MAUDE data represents reports of adverse events involving medical devices. This maude entry was filed from a 03,05,07 report with the FDA on 2012-03-02 for NBCA LIQUID EMBOLIC KIT 631XXX manufactured by Cordis Neurovascular, Inc..
[2494203]
During a literature search the following article was found: journal of neurointerventional surgery march 2011 3 (1) (pp 21-24) "vascular inflammation with eosinophils after the use of n-butyl cyanoacrylate liquid embolic system", quinn j. C. , mittal n. , baisre a. , cho e. S. , sharer l. R. , candhi c. , prestigiacoma c. J. The article reported three cases of restricted eosinophilic vasculitis secondary to nbca sensitization. The cases of three patients are reported who underwent endovascular embolization with n-bca, followed by resection in two and post-embolization hemorrhage with emergent evacuation in one, with histologic demonstration of an eosinophilic vasculitis found in resected avm specimens. This is probably the first report of this tissue reaction, which may have theoretically serious clinical implications. Clinical presentation: in this series, three patients (2 women, 1 man) presented with intracranial avms (spetzler-martin i-iii) with the lesions located in the frontal lobe in two of the patients and in the parietal lobe in one. All patients presented with headache, and one also had new-onset seizures. Intervention: all patients underwent embolization with n-bca before a planned, staged surgical resection of the embolized avms.
Patient Sequence No: 1, Text Type: D, B5
[9656281]
One patient had four embolizations over a 5-month period, one had three embolizations over 3 months complicated by hemorrhage after embolization requiring emergent evacuation of the hematoma, and the third patient had a single embolization. In all three patients, surgical and autopsy specimens showed an inflammatory response within the embolized vasculature with a prominent eosinophilic infiltrate. Conclusion: the eosinophilic vasculitis seen in the pathology specimens may represent a previously undocumented hypersensitivity reaction following exposure to n-bca, with the potential for adverse sequelae, including increased risk of hemorrhage as was seen in one of our patients. Journal of neurointerventional surgery march 2011 3 (1) (pp 21-24)? Vascular inflammation with eosinophils after the use of n-butyl cyanoacrylate liquid embolic system? , quinn j. C. , mittal n. , baisre a. , cho e. S. , sharer l. R. , candhi c. , prestigiacoma c. J. Reported three cases of restricted eosinophilic vasculitis secondary to nbca sensitization. All patients presented with headache. One of these cases was complicated by hemorrhage after embolization. With follow-up investigation it was reported by the contact author that the brand used was trufill nbca. Case 2 reported a man presenting with new-onset seizures was diagnosed with a 3. 5 cm left posterior frontal avm (spetzleremartin iii). The patient underwent three stages of n-bca embolization over the next 3 months at 40% concentration in lipiodol. A total of two pedicles were embolized over the three stages. Immediately after the third stage of embolization the patient developed an intracerebral hemorrhage and underwent emergent craniotomy for evacuation of the hematoma. No evidence of venous occlusion or vascular perforation was noted. Postoperatively the patient had a devastated neurologic examination and after discussion with the patient's family the decision was made to withdraw care. Postmortem microscopic examination of the resected avm and hematoma revealed a dense granulocytic infiltrate in vessel walls with many scattered eosinophils. No peripheral eosinophilia was noted on routine blood examination and the patient was also without signs of systemic involvement. The article reports that while the aberrant avm vasculature itself led to higher propensity for rupture, it is likely that the inflammatory response created by the widespread vasculitis played a part in the rupture; however, it is reported that this is difficult to prove with certainty. Potential deleterious effects of the vasculitic reaction described include increased vessel wall weakness and fragility and propensity for rupture. On hundred fifty-eight patients with varying grades of avms were treated with n-bca embolization, followed by open resection between 2002 and 2008. All specimens obtained during resection were sent for pathologic review. Histopathologic examination of the avms demonstrated the histopathologic progression as has been previously described. Unique to this series of three patients among the 158 cases reviewed was the presence of a prominent eosinophilic infiltrate affecting the endothelium and extending into the media of the embolized vessels, suggesting a separate inflammatory/immunological process in addition to the natural progression which has been previously described. Other portions of the non-embolized avm did show a similar eosinophilic infiltrate, arguing that this is probably a non-focal reaction. In all cases, there was no evidence of peripheral eosinophilia or any clinical signs of an underlying systemic cause for a cns restricted eosinophilic infiltrate, although dedicated serologic testing was not done in these patients. The presence of eosinophils in the chronic inflammatory milieu probably represents a restricted eosinophilic vasculitis caused by host sensitization to n-bca epitopes. The article states that the clinical consequences of the reported inflammatory/immunological response are difficult to assess in the series for a number of reasons, including the patient had baseline neurological deficits from their primary vascular malformations, the exposure time to nbca was relatively short, and for two patients, all embolized vasculature was resected during the stated surgical procedure. It further reports that because this reaction was described in patients in whom a staged resection was planned, it is entirely possible that the clinical sequel of n-bca exposure did not have time to manifest itself. It is reported that the implications of these findings may be more relevant in cases where n-bca embolization is to be used as a monotherapy or in cases where not all the embolic agent is fully resected. The authors hypothesize that the three cases of restricted eosinophilic vasculitis are secondary to n-bca sensitization and that they believe this may represent a rare but significant reaction in some patients has the potential to lead to increased rupture risk and, potentially, other neurological sequelae. The product is not available for evaluation and testing. Additional information will be submitted within 30 days upon receipt. This is one of four products reported in the same journal article/literature search. Please reference mfr. Report # 1058196-2012-00101; # 1058196-2012-00102; # 1058196-2012-00103; and # 1058196-2012-00104.
Patient Sequence No: 1, Text Type: N, H10
[9957093]
Please note that the product catalog number was corrected. (b)(6) reported three cases of restricted eosinophilic vasculitis secondary to nbca sensitization. One of these cases was complicated by hemorrhage after embolization. With follow-up investigation it was reported by the contact author that the brand used was trufill nbca. One man presenting with new-onset seizures was diagnosed with a 3. 5 cm left posterior frontal avm (spetzleremartin iii). The patient underwent three stages of n-bca embolization over the next (b)(6) months at 40% concentration in lipiodol. A total of two pedicles were embolized over the three stages. Immediately after the third stage of embolization the patient developed an intracerebral hemorrhage and underwent emergent craniotomy for evacuation of the hematoma. No evidence of venous occlusion or vascular perforation was noted. Postoperatively the patient had a devastated neurologic examination and after discussion with the patient's family the decision was made to withdraw care. Postmortem microscopic examination of the resected avm and hematoma revealed a dense granulocytic infiltrate in vessel walls with many scattered eosinophils. No peripheral eosinophilia was noted on routine blood examination and the patient was also without signs of systemic involvement. The article reports that while the aberrant avm vasculature itself led to higher propensity for rupture, it is likely that the inflammatory response created by the widespread vasculitis played a part in the rupture; however, it is reported that this is difficult to prove with certainty. Potential deleterious effects of the vasculitic reaction described include increased vessel wall weakness and fragility and propensity for rupture. (b)(4) patients with varying grades of avms were treated with n-bca embolization, followed by open resection between 2002 and 2008. All specimens obtained during resection were sent for pathologic review. Histopathologic examination of the avms demonstrated the histopathologic progression as has been previously described. Unique to this series of three patients among the (b)(4) cases reviewed was the presence of a prominent eosinophilic infiltrate affecting the endothelium and extending into the media of the embolized vessels, suggesting a separate inflammatory/immunological process in addition to the natural progression which has been previously described. Other portions of the non-embolized avm did show a similar eosinophilic infiltrate, arguing that this is probably a non-focal reaction. In all cases there was no evidence of peripheral eosinophilia or any clinical signs of an underlying systemic cause for a cns restricted eosinophilic infiltrate, although dedicated serologic testing was not done in these patients. The presence of eosinophils in the chronic inflammatory milieu probably represents a restricted eosinophilic vasculitis caused by host sensitization to n-bca epitopes. The article states that the clinical consequences of the reported inflammatory/immunological response are difficult to assess in the series for a number of reasons, including the patient had baseline neurological deficits from their primary vascular malformations, the exposure time to nbca was relatively short, and for two patients, all embolized vasculature was resected during the stated surgical procedure. It further reports that because this reaction was described in patients in which a staged resection was planned, it is entirely possible that the clinical sequel of n-bca exposure did not have time to manifest itself. It is reported that the implications of these findings may be more relevant in cases where n-bca embolization is to be used as a monotherapy or in cases where not all the embolic agent is fully resected. The authors hypothesize that the three cases of restricted eosinophilic vasculitis are secondary to n-bca sensitization and that they believe this may represent a rare, but significant reaction in some patients has the potential to lead to increased rupture risk and, potentially, other neurological sequelae. The product was not returned for inspection. The lot number of the trufill nbca glue is not known; therefore, a device history record review cannot be completed. These procedures are performed in vessels with existing abnormalities and as reported, the aberrant avm vasculature itself leads to higher propensity for rupture. The authors report that the implications of the findings of eosinophilic vasculitis may be more relevant in cases where n-bca embolizations is to be used as a monotherapy or in cases where not all the embolic agent is fully resected. The instructions for use outlines that trufill nbca liquid embolic system is indicated for the embolization of cerebral avms when presurgical devascularization is desired. It further warns that the safety and efficacy of this product as a long-term implant has not been established. It is contraindicated for use with previous history of reactions to components. The observed infection/inflammation and hemorrhage are outlined in the instructions for use as adverse events that may be associated with embolization procedures (including those observed during the clinical study), and may occur at any time during or after the procedure. Therefore, no corrective actions will be taken at this time.
Patient Sequence No: 1, Text Type: N, H10
| Report Number | 1058196-2012-00103 |
| MDR Report Key | 2475772 |
| Report Source | 03,05,07 |
| Date Received | 2012-03-02 |
| Date of Report | 2012-02-20 |
| Date of Event | 2012-02-02 |
| Date Mfgr Received | 2012-04-16 |
| Date Added to Maude | 2012-03-05 |
| Event Key | 0 |
| Report Source Code | Manufacturer report |
| Manufacturer Link | Y |
| Number of Patients in Event | 0 |
| Adverse Event Flag | 3 |
| Product Problem Flag | 3 |
| Reprocessed and Reused Flag | 3 |
| Health Professional | 3 |
| Initial Report to FDA | 3 |
| Report to FDA | 0 |
| Event Location | 0 |
| Manufacturer Contact | MRS. LINA ALZATE |
| Manufacturer City | MIAMI LAKES FL 330142802 |
| Manufacturer Country | US |
| Manufacturer Postal | 330142802 |
| Manufacturer Phone | 7863136492 |
| Manufacturer G1 | CORDIS NEUROVASCULAR, INC. |
| Manufacturer Street | 14700 NW 57TH COURT |
| Manufacturer City | MIAMI LAKES FL 33014 |
| Manufacturer Country | US |
| Manufacturer Postal Code | 33014 |
| Single Use | 3 |
| Remedial Action | OT |
| Previous Use Code | 3 |
| Event Type | 3 |
| Type of Report | 3 |
| Brand Name | NBCA LIQUID EMBOLIC KIT |
| Generic Name | CNV_NBCA (MFE) |
| Product Code | KGG |
| Date Received | 2012-03-02 |
| Model Number | NA |
| Catalog Number | 631XXX |
| Lot Number | UNK |
| ID Number | NA |
| Operator | HEALTH PROFESSIONAL |
| Device Availability | N |
| Device Age | DA |
| Device Eval'ed by Mfgr | R |
| Device Sequence No | 1 |
| Device Event Key | 0 |
| Manufacturer | CORDIS NEUROVASCULAR, INC. |
| Manufacturer Address | 14700 NW 57TH COURT MIAMI LAKES FL 33014 US 33014 |
| Patient Number | Treatment | Outcome | Date |
|---|---|---|---|
| 1 | 0 | 1. Death | 2012-03-02 |