Decision Making in Neurovascular Disease

Decision Making in Neurovascular Disease

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Neurovascular medicine has emerged as an established, semi-independent subspecialty of neurology and neurosurgery. Decision Making in Neurovascular Disease focuses on the challenging process of determining the best approach for managing patients with intracranial atherosclerosis, carotid artery disease, stroke, aneurysms, arteriovenous malformations, arteriovenous fistulae, cavernous malformations, and hypervascular tumors. Leonardo Rangel-Castilla, Robert Spetzler, esteemed coauthors, and an impressive cadre of experts discuss highly divergent modalities including medical management, open cerebrovascular, endovascular, radiosurgery, and combined/multimodality alternatives.

The book is organized into seven sections: Ischemic Stroke and Vascular Insufficiency, Aneurysms – Anterior Circulation, Aneurysms – Posterior Circulation, Aneurysms – Other, Arteriovenous Malformations and Fistula, Cavernous Malformations, and Hypervascular Tumors. Chapters include an introduction, decision-making algorithm, whether to treat, conservative management, anatomical considerations, clinical and imaging evaluation, differential diagnosis, treatment options, images, clinical and radiographic follow-up, and suggested reading.

Key highlights

Simple algorithms accompanying 71 chapters supported by the latest, most updated information in the literature
More than 375 radiologic images help elucidate disease-specific treatment decision making
Step-by-step guidance, clinical pearls, surgical nuances, complication avoidance, and evidence-based outcomes provide in-depth understanding
Point/counterpoint expert commentary on each case provides balanced insights on potential implications of specific treatments
This essential step-by-step book is a must-have for residents and fellows in neurosurgery, neurology, endovascular, interventional radiology, vascular neurology, and neurocritical care, as well as veteran clinicians in these specialties

Update: Nicardipine

Nicardipine

Nicardipine was approved by the FDA in December 1988. The patent for both Cardene and Cardene SR expired in October 1995.

Nicardipine hydrochloride (Cardene) belongs to the class of calcium channel blockers.

It is available in oral and intravenous formulations.

see Intraventricular nicardipine.

Ampules contain 25 mg and must be diluted before.

Does not require arterial line. Does not produce intracranial hypertension. Does not reduce heart rate 1).

May be used in conjunction with e.g. labetalol or esmolol if that is desired.

Its mechanism of action and clinical effects closely resemble those of nifedipine and the other dihydropyridines (amlodipine, felodipine), except that nicardipine is more selective for cerebral and coronary blood vessels.

Furthermore, nicardipine does not intrinsically decrease myocardial contractility and may be useful in the management of congestive heart failure. Nicardipine also has a longer half-life than nifedipine. It has been used in percutaneous coronary intervention.

Indications

Intravenous nicardipine is commonly used for blood pressure reduction in patients with acute stroke.

see Nicardipine for aneurysmal subarachnoid hemorrhage.

Endovascular approaches with balloon angioplasty and intra-arterial nimodipine, nicardipine, and milrinone have shown consistent benefits 2).

Side effects

Headache

Nausea

Hypotension

Reflex tachycardia.

Phlebitis is significantly associated with administration of a maximum concentration of nicardipine greater than 130 µg/mL 3).

Intravenous nicardipine-related phlebitis was retrospectively analyzed. From July 2015, a simple proposition was made to dilute maximum intravenous nicardipine concentration to lower than 130 µg/mL. The maximum intravenous nicardipine concentration and the incidence of phlebitis were compared between patients treated from July 2014 to June 2015 (preproposition group) and patients treated from July 2015 to June 2016 (postproposition group).

A total of 300 patients (preproposition group, 138; postproposition group, 162) were included. The postproposition group demonstrated significantly lower maximum intravenous nicardipine concentration (in µg/mL, 76.9, 47.6-104.5 versus 130.4, 69.8-230.8; P < .001) and incidence of phlebitis (9.9%, 16/162 vs. 30%, 42/138; P < .001) than the preproposition group. Multivariable logistic regression analysis revealed that the maximum intravenous nicardipine concentration lower than 130 µg/mL (odds ratio [OR] .15; 95% confidence interval [CI] .06-.35; P < .001) and National Institutes of Health Stroke Scale on admission (OR .95; 95% CI .91-.99; P = .007) were the statistically significant independent factors for phlebitis, which indicated the usefulness of the proposition to dilute maximum intravenous nicardipine concentration to lower than 130 µg/mL.

The simple and appropriate proposition about nicardipine administration lowered maximum nicardipine concentration and reduced the incidence of nicardipine-related phlebitis in patients with acute stroke 4).

Dosing

IV: 5 mg/hr by slow infusion (50 mL/hr) initially; may be increased by 2.5 mg/hr every 15 minutes; not to exceed 15 mg/hr.

Off label 10 mg/hr may be used in situations where urgent reduction of arterial hypertension is needed.

Decrease to 3 mg/hr once control is achieved.

Effects on cerebrovascular hemodynamics

Few studies have described its effects on cerebrovascular hemodynamics as measured by transcranial Doppler (TCD) waveform analysis and pulsatility index (PI).

Lahiri et al., report examples of a consistent but paradoxical finding associated with nicardipine that suggests intracranial vasoconstriction, contrary to what is expected from a vasodilator.

The data presented are from a convenience sample of patients who underwent TCD monitoring before, after, or during nicardipine administration. In each case, TCD waveform morphologies and PIs were compared.

The TCD waveforms during nicardipine infusion are characterized by a prominent systolic peak and dicrotic notch. Systolic deceleration was more pronounced and PIs were significantly elevated in patients who were on nicardipine (p < 0.001). This finding was not evident when patients were not on nicardipine.

This study provides the first evidence of paradoxical intracranial vasoconstriction associated with intravenous nicardipine. In the authors’ experience, this finding is consistently encountered in the vast majority of patients who are treated with intravenous nicardipine, and is contradictory to what is expected from a vasodilator. Future studies are needed to confirm this finding in larger populations and diverse clinical settings and to examine mechanisms that explain this phenomenon 5).

1)

Badjatia N, Topcuoglu MA, Pryor JC, Rabinov JD, Ogilvy CS, Carter BS, Rordorf GA. Preliminary experience with intra-arterial nicardipine as a treatment for cerebral vasospasm. AJNR Am J Neuroradiol. 2004 May;25(5):819-26. PubMed PMID: 15140728.
2)

Rao GS, Muthuchellappan R. Cerebral vasospasm: current understanding. Curr Opin Anaesthesiol. 2016 Oct;29(5):544-51. doi: 10.1097/ACO.0000000000000370. Review. PubMed PMID: 27341013.
3)

Kawada K, Ohta T, Tanaka K, Kadoguchi N, Yamamoto S, Morimoto M. Risk Factors of Nicardipine-Related Phlebitis in Acute Stroke Patients. J Stroke Cerebrovasc Dis. 2016 Oct;25(10):2513-8. doi: 10.1016/j.jstrokecerebrovasdis.2016.06.028. Epub 2016 Jul 14. PubMed PMID: 27423368.
4)

Kawada K, Ohta T, Tanaka K, Miyamoto N. Reduction of Nicardipine-Related Phlebitis in Patients with Acute Stroke by Diluting Its Concentration. J Stroke Cerebrovasc Dis. 2018 Mar 5. pii: S1052-3057(18)30064-8. doi: 10.1016/j.jstrokecerebrovasdis.2018.02.013. [Epub ahead of print] PubMed PMID: 29519742.
5)

Lahiri S, Nezhad M, Schlick KH, Rinsky B, Rosengart A, Mayer SA, Lyden PD. Paradoxical cerebrovascular hemodynamic changes with nicardipine. J Neurosurg. 2018 Apr;128(4):1015-1019. doi: 10.3171/2016.11.JNS161992. Epub 2017 Apr 21. PubMed PMID: 28430036.

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

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This book introduces the latest advances relating to the pathophysiology, biophysics, monitoring and treatment of traumatic brain injury, hydrocephalus, and stroke presented at the 16th International Conference on Intracranial Pressure and Neuromonitoring (the “ICP Conference”), held in Cambridge, Massachusetts, in June 2016 in conjunction with the 6th Annual Meeting of the Cerebral Autoregulation Research Network. Additionally, the conference held special sessions on neurocritical care informatics and cerebrovascular autoregulation. The peer-reviewed papers included were written by leading experts in neurosurgery, neurointensive care, anesthesiology, physiology, clinical engineering, clinical informatics and mathematics who have made important contributions in this translational area of research, and their focus ranges from the latest research findings and developments to clinical trials and experimental studies. The book continues the proud tradition of publishing key work from the ICP Conferences and is a must-read for anyone wishing to stay abreast of recent advances in the field.

Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

Neurocritical Care, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

by Alejandro A. Rabinstein MD FAAN

List Price: $138.99
This issue of Neurosurgery Clinics, edited by Alejandro A. Rabinstein, will focus on Neurocritical Care. Topics will include Anoxic-Ischemic Brain Injury, Practical Approach to Posttraumatic Intracranial Hypertension According to Pathophysiologic Reasoning, Management of Traumatic Brain Injury: An Update, Cortical Spreading Depression and Ischemia in Neurocritical Patients, Targeted Temperature Management in Brain-Injured Patients, Herpes Virus Encephalitis in Adults: Current Knowledge and Old Myths, Primary Acute Neuromuscular Respiratory Failure, Intensive Care Unit–Acquired Weakness, Recent Advances in the Acute Management of Intracerebral Hemorrhage, New Developments in Refractory Status Epilepticus, Acute Cardiac Complications in Critical Brain Disease, Nosocomial Infections in the Neurointensive Care Unit, Neurologic Complications of Solid Organ Transplantation, and Shared Decision Making in Neurocritical Care.

Seven Bypasses: Tenets and Techniques for Revascularization

Seven Bypasses: Tenets and Techniques for Revascularization

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Seven Bypasses: Tenets and Techniques for Revascularization is the third book in a trilogy of bravura, technical nuance, and strategy by master neurosurgeon Michael Lawton. Like his first two books on aneurysms and AVMs, Seven Bypasses provides unparalleled firsthand insights and guidance on complex pathologies in vascular neurosurgery. The fundamentals of microsurgical anastomosis and the craft of bypass surgery are explored in depth with clinical pearls in every chapter.

Lawton eloquently reveals the art of cerebral revascularization in exquisite, metaphorical detail. The surgeon performing bypass surgery is like an architect envisioning and building a beautiful structure. A bypass is designed to fit the patient’s unique anatomy; blueprints designate anastomotic sites, connections, and conduits; the anastomoses are constructed; and the bypass is brought to life with pulsations, flow, and reperfusion. The book highlights Lawton’s aesthetic, which has evolved from the common STA-MCA bypasses to IC-IC bypasses and elaborate arterial reconstructions.

Key Highlights

  • Stepwise discussion of the three anastomoses that form the building blocks of all bypasses: end-to-side, side-to-side, and end-to-end anastomoses
  • Ten tenets delineate nuances of bypass: dexterity, preparing donors and recipients, establishing a working zone, temporary arterial occlusion, arteriotomy, suturing technique, tissue handling, knot tying, patency, and aneurysm occlusion
  • Step-by-step guidance on the seven bypasses: EC-IC bypass, EC-IC interpositional bypass, arterial reimplantation, in-situ bypass, reanastomosis, IC-IC interpositional bypass, and combination bypass
  • Strategies and algorithms for aneurysms organized by specific anatomical sites, including the MCA and the Sylvian cistern, ACA and the interhemispheric cistern, basilar artery and the basal cisterns, and PICA and the cisterna magna
  • More than 1,500 radiographs, operative photographs, and exquisite illustrations drawn by artist Kenneth Xavier Probst elucidate anatomy, surgical principles, and clinical cases

Dr. Lawton has bequeathed a remarkable treasure of knowledge to current and future generations of neurosurgeons and their patients. The Seven series is destined to be an enduring classic for residents, fellows, and neurosurgeons specializing in the treatment of cerebrovascular disease, and for those who believe that manual dexterity and technical skill still matter.