Type II Endoleak:Transperitoneal Sacotomy and Ligation of Side Branch Endoleaks Responsible for Aneurysm Sac Expansion

2002 ◽  
Vol 9 (4) ◽  
pp. 539-542 ◽  
Author(s):  
Robert J. Hinchliffe ◽  
Ravinder Singh-Ranger ◽  
Simon C. Whitaker ◽  
Brian R. Hopkinson
Keyword(s):  
Side Branch ◽  
Type Ii

Sac Embolization and Side Branch Embolization for Preventing Type II Endoleaks After Endovascular Aneurysm Repair: A Meta-analysis

2019 ◽  
Vol 27 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Qiyi Li ◽  
Peiyong Hou
Keyword(s):  
Randomized Trials ◽  
Meta Analysis ◽  
Endovascular Aneurysm Repair ◽  
Side Branch ◽  
Type I ◽  
Type Ii ◽  
Related Complication ◽  
Type Ii Endoleak ◽  
Random Effects Models ◽  
Aneurysm Repair

Purpose:To investigate the efficacy and safety of preoperative side branch embolization or intraoperative sac embolization for preventing type II endoleaks after endovascular aneurysm repair (EVAR). Materials and Methods: A systematic literature search of MEDLINE and EMBASE was performed to identify studies that evaluated the outcomes of sac embolization vs no embolization or side branch embolization vs no embolization in patients who received EVAR. Among the 904 studies screened, 17 studies with 2084 participants were included in this review. Outcome measures included the type II endoleak rate, the reintervention rate for type II endoleaks, the incidence of types I/III endoleaks, and the rate of complications. Fixed (no heterogeneity) or random effects models were constructed for each outcome; the results are presented as the odds ratio (OR) with 95% confidence interval (CI). Results: The sac embolization group had significantly lower type II endoleak (OR 0.21, 95% CI 0.13 to 0.34, p<0.001) and reintervention (OR 0.15, 95% CI 0.07 to 0.33, p<0.001) rates than the no embolization group. No significant differences between the 2 groups were found for the type I/III endoleak rate (OR 0.57, 95% CI 0.23 to 1.37, p=0.21) or complication rate (OR 1.22, 95% CI 0.32 to 4.70, p=0.77). Compared with no embolization, side branch embolization was also associated with a decrease in type II endoleak (OR 0.35, 95% CI 0.21 to 0.60, p<0.001) and reinterventions (OR 0.10, 95% CI 0.04 to 0.27, p<0.001). One severe procedure-related complication (fatal colon ischemia) was reported in the side branch embolization group. Conclusion: Sac embolization and side branch embolization are safe and effective in preventing type II endoleaks. Further randomized trials are needed to directly compare the clinical outcomes of these procedures.

Systematic review and meta-analysis of prophylactic aortic side branch embolization to prevent type II endoleaks

2020 ◽  
Vol 72 (5) ◽  
pp. 1783-1792.e1 ◽  
Author(s):  
Hok Yee Harry Yu ◽  
David Lindström ◽  
Anders Wanhainen ◽  
Gustaf Tegler ◽  
Baderkhan Hassan ◽  
...  
Keyword(s):  
Systematic Review ◽  
Meta Analysis ◽  
Side Branch ◽  
Type Ii

Type II Endoleak: Transperitoneal Sacotomy and Ligation of Side Branch Endoleaks Responsible for Aneurysm Sac Expansion

2002 ◽  
Vol 9 (4) ◽  
pp. 539-542 ◽  
Author(s):  
Robert J. Hinchliffe ◽  
Ravinder Singh-Ranger ◽  
Simon C. Whitaker ◽  
Brian R. Hopkinson
Keyword(s):  
Computed Tomographic Angiography ◽  
Postoperative Recovery ◽  
Side Branch ◽  
Type Ii ◽  
Type Ii Endoleak ◽  
Computed Tomographic ◽  
Abdominal Aortic ◽  
The Face ◽  
Laparoscopic Techniques ◽  
Tomographic Angiography

Purpose: To demonstrate aneurysm sac expansion in the face of a type II endoleak and its treatment with open ligation of multiple side branch endoleaks. Case Report: An 81-year-old patient had undergone elective endovascular repair of a 6.3-cm infrarenal abdominal aortic aneurysm in September 1999. Routine spiral computed tomographic angiography at 10 months disclosed a type II endoleak; the aneurysm sac diameter had grown to 7.4 cm. Selective angiography revealed multiple lumbar endoleaks and a patent inferior mesenteric artery. Laparotomy and sacotomy was performed, confirming the presence of pulsatile type II endoleaks, which were ligated successfully. The patient made a full postoperative recovery. Conclusions: Type II endoleaks may cause aneurysm expansion. Open repair of multiple type II endoleaks is feasible and may be useful where endovascular or laparoscopic techniques are at high risk of procedural failure, such as multiple endoleak channels.

Aortic Side Branch Embolization before Endovascular Aneurysm Repair: Incidence of Type II Endoleak

2001 ◽  
Vol 12 (3) ◽  
pp. 337-341 ◽  
Author(s):  
Derek Alan Gould ◽  
Richard McWilliams ◽  
Richard David Edwards ◽  
Janis Martin ◽  
Donagh White ◽  
...  
Keyword(s):  
Endovascular Aneurysm Repair ◽  
Side Branch ◽  
Type Ii ◽  
Type Ii Endoleak ◽  
Aneurysm Repair

Type II Solar Radio Bursts over Solar Cycle 21

1994 ◽  
Vol 144 ◽  
pp. 283-284
Author(s):  
G. Maris ◽  
E. Tifrea
Keyword(s):  
Solar Radio ◽  
Interplanetary Space ◽  
Impulsive Phase ◽  
Radio Bursts ◽  
Type Ii ◽  
Solar Radio Bursts ◽  
Strong Energy ◽  
Mass Ejection ◽  
Geophysical Effect ◽  
Radio Event

The type II solar radio bursts produced by a shock wave passing through the solar corona are one of the most frequently studied solar activity phenomena. The scientific interest in this type of phenomenon is due to the fact that the presence of this radio event in a solar flare is an almost certain indicator of a future geophysical effect. The origin of the shock waves which produce these bursts is not at all simple; besides the shocks which are generated as a result of a strong energy release during the impulsive phase of a flare, there are also the shocks generated by a coronal mass ejection or the shocks which appear in the interplanetary space due to the supplementary acceleration of the solar particles.

Heat-Etching with a Bullivant Type II Simple Freeze-Cleave Device

1970 ◽  
Vol 28 ◽  
pp. 106-107 ◽  
Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt
Keyword(s):  
New Zealand ◽  
General Hospital ◽  
Massachusetts General Hospital ◽  
Type I ◽  
Type Ii ◽  
Collaborative Effort ◽  
Temperature And Pressure ◽  
The University

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

Mitochondria microcrystals deposition in some inherited diseases of lipid metabolism.

1978 ◽  
Vol 36 (2) ◽  
pp. 256-257
Author(s):  
S. Laoussadi ◽  
A. Kahan ◽  
G. Aubouy ◽  
F. Delbarre
Keyword(s):  
Synovial Tissue ◽  
Storage Disease ◽  
Metabolic Diseases ◽  
Uranyl Acetate ◽  
List Type ◽  
Type Ii ◽  
Type Number ◽  
Lipid Storage Disease ◽  
Thin Sections ◽  
Mean Size

Several patients with Fabry's, Gaucher's diseases and hyperlipoproteinemia type II and with arthropatic manifestations were observed.As no histological explanation for these symptoms was available,an ultrastructural study of synovial tissue was done to establish an anatomoclinical relation.Material and Methods :synovial membrane samples were obtained by needle biopsies of the knee from three patients with arthropatic manifestations of each disease.They were fixed in 5% glutaraldehyde, postfixed in 1% osmium tetraoxyde and embedded in Epon 812. Thin sections coloured by uranyl acetate and lead citrate were observed with an Elmiskop I Siemens electron microscope.Two important phenomena were observed in synovial tissue:Specific patterns of each lipid storage disease,which are now well known.In all the three metabolic diseases, hydroxyapatite-like crystals were found. They are characterized by their intramitochondrial localization, without any relation with cristae,an anarchic disposition and a mean size of 550 A.Crystals may be found also free in the cytoplasm of synoviocytes Some micrographs suggest an evolution in four steps :a. mitochondria with only a few microcrystalsb. mitochondria stuffed with these structuresc. disruption of mitochondria membranesd. microcrystals appear free in the cytoplasm

Labelling of non-A, non-B hepatitis infected chimpanzee hepatocytes with nuclease-gold conjugates

1984 ◽  
Vol 42 ◽  
pp. 250-251
Author(s):  
G. D. Gagne ◽  
M. F. Miller ◽  
D. A. Peterson
Keyword(s):  
Endoplasmic Reticulum ◽  
Experimental Infection ◽  
Uranyl Acetate ◽  
Type I ◽  
Cellular Injury ◽  
Type Ii ◽  
Tubular Structures ◽  
Type Iii ◽  
Type Iv ◽  
Infected Chimpanzee

Experimental infection of chimpanzees with non-A, non-B hepatitis (NANB) or with delta agent hepatitis results in the appearance of characteristic cytoplasmic alterations in the hepatocytes. These alterations include spongelike inclusions (Type I), attached convoluted membranes (Type II), tubular structures (Type III), and microtubular aggregates (Type IV) (Fig. 1). Type I, II and III structures are, by association, believed to be derived from endoplasmic reticulum and may be morphogenetically related. Type IV structures are generally observed free in the cytoplasm but sometimes in the vicinity of type III structures. It is not known whether these structures are somehow involved in the replication and/or assembly of the putative NANB virus or whether they are simply nonspecific responses to cellular injury. When treated with uranyl acetate, type I, II and III structures stain intensely as if they might contain nucleic acids. If these structures do correspond to intermediates in the replication of a virus, one might expect them to contain DNA or RNA and the present study was undertaken to explore this possibility.

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