Our retrospective data indicated that IVN tumors were twice as common as SVN tumors. The nerve of origin did not affect facial nerve outcomes but did impact hearing preservation rates. Patients with tumors <1 cm in size had the best chance for hearing preservation. Overall facial nerve preservation was excellent with >90% achieving HB 1 to 3 function at final follow-up.
Cerebrospinal fluid leak rates were similar in patients undergoing TL, SO, and MCF approaches, and CSF rhinorrhea was not decreased by ET packing. Patients whose ETs are packed with Proplast are at risk for extrusion and otorrhea years after their initial VS resection.
Although a reporting expectation increased the total number of reports, the majority of IMRs did not maintain a 1 or more PSE report per month despite positive attitudes.
Nodular regenerative hyperplasia (NRH) is an uncommon condition, but an important cause of noncirrhotic intrahepatic portal hypertension (NCIPH), characterized by micronodules of regenerative hepatocytes throughout the liver without intervening fibrous septae. Herein, we present a case of a thirty-seven-year-old female with systemic lupus erythematosus (SLE) who was discovered to have significant esophageal varices on endoscopy for dyspepsia. Her labs revealed a slight elevation in the alkaline phosphatase and mild thrombocytopenia. Abdominal MRI revealed seven focal hepatic masses, splenomegaly, no ascites, and a patent portal vein. Ultrasound-guided core biopsy was reported as focal nodular hyperplasia. However, her varices persisted despite treatment with beta-blockers and four additional upper endoscopies with banding. She was subsequently referred for a surgical opinion. At that time, given her history of SLE, azathioprine use, and portal hypertension, suspicion for NRH was raised. Given her normal synthetic function and lack of parenchymal liver disease, the patient was offered surgical shunting. During shunt surgery, a liver wedge biopsy was also performed and this confirmed NRH. An upper endoscopy six weeks after shunting verified complete resolution of varices. Currently, fifteen months after surgery duplex ultrasonography demonstrates shunt patency and the patient is without recurrence of her portal hypertension.
Introduction:A novel case is reported of upper gastrointestinal (UGI) bleeding from sinistral portal hypertension, caused by a left gastric artery (LGA) pseudoaneurysm (PA) compressing the splenic vein (SV) that was successfully treated with PA embolization.Case report:A 41-year-old man with previous medical history of recurrent, alcoholic pancreatitis presented with several episodes of hematemesis and abdominal pain for 48 hours. Physical examination revealed a soft abdomen, with no abdominal bruit, no pulsatile abdominal mass, and no stigmata of chronic liver disease. The hemoglobin declined acutely from 12.3 to 9.3 g/dL. Biochemical parameters of liver function and routine coagulation profile were entirely within normal limits. Abdominal CT revealed a 5-cm-wide peripancreatic mass compressing the stomach and constricting the SV. Esophagogastroduodenoscopy showed blood oozing from portal hypertensive gastropathy, small nonbleeding gastric cardial and fundal varices, gastric compression from the extrinsic mass, and no esophageal varices. MRCP and angiography showed that the mass was vascular, arose from the LGA, compressed the mid SV without SV thrombosis, and caused sinistral portal hypertension. At angiography, the PA was angioembolized and occluded. The patient has been asymptomatic with no further bleeding and a stable hemoglobin level during 8 weeks of follow-up.Discussion:Literature review of the 14 reported cases of LGA PA revealed that this report of acute UGI bleeding from sinistral portal hypertension from a LGA PA constricting the SV is novel; one previously reported patient had severe anemia without acute UGI bleeding associated with sinistral portal hypertension from a LGA PA.Conclusion:A patient presented with UGI bleeding from sinistral portal hypertension from a LGA PA compressing the SV that was treated by angiographic obliteration of the PA which relieved the SV compression and arrested the UGI bleeding. Primary therapy for this syndrome should be addressed to obliterate the PA and not the secondarily constricted SV.
A biliary enteric fistula (BEF) is a rare, abnormal communication between any segment of the biliary tree with any portion of the small or large intestine. BEF is more frequently diagnosed with the increasingly widespread use of endoscopic retrograde cholangiopancreatography. Different theories have been postulated regarding the etiology of this fistula formation, with the most likely cause being gallstones. Treatment modalities, ranging from conservative management to surgical reconstruction, show varying levels of success. We present a case of BEF secondary to large common bile duct stones, successfully treated with endoscopic sphincterotomy (EST) followed by papillary balloon dilatation, and we briefly discuss large stone retrieval in the setting of atypical anatomy.
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