We describe in this paper a rare case of a 45-year-old male with a common stem origin of the left gastric artery (LGA), right inferior phrenic artery (RIPA), and left inferior phrenic artery (LIPA), in association with the presence of a hepatosplenomesenteric trunk (HSMT) arising from the abdominal aorta (AA), as revealed by routine multidetector computed tomography (MDCT) angiography. The common stem origin of the LGA, RIPA, and LIPA had an endoluminal diameter of 3.3 mm, the LGA of 2.8 mm. The endoluminal diameter of the RIPA and LIPA was at the origin of approximately 1 mm, complicating selective chemoembolization of the liver parenchyma.
The authors report a case of a 44-year-old male found to have unusual origins of the celiac trunk (CT) and superior mesernteric artrery (SMA) as revealed by routine multidetector computed tomograph (MDCT) angiography. The CT and SMA originate from the thoracic aorta (TA) 21 mm and 9 mm above the aortic hiatus, respectively. The median arcuate ligament (MAL) is located at the level of the L1-L2 intervertebral disc. The course of the CT descends in the thoracic cavity making a 14° acute downward angle in front of the TA; below the level of the MAL, the CT descends, making an angle of 47°. The course of the SMA descends at both the thoracic and abdominal level making an angle of 17°, and having an aortomesenteric distance of 9 mm at the level of the third part of the duodenum. In the present case, the supradiaphragmatic origin of the CT and the SMA was determined by their incomplete caudal descent, associated with a pronounced apparent descent of the diaphragm. A thoracic origin of the CT and SMA and the acute downward aortomesenteric angle (17°) associated with a reduced aortomesenteric distance at the level of the third part of the duodenum (9 mm), although no clinical signs are present, may predispose the patient to develop simultaneously a triple syndrome: the compression of CT by MAL (celiac axis compression syndrome), the compression of SMA by MAL (superior mesenteric artery compression syndrome), and the compression of the duodenum by the SMA (superior mesenteric artery syndrome).
Aim: Contrast enhanced ultrasound (CEUS) improved the characterization of focal liver lesions (FLLs), but is an operatordependent method. The goal of this paper was to test a computer assisted diagnosis (CAD) prototype and to see its benefit in assisting a beginner in the evaluation of FLLs.Material and method: Our cohort included 97 good quality CEUS videos[34% hepatocellular carcinomas (HCC), 12.3% hypervascular metastases (HiperM), 11.3% hypovascular metastases (HipoM), 24.7% hemangiomas (HMG), 17.5% focal nodular hyperplasia (FNH)] that were used to develop a CAD prototype based on an algorithm that tested a binary decision based classifier. Two young medical doctors (1 year CEUS experience), two experts and the CAD prototype, reevaluated 50 FLLs CEUS videos (diagnosis of benign vs. malignant) first blinded to clinical data, in order to evaluate the diagnostic gap beginner vs. expert. Results: The CAD classifier managed a 75.2% overall (benign vs. malignant) correct classification rate. The overall classification rates for the evaluators, before and after clinical data were: first beginner-78%; 94%; second beginner-82%; 96%; first expert-94%; 100%; second expert-96%; 98%. For both beginners, the malignant vs. benign diagnosis significantly improved after knowing the clinical data (p=0.005; p=0,008). The expert was better than the beginner (p=0.04) and better than the CAD (p=0.001). CAD in addition to the beginner can reach the expert diagnosis. Conclusions: The most frequent lesions misdiagnosed at CEUS were FNH and HCC. The CAD prototype is a good comparing tool for a beginner operator that can be developed to assist the diagnosis. In order to increase the classification rate, the CAD system for FLL in CEUS must integrate the clinical data.
(1) Objective: This review paper aims to discuss multiple aspects of cerebral venous thrombosis (CVT), including epidemiology, etiology, pathophysiology, and clinical presentation. Different neuroimaging methods for diagnosis of CVT, such as computer tomography CT/CT Venography (CTV), and Magnetic Resonance Imaging (MRI)/MR Venography (MRV) will be presented. (2) Methods: A literature analysis using PubMed and the MEDLINE sub-engine was done using the terms: cerebral venous thrombosis, thrombophilia, and imaging. Different studies concerning risk factors, clinical picture, and imaging signs of patients with CVT were examined. (3) Results: At least one risk factor can be identified in 85% of CVT cases. Searching for a thrombophilic state should be realized for patients with CVT who present a high pretest probability of severe thrombophilia. Two pathophysiological mechanisms contribute to their highly variable clinical presentation: augmentation of venular and capillary pressure, and diminution of cerebrospinal fluid absorption. The clinical spectrum of CVT is frequently non-specific and presents a high level of clinical suspicion. Four major syndromes have been described: isolated intracranial hypertension, seizures, focal neurological abnormalities, and encephalopathy. Cavernous sinus thrombosis is the single CVT that presents a characteristic clinical syndrome. Non-enhanced CT (NECT) of the Head is the most frequently performed imaging study in the emergency department. Features of CVT on NECT can be divided into direct signs (demonstration of dense venous clot within a cerebral vein or a cerebral venous sinus), and more frequently indirect signs (such as cerebral edema, or cerebral venous infarct). CVT diagnosis is confirmed with CTV, directly detecting the venous clot as a filling defect, or MRI/MRV, which also realizes a better description of parenchymal abnormalities. (4) Conclusions: CVT is a relatively rare disorder in the general population and is frequently misdiagnosed upon initial examination. The knowledge of wide clinical aspects and imaging signs will be essential in providing a timely diagnosis.
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