Elevated Venous Pressure Research Articles

The Efficacy of Carvedilol in Comparison to Propranolol in Reducing the Hepatic Venous Pressure Gradient and Decreasing the Risk of Variceal Bleeding in Adult Cirrhotic Patients: A Systematic Review.

The most common cause of portal hypertension is liver cirrhosis. Portal hypertension causes many complications in cirrhotic patients; a significant complication is the formation of varices and the subsequent life-threatening variceal bleeding due to elevated portal venous pressures. Hepatic venous pressure gradient (HVPG) is the gold standard for measuring portal hypertension and guides management. Pharmacological treatments lower the HVPG, preventing the progression of varices and subsequent variceal bleeding. The pharmacological treatments frequently used in primary and secondary prophylaxis of a variceal bleed are nonselective beta (β)-adrenergic blockers. Propranolol was the first nonselective β-adrenergic blocker used for lowering HVPG and has been well studied. However, in the past decade, clinical trials have shown that carvedilol has been more effective. This study aims to establish whether carvedilol is more effective than propranolol in reducing the hepatic venous pressure gradient and decreasing the risk of variceal bleeding in adult cirrhotic patients. A systematic review has been conducted to gather relevant clinical trials comparing drugs and their effects on HVPG. Four databases: PubMed (Medical Literature Analysis and Retrieval System Online (MEDLINE)), Google Scholar, the Cochrane Library, and ScienceDirect, were analyzed, and records from January 1, 1999, to January 1, 2023, were chosen. There were a total of 1,235 potentially eligible records across the four databases. Using the eligibility criteria for this systematic review, seven studies of 533 patients were included. Across all seven clinical trials, it was found that carvedilol reduced HVPG more than propranolol and decreased the risk of variceal bleeding in adult cirrhotic patients.

Noninvasive, patient-specific computational fluid dynamics simulations of dural venous sinus pressures in idiopathic intracranial hypertension

BackgroundThe pathophysiology of Idiopathic Intracranial Hypertension (IIH) is poorly understood, making the disease difficult to properly diagnose and treat. Endovascular venous stenting has emerged as an effective non-invasive treatment option for a select cohort of IIH patients with venous sinus stenosis and elevated venous sinus pressure gradient. Unfortunately, current methods of determining patient eligibility for stenting treatment depend on highly invasive and insufficient measurement methods such as venous manometry, which can only measure pressure gradients and not other components of the complex 3D hemodynamic environment. Thus, there is a need for a non-invasive methodology for determining the 3D flow environment of the dural venous sinuses. ObjectiveTo develop a novel method of non-invasive, patient-specific computational fluid dynamic (CFD) simulation of venous sinus hemodynamics for evaluating stenting eligibility. MethodA patient with IIH and elevated sinus pressure gradient underwent MR venography, phase-contrast MR venography, and venous manometry. Patient-specific dural venous anatomy was segmented from the MR venography to construct 3D models of the venous sinuses. 3D transient patient-specific computational fluid dynamic simulations were conducted using flow velocities measured with phase-contrast MR venography as boundary conditions. ResultsSuccessful computational simulations were completed, allowing for the calculation of the spatio-temporal evolution of blood flow through the dural venous sinuses, and the quantitative examination of pressure gradients. Calculated pressure gradients from CFD were validated against venous manometry with an error of only ∼5%. ConclusionsWe have successfully developed time-resolved, patient-specific 3D computational simulations of the dural venous sinuses without assumptions at the boundary conditions for the first time. The methodology can accurately and non-invasively measure venous pressure gradients. This preliminary study serves as a proof of concept for our method to be used as a diagnostic tool for determining venous stenting eligibility, as well as a tool for advancing the general understanding of IIH pathophysiology. Statement of SignificanceThe pathophysiology of Idiopathic Intracranial Hypertension (IIH) is poorly understood making the disease difficult to properly diagnose and treat. Endovascular venous stenting has emerged as an effective non-invasive treatment option for a select cohort of IIH patients with venous sinus stenosis and elevated venous sinus pressure gradient. Our work provides a method for noninvasively determining eligibility for venous sinus stenting, avoiding costly and invasive venous manometry.

Acute fetal cardiovascular adaptation to artificial placenta in sheep model.

To describe the acute cardiovascular adaptation of the fetus after connection to an artificial placenta (AP) in a sheep model, using ultrasound and invasive and non-invasive hemodynamic assessment. This was an experimental study of 12 fetal sheep that were transferred to an AP system, consisting of a pumpless circuit with umbilical cord connection, at 109-117 days' gestation. The study was designed to collect in-utero and postcannulation measurements in all the animals. The first six consecutive fetuses were fitted with intravascular catheters and perivascular probes to obtain invasive physiological data, including arterial and venous intravascular pressures and perivascular blood flows, with measurements taken in utero and at 5 and 30 min after cannulation. These experiments were designed with a survival goal of 1-3 h. The second set of six fetuses were not fitted with catheters, and experiments were aimed at 3-24 h of survival. Echocardiographic assessment of cardiac anatomy and function, as well as measurements of blood flow and pre- and postmembrane pressures recorded by circuit sensors in the AP system, were available for most of the fetuses. These data were acquired in utero and at 30 and 180 min after cannulation. Compared with in-utero conditions, the pulsatility index at 30 and 180 min after connection to the AP system was reduced in the umbilical artery (median, 1.36 (interquartile range (IQR), 1.06-1.50) vs 0.38 (IQR, 0.31-0.50) vs 0.36 (IQR, 0.29-0.41); P < 0.001 for extreme timepoints) and the ductus venosus (median, 0.50 (IQR, 0.41-0.67) vs 0.29 (IQR, 0.22-0.33) vs 0.36 (IQR, 0.22-0.41); P = 0.011 for extreme timepoints), whereas umbilical venous peak velocity increased (median, 20 cm/s (IQR, 18-22 cm/s) vs 39 cm/s (IQR, 31-43 cm/s) vs 43 cm/s (IQR, 34-54 cm/s); P < 0.001 for extreme timepoints) and flow became more pulsatile. Intravascular monitoring showed that arterial and venous pressures increased transiently after connection, with median values for mean arterial pressure at baseline, 5 min and 30 min of 43 mmHg (IQR, 35-54 mmHg), 72 mmHg (IQR, 61-77 mmHg) and 58 mmHg (IQR, 50-64 mmHg), respectively (P = 0.02 for baseline vs 5 min). Echocardiography showed a similar transient elevation of fetal heart rate at 30 and 180 min after connection compared with in utero (median, 145 bpm (IQR, 142-156 bpm) vs 188 bpm (IQR, 171-209 bpm) vs 175 bpm (IQR, 165-190 bpm); P = 0.001 for extreme timepoints). Fetal cardiac structure and function were mainly preserved; median values for right fractional area change were 36% (IQR, 34-41%) in utero, 38% (IQR, 30-40%) at 30 min and 37% (IQR, 33-40%) at 180 min (P = 0.807 for extreme timepoints). Connection to an AP system resulted in a transient fetal hemodynamic response that tended to normalize over hours. In this short-term evaluation, cardiac structure and function were preserved. However, the system resulted in non-physiologically elevated venous pressure and pulsatile flow, which should be corrected to avoid later impairment of cardiac function. © 2023 International Society of Ultrasound in Obstetrics and Gynecology.

Unraveling the pathophysiology of lower-limb postthrombotic syndrome in adolescents: a proof-of-concept study.

A better understanding of the pathophysiology of pediatric postthrombotic syndrome (PTS) is needed to develop strategies to treat this condition. We investigated calf pump function, exercise capacity, balance in power output, and changes in limb muscle oxygen saturation (SmO2) and fluid content during exercise in 10 pediatric patients with unilateral lower-limb PTS, and in age- and sex-matched controls (1:1-1:2 ratio). Outcomes were investigated usingbioimpedance spectroscopy, torque-sensing pedals, and near-infrared spectroscopy during incremental- and constant-load cycling tests. The median age at participation was 17years (25th-75th percentile, 15-18 years); 68% of participants were females. The median CAPTSure score in the affected leg of affected participants was 35 points (25th-75th percentile, 24-46 points), indicating moderate/severe PTS; 20% of patients had a history of central venous catheter-related thrombosis. Increasing PTS severity was associated with higher calf pump venous volume and higher ejection volume, leading to compensated calf pump performance. We found no evidence of PTS impact on exercise capacity. Leg contribution to power output was similar in affected and unaffected legs. However, the PTS-affected legs showed lower SmO2 during active cycling and recovery with increasing PTS severity, indicating impaired microvascular function in the muscle. These findings suggest that PTS severity is associated with impaired blood flow, presumably from elevated venous pressure during and after exercise. The fact that microvascular function is impaired in young patients with PTS underscores the relevance of developing strategies to mitigate the effects of this chronic vascular disease to minimize its deleterious effects as children grow older.

A 48-year-old female with chronic, progressive bilateral vision loss and dyspnea.

To describe a unique case of isolated, bilateral serous retinal detachments associated with primary pulmonary arterial hypertension. Case report. A 48-year-old woman with primary pulmonary arterial hypertension presented with bilateral vision loss. She was found to have bilateral serous retinal detachments in the macula with accumulation of the fibrinous material. Optical coherence tomography demonstrated intraretinal and subretinal fluid, hyperreflective material in the subretinal space, and choroidal engorgement. Fluorescein angiography demonstrated pooling in the maculas, an area of blockage corresponding with the area of subretinal exudative material, and a petalloid pattern of leakage in the maculas without evidence of retinal vascular leakage. Her ocular symptoms improved with aggressive medical management of her pulmonary arterial hypertension with the addition of eplerenone. Primary pulmonary arterial hypertension results in chronically elevated systemic venous pressure, leading to both systemic and ocular symptoms. It is important to consider this systemic condition in the differential diagnosis of serous retinal detachments to provide adequate multidisciplinary management.

Does High-Intensity Exercise Cause Acute Liver Injury in Patients with Fontan Circulation? A Prospective Pilot Study.

The Fontan procedure results in chronic hepatic congestion and Fontan-associated liver disease (FALD) characterized by progressive liver fibrosis and cirrhosis. Exercise is recommended in this population, but may accelerate the progression of FALD from abrupt elevations in central venous pressure. The aim of this study was to assess if acute liver injury occurs after high-intensity exercise in patients with Fontan physiology. Ten patients were enrolled. Nine had normal systolic ventricular function and one had an ejection fraction < 40%. During cardiopulmonary exercise testing, patients had near-infrared spectroscopy (NIRS) to measure oxygen saturation of multiple organs, including the liver, and underwent pre- and post-exercise testing with liver elastography, laboratory markers, and cytokines to assess liver injury. The hepatic and renal NIRS showed a statistically significant decrease in oxygenation during exercise, and the hepatic NIRS had the slowest recovery compared to renal, cerebral, and peripheral muscle NIRS. A clinically significant increase in shear wave velocity occurred after exercise testing only in the one patient with systolic dysfunction. There was a statistically significant, albeit trivial, increase in ALT and GGT after exercise. Fibrogenic cytokines traditionally associated with FALD did not increase significantly in our cohort; however, pro-inflammatory cytokines that predispose to fibrogenesis did significantly rise during exercise. Although patients with Fontan circulation demonstrated a significant reduction in hepatic tissue oxygenation based on NIRS saturations during exercise, there was no clinical evidence of acute increase in liver congestion or acute liver injury following high-intensity exercise.

Venous dysfunction in obstructive hypertrophic cardiomyopathies: Results from the “HCM-Vein” pilot study

Hypertrophic cardiomyopathies (HCM) can be complicated by left ventricular outflow-tract obstruction (LVOTO) responsible for disabling exercise symptoms, a phenomenon influenced by hemodynamic factors including venous return. We aimed to evaluate venous dysfunction in obstructive HCM patients compared to healthy controls, and to investigate the relationship between venous dysfunction parameters and LVOTO in HCM. This is a clinical, monocentric, prospective, pilot study, in a tertiary care center. We investigated venous function using venous air plethysmography, and endothelial function. Among the 30 symptomatic obstructive HCM patients, 30% (n=9) presented abnormal venous residual volume fraction (RVFv) which translates in elevated ambulatory venous pressure vs. 0% in the 10 healthy controls (p<0.05). Comparing obstructive HCM patients with abnormal RVFv (n=9) to other obstructive HCM patients with normal RVFv (n=21), there were no significant differences in terms of age, sex (67% male), and classical echocardiographic parameters both at rest and during exercise, except for left ventricular end-diastolic volume index which was significantly lower in the group with abnormal RVFv compared to the other HCM patients (40.1±9.0ml/m2 vs. 50.2±10.6ml/m2, p=0.01). Fifty six percent of obstructive HCM patients with abnormal RVFv had an absolute increase in Willebrand factor (vs. 26% of other obstructive HCM patients, p<0.05). In this pilot monocentric study, venous insufficiency was observed in about 30% of symptomatic obstructive HCM patients. Patients with venous insufficiency had more frequently a smaller LV cavity volume. Due to the small sample size, this study is only hypothesis-generating, and further investigations are needed.

Point-of-care ultrasound in diagnosis and management of congestive nephropathy.

Congestive nephropathy is kidney dysfunction caused by the impact of elevated venous pressures on renal hemodynamics. As a part of cardiorenal syndrome, the diagnosis is usually made based on history and physical examination, with findings such as jugular venous distension, a third heart sound, and vital signs as supporting findings. More recently, however, these once though objective measures have come under scrutiny for their accuracy. At the same time, bedside ultrasound has increased in popularity and is routinely being used by clinicians to take some of the guess work out of making the diagnosis of volume overload and venous congestion. In this mini-review, we will discuss some of the traditional methods used to measure venous congestion, describe the role of point-of-care ultrasound and how it can ameliorate a clinician's evaluation, and offer a description of venous excess ultrasound score, a relatively novel scoring technique used to objectively quantify congestion. While there is a paucity of published large scale clinical trials evaluating the potential benefit of ultrasonography in venous congestion compared to gold standard invasive measurements, more study is underway to solidify the role of this objective measure in daily clinical practice.

Abstract Number ‐ 74: Venous Thrombectomy as Treatment for Central Venous Sinus Thrombosis presenting as symptomatic Idiopathic Intracranial Hypertension

Introduction Thrombosis of the cerebral venous sinus (CVST) is an uncommon form of stroke which primarily affects young adults, usually females. Patients with CVST present with either symptoms related to increased intracranial pressure secondary to venous congestion or focal brain injury from infarction or haemorrhage. Treatment of CVST currently involves anticoagulation with venous thrombectomy (VT) used as salvage therapy in refractory CVST. However, the clinical outcomes of patients with symptoms of idiopathic intracranial hypertension (IIH), secondary to CVST, pre‐ and post‐ VT has not been documented. In this case study we present two cases where patients presented with symptoms of IIH secondary to CVST who subsequently underwent VT salvage therapy. Methods We retrospectively analysed institutional data of patients who underwent VT for CVST from 2017–2022. Patients who presented with well documented symptoms of IIH without cerebral infarction or haemorrhage were included. Clinical outcomes including neuroimaging, retinal nerve fibre layer (RNFL) thickness from optical coherence tomography (OCT), visual acuity and use of medications including acetazolamide and anticoagulation were recorded. The technical aspects of the VT procedure are also described. Results Two patients were identified (2 women) that fit the study criteria. Both patients were taking the oral contraceptive pill. They both presented similarly with papilledema and symptoms of IIH including; headache, diplopia and nausea. There was symptomatic progress in both patients despite medical management with anticoagulation and acetazolamide. Patient A, a 39‐year‐old lady, was found to have a severe sagittal sinus thrombosis involving the entire sinus. Her lumbar puncture revealed an opening pressure of 31 cmH2O. She underwent urgent VT which revealed a highly organised thrombus and as such minimal change was achieved with repeated passes, however, her post‐op imaging showed partial recanalization of the right transverse sinus. Patient B, a 26‐year‐old lady, had a partially occlusive right transverse sinus thrombosis extending into the jugular vein. Manometry revealed elevated venous pressures. She underwent VT with alteplase injection to the site of thrombosis. After multiple passes, recanalization of the right transverse sinus was achieved. Post‐operative OCTs demonstrated a significant reduction in RNFLs bilaterally in both patients. Both patients also experienced resolution of symptoms over a few days and remained asymptomatic with gradually decreasing doses of acetazolamide. Conclusions VT may be a safe and effective treatment option in patients with medically refractory CVST who present with symptoms of IIH. In both patients there was marked improvement in symptoms and RNFL thickness after the procedure.

Topical netarsudil for treatment of glaucoma with elevated episcleral venous pressure: A pilot investigation in sturge-weber syndrome.

Topical netarsudil 0.02% may reduce intraocular pressure (IOP) by decreasing episcleral venous pressure (EVP), which carries theoretical utility for glaucoma associated with elevated EVP. A role for netarsudil in patients with elevated EVP is evaluated in a pilot investigation using a cohort of individuals with Sturge-Weber syndrome (SWS). Retrospective study of patients with SWS and glaucoma who were treated with netarsudil. Five patients (six eyes) were identified. Data collected included demographics, visual acuity, IOP, glaucoma medical and surgical treatments, and adverse effects of netarsudil. Mean age was 13.6 ± 8.5 years. EVP elevation was presumed based on clinical stigmata and/or historical features. Mean number of baseline glaucoma medications was 3.3 ± 1.2. There was a significant reduction in the IOP at netarsudil initiation (mean 26.2 ± 4.5 mmHg) to 1 month of netarsudil therapy (mean 20.2 ± 3.8 mmHg, p = 0.0283) and latest IOP on netarsudil (mean 17.6 ± 1.4 mmHg, p = 0.0034). Mean duration of netarsudil therapy was 18.7 ± 11.8 months. Three patients required additional glaucoma procedures; one patient required an additional glaucoma medication. Three eyes (50%) developed conjunctival hyperemia. One patient discontinued netarsudil at 29 months, to reduce drop burden. Netarsudil can effectively reduce IOP in patients with SWS, even when used as a fourth or fifth glaucoma medication. A possible role for netarsudil in the management of patients with elevated EVP is suggested pending further future investigations.

PS-BPB10-6: THE RELATION BETWEEN PERICYTE DETACHMENT AND INTERSTITIAL FIBROSIS IN DAHL SALT-SENSITIVE HYPERTENSIVE (DAHLS) RATS

Background: Congestive heart failure produces the state of fluid volume overload, central venous pressure (CVP) elevation, and consequently renal venous pressure (RVP) elevation. We have recently developed a novel rat unilateral renal venous congestion model, in which ligation of the inferior vena cava between both renal veins artificially induced renal congestion in the left kidney only. In this model, pericyte detachment and pericyte-myofibroblast transition (PMT) around the vasa recta were involved in interstitial injury and fibrosis. Dahl salt-sensitive hypertensive (DahlS) rats on high salt diets exhibit hypertension, congestive heart failure, fluid volume overload, CVP and RVP elevation, and renal damage, considering to be a non-artificial renal congestion model. The relation, however, between renal interstitial injury and fibrosis, elevated RVP, and pericyte detachment in DahlS rats has not been reported. In the present study, we assessed the relation of pericyte detachment around the vasa recta and PMT with interstitial fibrosis in DahlS rats. Methods: Eight-week-old DahlS rats (Dahl/Mcwi) were divided into three groups: normal diet, 4% NaCl diet, and 8% NaCl diet groups, and their kidneys were analyzed after 2 weeks. Total mRNA and protein expression levels were quantified by real-time PCR and western blot, respectively. Tubulointerstitial damage and fibrosis were identified by histological analysis. Furthermore, we evaluated pericyte detachment around the vasa recta by low-vacuum scanning electron microscopy (LV-SEM). Results: The expression of KIM1, a tubulointerstitial damage marker; CNN1 and αSMA, interstitial fibrosis markers; and TAGLN, a smooth muscle protein22 and PMT marker; was significantly increased in a salt-dependent manner in DahlS rats. In histological analysis, hyperplasia of the extracellular matrix and renal tubular injury were detected in 4% and 8% NaCl diet groups. The positive area of PMT markers in the interstitial space around the vasa recta was also increased in the NaCl diet groups. Pericyte detachment from the vasa recta was observed in the NaCl diet groups by LV-SEM. Conclusions: Pericyte detachment and PMT are involved in tubulointerstitial injury and fibrosis of DahlS rats. Renal venous congestion and subsequent physiological changes could have a role in renal damage and fibrosis. Arterial hypertension has been emphasized for a long time in renal injury, and venous hypertension must also be focused on with the concept of renal congestion. Further understanding of this concept may lead to new therapeutic strategies for renal injury.

Effect of drysuit seals on intraocular pressure in non-immersed scuba divers

Objective: This study quantifies the change in intraocular pressure (IOP) secondary to wearing neck seals in scuba diving drysuits. Previous work demonstrates significant pressures exerted by these seals; we hypothesize that they would reduce craniofacial venous drainage and increase IOP through elevation of episcleral venous pressure. Methods: IOP was measured in 33 divers before and while wearing a drysuit using rebound tonometry. The drysuit neck seal pressures were measured using a manometer. A paired two-sample t-test was used to compare IOP before and after drysuit donning. Pearson correlation coefficients were calculated between neck sealing pressures and IOP by side. Results: The mean IOP in the right eye was similar pre- and post-drysuit donning, with baseline mean 15.9 mmHg (3.7 mmhg) versus 15.4 mmHg (4.3 mmHg), p=0.4074. Similarly, the mean IOP in the left eye was also similar, with mean pre-donning IOP 15.6 (3.8 mmHg) versus 15.4 mmHg (4.7 mmHg) post-donning, p=0.7467. The mean right and left neck seal pressures were 23.66 (10.60) mmHg and 23.67 (7.87) mmHg, respectively. Only correlation between right neck sealing pressure for silicone neck seals and right IOP, pre- and post-donning was significant (pre: 0.97, p-value 0.0284, post: 0.98, p-value 0.0187). Conclusion: No significant difference overall was detected in IOP with drysuit donning.

Venous Doppler to Assess Congestion: A Comprehensive Review of Current Evidence and Nomenclature.

Organ congestion from venous hypertension is an important pathophysiological mechanism mediating organ injury in several clinical contexts including critical illness, congestive heart failure and end-stage chronic kidney disease. However, the practical evaluation of venous congestion is often challenging at the bedside because of the limitations of traditional methods. Point-of-care ultrasound (POCUS) enables the clinician to assess venous velocity profiles during the cardiac cycle using Doppler modalities. Venous Doppler profile abnormalities at multiple sites are detected when elevated venous pressure results in hemodynamic changes within the systemic venous circulation. The detection of these abnormal Doppler profiles may identify patients with clinically significant systemic venous congestion. These patients have been reported to be at increased risk of medical complications. Improving the evaluation of venous congestion may lead to individualized treatment and improved patient outcomes. In this review, we describe the physiologic principles necessary to understand venous Doppler assessment. We also propose a nomenclature for the description of venous Doppler profiles. Finally, we provide a narrative review of the current clinical evidence related to use of venous Doppler assessment in various clinical contexts.

Constrictive Pericarditis Secondary to Tuberculosis Infection: Literature Review

Tuberculous pericarditis is produced by Mycobacterium tuberculosis, accounting for 1% of all forms of tuberculosis. Its prevalence varies according to coinfection with HIV. Mortality varies between 17 and 40%. In the US, the prevalence is low compared to developing countries. This article aims to review the literature on pericarditis caused by tuberculosis (TBP), its prevalence in the US, clinical manifestations, diagnosis, and treatment. Among the most frequent clinical manifestations are dyspnea, fever, chest pain, and cough. TBP should be suspected in patients at high risk of exposure to tuberculosis. There are multiple lab tests for diagnosis, and its primary treatment is triple therapy with isoniazid, rifampin, and streptomycin or ethambutol. In case of persistent elevation of systemic venous pressure, surgical intervention is indicated. The clinical presentation was found to be variable.

Case of Elevated Dialysis Access Venous Pressures From Cephalic Arch Pseudo-Stenosis

Case of Elevated Dialysis Access Venous Pressures From Cephalic Arch Pseudo-Stenosis

Right ventricular failure in left heart disease: from pathophysiology to clinical manifestations and prognosis.

Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction and/or overload of the right heart structures, predominantly the right ventricle (RV), resulting in systemic venous hypertension, peripheral oedema and finally, the impaired ability of the right heart to provide tissue perfusion. Pathogenesis of RHF includes the incompetence of the right heart to maintain systemic venous pressure sufficiently low to guarantee an optimal venous return and to preserve renal function. Virtually, all myocardial diseases involving the left heart may be responsible for RHF. This may result from coronary artery disease, hypertension, valvular heart disease, cardiomyopathies and myocarditis. The most prominent clinical signs of RHF comprise swelling of the neck veins with an elevation of jugular venous pressure and ankle oedema. As the situation worsens, fluid accumulation becomes generalised with extensive oedema of the legs, congestive hepatomegaly and eventually ascites. Diagnosis of RHF requires the presence of signs of elevated right atrial and venous pressures, including dilation of neck veins, with at least one of the following criteria: (1) compromised RV function; (2) pulmonary hypertension; (3) peripheral oedema and congestive hepatomegaly. Early recognition of RHF and identifying the underlying aetiology as well as triggering factors are crucial to treating patients and possibly reversing the clinical manifestations effectively and improving prognosis.

S3168 Sinusoidal Obstruction Syndrome: A Known and Often Missed Complication of Oxaliplatin Therapy

Introduction: Sinusoidal obstruction syndrome (SOS) is caused by sinusoidal endothelial injury due to hematopoietic cell transplantation, liver irradiation or exposure to chemotherapy such as oxaliplatin and may occur days to weeks following exposure. SOS can be a life-threatening complication and its presentation may include jaundice, volume overload or hepatic failure. We present the case of a 32-year-old male with gastroesophageal adenocarcinoma who underwent oxaliplatin-based chemotherapy and developed SOS. Case Description/Methods: A 32-year-old male with no significant medical history presented with dysphagia and weight loss. Esophagogastroduodenoscopy showed a mass at the gastroesophageal junction. He underwent diagnostic laparoscopy which showed peritoneal metastasis. Tissue biopsy was consistent with stage 4 gastroesophageal junction adenocarcinoma. He was started on 5-fluorouracil (5-FU), oxaliplatin and nivolumab. The patient developed thrombocytopenia and moderate aminotransferase elevation after 6 cycles of chemotherapy. An abdominal ultrasound obtained after 10 of 12 cycles of chemotherapy showed portal hypertension. Subsequent abdominal imaging showed worsening ascites (serum ascites to albumin gradient > 1.1), anasarca and splenomegaly. Transjugular liver biopsy showed elevated portal hepatic venous pressure gradient, focal sinusoidal dilatation and centrizonal ischemic changes suggesting drug induced hepatopathy, and a diagnosis of oxaliplatin induced SOS was made. The patient was not a candidate for defibrotide and was treated conservatively. He continued to have worsening ascites with severe direct hyperbilirubinemia and moderately elevated aminotransferases without biliary obstruction (Figure). Discussion: Oxaliplatin-based chemotherapies are known to cause the potentially life-threatening complication of SOS which is oftentimes missed. Our patient developed signs and symptoms suggestive of SOS by cycle 10 of oxaliplatin therapy. These changes included thrombocytopenia, elevated liver associated enzymes, volume overload and portal hypertension. He went on to complete 12 cycles of oxaliplatin with eventual worsening of his portal hypertension related symptoms and worsening of his hepatic function. This case highlights the importance of having a high index of suspicion for the development of SOS with plans to pursue patient-centered discussions regarding alternative chemotherapeutic regimens, instituting prophylactic therapies and timely SOS screening protocols.Figure 1.: Timeline of events leading up to SOS diagnosis.

SUPERIOR VENA CAVA SYNDROME DUE TO A MEDIASTINAL MASS WITH RIGHT ATRIAL INVOLVEMENT

SUPERIOR VENA CAVA SYNDROME DUE TO A MEDIASTINAL MASS WITH RIGHT ATRIAL INVOLVEMENT

The natural history of patients with compensated cirrhosis and elevated hepatic venous pressure gradient.

Portal hypertension is a major complication of liver cirrhosis. Hepatic venous pressure gradient (HVPG) appears to be one of the best surrogates of clinical outcomes. However, the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear. We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, non-bleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepato-pulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement. Patients with high HVPG without evidence of clinical decompensation had significantly lower model for end stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, P = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow-up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 mmHg and 18 mmHg, respectively) differentiated patients who remained compensated vs. those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 g/dL vs. 2.6 g/dL, respectively, P = 0.05). A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long term follow-up.

Outcomes of medical and surgical management in eyes with idiopathic elevated episcleral venous pressure.

Idiopathic elevated episcleral venous pressure (IEEVP) is a rare cause of secondary glaucoma and is a diagnosis of exclusion. The aim of this study was to describe the clinical presentation and analyze the outcomes of medical and surgical management in eyes diagnosed with idiopathic elevated episcleral venous pressure. A retrospective analysis of eyes diagnosed with IEEVP over a 5-year period between April 2012 and March 2016 was performed. The demographic details, medical history, and clinical course of the cases were obtained from the medical records. Data pertaining to the severity of glaucomatous damage, response to medical management, need for surgical intervention, and their outcomes were analyzed. Fifteen eyes of 13 patients were included. Thirteen eyes (86.6%) had open angle configuration. Among the 13 eyes that had glaucoma, eight eyes (61.5%) had severe glaucoma, four eyes (30.7%) had moderate glaucoma, and one eye (7.6%) had mild glaucoma. The median follow-up was 210 days. Seven of the 15 eyes (46.6%) required a glaucoma filtration procedure, and three underwent prophylactic sclerotomies. 71.4% of these eyes had complete success. One out of the seven operated eyes required choroidal drainage post-operatively. IEEVP is an extremely rare condition and presents with raised intra-ocular pressure and tortuous episcleral vessels. The management of IEEVP is similar to that of primary open angle glaucoma. Uveal effusion is to be anticipated, and hence, combining trabeculectomy with prophylactic sclerotomies is advisable.