increments of 1.5 mmHg or greater, and resected liver segments of 3 or more to be independent predictors of PHLF. Conclusions. Acute PVPG increase after hepatectomy is associated with a higher risk of PHLF in Child–Pugh A patients.

A228 WHEN ASCITES & VARICEAL BLEEDING ARE NOT FROM CIRRHOSIS: A CASE OF MUTIPLE ARTERIOPORTAL FISTULAE CAUSING PORTAL HYPERTENSION

Background Portal hypertension is usually due to increased resistance from cirrhosis. However, pressures can also be elevated due to increased flow. Aims To describe a peculiar case of non-cirrhotic portal hypertension. Methods A case report and literature review was performed. Results A 47-year-old previously well man presented with a 6 month history of rapidly progressive weight loss, ascites and variceal bleed. Workup ruled out common causes of primary liver disease. Initial imaging demonstrated a heterogenous liver, splenomegaly, ascites, patent hepatic/portal veins and multiple poorly defined low-density hepatic lesions with the largest measuring 2.1 cm. Transient elastography was 7.3 kPa (F1-mild fibrosis). At transjugular liver biopsy, hepatic venogram ruled out Budd-Chiari and hepatic vein pressure gradient was normal at 3–4 mmHg. Histology unfortunately showed hemangioma. A percutaneous liver biopsy suggested nodular regenerative hyperplasia, minimal fibrosis and mild cholestasis. Given worsening ascites, hyponatremia and 7 months of rapidly progressive decline, transjugular intrahepatic portosystemic shunt (TIPSS) was inserted. Intra-procedure, portal vein pressure was noted to be 51 mmHg, with a portosystemic gradient of 42 mmHg. Although numerous abdominal CT and MRI did not show AV shunting, ultrasound post-TIPSS showed hepatic pseudoaneurysms & arterioportal fistulae (APF). Direct angiogram showed numerous hepatic pseudoaneurysms and intrahepatic fistulae making embolization impossible. CT showed no evidence of pseudoaneurysms or fistulae outside of the liver. Workup for autoimmune rheumatological diseases and congenital telangiectatic syndromes were negative. Given the high pressures being directed through the new TIPSS, right heart failure is an ongoing concern. APF are rarely encountered causes of presinusoidal portal hypertension, with communications most commonly arising from the hepatic (65%) & splenic arteries (11%) & the portal vein. Causes include traumatic (28%), iatrogenic (16%), vascular/telangiectatic malformations (15%), tumors (15%), aneurysms (14%) & congenital disease. Endovascular embolization can be used to treat single lesions. In complex cases with mulitple APF, surgery and/or liver transplantation may be required. Conclusions We report a rare case of non-cirrhotic portal hypertension due to increased flow rather than increased resistance secondary to APF. Funding Agencies None

Decompensated Acute Heart Failure Accompanied with Cardiac Cirrhosis and Chronic Disease Anemia in Child

Continuous heart failure can lead to complications to other systems, one of which is the hepatic system. Heart failure results in venous congestion in the portal vein so that the portal vein pressure increases, which is called portal hypertension. Portal hypertension causes fluid to pass through the walls of blood vessels and into the tissues. Management of decompensatory heart failure accompanied by comorbid disease in cardiac cirrhosis includes drugs management that does not aggravate the liver, namely angiotensin converting enzyme inhibitors and loop diuretic agents. Also, non-pharmacological management such as resting position and a diet sufficient in protein and low salt help improve the patient's general condition. This case report aims to present a decompensated heart failure accompanied by cardiac cirrhosis and anaemia of chronic disease in a child.

Percutaneous transhepatic portal vein stenting as rescue treatment for recurrent oesophageal variceal bleeding in a 31-year-old woman with haepatocellular carcinoma in a non-cirrhotic liver

A 31-year-old woman with hepatocellular carcinoma suffered from recurrent oesophageal variceal bleeding due to portal hypertension, which was caused by severe compression of the portal vein by metastatic lymph nodes. Endoscopic band ligation and pharmacological treatment did not suffice to prevent recurrence of variceal bleeding. Eventually, after the fifth variceal bleeding within 6 months, the patient was admitted to the intensive care unit in a haemodynamic shock. A Sengstaken-Blakemore tube was inserted and all treatment options were discussed, but only percutaneous transhepatic recanalisation of the portal vein with stent placement to reduce portal vein pressure was thought to be feasible with any chance to relieve portal vein pressure. After successful portal vein stenting, our patient did not have any recurrent bleeding in the remaining year of her life. We suggest that percutaneous transhepatic portal vein stenting may be a feasible and adequate last line treatment for complications of portal hypertension.

Effects of propofol and sevoflurane on hepatic blood flow: a randomized controlled trial

Background Maintaining adequate perioperative hepatic blood flow (HBF) supply is essential for preservation of postoperative normal liver function. Propofol and sevoflurane affect arterial and portal HBF. Previous studies have suggested that propofol increases total HBF, primarily by increasing portal HBF, while sevoflurane has only minimal effect on total HBF. Primary objective was to compare the effect of propofol (group P) and sevoflurane (group S) on arterial, portal and total HBF and on the caval and portal vein pressure during major abdominal surgery. The study was performed in patients undergoing pancreaticoduodenectomy because - in contrast to hepatic surgical procedures - this is a standardized surgical procedure without potential anticipated severe hemodynamic disturbances, and it allows direct access to the hepatic blood vessels. Methods Patients were randomized according to the type of anesthetic drug used. For both groups, Bispectral Index (BIS) monitoring was used to monitor depth of anesthesia. All patients received goal-directed hemodynamic therapy (GDHT) guided by the transpulmonary thermodilution technique. Hemodynamic data were measured, recorded and guided by Pulsioflex™. Arterial, portal and total HBF were measured directly, using ultrasound transit time flow measurements (TTFM) and were related to hemodynamic variables. Results Eighteen patients were included. There was no significant difference between groups in arterial, portal and total HBF. As a result of the GDHT, pre-set hemodynamic targets were obtained in both groups, but MAP was significantly lower in group S (p = 0.01). In order to obtain these pre-set hemodynamic targets, group S necessitated a significantly higher need for vasopressor support (p < 0.01). Conclusion Hepatic blood flow was similar under a propofol-based and a sevoflurane-based anesthetic regimen. Related to the application of GDHT, pre-set hemodynamic goals were maintained in both groups, but sevoflurane-anaesthetized patients had a significantly higher need for vasopressor support. Trial registration Study protocol number is AGO/2017/002 – EC/2017/0164. EudraCT number is 2017–000071-90.Clin.trail.gov,NCT03772106, Registered 4/12/2018, retrospective registered.