Displaying 1-10 letters out of 24 published
The Influence of Angioarchitecture on Management of Pediatric Intracranial Arteriovenous Malformations
I have read, with great interest, the paper by Ellis et al. titled 'Angioarchitectural features associated with hemorrhagic presentation in pediatric cerebral arteriovenous malformations . The authors retrospectively reviewed the angiographic features of 135 pediatric patients, mean age 10.1 years (range 0-19 years), who were referred to Hospital for Sick Children in Toronto, Canada and Boston Children's Hospital over a period of 11 years from 2000 to 2011. The most common presenting symptoms were hemorrhage (64%), seizure (13%), and focal neurological deficits or headache (13%). The authors sought to identify angiographic features associated with AVM rupture at presentation. Multivariate logistic regression analysis identified smaller size (P<0.01), exclusive deep venous drainage (P=0.02), and infratentorial location (P=0.01) to be independent predictors of hemorrhagic presentation.
Given the relatively little information available regarding the natural history of pediatric compared to adult AVMs, this study represents an important contribution to the pediatric AVM literature. As the authors note, there is an increased tendency to aggressively treat AVMs, especially ruptured ones, presenting in children compared to those in adults due to the higher exposure to hemorrhage risk and hemorrhage- related morbidity and mortality by children. Given what is currently known regarding the natural history of AVMs, which is largely derived from adult patients, this rationale is seems valid . A Randomized Trial of Unruptured Brain AVMs (ARUBA) is a study of adult patients only . It is unknown whether the results of ARUBA, which are pending imminent publication, will alter the management of unruptured pediatric AVMs.
It would be very interesting to know how the patients described in this study were treated and whether hemorrhagic presentation and AVM angioarchitectural features influenced the treatment strategies. Although the method by which AVM obliteration is achieved is biased, at times significantly, by the treating physician and institution, no single modality, including endovascular embolization, microsurgical resection, and radiosurgery, has emerged superior to its counterparts. For example, AVMs with smaller size and exclusive deep venous drainage, which typically implies deep location, are ideal radiosurgery targets [4-5]. However, in the setting of AVM rupture, some may advocate for microsurgical resection in order to rapidly eliminate future hemorrhage risk. Additionally, the authors did not distinguish infratentorial location by brainstem versus cerebellum. Recently, the UCSF cerebrovascular group described cerebellar AVMs as anatomically distinct lesions from cerebral AVMs with a higher propensity for hemorrhagic presentation . Not surprisingly, cerebellar AVMs are significantly more conducive than brainstem AVMs to surgical resection therefore underscoring the importance of distinguishing the two locations.
In summary, the authors should be congratulated for identifying independent predictors of hemorrhagic presentation in a relatively large cohort of pediatric AVMs combined from two tertiary pediatric referral centers of international repute. Given the difficulty of obtaining prospective data regarding the natural history of pediatric AVMs, the cerebrovascular community will continue to rely on this study and others like it to guide decision-making for the management of these rare and complex vascular lesions.
1. Ellis, M.J., D. Armstrong, S. Vachhrajani, A.V. Kulkarni, P.B. Dirks, J.M. Drake, E.R. Smith, R.M. Scott, and D.B. Orbach, Angioarchitectural features associated with hemorrhagic presentation in pediatric cerebral arteriovenous malformations. J Neurointerv Surg, 2013. 5(3): p. 191-5. 2. Gross, B.A. and R. Du, Natural history of cerebral arteriovenous malformations: a meta-analysis. J Neurosurg, 2013. 118(2): p. 437-43. 3. Mohr, J.P., A.J. Moskowitz, C. Stapf, A. Hartmann, K. Lord, S.M. Marshall, H. Mast, E. Moquete, C.S. Moy, M. Parides, J. Pile-Spellman, R. Al-Shahi Salman, A. Weinberg, W.L. Young, A. Estevez, I. Kureshi, and J.L. Brisman, The ARUBA trial: current status, future hopes. Stroke, 2010. 41(8): p. e537-40. 4. Kano, H., D. Kondziolka, J.C. Flickinger, H.C. Yang, T.J. Flannery, N.R. Awan, A. Niranjan, J. Novotny, and L.D. Lunsford, Stereotactic radiosurgery for arteriovenous malformations, part 2: management of pediatric patients. J Neurosurg Pediatr, 2012. 9(1): p. 1-10. 5. Yen, C.P., S.J. Monteith, J.H. Nguyen, J. Rainey, D.J. Schlesinger, and J.P. Sheehan, Gamma Knife surgery for arteriovenous malformations in children. J Neurosurg Pediatr, 2010. 6(5): p. 426-34. 6. Rodriguez-Hernandez, A., H. Kim, T. Pourmohamad, W.L. Young, and M.T. Lawton, Cerebellar arteriovenous malformations: anatomic subtypes, surgical results, and increased predictive accuracy of the supplementary grading system. Neurosurgery, 2012. 71(6): p. 1111-24.
Conflict of Interest:
The Impact of Endovascular Onyx Embolization on Acutely Ruptured Intracranial Arteriovenous Malformations
I have read, with great interest, the paper by Stemer et al. titled 'Acute embolization of ruptured brain arteriovenous malformations' . The authors describe a cohort of 21 patients with ruptured intracranial arteriovenous malformations (AVM) who were treated with endovascular Onyx (ev3, Irvine, California, USA) embolization in the acute phase following hemorrhage. The median interval from hemorrhagic presentation to treatment was 4 days (range 0-19 days). Thirteen patients received a single treatment (62%), and eight patients were treated in more than one stage (38%). Complete occlusion was achieved in 11 patients (52%) including seven in one stage and four in multiple stages. There were two asymptomatic intraprocedural complications (10%) as well as two mortalities unrelated to treatment (10%).
Excluding three patients lost to follow-up and six patients who underwent post-embolization surgical resection, 12 patients had angiographic follow-up at a mean interval of 7.5 months. It would be interesting to know the number of AVMs, if any, which had post- embolization recanalization at follow-up as this is known to occur at varying time intervals following endovascular treatment. Despite high levels of initial enthusiasm for complete AVM cure with standalone endovascular embolization following the advent and subsequent widespread therapeutic use of permanent liquid embolic agents, especially Onyx, the role of embolization in the overall management of AVMs remains largely adjunctive.
Studies reporting high rates of complete AVM obliteration with embolization alone, approaching 50%, were subject to significant selection biases . Total obliteration rates of 10-20% with embolization alone are more reflective of less selected AVM cohorts . The effect of partial AVM treatment on the subsequent hemorrhage risk is still controversial with conflicting studies reporting improved and worsened outcomes of incompletely obliterated AVMs. With increasing evidence that embolization reduces AVM obliteration rates following radiosurgery, judicious use of endovascular therapy for AVMs is crucial to the optimal long-term management of these complex vascular lesions [4-6].
Early natural history studies of AVMs did not distinguish ruptured from unruptured lesions. However, several recent studies in the past decade have repeatedly demonstrated that the hemorrhage risk of ruptured AVMs is significantly higher than the hemorrhage risk of unruptured ones . Unlike intracranial aneurysms, for which the risk of acute repeat hemorrhage following initial rupture is well described, the acute rehemorrhage rate of ruptured AVMs is poorly defined. In a recent meta- analysis of over 3900 patients, Gross et al. reported an annual hemorrhage risk of 4.5% for ruptured AVMs compared to 2.2% for unruptured lesions . A follow-up duration of less than one year, such as in this study, is inadequate to compare treatment outcomes to the natural history.
In summary, the authors should be congratulated for demonstrating the feasibility and safety of endovascular Onyx embolization for the treatment of acutely ruptured AVMs. As the authors note, the study is significantly limited by the relatively small number of patients with angiographic follow-up and the relatively short duration of follow-up. Therefore it remains to be determined in larger cohorts with longer follow-up whether the strategy of acute embolization for ruptured AVMs is superior to current approaches which are largely conservative in the acute post- hemorrhage phase.
1. Stemer, A.B., W.O. Bank, R.A. Armonda, A.H. Liu, D.W. Herzig, and R.S. Bell, Acute embolization of ruptured brain arteriovenous malformations. J Neurointerv Surg, 2013. 5(3): p. 196-200. 2. Saatci, I., S. Geyik, K. Yavuz, and H.S. Cekirge, Endovascular treatment of brain arteriovenous malformations with prolonged intranidal Onyx injection technique: long-term results in 350 consecutive patients with completed endovascular treatment course. J Neurosurg, 2011. 115(1): p. 78-88. 3. van Rooij, W.J., M. Sluzewski, and G.N. Beute, Brain AVM embolization with Onyx. AJNR Am J Neuroradiol, 2007. 28(1): p. 172-7; discussion 178. 4. Schwyzer, L., C.P. Yen, A. Evans, S. Zavoian, and L. Steiner, Long-term Results of Gamma Knife Surgery for Partially Embolized Arteriovenous Malformations. Neurosurgery, 2012. 71(6): p. 1139-48. 5. Ding, D., C.P. Yen, Z. Xu, R.M. Starke, and J.P. Sheehan, Radiosurgery for patients with unruptured intracranial arteriovenous malformations. J Neurosurg, 2013. 6. Andrade-Souza, Y.M., M. Ramani, D. Scora, M.N. Tsao, K. terBrugge, and M.L. Schwartz, Embolization before radiosurgery reduces the obliteration rate of arteriovenous malformations. Neurosurgery, 2007. 60(3): p. 443-51; discussion 451-2. 7. Stapf, C., H. Mast, R.R. Sciacca, J.H. Choi, A.V. Khaw, E.S. Connolly, J. Pile-Spellman, and J.P. Mohr, Predictors of hemorrhage in patients with untreated brain arteriovenous malformation. Neurology, 2006. 66(9): p. 1350-5. 8. Gross, B.A. and R. Du, Natural history of cerebral arteriovenous malformations: a meta-analysis. J Neurosurg, 2013. 118(2): p. 437-43.
Conflict of Interest:
I am glad to see that my letter has piqued the interest of interventional neuroradiologists like Dr. Jagadeesan. I agree with him that no one should be running a fellowship that does not have the volume to expose trainees to enough cases so that they may obtain the necessary experience to practice safely. However, I think he has misunderstood my point. As I stated about the original piece, "I have no objection to the logic and opinions expressed, and actually have no opinion on the issue for or against these fellowships." My only request was for the authors of the original article to disclose the fact (as Dr. Jagadeesan has nicely done in his own letter) that they may have potential conflicts of interest by way of already completed and reaping the potential rewards of the very same fellowship training that they now advocate curtailing, so that the reader may use this information when making up his or her own mind. I have no interest in standing between interventional neuroradiologists and their patients (unless one is trying to run over the other, in which case I hope I could intervene). As far as taxi drivers, I would applaud their specialty if one disclosed that he gotten his driver's license from the black market instead of completing the required training and tests - indeed, that information might affect my decision to ride in his or another cab.
Conflict of Interest:
CT Perfusion or Time Criteria for Endovascular Stroke Management?
Nohra Chalouhi M.D., Stavropoula Tjoumakaris M.D.,and Pascal Jabbour M.D.
We read with great interest the article by Turk et al assessing the safety and efficacy of endovascular stroke intervention based on CT perfusion (CTP) criteria. The authors are to be congratulated for this excellent report and for achieving remarkably high rates of favorable outcomes (42%) in stroke patients with poor neurological status (mean NIHSS, 18.2). They further categorize their patient population based on time from symptom onset and clearly show that patients treated after 8 h had no difference in outcomes or mortality than those treated before 8 h. The fact that time from symptom onset to intervention was as long as 16.4 h in the late group (>8h) lends further credence to their findings because the extent of salvageable brain tissue and the prospect of improvement significantly decrease with delayed recanalization.[2-4] This report adds substantially to the growing body of literature supporting the use of CTP in stroke patients and reinforces what we have always believed; specifically, CTP can optimize and guide patient selection for intraarterial therapy based on an individual's physiological parameters namely the extent of salvageable ischemic penumbra.
Although we agree with the authors about the merits of CTP and stress the importance of their results, we would like to bring to their attention that their conclusion may not be totally supported by the presented data. The authors have compared functional outcomes in patients treated <8 h and >8 h after symptom onset. Although all patients were selected for endovascular stroke intervention based on CTP criteria, they conclude that "physiologic imaging-guided patient selection rather than time for endovascular reperfusion in ischemic stroke may be effective and safe". We believe the only way to reach such a conclusion is to compare two groups of patients, one selected based on CTP criteria and the other based on time from symptom onset. Indeed, the authors do not discuss the study by Hassan et al published in 2010 that retrospectively compared 69 patients undergoing CTP-guided and 127 patients undergoing time-guided endovascular treatment. The authors of this study found no incremental benefit with the use of CTP, with similar rates of recanalization, intracranial hemorrhage, favorable outcomes, and in-hospital mortality in both groups. It should be noted, however, that only 40% of patients in their study underwent mechanical thrombectomy and that CTP-guided treatment at the primary author's institution was compared to time-guided treatment at a different institution, which could have influenced their results. Still, this is to our knowledge the only study that has compared time-guided to CTP-guide patient selection for acute stroke intervention. Randomized controlled trials comparing the 2 strategies are needed especially that many prominent centers still have not adopted CTP as a screening tool in this setting.
We would also like to highlight some of the potential shortcomings associated with CTP that were not discussed in this study. The inter- observer variability remains a great concern with CTP. Additionally, the optimal post-processing algorithm for defining penumbra and core infarct have yet to be determined, and thresholds for guiding therapy are still under investigation. The variation in reconstruction of CTP images and qualitative interpretation of salvageable tissue may lead to selection of a relatively heterogeneous population, leading to the inclusion of patients with limited salvageable tissue. False negatives and non interpretable imaging can occur with CTP due to low cardiac output, inappropriate slow rate of bolus administration, contrast extravasation in the subcutaneous tissue, patient movement, and operator inexperience.
Finally, despite the potential caveats of CTP imaging , Turk et al have clearly demonstrated that CTP allows effective treatment of many patients who otherwise would be destined for supportive management or end of life care due to presentation outside of the therapeutic window. We commend the authors for their rigorous work and await similar contributions that will help us determine the best approach for patient selection for acute stroke intervention.
References 1. Turk AS, Magarick JA, Frei D, et al. CT perfusion-guided patient selection for endovascular recanalization in acute ischemic stroke: a multicenter study. J Neurointerv Surg 2012 doi: neurintsurg-2012-010491 [pii] 10.1136/neurintsurg-2012-010491[published Online First: Epub Date]|. 2. Wardlaw JM, Murray V, Berge E, et al. Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis. Lancet 2012;379(9834):2364-72 doi: S0140-6736(12)60738-7 [pii] 10.1016/S0140-6736(12)60738-7[published Online First: Epub Date]|. 3. Hesselmann V, Niederstadt T, Dziewas R, et al. Reperfusion by combined thrombolysis and mechanical thrombectomy in acute stroke: effect of collateralization, mismatch, and time to and grade of recanalization on clinical and tissue outcome. AJNR Am J Neuroradiol 2012;33(2):336-42 doi: ajnr.A2746 [pii] 10.3174/ajnr.A2746[published Online First: Epub Date]|. 4. Vergouwen MD, Algra A, Pfefferkorn T, et al. Time Is Brain(stem) in Basilar Artery Occlusion. Stroke 2012 doi: STROKEAHA.112.666867 [pii] 10.1161/STROKEAHA.112.666867[published Online First: Epub Date]|. 5. Hassan AE, Zacharatos H, Rodriguez GJ, et al. A comparison of Computed Tomography perfusion-guided and time-guided endovascular treatments for patients with acute ischemic stroke. Stroke 2010;41(8):1673-8 doi: STROKEAHA.110.586685 [pii] 10.1161/STROKEAHA.110.586685[published Online First: Epub Date]|. 6. Hassan AE, Zacharatos H, Chaudhry SA, et al. Agreement in endovascular thrombolysis patient selection based on interpretation of presenting CT and CT-P changes in ischemic stroke patients. Neurocrit Care 2012;16(1):88 -94 doi: 10.1007/s12028-011-9577-9[published Online First: Epub Date]|. 7. Amenta PS, Ali MS, Dumont AS, et al. Computed tomography perfusion- based selection of patients for endovascular recanalization. Neurosurg Focus 2011;30(6):E6 doi: 10.3171/2011.4.FOCUS10296[published Online First: Epub Date]|.
Conflict of Interest:
Are there too many fellowships, or not enough training?
As a participant in the creation of the original ACGME ESNR fellowship training standards, I read the article concerning fellowship suspension with great interest (1). The paper is timely and thorough. It is unfortunate that the Neurointerventional world is dealing with so many unknowns. We do not seem to know how many we are, where we work, what we do, or where we were trained. The problem is very well summarized at the end of the paper. We seem to be spreading our patient population among too many practitioners, which subsequently restricts the number of patients available to each practitioner to stay in practice, make a living, and be proficient.
The first line states: "The purpose of any training program is to provide a supply of skilled workers to address an unmet demand for their services." The authors discuss numbers of procedures and extrapolate implications but do not discuss what the training was that got these people out into the world. Further, there is no clear statement as to what these unmet needs are. These workers might perhaps be skilled in certain areas, but not know anything about other subjects.
Adequacy of numbers is the primary thrust of the article. One endovascular neurosurgeon can possibly cover 5 different hospitals by themselves for aneurysms, AVMs etc., and could do 300 aneurysms per year easily. Most, but not all, neurointerventional fellowships provide an adequate number of aneurysms for training. But as correctly pointed out, the numerous auxiliary procedures that are necessary to be proficient in this profession, such as skull base tumor embolization, epistaxis, vertebroplasty, nerve root block or ablation, are not routinely performed at all institutions. AVMs might be completely ignored at many places. Endovascular spinal procedures are rare.
The gaping hole in fellowship training is acute ischemic stroke. Consistently complete training for all fellows continues to be a void in our profession and a gap in the entire premise of this statement. It is perfectly acceptable to produce specialists in aneurysm intervention as well as vertebroplasty, but we should not count them all in the same bucket and presume we have enough people to cover the nation for stroke. Everyone does not do everything nor do they want to. Many fellowship programs have inadequate caseload and resultant inadequate or poor training in acute stroke treatment. We should not just expect this specialized training to magically appear in fellowships where there is inadequate case volume to begin with. Therefore, what is the true number of interventionists that are available, trained, able, and willing to treat strokes?
The need for trained physicians to treat stroke is not based upon the number of strokes (as might be the case for aneurysms), but rather on the number of hospitals that need stroke coverage. The issue with stroke coverage is that there needs to be a minimal number of practitioners at each hospital to take call 24/7/365, no matter the number of cases: 1 per month or 1 per day. Another paper describes the necessity of stroke coverage as 2-3 interventionists per center for 24/7/365 coverage (2), contradicting the official SNIS stated position as well as EMTALA (Emergency Medical Treatment and Active Labor Act) that states that no requirement can be made for 24/7 coverage with less than 4 persons. If there is a need for 200 hospitals to have 24/7/365 coverage, then there needs to be at least 800 interventionists just at those hospitals alone.
The official SNIS position on stroke coverage is as follows: "Current staffing levels at Comprehensive Stroke Centers will rarely allow continuous immediate coverage for IA stroke therapy at all times, 365 days a year. Instantly available coverage on a continuous basis 24/7/365 should not be expected with fewer than 4 persons. Until adequate staffing levels are achieved, continuously available catheter-directed intra- arterial emergency stroke therapy is considered the "ideal", but is not mandatory in order to be classified as Comprehensive Stroke Center. Therefore, in agreement with federal regulations, IA stroke therapy might be available only a portion of the time as determined by local hospital conditions and staffing levels of qualified and appropriately trained personnel, and the institution still qualify as a Comprehensive Stroke Center." (SNIS executive committee, John Barr president, 2005). As we all know, there are very few hospitals that have 4 neurointerventionists.
There are probably fewer than 20 fellowships in the US that treat by endovascular techniques more than 50 strokes per year. Maybe 10. Even with 50 cases, a "fellow" can only "maybe" attain the SNIS mandated 10 cases as "primary operator" in his last few months. Thus, in the remaining 60-70 fellowships (90%?), the trainees will not get the required experience. There are numerous examples of fellowships that provide a certificate of competency for everything "neurointerventional" where the number of endovascular stroke cases can be counted on one hand... or one finger. How will these fellows get sufficient training, experience, and knowledge to have good outcomes when treating strokes when they are in private practice?
Foremost, I hope that this call for a moratorium in fellowships will be accompanied by an equally vigorous call for augmented and improved stroke training for fellows and our members. A recent SNIS webinar bemoaned the poor operator performance for intracranial stenting during SAMMPRIS. A recent article has documented "death and destruction" in endovascular stroke therapy (3). The failure of SAMMPRIS and the stoppage of IMS 3 only highlights the fact that we are not doing very well at this. As we all used to believe, IMS 3 should have been a slam-dunk. SNIS/SVIN should offer specialized intensive training courses that are, in actual fact, a responsibility of our professional organizations. Our societies need a plan for improved training and continuing education for our fellows and members in addition to a moratorium.
1) Fiorella D, Hirsch JA, Woo HH, et al. Should neurointerventional fellowship training be suspended indefinitely? J NeuroIntervent Surg 2012;4:315-318
2) Zaidat OO, Lazzaro M, McGinley E, et al. Demand-supply of neurointerventionalists for endovascular ischemic stroke therapy. Neurology 2012;79 (Suppl 1):S35-S41.
3) Cloft HJ. Death and Destruction in the Intra-Arterial Battle with Acute Ischemic Stroke. AJNR Am J Neuroradiol 32:1767-70.
Conflict of Interest:
MOC-and the Certification Industrial Complex: Taking money and providing no value
Hirsh and Meyers espouse that same party line of the many private non -governmental agencies (and academics who will personally benefit from this program) who wish to impose private interest group-unproven corporate interests upon practicing physicians. They continue to state MOC is "voluntary" and then describe the many ways these "non-profit" corporations (who earn handsomely and have over $400 million in assets and as great yearly gross receipts!) will see this product forced on physicians. HOWEVER, Working physicians do not want or even see any value in this unproven imposition:
The American Medical Association (AMA) developed the Physician's Recognition Award (PRA) in the late 1960's as the validation program for Continuing Medical Education (CME), embraced by most, but not all states, to validate physician "lifelong learning" as the educational component of re-licensure. Recently, the Federation of State Medical Boards (FSMB), Inc., a multimillion dollar, non-profit and non-governmental corporation, targeted the State of Ohio as the first of 11 pilot states to implement their corporate brand of MOL (Ohio., Calif., Colo., Del., Iowa, Mass., Mississippi, Okla., Ore., Va., Wis.). On May 19, 2012, the Ohio State Medical Association, as the first Ohio physician organization, formally resolved at the state meeting to oppose the FSMB MOL program. (1) OSMA recognized early that FSMB MOL was the unwarranted regulatory capture of physician licensure: the act of securing corporate income through legislation. (2) An intense battle over FSMB MOL ensued within the State Medical Board of Ohio (SMBO), zealously led by two FSMB board members, who also occupied the SMBO Executive Director and one senior Board member positions. On October 5, 2012, the OSMA drafted with 10 other state medical associations, representing over 15,000 physicians, a formal resolution of opposition directed to the SMBO. (3) The defeat of the FSMB MOL proposal by SMBO vote followed on October 11, 2012. In the aftermath, the two FSMB board members serving on the SMBO were formally reviewed. The Executive Director of the SMBO was ousted October 12th and formal investigations regarding violations of conflict of interests continue regarding the senior SMBO member. (4) Subsequent communications with legal offices of the SMBO and OSMA concluded that: 1) FSMB MOL was not advocated by any other corporate, government or consumer groups, no deficiency of AMA PRA CME programs or physician competency issues were identified in Ohio and 2) FSMB MOL initiative appeared solely promulgated by the FSMB as a corporate mandate. It continues to be actively advocated by FSMB in 9 states and must be either fought or approved in each state. FSMB MOL serves primarily corporate coffers and false reassurance through testing vs CME. Effective physician opposition is primarily possible via grass-roots resolutions at state level. We must inform and support all state organizations at this time regarding FSMB MOL, using this "Ohio experience" as evidence and instruction in opposing this regulatory capture of physicians, solely for corporate profits. (5) The assertions by the Certification industrial complex including the ABMS that MOC and MOL are "Done deals" is simple propaganda-nothing more!
References: 1) Ohio State Medical Association Statement on MOL. Available at: http://www.osma.org/files/pdf/facts-maintenance-of-licensure-final-.pdf Accessed 10/27/12
2)Kempen PM: Maintenance of Certification (MOC), Maintenance of Licensure (MOL), and Continuing Medical Education (CME):the Regulatory Capture of Medicine. Journal of American Physicians and Surgeons 2012; 17:72-5. Available at: http://www.jpands.org/vol17no3/kempen.pdf Accessed 10/27/12 3) Kumar D et al: Joint letter from 11 medical societies to the SMBO. Available at: http://www.itraumaohio.org/aws/OACEP/asset_manager/get_file/54757/2012.10.5_joint_mol_letter_to_medical_board.pdf Accessed 10/27/12 4) Alan Johnson In The Columbus Dispatch Thursday October 18, 2012 6:07 AM: State medical board ousts chief Available at: http://www.dispatch.com/content/stories/local/2012/10/18/state-medical- board-ousts-chief.html Accessed 10/27/12 5)Kempen PM: What to do about MOC and MOL? Available at: http://www.youtube.com/watch?v=WRS15Dmsk7E Accessed Nov 1, 2012
Conflict of Interest:
Abolishing Neurointerventional Fellowship Training: A Reality Check
I am not a neurosurgeon, neuroradiologist, nor interventionalist. In fact, I am not a regular reader of your journal. However, the article entitled "Should Neurointerventional Fellowship Training Be Suspended Indefinitely?" by David Fiorella, et al., was brought to my attention, unsolicited, by several different medical web sites. I have no objection to the logic and opinions expressed, and actually have no opinion on the issue for or against these fellowships. But I feel I must register my shock at what I see as a glaring omission by the journal.
The many authors do indicate their respective affiliations, and cumulatively list in their disclosure, "Competing interests: None." The most important disclosure, however, is not listed anywhere as a conflict of interest. Namely, how many of the authors are practicing, already fellowship-trained neurointerventionalists? In order to get a sense of any potential bias, I think the reader would want to know this fact about each author. Certainly, if most (or all) of the authors currently practice as neurointerventionalists, regardless of their arguments, some readers might feel that their position and recommendations simply represent an effort to restrict competition for their own advantage, and that the journal has given them a platform to advance this protectionist goal. If General Motors found themselves with a surplus of unsold cars and made the argument that there were too many autos already on the road, I might agree with that statement. But if their proposed solution was to ban further manufacture of cars so that they would have less competition unloading their inventories, I might object. Perhaps another company could produce cars that would be better (more efficient, safer, faster, etc.) and preventing them from doing so would hurt consumers, who would have fewer options. Similarly, while the authors may have correctly described the current problem (too many neurointerventionalists with not enough cases) their proposed solution (blocking further entries into the field) could be seen as self-serving. After all, maybe there are potential trainees or training programs who would introduce better practitioners (more efficient, safer, faster, etc.) into the market place, pressuring current (and future) neurointerventionalists to continue to improve the services they now deliver.
I invite each of the authors of the original article (and of any subsequent supportive letters) to make that disclosure: who among you are neurointerventionalists who have already enjoyed the benefits of fellowship training? Like any disclosure, this should not lessen your stated arguments; rather it will just allow the reader to know whence your recommendations are coming from. It only seems fair to be transparent. I'm just saying.
Conflict of Interest:
Re:Caution during use of DDAVP in IPSS
We thank the authors for their letter entitled, "Caution during use of DDAVP in IPSS," by Drs. Pecori Giraldi, Federici, and Cavagnini. The authors suggest that because of the hypercoagulable state that characterizes Cushing disease, DDAVP may not be safe since it has been shown to increase the level of von Willebrand factor (vWF) and could therefore lead to platelet adhesion and cause thromboembolism. The authors point to their own published work suggesting this effect (1). In this paper, the authors show that not only vWF levels increase, but also t-PA, likely to achieve a balance by activating fibrinolytic pathways. Therefore, increased risk of thromboembolic events in Cushing disease patients in the context of DDAVP administration is a theoretical consideration.
Thromboembolism is a rare complication of BIPSS and when reported, has been linked to lack of prophylaxis with IV heparin (2, 3). In our practice, we routinely heparinize patients undergoing BIPSS, whether they receive CRH or DDAVP to stimulate the pituitary (4). The case series previously reported where DDAVP was used rather than CRH do not indicate an increased risk of thromboembolic events (5-8). As the increased risk of thromboembolism is only a theoretical consideration, we can only use this available clinical data. Because the sensitivity of BIPSS is significantly increased by the use of CRH or DDAVP, the benefits of using DDAVP appear at this point to outweigh the theoretical risks. One possible positive outcome of the CRH shortage is that more data will be accumulated to determine whether there are unexpected negative effects of using DDAVP.
1. Pecori Giraldi F, Ambrogio AG, Fatti LM, Rubini V, Cozzi G, Scacchi M et al. Von Willebrand factor and fibrinolytic parameters during the desmopressin test in patients with Cushing's disease. Br.J.Pharmacol. 2011;71:132-6.
2. Blevins LS Jr, Clark RV, Owens DS. Thromboembolic complications after inferior petrosal sinus sampling in patients with Cushing's syndrome. Endocr Pract 1998; 4:365-367.
3. Obuobie K, Davies JS, Ogunko A, Scanlon MF. Venous thrombo- embolism following inferior petrosal sinus sampling in Cushing's disease. J Endocrinol Invest 2000; 23:542-544.
4. Deipolyi...Oklu et al. The role of bilateral inferior petrosal sinus sampling in the diagnostic evaluation of Cushing syndrome. Diagn Interv Radiol 2012; 18:132-138
5. Castinetti F, Morange I, Dufour H, et al. Desmopressin test during petrosal sinus sampling: a valuable tool to discriminate pituitary or ectopic ACTH-dependent Cushing's syndrome. Eur J Endocrinol 2007;157:271- 7.
6. Machado MC, de Sa SV, Domenice S, et al. The role of desmopressin in bilateral and simultaneous inferior petrosal sinus sampling for differential diagnosis of ACTH-dependent Cushing's syndrome. Clin Endocrinol (Oxf) 2007;66:136-42.
7. Malerbi DA, Mendonca BB, Liberman B, et al. The desmopressin stimulation test in the differential diagnosis of Cushing's syndrome. Clin Endocrinol (Oxf) 1993;38:463-72.
8. Salgado LR, Mendon??a BB, Pereira MAA, et al. Use of Desmopressin in Bilateral and Simultaneous Inferior Petrosal Sinus Sampling for Differential Diagnosis of ACTH-Dependent Cushing's Syndrome. The Endocrinologist 1997;7:135-40.
Conflict of Interest:
Caution during use of DDAVP in IPSS
Dear Sir, we have read with great interest the paper by Deipolyi and co-workers on the use of desmopressin during inferior petrosal sinus sampling (IPSS) in alternative to corticotropin-releasing hormone (CRH) for the diagnostic work-up of Cushing's disease (1). As the Authors report, evidence collected in small series suggests that desmopressin achieves an equivalent diagnostic accuracy to CRH, thus appears a tempting and less expensive alternative. It is worth recalling, however, that desmopressin is also a potent haemostatic agent and that patients with Cushing's syndrome are at increased risk for thromboembolic events (2), some even occuring during IPSS performed at expert centers (3). In this context, we have recently observed that endothelial factors are released upon administration of desmopressin to patients with Cushing's disease (4), although the dose used for diagnostic purposes is roughly half the haemostatic dosage. The magnitude of the increase in von Willebrand factor, a promoter of platelet adhesion to the subendothelium in the early phases of haemostasis, was comparable to the one observed in healthy subjects and possibly counterbalanced by increased fibrinolytic factors but to what extent these changes might affect general haemostatic processes remains to be ascertained. As a consequence, as long as no further evidence is available on the safety of this haemostatic agent during endovascular damages, procedures which are per se at risk for vascular events, extreme caution should be exercised when using desmopressin instead of CRH during IPSS.
References 1. Deipolyi AR, Hirsch JA, Oklu R. Bilateral inferior petrosal sinus sampling with desmopressin. J.Neurointervent.Surg. 2012;doi10.1136/neurointsurg-2012-010437. 2. Stuijver DJF, van Zaane B, Feelders RA, Debeij J, Cannegieter SC, Hermus AR et al. Incidence of venous thromboembolism in patients with Cushing's syndrome: a multicenter cohort study. J.Clin.Endocrinol.Metab. 2011;96:3525-32. 3. Doppman JL. There is no simple answer to a rare complicaton of inferior petrosal sinus sampling. Am.J.Neuroradiology 1999;20:191-2. 4. Pecori Giraldi F, Ambrogio AG, Fatti LM, Rubini V, Cozzi G, Scacchi M et al. Von Willebrand factor and fibrinolytic parameters during the desmopressin test in patients with Cushing's disease. Br.J.Pharmacol. 2011;71:132-6.
Conflict of Interest:
The reply from Perez et al to my letter of March 2012 is misleading and wrong in two important regards.1 First, they state that their report of the use of the solitaire stent for thrombectomy was just a case report, "nothing else". 2 This is not true. In fact, they explicitly use this report, both in the abstract and conclusion to lay claim for developing the stentreiever concept for thrombectomy: "This was the first .. use of the Solitaire stent for this purpose and the ignition spark for the development of a whole new generation of devices". In addition, this report was titled a "Historical Vignette". This report was written to take credit for the development of stentreivers for acute stroke. To state, as they do in their response to my letter, that their paper makes no claims is clearly disingenuous.
Second, they dismiss the idea that the prior publication by Kelly et al -- reporting the use of an Enterprise stent (Codman Neurovascular, Rayhnam, MA) as a temporary endovascular bypass to achieve successful revascularization in a patient with an acute ischemic stroke and large vessel occlusion -- had any influence on their work. This claim is disingenuous as well. In their response, they state that " ... temporary bypass might have been a local and ephemeral phenomenon; however it did not cause to much commotion, at least in Europe." However, the technique of stent-retrieval, or any kind of temporary stenting for acute stroke is, in fact, part and parcel of "temporary endovascular bypass". The best evidence of this is that the authors presented their own original experience with the Solitaire at the 2010 International Stroke Conference in an abstract entitled "Temporary Endovascular Bypass for the treatment of ischemic stroke: Experience After 50 Patients". Clearly their work with the Solitaire stent in acute stroke was influenced by this prior report.
In summary, despite their claims, the concept of temporary stenting for acute stroke treatment preceded the authors' 2008 case. In their Historical Vignette and subsequent response to my prior letter, the authors are attempting to rewrite history. They do deserve credit for taking this concept and rapidly moving it forward in clinical practice, however. References: 1. Re: Perez et al 'Intracranial thrombectomy using the Solitaire stent: a historical vignette'. Derdeyn CP. J Neurointerv Surg. 2012 Mar;4(2):153-4; Author Response 154 2. Intracranial thrombectomy using the Solitaire stent: a historical vignette. P?rez MA, Miloslavski E, Fischer S, B?zner H, Henkes H. J Neurointerv Surg. 2011 Dec 14. 3. Kelly ME, Furlan AJ, Fiorella D. Recanalization of an acute middle cerebral artery occlusion using a self-expanding, reconstrainable, intracranial microstent as a temporary endovascular bypass. Stroke 2008;39:1770-3. 4. Liebig T, Lockau H, Stehle S, Dorn F, Prothmann S, Henkes HH. Temporary Endovascular Bypass in Acute Stroke: Experience After 50 Patients. Stroke 2010 Vol 41,1:e259-260.
Conflict of Interest:
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