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Anatomy of the Anterior Abdominal Wall
Published in Jeff Garner, Dominic Slade, Manual of Complex Abdominal Wall Reconstruction, 2020
The thoracic aorta gives rise to nine pairs of segmental arteries – the (3rd–11th) intercostal arteries and the (12th) subcostal arteries. These vessels follow the same course as the spinal nerves described earlier. The 10th and 11th intercostal arteries pass deep to the costal margin to supply the lateral zone and anastomose with the subcostal, superior epigastric and lumbar arteries. The intercostal arteries above this level do not enter the abdominal wall but terminate by anastomosing with the musculophrenic arteries and may contribute to the blood supply of the abdominal wall through this route. Remember that in patients who have undergone coronary artery bypass grafting the left internal thoracic artery is likely to have been disconnected from the superior epigastric artery, and flow into the vessel will be through this intercostal anastomosis. This may not be sufficient to support a TRAM flap.
Paper 4
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Inferior rib notching in aortic coarctation is caused by dilated intercostal vessels which act as collateral supply bypassing blood to the thoracic aorta distal to the coarctation. Unilateral left inferior rib notching is seen in aortic coarctation when there is an anomalous origin of the right subclavian artery distal to the coarctation. Anomalous origin of the left subclavian artery, a right-sided aortic arch with an anomalous left subclavian artery and a stenosed left subclavian artery are all potential causes of unilateral right inferior rib notching. The costocervical trunks are important anatomically as they arise directly from the subclavian arteries on both sides and supply the first and second intercostal arteries. The other intercostal arteries arise directly from the thoracic aorta, hence there is sparing of the first and second ribs from rib notching with aortic coarctation.
The Liver (LR)
Published in Narda G. Robinson, Interactive Medical Acupuncture Anatomy, 2016
Anterior intercostal arteries: Derived from the musculophrenic arteries (branches of the internal thoracic arteries), the 6th and 7th anterior intercostal arteries supply the 6th and 7th intercostal muscles, respectively, along with the pectoral muscles, the breasts, and the skin.
Hybrid Reconstruction of the Aortic Arch Using a Double-Branched Stent-Graft in a Canine Model
Published in Journal of Investigative Surgery, 2019
Fan Qiao, Cunhua Su, Qingqi Han, Mengwei Tan, Jun Wang, Yang Liu, Fanglin Lu, Lin Han, Zhiyun Xu
Gross morphometric observation of the target aorta showed that the stent-graft was firmly attached to the corresponding native aortic wall. In each dog, the luminal surface of the endoprosthesis had a thin, but full coverage layer of uniform yellow-white neo-intima, without any loosely attached mural thrombus. The proximal 2–4 pairs of intercostal arteries were always occluded by the graft. Representative microscopic images of the target aorta in both the experimental and normal animals are shown in Figures 5 and 6. As shown in Figure 5, sections of the graft-supporting segments of the aorta from the experimental group stained with H&E stain showed a normal arrangement of the media, adventitia, and circumferential, intimal proliferation with or without neo-microvessels, as compared with the sections from normal aorta. VVG-stained sections of the graft-supporting vessels from the experimental animals showed a normal distribution and density of the elastic fibers and collagen bundles in the medial and adventitial layer (Figure 6). Proliferated intima with an increased average thickness was noted. Moreover, the integrity of the internal elastic lamina in the experimental animals was moderately distorted by the extrusion of proliferated intima.
Acute necrotizing esophagitis presenting with severe lactic acidosis and shock
Published in Baylor University Medical Center Proceedings, 2018
Kenneth Iwuji, Sarah Jaroudi, Arpana Bansal, Ana Marcella Rivas
Although the etiology of acute esophageal necrosis is hypothesized to be multifactorial, vascular compromise seems to be a mainstay.2 The “two-hit” hypothesis describes an initial low flow state due to a vasculopathy or hemodynamic instability that leaves the esophageal mucosal barriers susceptible to gastric acid reflux insults in the setting of gastric outlet obstruction. The esophagus has an intricate vascular supply that is rarely susceptible to ischemia but in the case of the two-hit hypothesis can reveal transient necrosis that will rapidly recover with restoration of flow. The blood supply is distributed among segments of the esophagus, with the distal segment known as a “watershed” area where acute esophageal necrosis tends to be detected. The upper esophagus is supplied by the descending branches of the inferior thyroid arteries. The middle esophagus receives its blood supply from branches off the descending aorta that include the bronchial arteries, right third or fourth intercostal arteries, and esophageal arteries. Lastly, the distal esophagus derives its supply from the branches off the left gastric artery or left inferior phrenic artery. In addition, numerous contributions are derived from surrounding arteries leading to a rich vascular supply.2 This rich arterial connection makes ischemic esophagus necrosis a rare finding.
Recognition of alpha-mannan by dectin 2 is essential for onset of Kawasaki disease-like murine vasculitis induced by Candida albicans cell-wall polysaccharide
Published in Modern Rheumatology, 2020
Toshiaki Oharaseki, Yuki Yokouchi, Yasunori Enomoto, Wakana Sato, Kenichi Ishibashi, Noriko Miura, Naohito Ohno, Kei Takahashi
The coronary arteries dilate when the inflammation causes destruction of the internal elastic lamina and/or the medial smooth muscle, but the lumen often shows stenosis due to fibrocellular intimal thickening. That may also lead to myocardial infarction. Besides the coronary arteries, there is also involvement of the bifurcations of such medium-sized arteries as the renal arteries, common iliac artery, intercostal arteries, etc. and the nearby aorta. The inflammation in this model follows an acute, transient course. The histological time-phases of the vasculitis in the various organs are synchronous, so there is no mixing of acute inflammation and vasculitis scars such as seen in PAN.