Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen. A brief overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.
Pathologic increase in portal pressure can be caused by increased resistance to blood flow at the level of the portal vein (pre-hepatic), hepatic sinusoids (hepatic) or hepatovenous outflow (post-hepatic). This results in recruitment and dilatation of tiny portosystemic collateral pathways, diverting portal venous blood flow to low pressure systemic veins. Based on the location of the causative factor of portal venous resistance, different collateral pathways and shunts may develop, resulting in unique syndromes of portal hypertension and in-turn requiring unique treatment options. Knowledge of the common and less-common portosystemic collateral pathways have important implication for clinicians and interventionalists. The objective of this pictorial review is to illustrate the various collateral pathways using diagrammatic and conventional non-invasive and invasive radiologic examples. Additionally, we will briefly address minimally invasive interventional techniques used to treat the sequelae of portal hypertension.
BackgroundComputed tomographic angiography (CTA) has emerged as the defacto imaging test to rule out acute aortic dissection; however, it is not without flaws. We report a case of a false-positive CTA with respect to Stanford Type A aortic dissection.CaseA 52 year-old male presented with sudden onset shortness of breath. He denied chest pain. Due to severe hypertension and an Emergency Department bedside ultrasound suggesting an intimal flap in the aorta, CTA was requested to better assess the ascending aorta and was interpreted as consistent with Stanford Type A aortic dissection with thrombosis of the false lumen in the ascending aorta. However, intra-operative imaging (TEE and epi-aortic scanning) did not identify an intimal flap or dissection, and neither did definitive surgical inspection of the aorta. The suspected aortic dissection and thrombosed false lumen were not visualized on repeat CTA two days later.DiscussionFalse positive diagnosis of Stanford Type A aortic dissection on CTA can be the result of technical factors, streak artifacts, motion artifacts, and periaortic structures. In this case, non-uniform arterial contrast enhancement secondary to unrecognized biventricular dysfunction resulted in the false positive CTA appearance of an intimal flap and mural thrombus. Intra-operative TEE and epi-aortic scanning were proven correct in excluding aortic dissection by the standard of definitive surgical inspection of the aorta.
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