Anatomic variations are often responsible for a variety of clinical conditions. In this review we investigate compression of the celiac artery and the superior mesenteric artery by the median arcuate ligament (MAL), diaphragmatic crura, or the celiac nerve plexus. This clinical condition known as celiac artery compression syndrome (CACS) has proven controversial in definition and relevance. This condition was first described as chronic abdominal pain because of the mesenteric ischemia caused by extrinsic compression of the celiac artery. Dunbar and others presented surgical approaches to decompress the celiac artery by releasing the MAL. Definitive answers have been sought to classify and relieve the clinical symptoms patients experience postprandially. Persistent symptoms following surgical treatment for CACS have led investigators to question the existence of this disease. Advances in technology such as angiographic MRI and color duplex ultrasonography have refreshed the importance of considering compression of the celiac artery during differential diagnoses. Because of the varying anatomic etiologies of disease, it is not possible to pinpoint a single cause for CACS. Potential etiologies for compression of the celiac artery include a "high take off" origin of the celiac artery compressed by normal diaphragmatic crura and MAL, a normal origin of the celiac artery with long diaphragmatic crura and MAL, large bilaterally fused celiac ganglia (with or without the involvement of the superior mesenteric ganglia) compressing the celiac trunk, celiacomesenteric trunk compression by diaphragmatic crura and MAL, or combinations of the above mentioned entities. In this review we describe potential sources of compression of the celiac artery by regional structures and treatments of CACS in an effort to justify the relevance of CACS in modern medicine.

Anomalies in the course and drainage of the Inferior Vena Cava (IVC) may complicate normal functioning, correct diagnosis, and therapeutic interventions within the abdomen. Development of the IVC occurs during the 4th to 8th week of gestation, and due to its developmental complexity, there are many opportunities for malformations to occur. Although most IVC anomalies are clinically silent and are usually discovered incidentally on abdominal imaging, aberrations may be responsible for formation of thrombosis, back pain, and anomalous circulation of blood to the heart. In this review, we will discuss the most common variations and abnormalities of the IVC, which include the posterior cardinal veins, the subcardinal veins, the supracardinal veins, persistent left IVC, IVC duplication, situs inversus, left retroaortic renal vein, left circumaortic renal collar, scimitar syndrome, and IVC agenesis. For each abnormality outlined above, we aim to discuss relevant embryology and potential clinical significance with regards to presentation, diagnosis, and treatment as is important for radiologists, surgeons, and clinicians in current clinical practice.

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: Risk, IV.