Balloon-Assisted Portal Vein Embolization Using n-Butyl-2-Cyanoacrylate-Lipiodol-Iopamidol Mixture in Swine: A Comparison of 2 Formulations.

PURPOSE: To compare 2 ratios of n-butyl-2-cyanoacrylate (nBCA)-ethiodized oil (Lipiodol)-iopamidol (NLI) in balloon-assisted portal vein embolization (PVE) in swine. MATERIALS AND METHODS: In an in vitro study, NLI prepared at a ratio of 2:3:1 (NLI231) or 1:4:1 (NLI141) was injected into 2.5- or 10-mL syringes filled with swine blood, and the viscosity of NLI was measured to determine an appropriate balloon occlusion time. Two portal vein branches in 8 female swine (n = 16 vein branches) were embolized with NLI231 (n = 8) or NLI141 (n = 8) under balloon occlusion. Portal venography was performed before, immediately after, and 3 days after PVE to evaluate the migration of NLI and the recanalization of embolized portal vein branches. Then, the livers were removed for histopathologic evaluation. RESULTS: The times to peak viscosity of NLI231 in the 2.5- and 10-mL syringes were 55.8 seconds (SD ± 7.0) and 85.2 seconds (SD ± 6.3), and those to peak viscosity of NLI141 were 129.2 seconds (SD ± 11.8) and 254.0 seconds (SD ± 21.8), respectively. No migration of NLI231 was observed in all 8 procedures immediately or 3 days after PVE. Migration of NLI141 was observed in 6 of 8 procedures within 3 days after PVE. The migration frequency of the embolic material was lower in the NI231 group than in the NLI141 group (0/8 vs 6/8; P = .051). Histologically, NLI231 occupied the portal veins without any thrombi, whereas NLI141 was accompanied by thrombi in the portal veins. CONCLUSIONS: NLI231 may be more suitable than NLI141 for balloon-assisted PVE in swine.

Massive cerebral air embolism following percutaneous transhepatic biliary drainage: A case report.

RATIONALE: Cerebral air embolism from portal venous gas rarely occurs due to invasive procedures (e.g., endoscopic procedures, liver biopsy, or percutaneous transhepatic biliary drainage) that disrupt the gastrointestinal or hepatobiliary structures. Here, we report a rare case of fatal cerebral air embolism following a series of percutaneous transhepatic biliary drainage tube insertions. PATIENT CONCERNS: A 50-year-old woman with a history of cholecystectomy, liver wedge resection, and hepaticojejunostomy for gallbladder cancer presented with altered mental status 1 week after percutaneous transhepatic biliary drainage tube placement. DIAGNOSES: Extensive cerebral air embolism and acute cerebral infarction. INTERVENTIONS: Brain computed tomography and magnetic resonance imaging, hyperbaric oxygen therapy, medical therapy. OUTCOMES: Despite the use of hyperbaric oxygen therapy and medical treatment including vasopressors, the patient eventually died due to massive systemic air embolism. LESSONS: To date, there have been no reports of cerebral air embolism due to percutaneous transhepatic biliary drainage with pronounced radiologic images. We reviewed previously reported fatal cases associated with endoscopic hepatobiliary procedures and assessed the possible mechanisms and potential causes of air embolism.

Delayed-Onset Portal Venous Thrombosis After Ingestion of 3% Hydrogen Peroxide.

BACKGROUND: Identification of portal venous gas on radiographic imaging is well documented after the ingestion of hydrogen peroxide, as is its resolution after hyperbaric therapy. Although hyperbaric therapy may resolve the gastrointestinal symptoms associated with the presence of portal venous gas, the principle rationale for performing hyperbaric therapy is to prevent subsequent central nervous system oxygen embolization. CASE REPORT: We describe a patient with portal venous gas identified by computed tomography after the ingestion of 3% hydrogen peroxide, managed without hyperbaric therapy, who subsequently developed portal venous thrombosis. We are not aware of this complication being previously described from hydrogen peroxide ingestion. The case is complicated by the coexistence of a self-inflicted stab wound, leading to exploratory laparotomy in a patient predisposed to arterial vascular occlusion. Why Should an EmergencyPhysicianBeAware of This? Emergency physicians will encounter patients after the ingestion of hydrogen peroxide who, despite not having symptoms of central nervous system emboli, have portal venous gas identified on radiographic imaging. Being aware that the principle rationale for prophylactic utilization of hyperbaric therapy is to prevent subsequent central nervous system emboli, and that in at least one case, delayed-onset portal venous thrombosis has occurred without hyperbaric therapy may help contribute to clinical decision-making.

Application of a new hyperbaric oxygen therapy protocol in patients with arterial and venous gas embolism due to hydrogen peroxide poisoning.

Hydrogen peroxide (H2O2) ingestion can cause vascular gas embolism (GE). Hyperbaric oxygen therapy (HBO2) is known to improve neurological abnormalities in patients with arterial gas embolism (AGE). Previously, HBO2 based on the U.S. Navy Table 6 diving protocol has been adopted for treating AGE and preventing the progression of portal venous GE, caused by H2O2 ingestion, to AGE. However, the indication and protocol for HBO2 have not been established for GE related to H2O2 ingestion. Herein, we describe a case in which GE caused by H2O2 ingestion was treated using HBO2 with a short protocol. A 69-year-old female patient presented with abdominal pain, vomiting, and transient loss of consciousness after ingesting 35% H2O2. Computed tomography revealed gastric wall and portal venous gas. She was administered an HBO2 protocol with 2.8-atmosphere absolute (ATA) compression for 45 minutes. This was followed by a 2.0-ATA treatment for 60 minutes with a five-minute air break, after which all gas bubbles disappeared. After HBO2 treatment, brain magnetic resonance imaging revealed focal cytotoxic edema lesions; however, the patient was discharged without additional symptoms.

Induction of Contralateral Hepatic Hypertrophy by Unilobar Yttrium-90 Transarterial Radioembolization versus Portal Vein Embolization: An Animal Study.

PURPOSE: To compare hepatic hypertrophy in the contralateral lobe achieved by unilobar transarterial radioembolization (TARE) versus portal vein embolization (PVE) in a swine model. METHODS: After an escalation study to determine the optimum dose to achieve hypertrophy after unilobar TARE in 4 animals, 16 pigs were treated by TARE (yttrium-90 resin microspheres) or PVE (lipiodol/n-butyl cyanoacrylate). Liver volume was calculated based on CT before treatment and during 6 months of follow-up. Independent t-test (P < .05) was used to compare hypertrophy. The relationship between hypertrophy after TARE and absorbed dose was calculated using the Pearson correlation. RESULTS: At 2 and 4 weeks after treatment, a significantly higher degree of future liver remnant hypertrophy was observed in the PVE group versus the TARE group, with a median volume gain of 31% (interquartile range [IQR]: 16%-66%) for PVE versus 23% (IQR: 6%-36%) for TARE after 2 weeks and 51% (IQR: 47%-69%) for PVE versus 29% (IQR: 20%-50%) for TARE after 4 weeks. After 3 and 6 months, hypertrophy converged without a statistically significant difference, with a volume gain of 103% (IQR: 86%-119%) for PVE versus 82% (IQR: 70%-96%) for TARE after 3 months and 115% (IQR: 70%-46%) for PVE versus 86% (IQR: 58%-111%) for TARE after 6 months. A strong correlation was observed between radiation dose (median 162 Gy, IQR: 139-175) and hypertrophy. CONCLUSIONS: PVE resulted in rapid hypertrophy within 1 month of the procedure, followed by a plateau, whereas TARE resulted in comparable hypertrophy by 3-6 months. TARE-induced hypertrophy correlated with radiation absorbed dose.

Imaging Changes and Clinical Complications After Drug-Eluting Bead Versus Conventional Transarterial Chemoembolization for Unresectable Hepatocellular Carcinoma: Multicenter Study.

BACKGROUND. Drug-eluting bead transarterial chemoembolization (DEB-TACE) has emerged as an alternative to conventional TACE (cTACE) for treatment of hepatocellular carcinoma (HCC), although selection between the approaches remains controversial. OBJECTIVE. The purpose of this study was to compare DEB-TACE and cTACE in the treatment of patients with unresectable HCC in terms of hepatobiliary changes on imaging and clinical complications. METHODS. This retrospective study included 1002 patients (871 men, 131 women; mean age, 59 ± 12 years) from three centers who had previously untreated unresectable HCC and underwent DEB-TACE with epirubicin (780 procedures in 394 patients) or cTACE with ethiodized oil mixed with doxorubicin and oxaliplatin (1187 procedures in 608 patients) between May 2016 and November 2018. Among these patients 83.4% had hepatitis B-related liver disease, 57.6% had Barcelona Clinic Liver Cancer (BCLC) stage A or B HCC, and 42.4% had three or more nodules. Mean tumor size was 6.3 ± 4.2 cm. Hepatobiliary changes and tumor response were evaluated with CT or MRI 1 month after TACE. Clinical records were reviewed for adverse events. RESULTS. Bile duct dilatation (p < .001) and portal vein narrowing (p = .006) on imaging and liver failure (p = .03) and grade 3 abdominal pain (p < .001) in clinical follow-up occurred at higher frequency in the DEB-TACE group (15.5%, 4.6%, 2.3%, and 6.1%) than in the cTACE (7.4%, 1.6%, 0.7%, and 2.1%) group. Higher frequency of bile duct dilation in patients who underwent DEB-TACE was observed in subgroup analyses that included patients with BCLC stage A or B HCC (p = .001), with cirrhosis (p < .001), without cirrhosis (p = .04), and without main portal vein tumor thrombus (p = .002). Total bilirubin level 1 month after treatment was 1.5 ± 2.4 mg/dL (95% CI, 1.2-1.8 mg/dL) for DEB-TACE versus 1.3 ± 2.0 mg/dL (95% CI, 1.1-1.5 mg/dL) for cTACE (p = .02). The cTACE and DEB-TACE groups did not differ in other manifestations of postembolization syndrome or systemic toxicity (p > .05). Local tumor disease control rates did not differ between the cTACE and DEB-TACE groups (1 month, 96.7% vs 98.5%, p = .06; 3 months, 81.8% vs 82.4%, p = .87), but overall DCR was significantly higher in the cTACE than in the DEB-TACE group (1 month, 87.5% vs 80.0%, p = .001; 3 months, 78.5% vs 72.1%, p = .02). CONCLUSION. Compared with cTACE, DEB-TACE was associated with greater frequency of hepatobiliary injury and severe abdominal pain. CLINICAL IMPACT. Greater caution and closer follow-up are warranted for patients who undergo DEB-TACE for unresectable HCC than for those who undergo cTACE.

Successful management of portal vein thrombosis in a Yorkshire Terrier with protein-losing enteropathy.

BACKGROUND: Portal vein thrombosis (PVT) is a rare presentation in dogs with protein-losing enteropathy (PLE). Rivaroxaban, an oral, selective, direct factor Xa inhibitor, has not been reported to be administrated for canine PVT and the effect is unclear in dogs with PLE. CASE PRESENTATION: An 11-year-old Yorkshire Terrier presented with moderate ascites. The dog had severe hypoalbuminemia (1.2 g/dL), and a portal vein thrombus was confirmed on computed tomographic angiography (CTA). On endoscopic examination, it became apparent that the hypoalbuminemia was caused by PLE, which was consequent of lymphatic dilation and lymphoplasmacytic enteritis. Therefore, the dog was initially treated with oral administrations of spironolactone and clopidogrel, with dietary fat restriction. However, a follow-up CTA showed no changes in the ascites, thrombus, and portal vein to aorta (PV/Ao) ratio. Therefore, the dog was additionally prescribed rivaroxaban and low-dose prednisolone for the portal vein thrombus and hypoalbuminemia due to lymphoplasmacytic enteritis, respectively. Following the treatment, the PV/Ao ratio decreased because of a decrease in the thrombus and the ascites disappeared completely with an elevation of albumin concentration (1.9 g/dL). CONCLUSIONS: This case report demonstrated that oral administration of rivaroxaban combined with low-dose glucocorticoid was effective management for PVT in a dog with PLE.

Clinical management of type C hepatic encephalopathy.

Type-C hepatic encephalopathy is a complex neurological syndrome, characteristic of patients with liver disease, causing a wide and complex spectrum of nonspecific neurological and psychiatric manifestations, ranging from a subclinical entity, minimal hepatic encephalopathy, to a deep form in which a complete alteration of consciousness can be observed: overt hepatic encephalopathy. Overt hepatic encephalopathy occurs in 30-40% of patients. According to the time course, hepatic encephalopathy is subdivided into episodic, recurrent and persistent. Diagnostic strategies range from simple clinical scales to more complex psychometric and neurophysiological tools. Therapeutic options may vary between episodic hepatic encephalopathy, in which it is important to define and treat the precipitating factor and hepatic encephalopathy and secondary prophylaxis, where the standard of care is non-absorbable disaccharides and rifaximin. Grey areas and future needs remain the therapeutic approach to minimal hepatic encephalopathy and issues in the design of therapeutic studies for hepatic encephalopathy.

Measuring the density of iodine depositions: Detecting an invisible residual tumor after conventional transarterial chemoembolization.

PURPOSE: The purpose of this study is to evaluate the use of density measurements in the diagnosis of an underlying residual tumor beyond iodine depositions after Lipiodol-based conventional transarterial chemoembolization (cTACE). METHOD AND MATERIALS: Thirty follow-up CT scans of 20 patients 6-12 weeks after Lipiodol-based cTACE, receiving a digital subtraction angiography at the same time, were analyzed. Reference for the detection of a residual tumor was the angiography, and a visible contrast enhancement was categorized as a residual tumor (n = 16 with residual tumor; n = 14 without residual tumor). The density of the iodine depositions was measured in all containing slices in non-contrast-, arterial- and portal venous-phase CT scans, with a slice thickness of 5.00 mm. The mean density of the iodine deposition during the portal venous phase was subtracted from the mean density of the arterial phase to calculate the density changes (a positive enhancement score represents washout in the portal venous phase). In addition, a quotient relating to the non-contrast measurement was evaluated. RESULTS: Patients with a residual tumor displayed significantly higher enhancement scores in favor of density reduction between the arterial and portal venous phases, compared to patients without a residual tumor (1.41 ± 3.59, n = 14 vs. -13.97 ± 2.88, n = 16; p-value < 0.01). Furthermore, 87.75% of patients with an enhancement score higher than -1.00 (n = 9) had a residual tumor, whereas 100.00% of patients with an enhancement score lower than -20.00 (n = 6) were shown to be tumor-free. The enhancement score quotient resulted in similar findings. CONCLUSION: After cTACE in patients with hepatocellular carcinoma (HCC), the presence of a viable tumor correlated with enhancement scores based on the density measurements of iodine depositions in different phases of the CT scan. Low enhancement scores were associated with completely treated tumors and can aid the decision process to avoid possibly unnecessary angiographies.

Low-molecular-weight heparin followed by rivaroxaban for acute occlusive portomesenteric vein thrombosis in a cirrhotic patient treated with multiple endoscopic variceal procedures.

Acute portomesenteric vein thrombosis is potentially lethal. In the present paper, a cirrhotic patient with a previous history of esophageal variceal bleeding presented with acute occlusive portomesenteric vein thrombosis, but achieved complete recanalization by low-molecular-weight heparin followed by rivaroxaban. Notably, no bleeding episode occurred during anticoagulation therapy. This case supported early initiation of anticoagulation in such patients.

Randomized controlled trial of rivaroxaban versus warfarin in the management of acute non-neoplastic portal vein thrombosis.

BACKGROUND AND AIM: Anticoagulation therapy is the main line of treatment for acute portal vein thrombosis (PVT) in the absence of cirrhosis. However, the use of this therapy in cirrhotic PVT is still with doubtful evidence. We aimed to evaluate the efficacy and safety of rivaroxaban compared to warfarin for the management of acute non-neoplastic PVT in Hepatitis C virus (HCV)-related compensated cirrhosis. METHODS: Out of 578 patients with chronic HCV infection, 80 patients with acute PVT who had undergone splenectomy due to hypersplenism and 4 patients with acute PVT due to portal pyemia were selected. The patients were randomly assigned (1:1) to the study group (n = 40), in which the patients received rivaroxaban 10 mg/12 h, or the control group (n = 40), in which the patients received warfarin. RESULTS: In the rivaroxaban group, the resolution of PVT was achieved in 34 patients (85%) within 2.6 ±â€¯0.4 months and delayed, partial recanalization after 6.7 ±â€¯1.2 months (n = 6.15%). Complications such as major bleeding, abnormal liver functions, death, or recurrence did not occur during treatment, and patients in this group showed improved short-term survival rate (20.4 ±â€¯2.2 months) compared to the survival rate in the control group (10.6 ±â€¯1.8 months) in which warfarin achieved complete resolution in 45% of patients. Complications such as severe upper GI tract bleeding (43.3%), hepatic decompensation (22.5%), progression to mesenteric ischemia (12.5%), recurrence (10%), and death (20%) were observed in the control group. The duration until complete resolution of thrombus correlated with age, the extent of the thrombus, creatinine level, and MELD score. The recurrence after complete resolution of thrombus correlated with age, the extent of the thrombus, thrombogenic gene polymorphism, and the use of warfarin. CONCLUSION: Rivaroxaban was effective and safe in acute HCV-related non-neoplastic PVT with improved short-term survival rate; ClinicalTrials.gov Identifier: NCT03201367.

Accidental Concentrated Hydrogen Peroxide Ingestion Associated with Portal Venous Gas.

A case of a 52-year old male patient who presented to the emergency department with severe nausea and vomiting following accidental ingestion of H2O2. A computed tomography (CT) abdomen performed at our institution demonstrated extensive portal venous gas throughout the liver with few gas droplets seen in the extrahepatic portal vein portion. Pneumatosis was also noted in the wall of the gastric antrum. Upper GI Endoscopy was done revealing diffuse hemorrhagic gastritis and mild duodenal bulb erosion. The patient was treated with hyperbaric oxygen. On the second day of admission, the patient was able to eat without difficulty or pain. Accidental ingestion of high concentration H2O2 solution has been shown to cause extensive injury to surrounding tissues. The injury occurs via three main mechanisms: corrosive damage, oxygen gas formation, and lipid peroxidation. We report a case of accidental ingestion of a highly concentrated (35%) solution of H2O2 causing portal venous gas.

Evaluation of the relationship between hepatocellular carcinoma location and transarterial chemoembolization efficacy.

AIM: To evaluate the relationship between the location of hepatocellular carcinoma (HCC) and the efficacy of transarterial chemoembolization (TACE). METHODS: We evaluated 115 patients (127 nodules), excluding recurrent nodules, treated with TACE between January 2011 and June 2014. TACE efficacy was evaluated according to mRECIST. The HCC location coefficient was calculated as the distance from the central portal portion to the HCC center (mm)/liver diameter (mm) on multiplanar reconstruction images rendered (MPR) to visualize bifurcation of the right and left branches of the portal vein and HCC center. The HCC location coefficient was compared between complete response (CR) and non-CR groups in Child-Pugh grade A and B patients. RESULTS: The median location coefficient of HCC among all nodules, the right lobe, and the medial segment was significantly higher in the CR group than in the non-CR group in the Child-Pugh grade A patients (0.82 vs 0.62, P < 0.001; 0.71 vs 0.59, P < 0.01; 0.81 vs 0.49, P < 0.05, respectively). However, there was no significant difference in the median location coefficient of the HCC in the lateral segment between in the CR and in the non-CR groups (0.67 vs 0.65, P > 0.05). On the other hand, in the Child-Pugh grade B patients, the HCC median location coefficient in each lobe and segment was not significantly different between in the CR and in the non-CR groups. CONCLUSION: Improved TACE efficacy may be obtained for HCC in the peripheral zone of the right lobe and the medial segment in Child-Pugh grade A patients.

Elimination of CT-detected gas bubbles derived from decompression illness with abdominal symptoms after a short hyperbaric oxygen treatment in a monoplace chamber: a case report.

We report the case of a 54-year-old male compressed-air worker with gas bubbles detected by computed tomography (CT). He had complained of strong abdominal pain 30 minutes after decompression after working at a pressure equivalent to 17 meters of sea water for three hours. The initial CT images revealed gas bubbles in the intrahepatic portal vein, pulmonary artery and bilateral femoral vein. After the first hyperbaric oxygen treatment (HBO2 at 2.5 atmospheres absolute/ATA for 150 minutes), no bubbles were detected on repeat CT examination. The patient still exhibited abdominal distension, mild hypesthesia and slight muscle weakness in the upper extremities. Two sessions of U.S. Navy Treatment Table 6 (TT6) were performed on Days 6 and 7 after onset. The patient recovered completely on Day 7. This report describes the important role of CT imaging in evaluating intravascular gas bubbles as well as eliminating the diagnosis of other conditions when divers or compressed-air workers experience uncommon symptoms of decompression illness. In addition, a short treatment table of HBO2 using non-TT6 HBO2 treatment may be useful to reduce gas bubbles and the severity of decompression illness in emergent cases.

Jugular and Portal Vein Volume, Middle Cerebral Vein Velocity, and Intracranial Pressure in Dry Immersion.

BACKGROUND: The objective was to determine if short term exposure to dry immersion (DI) results in a cephalic fluid shift similar to what has been observed with spaceflight. METHODS: Data were collected from 10 individuals at rest and during the first 2 h of dry immersion. Jugular vein (JV), portal vein (PV), and thyroid volume were measured using 3D echography. Middle cerebral vein velocity (MCVv) was determined using transcranial Doppler ultrasound. The cochlear response to audio stimulation was used to derive an estimate of intracranial pressure (dICP). RESULTS: After 2 h of DI, there was a significant increase (mean ± SD) in JV (2.21 ± 1.10 mL), PV (1.05 ± 0.48 mL), and thyroid (0.428 ± 0.313 mL) volume. MCVv was also significantly increased with DI (3.90 ± 5.03 cm · s-1). There was no change in dICP with DI in part due to large individual variability. The range of dICP changes appeared to be related to MCVv, with participants with the largest increase in MCVv also showing increased dICP. DISCUSSION: The results suggest that DI induces a significant cephalic fluid shift similar to what is observed with spaceflight. The increased thyroid volume suggests that cerebral tissue may also be subjected to similar fluid filtration, with implications for changes in intracranial pressure. However, despite all participants having an increase in JV and thyroid volume, only half showed an increase in dICP, suggesting that increased venous pooling alone is not sufficient to cause increased intracranial pressure.Arbeille P, Avan P, Treffel L, Zuj K, Normand H, Denise P. Jugular and portal vein volume, middle cerebral vein velocity, and intracranial pressure in dry immersion. Aerosp Med Hum Perform. 2017; 88(5):457-462.