False lumen

A Intimal tear -Hntimal flap True lumen "False lumen... 

ADs occur due to a tear of the aortal intima and the inner layers of the media. This entry, which is most common in the lateral wall of the ascending aorta or in the aortic isthmus, leads to blood flow into the aortic wall and a consecutive separation of the media creating a false lumen. This lumen is separated from the true lumen by the dissection membrane. 

The differentiation of dissections with and without reentry is of cHnical relevance, since the risk of rupture is significantly higher in communicating dissections with a flow in the false lumen than in noncommunicating dissections with a thrombosed false lumen (Takahashi and Stanford 2005). It can be achieved by an additional nonenhanced scan or by additional late phases (70-120 s). 

The distinction between the true and false lumen is indispensable before endovascular aortic reconstruction (EVAR). Those lumens show the following characterizations ... 

The true lumen is characterized by an early and strong contrast enhancement and by continuity into the aortic sections, which are not affected by the dissection. It often shows a smaller diameter than the false lumen. 

The false lumen is characterized by a mostly sickleshaped configuration. Intimal flaps can be seen in some patients as small intraluminal lines looking like a cobweb, ( cobweb sign ). This sign is specific for the false lumen and can sometimes simplify the differentiation. 

Fig. 23.7a c. Stanford type A dissection with two separate false lumens. Axial (a) and coronary (b) standard MPR and a VR of the data in coronary and sagittal orientations (c). The lateral false lumen is partially thrombosed and shows a significant decrease of the blood flow. The medial false lumen shows a... 

The challenge for spinal artery CTA is to provide sufficient arterial enhancement but to scan before arrival of contrast medium in the venous system. An ROI of the bolus tracking system placed in the ascending aorta might be affected by inflow artifacts of the SVC and may result in a mistimed early scan. Therefore, placement of the ROI in the aortic arch or descending aorta is recommended. In the presence of aortic dissection, caution should be taken that the ROI is not too big or positioned in the false lumen or across the dissection membrane, respectively. In these cases, manual start of the scan should be considered. The Hounsfield unit threshold should be around 100 HU above baseline. Scan start is usually delayed by time for table movement (<3 s), which is usually right above the origin of the vertebral arteries. An additional scan delay of 3 s is recommended for scanners with equal to or more than 16 rows and rotation time equal or less than 0.4 s. Hounsfield unit values of attenuated blood in the thoracic aorta should never be lower than within the pulmonary trunk. 

The presence of cranial neuropathy may result in a misdiagnosis of brainstem stroke. Cranial nerve palsies may result from local pressure from the false internal carotid artery lumen, thromboembolism or hemodynamic compromise to the blood supply of the nerve. Cranial nerve III receives its blood supply from the ophthalmic artery, branches of the internal carotid or the posterior cerebral artery and, consequently, may rarely become ischemic after carotid dissection. 

The absolute level of ammonia and its metabolites, such as glutamine, in the blood or cerebrospinal fluid in patients with hepatic encephalopathy correlates only roughly with the presence or severity of the neurologic signs and symptoms. y-Aminobutyric acid (GABA), an important inhibitory neurotransmitter in the brain, is also produced in the gut lumen and is shunted into the systemic circulation in increased amounts in patients with hepatic failure. In addition, other compounds (such as aromatic amino acids, false neurotransmitters, and certain short-chain fatty acids) bypass liver metabolism and accumulate in the systemic circulation, adversely affecting central nervous system function. Their relative importance in the pathogenesis of hepatic encephalopathy remains to be determined. 

Classification of intracranial aneurysms may be based on morphology, size, location and etiology. The majority of intracranial aneurysms are true aneurysms containing all layers or components of the normal vessel wall. In contrast, in false aneurysms or pseudoaneurysms, the vascular lumen does not enlarge, although the external diameter of the abnormal segment may be increased. These aneurysms are rare within the skull. 

Vessel wall calcifications may deteriorate the visualization of the coronary artery lumen through the effect of blooming. The blooming artifact results in an artificial obscuring of the vessel lumen, causing an overestimation of the degree of stenosis. This overestimation leads to false-positive findings that are associated with a dechne in the specificity and positive... 

A soft plaque at the initial stage of calcification may have an overall density of less than 400 HU. Should we now fill the vascular lumen with more than 400 HU of iodine contrast, some of the calcified structures adjacent to the lumen might be obscured and undiscernible from lumen territory on cross-sectional cuts (Fig. 16.3). This may potentially result in false-negative findings on coronary angiograms, which would constitute a worst-case scenario for the current clinical appHcation of the modahty. 

CTA enables the diagnosis of AD and its differentiation according to the Stanford classification, with a sensitivity and specificity of over 99% (Hayter et al. 2006). RadiologicaUy, the primary intimal tear (entry) and the extension of the AD should be located. Additionally, distal connections between the false and the true lumen (reentries) have to be located. In case of a circumferential dissection, there is an intimo-intimal intussusception and a floating true lumen in the center. A missing contrast enhancement of the lumen arises either from a significant reduction of the blood flow or from a thrombosis. 

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