Purpose: Neurofibromatosis type 1 (NF1) is an autosomal-dominant disorder found in approximately 1 of every 3000 individuals. Neurofibromatosis type 1 can have vascular manifestations including aneurysms, stenoses, and arteriovenous malformations. The purpose of this article is to describe the clinical manifestations of NF1 vasculopathy, discuss therapeutic options, and highlight endovascular therapies from our institutional experience. Materials and Methods: The radiology information system was searched for cases of NF1. Cases with vasculopathy managed with endovascular therapies were included. Demographics, clinical histories, procedural details, and outcomes were recorded. A review of the literature for the management strategies of NF1 vasculopathy was performed. Results: Two pediatric patients with NF1 were identified, both of whom presented with hypertension found to be secondary to renal artery stenosis. One of the patients also had infrarenal aortic narrowing. Both patients were successfully treated with balloon angioplasty, resulting in improved blood pressures. The review of the literature identified case series of pharmacologic, surgical, and endovascular therapies, although, endovascular therapies appear to be preferred due to lower morbidity and mortality. Conclusions: NF1 vasculopathy is a rare condition that most often presents with hypertension due to renal artery stenosis. In these situations, endovascular management is the preferred approach.

BackgroundSeveral peritoneal dialysis catheter (PDC) placement techniques have been described. The objective of this study was to compare the fluoroscopy and ultrasound guidance technique with the laparoscopic technique.MethodsWe retrospectively reviewed the medical records of 260 patients who had their first PDC placed between January 2005 and June 2016. We compared the outcomes of the fluoroscopic and ultrasound-guided catheter placement technique (radiologic group, n = 50) with the laparoscopic catheter placement technique (laparoscopic group, n = 190). The primary endpoint was complication-free catheter survival at 365 days. Secondary endpoints were complication-free catheter survival at 90 days, overall catheter survival at 90 and 365 days, median days to first complication and median days to catheter removal.ResultsIn the radiologic group, the complication-free catheter survival at 90 and 365 days was 64% and 48%, respectively, while in the laparoscopic group it was 71% (P = 0.374) and 53% (P = 0.494), respectively. Catheter malfunction was significantly higher in the laparoscopic group (30%) compared with the radiologic group (16%, P = 0.048). The overall catheter survival at 90 and 365 days was 76% and 52%, respectively, in the radiologic group, while in the laparoscopic group it was 88% (P = 0.0514) an 48% (P = 0.652), respectively. There was no significant difference in the median days to first complication and the median days to catheter removal between the two groups (P = 0.71).ConclusionThe technique of fluoroscopic and ultrasound-guided PDC placement is a clinically effective and safe alternative to laparoscopic catheter placement with similar survival and complication rates.

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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.