Academic literature on the topic 'Sac thrombosis'
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Journal articles on the topic "Sac thrombosis"
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Cojocari, Vladimir, Vasile Culiuc, Florin Bzovii, Dumitru Casian, and Eugen Gutu. "Giant thrombosed saphenofemoral junction aneurysm: A case report." SAGE Open Medical Case Reports 5 (January 1, 2017): 2050313X1774101. http://dx.doi.org/10.1177/2050313x17741012.
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Introduction: Although saphenofemoral junction aneurysms are not so rare, only scarce of the published cases reported thrombosis of the aneurysmal sac and saphenous trunk. Presentation of case: A 65-year-old male with varicose disease, developed acute ascending superficial vein thrombosis of the left greater saphenous vein, involving the 6-cm saphenofemoral junction aneurysm. The patient underwent common femoral vein thrombectomy, aneurysm removal, and greater saphenous vein excision with uneventful postoperative course. Conclusion: Thrombosed giant saphenofemoral junction aneurysms require emergent surgical intervention aimed at preventing potential progression to deep vein thrombosis and pulmonary embolism.
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Warschewske, G., G. Benndorf, Th Lehmann, and W. Lanksch. "Spontaneous Thrombosis of an Intracranial Giant Aneurysm." Interventional Neuroradiology 5, no. 4 (December 1999): 327–32. http://dx.doi.org/10.1177/159101999900500410.
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Spontaneous thrombosis in giant aneurysms is known, whereas complete occlusion of such aneurysms in a short period of time is rarely reported. We present the case of a 50-year-old man with a giant anuersym arising from the anterior communicating artery (ACA) producing significant mass effect with clinical consequences. The digital subtraction arteriogram (DSA) showed a patent lumen of about 20 mm and a very small neck leading to extremely slow blood flow inside the sac and stagnation of contrast. During catheterization for endovascular occlusion four weeks later, the arteriogram revealed complete disappearance of the aneurysm, while the patient remained clinically stable. The patient was operated upon and the thrombosed sac was removed with no complications. He was discharged one week later and recovered completely from his symptoms within three months.
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Victory, Jesse, Syed Ali Rizvi, Enrico Ascher, and Anil Hingorani. "Ruptured abdominal aortic aneurysm after endovascular aortic aneurysm repair thrombosis." Vascular 25, no. 3 (November 24, 2016): 333–35. http://dx.doi.org/10.1177/1708538116679330.
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Background Complete thrombosis of an aortic endograft after an endovascular aortic aneurysm repair is a rare complication. The majority of thrombotic events occur in the iliac limbs. Case presentation We present the case of a patient who presented with acute limb ischemia as the result of a thrombosed infra-renal aortic endograft. After restoration of blood flow to the lower extremities with an axillary to bi-femoral artery bypass, the patient was lost to follow-up. The patient returned two years later with a ruptured abdominal aortic aneurysm due to a type 1A endoleak. Discussion We propose that all patients after endovascular aortic aneurysm repair, including those with a thrombosed aortic endograft, continue to undergo regular graft surveillance. This case report highlights the importance of continued surveillance of the aortic sac, even after total thrombosis of the endovascular aortic aneurysm repair.
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Davis, Renee, Kurt Stahlfeld, and Harry W. Sell. "Congenital peritoneal encapsulation and superior mesenteric vein thrombosis: A case report." SAGE Open Medical Case Reports 10 (January 2022): 2050313X2211324. http://dx.doi.org/10.1177/2050313x221132436.
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Congenital peritoneal encapsulation is a rare entity characterized by an accessory peritoneal membrane that forms during embryonic development. Congenital peritoneal encapsulation is generally asymptomatic but can cause intermittent, colicky abdominal pain related to subacute small bowel obstruction. Diagnosis is made incidentally or upon surgical exploration for chronic abdominal complaints as preoperative imaging is typically nonspecific. We report a case of a 49-year-old male with epigastric abdominal pain, constipation, and superior mesenteric vein thrombosis on imaging. Upon exploratory laparotomy, the small bowel was covered by an accessory peritoneal sac consistent with congenital peritoneal encapsulation. The accessory sac was excised completely, and the patient recovered well. Although rarely causing significant gastrointestinal symptoms, congenital peritoneal encapsulation is an anomaly that requires surgical intervention.
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Papakostas, John C., Emmanouil Theodoropoulos, George Karydas, and Petros K. Chatzigakis. "Contained rupture of a celiac artery aneurysm treated with aortic endograft deployment and assisting percutaneous coil and thrombin infusion." Vascular 21, no. 3 (May 13, 2013): 183–88. http://dx.doi.org/10.1177/1708538113478735.
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In this report we present a case of a ruptured celiac artery aneurysm (CAA) with a thrombosed distal neck, which was treated as an emergently with a deployment of a tube thoracic endograft to the descending thoracic and upper abdominal aorta. The initial treatment was assisted with a second stage percutaneous, transhepatic, ultrasound guided needle infusion of coil and thrombin to the aneurysmal sac due to type Ib endoleak, with immediate thrombosis of the aneurysm. This technique, although not standard, could also be considered as a useful choice for the treatment of CAAs with wide proximal and patent distal neck.
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Antoniou, A., Schiro, V. Smyth, Murray, Farquharson, and Serracino-Inglott. "Multilayer stent in the treatment of popliteal artery aneurysms." Vasa 41, no. 5 (August 1, 2012): 383–87. http://dx.doi.org/10.1024/0301-1526/a000227.
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Endovascular repair of popliteal artery aneurysms is an emerging treatment in high risk surgical patients. The location in a functionally demanding anatomical area creates limitations in terms of endograft patency. Technological advancements have been conscripted in an effort to circumvent such constraints. The multilayer stent technology effects through haemodynamic modulation. We used the multilayer stent to treat 6 asymptomatic popliteal artery aneurysms in 3 patients. All procedures were successfully accomplished without any complications. Over a mean follow up period of 9 months, thrombosis occurred in two limbs, and blood flow was restored with thrombolysis, achieving a primary and secondary patency rate at 6 months of 67 % and 100 %, respectively. Partial or complete thrombosis of the aneurysm sac was achieved in all aneurysms. Even though the use of the multilayer stent in popliteal artery aneurysms was safe in the short term, our experience showed that close surveillance is required.
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Zhang, Xiaoxi, Qiao Zuo, Haishuang Tang, Gaici Xue, Pengfei Yang, Rui Zhao, Qiang Li, et al. "Stent assisted coiling versus non-stent assisted coiling for the management of ruptured intracranial aneurysms: a meta-analysis and systematic review." Journal of NeuroInterventional Surgery 11, no. 5 (March 6, 2019): 489–96. http://dx.doi.org/10.1136/neurintsurg-2018-014388.
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PurposeTo compare the safety and efficiency of stent assisted coiling (SAC) with non-SAC for the management of ruptured intracranial aneurysms.MethodsA meta-analysis that compared SAC with coiling alone and balloon assisted coiling was conducted by database searching. The primary outcomes of this study were immediate occlusion and progressive thrombosis rate, overall perioperative complication rate, and angiographic recurrence. Secondary outcomes included mortality at discharge, hemorrhagic and ischemic complications, and favorable clinical outcome at discharge and at follow-up.ResultsEight retrospective cohort studies with 1408 ruptured intracranial aneurysms (SAC=499; non-SAC=909) were included. The SAC group tended to show a lower immediate complete occlusion rate than the non-SAC group (54.3% vs 64.2%; RR 0.90; 95% CI 0.83 to 0.99; I2=17.4%) and achieved a significantly higher progressive complete rate at follow-up (73.4% vs 61.0%; RR 1.30; 95% CI 1.16 to 1.46; I2=40.5%) and a lower recurrence rate (4.8% vs 16.6%; RR 0.28; 95% CI 0.16 to 0.50; I2=0.0%). With respect to safety concerns, overall perioperative complications in the SAC group were significantly higher (20.2% vs 13.1%; RR 1.70; 95% CI 1.36 to 2.11; I2=0.0%). However, no significant difference was found for mortality rate at discharge (6.3% vs 6.2%; RR 1.29; 95% CI 0.86 to 1.94; I2=0.0%), or favorable clinical outcome rate at discharge (73.4% vs 74.2%; RR 0.95; 95% CI 0.88 to 1.02; I2=12.1%) and at follow-up (85.6% vs 87.9%; RR 0.98; 95% CI 0.93 to 1.02; I2=0.0%; P=0.338).ConclusionsSAC has a lower recurrence rate than non-SAC. Nevertheless, further validation by well designed prospective studies is warranted for determining whether stents improve angiographic outcome without an increased complication rate or unfavorable clinical outcome.
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Slater, Lee-Anne, Cathy Soufan, Michael Holt, and Winston Chong. "Effect of flow diversion with silk on aneurysm size: A single center experience." Interventional Neuroradiology 21, no. 1 (February 2015): 12–18. http://dx.doi.org/10.1177/1591019915576433.
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Alterations in aneurysm size and mass effect can result in alleviation or aggravation of symptoms. We assessed the effects of flow diversion with SILK stents on aneurysm sac size and associated factors. A retrospective evaluation of 14 aneurysms treated with SILK stents alone with MRI follow-up was performed. Aneurysm sac size was measured using the sequence best demonstrating the sac. Aneurysm characteristics and flow-related enhancement on time of flight images were documented. Clinical histories were reviewed for evolution of symptoms. Complete collapse of the aneurysm sac was demonstrated at three and 18 months in 2/14 aneurysms. Increase in size was observed in 2/14 aneurysms with associated persistent flow on time of flight MRA. Blister formation with aggravation of symptoms was observed in one aneurysm, and subsequent decrease in size occurred after treatment with a second SILK. The other aneurysm which increased in size initially continued to enlarge asymptomatically despite retreatment with a second SILK, however at 24 months thrombosis of the sac and decrease in size was observed. The remaining 10/14 aneurysms decreased in size. Nine had corresponding MRA occlusion and the tenth demonstrated decreased but persistent flow on the time of flight MRA. No aneurysm with MRA occlusion increased in size. Decrease in sac size was associated with MRA occlusion in our study. Persistence of flow and blistering were associated with increased sac size. As previously demonstrated flow diversion may be effective in the treatment of large aneurysms presenting with mass effect, however rates of sac obliteration in this small series were not as high as previously reported.
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Motataianu, Anca, Smaranda Maier, Sebastian Andone, Laura Barcutean, Georgiana Serban, Zoltan Bajko, and Adrian Balasa. "Ischemic Stroke in Patients with Cancer: A Retrospective Cross-Sectional Study." Journal of Critical Care Medicine 7, no. 1 (January 1, 2021): 54–61. http://dx.doi.org/10.2478/jccm-2021-0002.
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Abstract Introduction An increasing trend of cancer associated stroke has been noticed in the past decade. Objectives To evaluate the risk factors and the incidence of neoplasia in stroke patients. Material and Method A retrospective, observational study was undertaken on 249 patients with stroke and active cancer (SAC) and 1563 patients with stroke without cancer (SWC). The general cardiovascular risk factors, the site of cancer, and the general clinical data were registered and evaluated. According to the “Oxfordshire Community Stroke Project” (OCSP) classification, all patients were classified into the clinical subtypes of stroke. The aetiology of stroke was considered as large-artery atherosclerosis, small vessel disease, cardio-embolic, cryptogenic or other determined cause. Results The severity of neurological deficits at admission were significantly higher in the SAC group (p<0.01). The haemoglobin level was significantly lower, and platelet level and erythrocyte sedimentation rate were significantly higher in the SAC group. Glycaemia, cholesterol and triglycerides levels were significantly higher in the SWC group. The personal history of hypertension was more frequent in the SWC group. In the SAC group, 28.9% had a cryptogenic aetiology, compared to 9.1% in SWC group. Cardio-embolic strokes were more frequent in the SAC group (24%) than the SWC group (19.6%). In the SAC group, 15,6% were diagnosed with cancer during the stroke hospitalization, and 78% of the SAC patients were without metastasis. Conclusions The most frequent aetiologies of stroke in cancer patients were cryptogenic stroke, followed by large-artery atherosclerosis. SAC patients had more severe neurological deficits and worse clinical outcomes than SWC patients. Stroke in cancer patients appears to be more frequently cryptogenic, probably due to cancer associated thrombosis. The association between stroke and cancer is important, especially in stroke of cryptogenic mechanism, even in the presence of traditional cardiovascular risk factors.
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Raval, Bharat, J. Timothy Hall, and Harris Jackson. "CT Diagnosis of Fluid in Lesser Sac Mimicking Thrombosis of Inferior Vena Cava." Journal of Computer Assisted Tomography 9, no. 5 (September 1985): 956–58. http://dx.doi.org/10.1097/00004728-198509000-00023.
Full textDissertations / Theses on the topic "Sac thrombosis"
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AHMED, MOHAMED MOHAMED NORAH. "The innovation of Multilayered Aneurysm Repair Stents (MARS) in treatment of thoraco-abdominal aneurysms." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41912.
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Background
Morbidity and mortality from Thoraco-abdominal aneurysms are tremendous. Preoperative assessment in predicting cardiac and pulmonary risk factors in order to reduce cardiopulmonary complications, paraplegia, and renal failure are the main determinants of postoperative mortality and therefore gained substantial attention during the last decades.(Jacobs MJ et al.,2007)
Left heart by-pass, CSF drainage and epidural cooling have significantly reduced the paraplegia rates. Monitoring MEPs allowed detection of cord ischemia,(spinal cord ischemic injury, SCII) guiding aggressive surgical strategies to restore spinal cord blood supply and reduce neurological deficit. It’s believed that these protective measures should be included in the surgical protocol of TAAA repair type II cases. (Jacobs MJ et al.,2007)
Renal and visceral ischemia can be reduced significantly by continuous perfusion during TAAA repair. (Jacobs MJ et al.,2007)
Obviously endovascular modalities have been successfully applied in TAAA patients, the majority apart of hybrid procedures. Technological innovations will eventually cause a shift from open to minimal invasive surgical repair. (Jacobs MJ et al.,2007)
The multilayer aneurysm repair system (MARS) is a flow modulator and part of the fluid smart© technology platform developed by Cardiatis, Isne-Belgium. The MARS is self-expanding and composed of multiple cobalt alloy interconnected braided layers the 3D geometrical configuration gurantees an optimal porosity range for stent from 2 to 50mm in diameter providing unique flow modulating features. The innovative multilayer flow modulating device offers a paradigm shift approach to the treatment of these complicated aneurysms by physiologically (rather than mechanically ) excluding aneurysms from the circulation, while keeping branches patent and preserving critical collateral circulation.(C.Vaislic et al.,2011)
Its 3D geometrical and structural gives rise to several important hemodynamic and biological effects i.e, in a secular aneurysm it reduces the vortex velocity within the aneurysm sac creating a remodeled organized thrombus, it transforms turbulent flow into laminar flow preserving collateral circulation when over stenting collaterals or in a fusiform aneurysm, it accelerates and channels the flow into a branching aneurysm open branch enhancement and accelerates shear flow along the parent vessel, resulting in inhibition of intimal hyperplasia. (C.Vaislic et al.,2011)
Theoretical basic principles of the device are very attractive and the most important of which is preserving the collaterals and improving their flow. Sac thrombosis and sac shrinkage don’t

usually occur immediately, several factors could play a role as collateral branches and this should be studied and determined preoperatively.(M.Henry,2011)
Preliminary clinical results are satisfactory and promising but larger experience and longer follow up are still needed. (M.Henry,2011)
Hypothesis
The results of endovascular treatment for thoraco-abdominal aneurysms are now comparable with the open surgical procedure. However, endovascular repair in the thoraco-abdominal aorta has been limited due to the complexity of keeping the side branches (intercostals ,renal, visceral) perfused. Attempts are being made to adapt endoluminal stent-graft by using custom fenestrations and branched graft. While preliminary data showed concept feasibility, this technique is still investigational and requires highly skilled operator and custom made devices for each patient.
Aim of the work
1- To study the availability of the new technique in management of TAAA.
2- To shed lights on the technique of deploying the new device.
3- To review the outcome and complications of this new device before introducing this
technique as a standard utility.
4- To shed lights over the new evolving biomedical technology in vascular surgery
This will be supported by the French STRATO trial and by a number of cases done at multi- european centers
Keywords
Thoraco-abdominal aneurysms, Multilayer Aneurysm Repair System (MARS) Intimal hyperplasia, Sac shrinkage, Sac thrombosis, Ischemia
References
1- Jacobs MJ, Mommertz G, koeppel TA, Langer S, Nijenhuis RJ, Mess WH, Schurink GW. Surgical repair of TAAA. J Cardiovasc Surg Torino(2007) Feb; 48 (1) :49-58
2- C.Vaislic, A.Benjelloun ,J.-N.Fabiani, J.-F.Bonneville, S.Chocron. multilayered flow modulator treatment of thoraco-abdominal aortic aneurysms.Controversies and vascular updates (2011)JAN;74:443-449
3- M.Henry,MD. The Multilayer Stent. First human study.(2011), ISET presentation.
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Gómez, Puerta José Alfredo. "Antiphospholipid Syndrome: Expanding the Spectrum of Autoimmune Thrombosis." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/2227.
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The antiphospholipid syndrome (APS) is an acquired prothrombotic syndrome characterized by venous or arterial thromboses and pregnancy morbidity. It can present as primary APS without any discernable underlying disease, or in association with systemic autoimmune disease [usually systemic lupus erythematosus (SLE)], infections (mainly chronic viral infections) and malignant process, among others. It may also occur rapidly over days or weeks, when it is known as "catastrophic" APS (CAPS).The first study described one of the largest known cohorts of patients with primary APS from 4 different referral centers. The final study sample included 128 patients with primary APS with a median age of 42 years and mean follow-up of 9 years. After a median disease duration of 8.2 years, 110 (86%) patients remained with primary APS; 11 (8%) patients developed SLE; 6 (5%), LLD; and 1 (1%), myasthenia gravis. At the end of the study, 113 (88%) patients were alive and 15 (12%) patients had died. Our study confirms that progression from primary APS to SLE or LLD is unusual, even after a long follow-up.
In the second study, we evaluated 120 cases of antiphospholipid antibodies associated with malignancies with a mean age of 56 years, The main hematological malignancies found were B-cell lymphoma, spleen lymphoma and chronic myeloid leukemia. The main solid tumors were renal cell carcinoma, primary tumor of unknown origin, lung adenocarcinoma and breast carcinoma. Around one third of patients achieved aPL remission after treatment.
In the third study, we analyzed 15 cases of CAPS that appeared during pregnancy or the puerperium with a mean age at the time of the CAPS event of 27 years. In 7 of the 14 (50%) cases, CAPS appeared during pregnancy, in 6 (43%) cases it presented during puerperium and in 1 (7%) after curettage for a fetal death. The main clinical and serological characteristics were similar to those of patients with CAPS triggered by other factors, however we found some particular features including placental infarctions, pelvic vein thrombosis and myometrial thrombotic microangiopathy and HELLP syndrome.
Final conclusion: Primary APS is a widely recognized distinct entity which rarely progresses to SLE, even after long-term follow-up. APS may also be associated with other chronic disorders, such as solid tumors or hematological malignancies. In cases with the life-threatening variant of APS known as CAPS, pregnancy and the puerperium are periods of high susceptibility for the development of this often fatal form of presentation.
"SINDROME ANTIFOSFOLIPIDICO: EXPANDIENDO EL ESPECTRO CLÍNICA DE LA TROMBOSIS AUTOINMUNE"
El síndrome antifosfolipídico (SAF) es un síndrome protrombótico adquirido caracterizado por trombosis venosas y arteriales y pérdidas fetales recurrentes. Puede estar presente como SAF "primario" cuando no esta asociado a ninguna enfermedad autoinmune [fundamentalmente el lupus eritematoso sistémico (LES)] o en asociación a otros procesos tales como infecciones y procesos neoplásicos, entre otros. También puede manifestarse de una forma acelerada en días o semanas, caracterizado por trombosis de pequeños órganos y fallo multiorgánico, lo que se conoce como SAF "catastrófico".
En el primer estudio se analizó una de las series más amplia y con más largo seguimiento de pacientes con SAF primario. Se incluyeron 128 pacientes con un seguimiento medio de 9 años. Después de una duración media de la enfermedad de 8 años, 110 (86%) pacientes continúan con el diagnóstico de SAF primario, 11 (8%) pacientes desarrollaron un LES, 6 (5%) una forma incompleta de lupus ("lupus-like disease") y 1 (1%) paciente desarrolló una miastenia gravis. La presencia del test de Coombs positivo confiere un riesgo estadísticamente significativo para el desarrollo de LES. . Nuestro estudio confirma que es inusual que un SAF primario evolucione hacia un LES o una forma incompleta de lupus, incluso tras un período largo de seguimiento.
En el segundo estudio se incluyeron un total de 120 casos con anticuerpos antifosfolipídicos (AAF) asociados a procesos neoplásicos. Las principales neoplasias hematológicas relacionadas a los AAF fueron el linfoma de células B, el linfoma esplénico y la leucemia mieloide crónica. Los principales tumores sólidos fueron el carcinoma de células renales, los tumores de primario desconocido, el adenocarcinoma de pulmón y el cáncer de mama. Alrededor de una tercera parte de los paciente negativizaron los AAF después del tratamiento de la neoplasia.
En el tercer estudio se analizaron 15 pacientes con SAF catastrófico que ocurrieron durante el embarazo o el puerperio. Las características clínicas generales del SAF catastrófico durante el embarazo o el puerperio fueron similares a las del SAF catastrófico desencadenado por otros factores a excepción de una tasa mayor de abortos previos. Sin embargo se encontraron una serie de características particulares, como el síndrome de HELLP, la trombosis placentaria, la microangiopatía trombótica de miometrio o la trombosis de la vena pélvica.
CONCLUSIÓN FINAL: El SAF primario es una entidad propia ampliamente reconocida que en raras ocasiones evoluciona a un LES, incluso tras un período largo de seguimiento. El SAF puede asociarse a una serie de procesos crónicos como lo son las neoplasias hematológicas y los tumores sólidos. En aquellos casos con la variante "catastrófica" del SAF, el embarazo y el puerperio, constituyen un período de alta susceptibilidad para el desarrollo de esta variante altamente letal del SAF.
Books on the topic "Sac thrombosis"
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Kahn, S. Lowell. Creation of a Flow-Modulating Stent Using Multilayered Wallstents for Aneurysm Exclusion. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0011.
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Abdominal aortic aneurysms (AAAs) are a common pathology that is found in 4–9% of patients in the developed world. Risk factors for AAAs include age, male sex, family history, comorbid cardiovascular disease, and smoking. Despite the male predominance of the disease, rupture occurs at a smaller diameter in females, and the outcomes are poorer in this subgroup. Flow-modulating stents are a relatively new development and consist of multilayered bare-metal self-expanding stents. Despite the inherent porosity of the stents, the interconnected stent matrix features flow-diverting properties that preserve luminal and branch vessel flow while simultaneously depressurizing the aneurysm sac, resulting in shrinkage and thrombosis. Flow-modulating stents are unavailable in the United States. This chapter discusses in vivo construction of a flow-modulating stent and its potential applications and complications.
Book chapters on the topic "Sac thrombosis"
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Dorn, Franziska. "Dural Arteriovenous Fistula of the Superior Petrosal Sinus: Postinterventional SAH and Edema of the Brainstem and Cerebellum due to Thrombosis of the Superior Petrosal Vein." In The Arteriovenous Malformations and Fistulas Casebook, 1–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-51200-2_34-1.
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Kirsch, Michael. "Posterior Communicating Artery Aneurysm: Giant Aneurysm of the Internal Carotid Artery, Acute SAH, Ruptured Wide Neck Aneurysm, Incorporation of the Fetal Origin of the Posterior Cerebral Artery, Coil Occlusion, Secondary Treatment of the Neck Remnant with a Single Derivo Flow Diverter, Intra-procedural Thrombosis, Intra-arterial Eptifibatide Infusion, Good Clinical Outcome." In The Aneurysm Casebook, 357–62. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-77827-3_11.
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Kirsch, Michael. "Posterior Communicating Artery Aneurysm: Giant Aneurysm of the Internal Carotid Artery, Acute SAH, Ruptured Wide Neck Aneurysm, Incorporation of the Fetal Origin of the Posterior Cerebral Artery; Coil Occlusion, Secondary Treatment of the Neck Remnant with a Single Derivo Flow Diverter, Intra-procedural Thrombosis, Intra-arterial Eptifibatide Infusion, Good Clinical Outcome." In The Aneurysm Casebook, 1–6. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70267-4_11-1.
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Kirsch, Michael. "Posterior Communicating Artery Aneurysm: Giant Aneurysm of the Internal Carotid Artery, Acute SAH, Ruptured Wide Neck Aneurysm, Incorporation of the Fetal Origin of the Posterior Cerebral Artery; Coil Occlusion, Secondary Treatment of the Neck Remnant with a Single Derivo Flow Diverter, Intra-procedural Thrombosis, Intra-arterial Eptifibatide Infusion, Good Clinical Outcome." In The Aneurysm Casebook, 1–6. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70267-4_11-2.
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Crowther, Mark A., and Thomas C. Abshire. "Hemostasis and thrombosis." In ASH-SAP (3rd EDITION), 361–407. American Society of Hematology, 2007. http://dx.doi.org/10.1182/ash-sap.2007.15.
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Moll, Stephan, and Janna M. Journeycake. "Thrombosis and thrombophilia." In ASH-SAP (4th EDITION), 179–215. American Society of Hematology, 2010. http://dx.doi.org/10.1182/ash-sap.2010.7.
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Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Headache." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0007.
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The sinister causes can be remembered using the mnemonic VIVID: . . . Vascular: subarachnoid haemorrhage (SAH), haematoma (subdural or extradural), cerebral venous sinus thrombosis, cerebellar infarct Infection: meningitis, encephalitis Vision-threatening: temporal arteritis, acute glaucoma, cavernous sinus thrombosis, pituitary apoplexy, posterior leucoencephalopathy Intracranial pressure (raised): space-occupying lesion (SOL; e.g. tumour, abscess, cyst), cerebral oedema (e.g. trauma, altitude), hydrocephalus, malignant hypertension, idiopathic intracranial hypertension Dissection: carotid dissection . . . The approach to headache is the same as that to pain anywhere in the body: you need to start by characterizing the pain. One useful way of doing this is by following another mnemonic, SOCRATES: . . . Site of pain, and has it moved since it began? Onset of pain—was it sudden or gradual, and did something trigger it? Character of pain—throbbing, dull ache, sharp stabbing? Radiation of pain—has the pain spread? . . . Attenuating factors—does anything make the pain better (e.g. position, medications)? Timing of pain—how long has it gone on for, has it been constant or coming and going? Is it worse at a particular time of the day? Exacerbating factors—does anything make the pain worse (e.g. lying down, standing up, coughing, fatigue)? Severity—on a scale of 0 to 10, where 10 is the worst pain ever (e.g. childbirth). In addition, you should enquire about the presence or absence of the following ‘red flags’: • Decreased level of consciousness. This is a worrying feature of any medical presentation. Combined with headache, SAH needs exclusion. If there is a history of head injury, it could suggest a subdural haematoma (fluctuating consciousness) or extradural haematoma (altered consciousness following a lucid interval). Meningitis and encephalitis can also affect consciousness. • Sudden onset, worst headache ever. Suggests SAH, with blood in the cerebrospinal fluid (CSF) irritating the meninges. It can be informative to ask the patient whether they remember the exact moment when the headache started—a very severe headache of almost instantaneous onset is characteristic of SAH. Patients describe it like, for example, ‘being hit on the back of the head with a bat’.
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Wilkinson, Ian B., Tim Raine, Kate Wiles, Anna Goodhart, Catriona Hall, and Harriet O’Neill. "Neurology." In Oxford Handbook of Clinical Medicine, 444–517. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199689903.003.0010.
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This chapter explores neurology, including lesion location, drugs and the nervous system, cerebral blood supply, testing peripheral nerves, dermatomes and peripheral nerves, headache, migraine, blackouts, vertigo and dizziness, hearing loss and tinnitus, acute bilateral leg weakness, abnormal involuntary movements (dyskinesia), stroke, transient ischaemic attack (TIA), subarachnoid haemorrhage (SAH), intracranial venous thrombosis (IVT), subdural haematoma, extradural (epidural) haematoma, delirium (acute confusional state), dementia, Alzheimer’s disease (AD), epilepsy, Parkinsonism, multiple sclerosis (MS), space-occupying lesions (SOL), idiopathic intracranial hypertension, Bell’s palsy, mononeuropathies, polyneuropathies, autonomic neuropathy, motor neuron disease (MND), bulbar palsy, cervical spondylosis, myopathy, myasthenia gravis (MG), Lambert–Eaton myasthenic syndrome (LEMS), neurofibromatosis, syingomyelia, and retroviruses and neurology.
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Massberg, Steffen, Julinda Mehilli, and Adnan Kastrati. "The role of bivalirudin in percutaneous coronary intervention." In Oxford Textbook of Interventional Cardiology, 440–56. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.025.
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Rapid progress has been made in interventional cardiology over the past years, and many patients with coronary artery disease, even those with complex lesions, are nowadays being treated with percutaneous coronary interventions (PCI). As a result, a major focus of current cardiovascular research is on reducing negative peri-procedural clinical events associated with PCI, particularly in high-risk patients. Among the most dangerous peri-procedural events are thrombotic complications, leading to recurrent myocardial or cerebral ischaemia, often with fatal outcome. Anticoagulant and antithrombotic treatment, therefore, is an integral part of current PCI strategies. It is needless to say that prevention of procedural thrombotic events with the use of anticoagulants occurs at the expense of severe bleeding complications. Hence, there has been a strong effort over recent years to develop and validate novel anticoagulant regimens that provide protection against thrombotic complications, but have only minor effects on normal haemostasis. Until recently, the standard anticoagulation therapy during PCI consisted in either unfractionated (UFH) or low-molecular-weight heparin (LMWH) that prevent coagulation indirectly by activation of antithrombin (AT). Once activated, AT inactivates thrombin and other proteases involved in blood clotting. However, only recently direct thrombin inhibitors (DTI) have been introduced as an alternative anticoagulant strategy in patients undergoing PCI. Bivalirudin is the most prominent member of the DTI class, directly inhibiting free- and clot-bound thrombin. Use of bivalirudin has recently been shown to result in a significant reduction of bleeding without an increase in thrombotic or ischaemic endpoints compared to heparin and glycoprotein (GP) IIb/IIIa inhibitors in patients presenting with acute coronary syndromes (ACS). This chapter will give an overview of the pharmacology and mechanism of action of bivalirudin and summarize results from recent clinical trials evaluating the use of bivalirudin in patients undergoing PCI.
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Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Limb weakness." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0032.
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The definition of weakness is important, because many patients who self-describe a ‘weak limb’ will actually have a clumsy limb (ataxia), a numb limb (reduced sensation), or a limb that is too painful to move. The time course of the onset of the symptoms in general reflects the time course of the underlying pathology: • Sudden onset (seconds to minutes) usually implies either trauma (e.g. displaced vertebral fractures due to major trauma) or certain vascular insults (e.g. stroke, transient ischaemic attack (TIA)). • Subacute onset (hours to days) suggests a progressive demyelination (e.g. Guillain–Barre syndrome, multiple sclerosis) or a slowly expanding haematoma (e.g. subdural haematoma). • Chronic onset (weeks to months), is consistent with pathologies such as a slow-growing tumour or motor neuron disease (progressive degeneration of motor neurons). As only acute and subacute limb weakness will present acutely to generalists in hospital (chronic onset cases will most likely be referred to neurology from primary care), we have limited the chapter to these cases. Limb movement requires an intact pathway from the cerebral cortex, down the corona radiata, internal capsule, and pons, along the corticospinal tract of the spinal cord, out along a nerve root, and down a peripheral nerve to the neuromuscular junction and muscle itself. If a patient has limb weakness, there must be a lesion somewhere in this pathway. Figure 26.2 gives the differential diagnosis for limb weakness. Mr Walker has presented with rapid onset of left-sided arm weakness. Key clues in the history to elicit include: • Exact time of onset? This is critical in suspected strokes because the window of time in which to confirm the diagnosis and administer thrombolysis (if appropriate) is only 4.5 hours from onset of symptoms (after that, you risk doing more harm than good to the patient). If you suspect a stroke in a patient within that time frame, call the thrombolysis team immediately. In this case, all we can say is that the onset was at some point in the 7 hours between 11 p.m. (when he went to sleep) and 6 a.m. (when he woke up), so we cannot confidently say the onset was within 4.5 hours.
Conference papers on the topic "Sac thrombosis"
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Babiker, Haithem, Youngjae Chun, Colin P. Kealey, Gregory P. Carman, Dan S. Levi, and David H. Frakes. "Experimental Fluid Dynamic Investigation of a Novel Hyper-Elastic Thin Film for Cerebral Aneurysm Treatment." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53999.
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Wide-neck and giant cerebral aneurysms are difficult to treat with conventional endovascular or surgical means [1]. Recently, stand-alone stent treatment has been explored as a viable treatment option for these aneurysms. Two goals of standalone stent design are to permit flexible conformation of the stent through tortuous vessels and to provide sufficient coverage across the aneurysmal neck [2]. Stents that achieve those goals can facilitate the long-term physiological processes that exclude the aneurysmal sac from circulation. Thrombosis within the sac is an important intermediate step, which may begin with the elimination of aneurysmal inflow [3].
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Kornberg, A., S. Kaufman, L. Silber, and J. Ishay. "THE EFFECT OF THE VENOM OF THE ORIENTAL HORNET ON COAGULATION FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644338.
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The extract from the venom sac of Vespa orientalis (VSE) inactivates exogenous and endogenous thromboplastin (Joshua and Ishay, Toxicon, 13:11-20,1975). The prolongation of both prothrombin time (PT) and recalcification time suggests inactivation of other factors. The aim of the present study is to investigate the effect of VSE on clotting factors. A lyophilized VSE with protein concentration of 5 mg/ml was used. Studies were performed in vitro with human plasma and in vivo in cats. Routine methods were employed for the assay of PT, activated tissue thromboplastin (APTT), thrombin time (TT), fibrinogen degradation products (FDP), fibrinogen and factors V,VII,VIII,IX,X. Human plasma was incubated with various concentrations of VSE (0,1,5,10,50,100 μg/ml) for 60 min and for various incubation times (0,5,15,30,+ 60,90,120 min) with 50 μg/ml VSE (n=8). 1 μg/ml VSE prolonged PT from 13.5 to 16 sec (p<0.05) and APTT from 62 to 180 sec. PT was maximal (17.7 sec) with 10 μg/ml and APTT (442 sec) with 50 μg/ml VSE. Factors V,VII,X decreased gradually from 94-105% to 11%,11% and 29% with 100 μg/ml VSE and VIII and IX to 1% even with 1 μg/ml VSE. After 5 min with constant concentration of VSE (50 μg/ml) PT was 14.9 sec (normal 13 sec) and APTT 165 sec (normal 54 sec). Both were maximal (17.5 and 298 sec) after 60 min. Factors VII and X decreased to 13% and 32% and VIII and IX to >1% after 60 min of incubation. Injection of 5 mg/kg VSE to cats (n=6-8) resulted in prolongation of PT from 9.4 to 11.2 sec and of APTT from 19.5 to 63 sec after 5 min. Both were maximal after 90 min (12.3 and 127 sec). Factors V,VII and X decreased from 100% to 7.6%, 13% and 37% and VIII and IX to 1% after 10 min. In all experiments TT and plasma fibrinogen were not affected and FDP were normal. Heating of VSE for 5 min at 80°C abolished completely the anticoagulant activity but dialysis for 24 hr at 4°C had no effect on it. The activity was eluted on Sephadex-25 both in void and post void volumes. The results show that VSE has a potent anticoagulant activity against various factors. Factors VIII and IX are markedly decreased. The effect on V, VII and X is moderate. Plasma fibrinogen is not affected. The nature and clinical significance of the anticoagulant activity merit further investigation.
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Muzangwa, L. G., K. Lien, V. Rana, M. Groth, and A. Iftikhar. "Catheter-Directed Thrombolysis: Treatment of Acute Portal Vein Thrombosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2937.
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Xiang, Jianping, Ding Ma, Adnan Siddiqui, and Hui Meng. "Flow Modification of Cerebral Aneurysm by Flow Diverter (Pipeline) With Different Packing Densities." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80764.
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Flow diverter, a braided fine mesh stent, is emerging as a novel device to treat wide-necked, fusiform, and giant cerebral aneurysms since these types of aneurysms are either untreatable otherwise or have high recurrence rate treated by endovascular coils. Flow diverter devices represent a major paradigm shift in the endovascular treatment of aneurysms from filling the aneurysm cavity to diverting blood flow away from aneurysm sac with parent vessel reconstruction. Due to its high flexibility, a flow diverter can be manipulated during deployment process to achieve better results; for example, an experienced neuro-interventionalist can manipulate the stent’s local metal coverage through coordinated movement of catheter pull-back, pusher advancement, and distal coil release to pack higher density for the aneurysm orifice region to divert more flow away from aneurysm, making aneurismal thrombosis quicker and easier. Pipeline embolization device is the first flow diverter approved by FDA. In this study, we investigate the flow modification of a wide-necked aneurysm by Pipeline with different packing densities.
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Seong, Jaehoon, Baruch B. Lieber, and Ajay K. Wakhloo. "Reduction of Intra-Aneurysmal Kinetic Energy by Intralumenal Flow Diverting Devices." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176377.
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Endovascular coiling is an acceptable treatment of intracranial aneurysms yet long term follow-ups suggest that endovascular coiling fails to achieve complete aneurysm occlusion particularly in wide-neck and giant aneurysms. Flow diverting devices can serve as an alternative to coils in endovascular bypass of human brain aneurysms for their exclusion from the cerebral circulation. They can redirect flow away from the aneurysm distally into the parent vessel thereby reestablishing physiological flow patterns. Placing of a flow diverting device across the aneurysm neck may be sufficient to occlude the aneurysm by promoting intra-aneurysmal thrombosis, however, conclusive evidence of its efficacy are still lacking. In this study [1], we investigated in vitro the efficacy of custom designed flow diverting devices and develop indices of their performance in an elastomeric model of the elastase-induced aneurysm in rabbit. The efficacy of custom designed flow divertors is investigated in terms of reducing the flow activity inside the sac. These custom made devices possess porosities that are similar to available stents, however, their pore densities are much higher. The results will help optimize the device that will be used in the animal model.
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Simeone, S., and E. Nadler. "High Risk Pulmonary Embolism Complicated by Systemic Thrombosis Requiring Systemic Thrombolysis and Multiple Endovascular Procedures." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2868.
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Broekmans, A. W., F. J. M. der Meer, and K. Briët. "TREATMENT OF CONGENITAL THROMBOTIC SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643718.
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Hereditary antithrombin III deficiency,protein C deficiency, and protein S deficiency predispose to the occurrence of venous thrombotic disease at a relatively youngage and often without an apparent cause. These disorders inherit as an autosomal dominant trait. Heterozygotes are at risk fosuperficial thrombophlebitis, thrombosis atnearly every venous site, and pulmonary embolism. Homozygous protein C deficiency may present itself with a purpura fulminans syndrome shortly after birth.In the acute phase of venous thromboembolism heparin is effective for preventing extension of the thrombotic process, and pulmonary embolism. In patients with antithrombin III deficiency the concomittant useof antithrombin III concentrate is controversial, although some patients may requirehigher doses of heparin.Substitution therapy is only indicated in homozygous protein C deficient patientswith purpura fulminans. Fresh frozen plasma i.v. is the treatment of choice, in a dosage of 10 ml/kg once or twice daily. The current prothrombin complex concentrates may induce new skin lesions and disseminated intravascular coagulation. After the lesions have been healed(mostly in 4 to6 weeks)coumarin therapy may effectively prevent new episodes of purpura fulminans, provided the prothrombin time is kept within 2,5 - 4,0 INR. Heparin is ineffective for preventing purpura fulminans due to homozygous protein C deficiency.The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. This is supported by the observation that patients may remain free of thrombosis during long-term treatment and may have recurrences shortly after the withdrawal of the coumarin drug. The therapeutic range for the prothrombin time should be within 2,0 - 4,0 INR, target value 3,0 INR. In the initial phase of oral anticoagulant therapy protein C deficient patients are prone to the development of coumarin induced hemorrhagic skin (tissue) necrosis.In the patients studied in Leiden, it occurred in about 3% of the treated patients. Heparin appears to be ineffective for the prevention of coumarin-induced skin necrosis; high loading doses of coumarin should be avoided and the prothrombin timeshouldbe checked dialy during the initial phase of oral anticoagulant treatment. Tissue necrosis may contribute to bleeding complications after fibrinolytic therapy, ashas been observed in two protein C deficient patients.In clinical situations with an increased risk for thrombosis such as surgery and pregnancy, heparin (in-low-doses) alone orin combination with coumarins have been used succesfully for the prevention of thrombosis. The need for antithrombin III concentrates in patients with hereditary antithrombin III deficiency in such situations is not substantiated.Although anabolic steroids are capable to increase the plasma concentrations of antithrombin III and of protein C in the respective deficiency states, its efficacy in preventing thrombotic episodes remains to be established.An optimal strategy for preventing thrombosis in congenital thrombotic syndromes is to identify still asymptomatic patients. In case of antithrombin III, protein C, and protein S deficiency this search is feasible. During risk situations for thrombosis patients are to be protected against the development of thrombosis.In Leiden pregnant women with one of the deficiencies are treated from the 14th week of pregnancy, initially with a shortacting coumarin drug, after the 34th week withheparin s.c. b.i.d. at therapeutic dosages,and after delivery coumarin therapy is reTnstituted during 6 weeks. The use of oralcontraceptives should be avoided, unlesspatients are under coumarin treatment. As long as deficient patients remain asymptomatic no antithrombotic treatment is indicated. After the first documented thromboticincident patients are treated indefinitelywith oral anticoagulants.
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Ghirardini, A., T. DiPaolantonio, S. Solinas, M. Papacchini, C. Cutrera, and G. Mariani. "CONCENTRATED DDAVP: FURTHER IMPROVEMENT FOR THE TREATMENT OF MILD F.VIII DEFICIENCIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644707.
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We have evaluated the pharmacological efficacy of a concentrated DDAVP preparation (40 μg/mL) (herein referred to as C-DDAVP) administered subcutaneously (s.c.) in mild (n=23) and moderate (n=2) hemophilia A patients. A comparison between the response to s.c. C-DDAVP and the "dilute" DDAVP (4 μg/ml) (administered s.c. in 16 patients with mild (n=13) and moderate (n=3) hemophilia A and i.v. in 18 patients with mild (n=16) and moderate (n=2) was also carried out. In all instances Desmopressin was given at a dose of 0.3 μg/kg b.w. in absence of bleeding. The increase of F. VIII:C (expressed as post/pre ratio) after s.c. C-DDAVP was 2,55 at 30', 3,50 at 60'and 3,21 at 120'. The comparison among the three schedules of DDAVP administration showed that s.c. C-DDAVP elicited an increase of F. VIII :C at least as high as that induced by the dilute DDAVP with differences not statistically significant.C-DDAVP was also administered s.c. in 4 patients with type I vWD (platelet normal subtype) with a normalization of bleeding time 60' after s.c. C-DDAVP, concomitant with a rise of activities related to F. VIII/vWF complex. Side effects were modest and transient. We can conclude that s.c. C-DDAVP is equally effective and safe in comparison with the dilute brand with the advantage of the minimal adminstration volume (<1 mL).
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Köhler, M., P. Hellstern, A. Harris, M. Hammer, and E. Wenzel. "A NEW DDAVP-PREPARATION FOR IMPROVEMENT OF SUBCUTANEOUS (S.C.) INJECTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644703.
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The s.c. administration of DDAVP was currently limited by the large volumes, which had to be injected. Thus, a new preparation containing 40 pg DDAVP per ml was investigated using a standard dose of 0.4 μg/kg body weight by s.c. injection. The pharmacokinetics of s.c. DDAVP and the resulting effects on the haemostatic system were assessed in 10 healthy male subjects in a placebo-controlled study. Peak levels of DDAVP, ranging from 480 to 638 pg/ml (median 505 pg/ml ) were found one hour after injection. DDAVP declined with a median (m) half-life of 3.1 h (range: 2.9- 3.6 h) . Maximum FV III levels were measured 1 or 2 h after DDAVP, the m increases were 2.7 and 3. Ox basal levels for FVIII:C and FVIII:Ag, respectively. A 2.1-fold increase of t-PA antigen was observed. The number of leucocytes significantly increased (absulute mean increment of 3.3x109 /I granulocytes) 4 h after DDAVP. These results were confirmed in plasmapheresis donors (N=13). Two bags of plasma were obtained after s.c. DDAVP with a mean content of 1.7 U/ml FVI11 :C and 1.9 U/ml ristocetin cofactor. The effect of s.c. DDAVP was was tested in 10 haemophilia A patients and 2 carriers of hemophilia A (m FVIII:C: 0.17 U/ml). The mean increase of FVIII:C was 2.3-fold (FVIII:Ag 2.5-fold) 1 h post injection. Eight bleeding episodes or operations were successfully treated with s.c. DDAVP, in one case postoperative haematoma occurred. In eight patients with uraemic bleeding the influence of s.c. DDAVP was investigated in the steady state. Bleeding time (BT) significantly shortened in 7 patients (before m BT: >15 min; 90 min after DDAVP BT: 6 min). Additionally, platelet count decreased while platelet retention increased.DDAVP, s.c. injected, was shown to be a safe and effective measure in bleeding disorders and may become a useful tool for conditioning of plasma or granulocyte donors.
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Mannucci, P. M., V. Vicente, I. Alberca, E. Sacchi, A. S. Harris, and A. Lindqvist. "SUBCUTANEOUS AND INTRAVENOUS ADMINISTRATION OF DESMOPRESSIN (DDAVP) TO HEMOPHILIACS: PLASMA PHARMACOKINETICS AND FACTOR VIII (VIII:C) RESPONSES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644706.
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Reported studies dealing with the clinical use of DDAVP in mild and moderate hemophilia A patients show a very large between-patient variability for the maximum increase of VIII:C after the drug given intravenously (i.v.) or subcutaneously (s.c.). By measuring DDAVP plasma levels with a sensitive and specific RIA method, we elected to evaluate whether or not between-patient response variability was related to the variability of DDAVP levels achieved in their plasma. To this purpose 14 moderate or mild hemophilic volunteers (baseline VIII : C 4 to 31 U/dL) were randomly given 0.3 pg/Kg of i.v. or s.c. DDAVP with a between-treatment interval of 15 - 30 days. Plasma DDAVP pharmacokinetics in relation to the routes of administration are shown in the table.Pack levels (Cmax) were higher after i.v. DDAVP (p < 0.02). Time to peak levels (tmax) was shorter for i.v. DDAVP (p < 0.001). There was no difference between i.v. and s.c. DDAVP for plasma time curve (AUC) and half-life (t½).The bioavailability of the s.c. route relative to the i.v. route was 85 ° 32%. Of further interest, was the greater variability of the i.v. pharmacokinetics compared to the s.c. data. These differences were reflected in the VIII:C response. Maximum VIII:C increase over baseline levels was 3.2 ° 2.4 fold (i.v.) and 3.2 ° 1.3 fold (s.c.) (n.s.).Thus the i.v. route gave a marginally greater response but the effect was more variable than the s.c. route. Finally, no significant correlation was found between the VIII:C response and plasma DDAVP levels for either route of administration (i.v. route r = 0.03, s.c. route r = 0.23).These findings establish the subcutaneous route to be bioequivalent in effect to the intravenous route with less variation. This study also demonstrates that the VIII:C response to DDAVP is neither a function of the rate of absorption of the corrpound into the body nor the magnitude of the plasma concentration.