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Medtronic is submitting this report to comply with fda reporting regulations under 21 cfr parts 4 and 803.This report is based upon information obtained by medtronic, which the company may not have been able to fully investigate or verify prior to the date the report was required by the fda.Medtronic has made reasonable efforts to obtain more complete information and has provided as much relevant information as is available to the company as of the submission date of this report.This report does not constitute an admission or a conclusion by fda, medtronic, or its employees that the device, medtronic, or its employee caused or contributed to the event described in the report.In particular, this report does not constitute an admission by anyone that the product described in this report has any ¿defects¿ or has ¿malfunctioned¿.These words are included in the fda 3500a form and are fixed items for selection created by the fda to categorize the type of event solely for the purpose of regulatory reporting.Medtronic objects to the use of these words and others like them because of the lack of definition and the connotations implied by these terms.This statement should be included with any information or report disclosed to the public under the freedom of information act.Any required fields that are unpopulated are blank because the information is currently unknown or unavailable.A good faith effort will be made to obtain the applicable information relevant to the report.If information is provided in the future, a supplemental report will be issued.
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Wael e.A.Saad, mark g.Davies, nael e.A.Saad, karin e.Westesson, nikhil c.Patel, lawrence g.Sahler, david e.Lee, takashi kitanosono, talia sasson, david l.Waldman; vascular and endovascular surgery; 2007; 41(1):19-26; catheter thrombolysis of thrombosed hepatic arteries in liver transplant recipients: predictors of success and role of thrombolysis; 10.1177/1538574406296210 medtronic received information in a literature article of five patients (mean age 47, 4 mal, 1 female) with liver transplantation had subsequent hepatic artery thrombosis (hat) between (b)(6) 1995 and (b)(6) 2006.A cragg-mcnamara infusion catheter was used for one of two types of pharmaceutical thrombolytic infusion.Either urokinase at 120 000 iu/hour or recombinant tissue plasminogen activator ( at 0.5 mg/hour for 16 to 24 hours.In conjunction with transcatheter intra-arterial thrombolysis infusion, peripheral intravenous heparin was infused to prevent pericatheter thrombosis at a rate of 250 to 400 units per hour. mechanical thrombolysis (thrombus maceration) of the intra-arterial thrombus was occasionally performed using a 0.018-inch guidewire before the placement of the infusion catheter/wire system.Case 1: at 71 days post-transplantation, the hepatic arteries were not depicted by doppler ultrasound (dus) and an angiogram confirmed hat.Guidewire manipulations in an attempt to fragment the thrombus, before commencing pharmacological thrombolysis, caused a perforation of the hepatic artery. a 4-mm balloon was inflated to tamponade the hepatic artery for 20 minutes.Post-tamponade angiogram demonstrated no contrast extravasation and continued hat.No further interventions were performed.Within 16 days a hepatic abscess developed that was treated with computed tomography (ct)¿ guided percutaneous drainage with antibiotics.The patient overcame his initial hepatic parenchymal necrosis and survived for 2 years without significant morbidity.Eventually the hepatic abscesses recurred, along with cholangitis, septic shock, and disseminated intravascular coagulopathy, and the patient died.Case2: hat was confirmed by angiography.A catheter was placed into the thrombosed hepatic artery and urokinase was instilled at 120 000 iu/hour.Ten hours later, an interval angiogram demonstrated partial resolution of the thrombus with continued filling defects in the distal intrahepatic arteries and a stenosis in the main hepatic artery distal to the surgical anastomosis.The flow in the hepatic artery was reestablished but was slow.Urokinase infusion was continued at the same rate for another 30 hours (40 hours total).A repeat angiogram demonstrated no change.After an attempt at angioplasty, the lesion failed due to inability to traverse the distal has with a balloon.At the end of the attempt, hat ensued and further attempts at revascularization of the graft were terminated.The patient underwent repeat transplantation within 2 days and has done well for 4 1/2 years after his re-transplant.Case 3: diagnosed with hat by dus 15 days after his orthotopic liver transplant (olt).This was confirmed by angiography.An infusion catheter was placed in the thrombosed hepatic artery.Urokinase was infused at 120 000 iu/hour for 24 hours.An interval angiogram the next day showed partial resolution of the thrombus with reestablished arterial flow and a stenosis at the surgical anastomosis.Angioplasty of this stenosis was attempted and failed due to inability to cross the lesion.Hat ensued after the attempted angioplasty and no further attempts were made.Within 6 days, a necrotic collection developed within the liver and multiple hepatic abscesses subsequently developed that were treated with antibiotics.A percutaneous transhepatic cholangiogram demonstrated a necrotic biliary tract, and an internal-external biliary drain was placed.The patient is 3 1/2 years out from this episode of hat without significant morbidity.Case 4: diagnosed with hat by dus 35 days after her olt.This was confirmed by angiography.Mechanical thrombolysis with a guidewire was performed with partial resolution of the thrombus.A hepatic artery infusion catheter was placed and urokinase was infused at 120 000 iu/hour for 17 hours.An interval angiogram demonstrated reestablishment of flow with minimal residual thrombus.An arterial kink and a significant vascular anastomotic stenosis were uncovered.Attempts to traverse the stenosis with a balloon over a guidewire failed.Urokinase was infused at the same rate for another 23 hours (total of 40 hours) with no additional improvement by angiography.The patient underwent revision of the surgical anastomosis and thrombectomy of the artery.Case 5: 7 days after his olt with an aorto-hepatic conduit was diagnosed with hat by dus and angiography.The arterial conduit and graft hepatic artery were negotiated with both angiographic catheter and guidewire with occasional contrast material injections.The intention of this is thrombus maceration and to evaluate the most distal extent of the thrombus.Tissue plasminogen activator (tpa) was transfused at 0.25 mg/hour via an infusion wire and 0.25 mg/hour via an infusion catheter (0.5 mg/hour, total).Peripheral iv heparin infusion at a rate of 250 u/hour was also administered.Twenty-four hours later, reestablishment of flow was achieved.This uncovered an arterial conduit anastomotic stenosis and a more distal critical stenosis.Balloon angioplasty did macerate the thrombus in the proximal arterial conduit; however, the operator could not traverse the proximal arterial conduit turn to resolve the surgical anastomosis and the more distal critical anastomosis (figure 1e).A dus in the angiography suite demonstrated a patent main and right hepatic artery with an arterial resistive index of 0.51 and 0.47, respectively.The left hepatic artery was not visualized by dus.The patient was taken to the operating room for a surgical revascularization.Intra-operative examination of the artery confirmed pulsatile flow and an arterial kink.During the open surgical revision, a fogarty thrombectomy yielded partial thrombus.After the surgical revascularization, dus evaluated demonstrated patent hepatic arteries with normal arterial ri (=0.50).The patient did well with no intrahepatic infarcts or abscesses or other major morbidities for the following 2 years.
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G3 510k information corrected.Medtronic is submitting this report to comply with fda reporting regulations under 21 cfr parts 4 and 803.This report is based upon information obtained by medtronic, which the company may not have been able to fully investigate or verify prior to the date the report was required by the fda.Medtronic has made reasonable efforts to obtain more complete information and has provided as much relevant information as is available to the company as of the submission date of this report.This report does not constitute an admission or a conclusion by fda, medtronic, or its employees that the device, medtronic, or its employee caused or contributed to the event described in the report.In particular, this report does not constitute an admission by anyone that the product described in this report has any ¿defects¿ or has ¿malfunctioned¿.These words are included in the fda 3500a form and are fixed items for selection created by the fda to categorize the type of event solely for the purpose of regulatory reporting.Medtronic objects to the use of these words and others like them because of the lack of definition and the connotations implied by these terms.This statement should be included with any information or report disclosed to the public under the freedom of information act.Any required fields that are unpopulated are blank because the information is currently unknown or unavailable.A good faith effort will be made to obtain the applicable information relevant to the report.If information is provided in the future, a supplemental report will be issued.
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