1.Current Management of the Growing Sac after Endovascular Aneurysm Repair.
Journal of the Korean Society for Vascular Surgery 2013;29(2):41-45
Endovascular aneurysm repair (EVAR) has become the preferred treatment for abdominal aortic aneurysm. EVAR results in sac exclusion and subsequent sac depressurization, which prevents aneurysm rupture and aneurysm related death. Its benefits have led to a widespread adaptation. However, EVAR has transformed abdominal aortic aneurysm from an ailment with the definitive cure (open surgical repair) into a chronic disease process with the need for a close, life-long surveillance and increased potential for secondary interventions. Following EVAR, endoleak can occur, and incidence varies widely ranging from 15% to 52%. Endoleak can lead to sac growth and concern for rupture. Treatment depends on the leak type. Type I and III endoleaks should be treated. There is general consensus that type II endoleaks can be monitored except in cases of sac enlargement >5 mm. Treatment of type V endoleak, or "endotension" is controversial. These endoleaks have been associated with the first generation high porosity Gore Excluder stent graft. In these cases, relining the stent graft with resultant halt of sac growth has been descried. With the next generation of low porosity Gore Excluder, endotension is a less commonplace. Nonetheless, sac growth in the absence of endoleak can occur with any stent graft system, and surgical conversion may be warranted. Needless to say, this decision is made on an individual case basis. Management of sac growth is varied and can generally be categorized by approach (transarterial, translumbar, transcaval, and laparoscopic) or by method of repair (embolization, proximal/distal extension, endostaple, and surgical conversion). Extension pieces are used to seal type I endoleaks wheng there is adequate neck length to extend the seal. Use of fenestrated or "chimney" grafts can extend coverage to the pararenal aorta. When there is insufficient additional neck to obtain the seal, a Palmaz stent or noncompliant balloon can be considered. Recent approval of an endovascular stapler is a novel method for treating type I endoleaks. Type II endoleak treatment is conceptually similar to the treatment of a vascular malformation. An attempt should be made to embolize the inflow and outflow vessels, as well as the endoleak nidus. Laparoscopic branch vessel ligation or sac plication has been described. Finally, rather than responding to the endoleaks that occur, a strategy of preemptive action to prevent their appearance should be considered, though this is not widely practiced. Aneurysm sac "thrombization" involves embolization of the sac with a combination of glue and coil during the time of initial stent graft implantation. This may decrease the subsequent development of endoleak. Preoperative ligation or embolization of a patent inferior mesenteric artery is performed at some centers. Finally, the aforementioned endostapler can be used to prevent future endoleak and graft migration, particularly in hostile neck anatomy.
Adhesives
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Aneurysm
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Aorta
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Aortic Aneurysm, Abdominal
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Chronic Disease
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Consensus
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Endoleak
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Endovascular Procedures
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Glycosaminoglycans
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Incidence
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Ligation
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Mesenteric Artery, Inferior
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Neck
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Porosity
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Rupture
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Stents
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Transplants
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Vascular Malformations
2.Temporal response of ovine fetal plasma erythropoietin induced by fetal hemorrhage.
Sa Jin KIM ; Robert A BRACE ; Gui Se Ra LEE ; Seung Hye RHO ; Jong Chul SHIN ; Dae Young JUNG ; Young YI ; Jin Woo KIM ; Soo Pyoung KIM
Korean Journal of Obstetrics and Gynecology 2000;43(3):457-460
OBJECTIVE: The ovine fetus responds to hemorrhage with a 10-20 fold increase in plasma erythropoietin (EPO) concentration at 24 hr and a return toward normal at 48 hr after the hemorrhage. The objective of the present study was more accurately to compare the magnitude and time course of the plasma EPO response after fetal hemorrhage. METHODS: Chronically catheterized, 12 of late gestation ovine fetus were gradually hemorrhaged 40% of their blood volume over 2 hr (1ml/min). Plasma was sampled for EPO concentration at 1, 2, 3, 4, 6, 8, 10, 12, 16, 20, 24, 30, 36 hr after initiating the hemorrhage were collected at these times. Radioimmunoassay was used to measure plasma EPO concentrations. Analysis of variance was used for statistical analysis. RESULT: After a slow hemorrhage in the ovine fetus (1ml/min over 2hr), plasma EPO concentration increased significantly at 4hr (2.3 times basal values), reached a maximum at 16 hr (33.3 times basal values), and declined thereafter. CONCLUSION: We studied change in time course of the fetal plasma EPO after slow hemorrhage and recent studies have shown that the fetal kidney, liver and placenta express EPO mRNA. These observation suggest that plasma EPO increase may be mediated by a tissue specific up-regulation of EPO transcription in the fetal kidney, liver and placenta. We have studied change in Epo mRNA expression in various fetal tissue after slow haemorrhage.
Blood Volume
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Catheters
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Erythropoietin*
;
Fetus
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Hemorrhage*
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Kidney
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Liver
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Placenta
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Plasma*
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Pregnancy
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Radioimmunoassay
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RNA, Messenger
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Sheep
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Up-Regulation
3.Validating lactate dehydrogenase (LDH) as a component of the PLASMIC predictive tool (PLASMIC-LDH)
Christopher Chin KEONG LIAM ; Jim Yu-Hsiang TIAO ; Yee Yee YAP ; Yi Lin LEE ; Jameela SATHAR ; Simon MCRAE ; Amanda DAVIS ; Jennifer CURNOW ; Robert BIRD ; Philip CHOI ; Pantep ANGCHAISUKSIRI ; Sim Leng TIEN ; Joyce Ching MEI LAM ; Doyeun OH ; Jin Seok KIM ; Sung-Soo YOON ; Raymond Siu-Ming WONG ; Carolyn LAUREN ; Eileen Grace MERRIMAN ; Anoop ENJETI ; Mark SMITH ; Ross Ian BAKER
Blood Research 2023;58(1):36-41
Background:
The PLASMIC score is a convenient tool for predicting ADAMTS13 activity of <10%.Lactate dehydrogenase (LDH) is widely used as a marker of haemolysis in thrombotic thrombocytopenic purpura (TTP) monitoring, and could be used as a replacement marker for lysis. We aimed to validate the PLASMIC score in a multi-centre Asia Pacific region, and to explore whether LDH could be used as a replacement marker for lysis.
Methods:
Records of patients with thrombotic microangiopathy (TMA) were reviewed. Patients’ ADAMTS13 activity levels were obtained, along with clinical/laboratory findings relevant to the PLASMIC score. Both PLASMIC scores and PLASMIC-LDH scores, in which LDH replaced traditional lysis markers, were calculated. We generated a receiver operator characteristics (ROC) curve and compared the area under the curve values (AUC) to determine the predictive ability of each score.
Results:
46 patients fulfilled the inclusion criteria, of which 34 had ADAMTS13 activity levels of <10%. When the patients were divided into intermediate-to-high risk (scores 5‒7) and low risk (scores 0‒4), the PLASMIC score showed a sensitivity of 97.1% and specificity of 58.3%, with a positive predictive value (PPV) of 86.8% and negative predictive value (NPV) of 87.5%. The PLASMIC-LDH score had a sensitivity of 97.1% and specificity of 33.3%, with a PPV of 80.5% and NPV of 80.0%.
Conclusion
Our study validated the utility of the PLASMIC score, and demonstrated PLASMIC-LDH as a reasonable alternative in the absence of traditional lysis markers, to help identify high-risk patients for treatment via plasma exchange.