DOCSLIB.ORG

Strategies for Preventing Vasospasm in the Intensive Care Unit

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Strategies for Preventing Vasospasm in the Intensive Care Unit 760 Aneurysmal Subarachnoid Hemorrhage: Strategies for Preventing Vasospasm in the IntensiveCareUnit Michael N. Diringer, MD1 Allyson R. Zazulia, MD1 1 Department of Neurology, Washington University School of Address for correspondence Michael N. Diringer, MD, Department of Medicine, St. Louis, Missouri Neurology, Washington University School of Medicine, Campus Box 8111, 660 S Euclid Avenue, St Louis, MO 63110 Semin Respir Crit Care Med 2017;38:760–767. (e-mail: [email protected]). Abstract This article addresses the intensive care unit (ICU) management of patients with aneurysmal subarachnoid hemorrhage (SAH), with an emphasis on the prevention of cerebral vasospasm and delayed cerebral ischemia (DCI), which are major contributors to morbidity and mortality. Interventions addressing various steps in the development of vasospasm have been attempted, with variable success. Enteral nimodipine remains the only approved measure to potentially prevent DCI. Since oral and intravenous administrations are limited by hypotension, direct administration via sustained-release pellets and intraventricular administration of sustained-release microparticles are Keywords being investigated. Studies of other calcium channel blockers have been disappointing. ► subarachnoid Efforts to remove blood from the subarachnoid space via cisternal irrigation, cisternal hemorrhage or ventricular thrombolysis, and lumbar cerebrospinal fluid drainage have met with ► aneurysm limited and variable success, and they remain an area of active investigation. Several ► vasospasm interventions that had early promise have failed to show benefit when studied in large ► hypertension trials; these include tirilazad, magnesium, statins, clazosentan, transluminal angio- ► treatment plasty, and hypervolemia. Subarachnoid hemorrhage (SAH) refers to bleeding that delayed cerebral ischemia (DCI).5,6 The focus of treatment is occurs primarily within the subarachnoid space. The most anticipating, preventing, and managing these secondary common cause of SAH is trauma, but among cases of spon- complications. taneous SAH, rupture of an intracranial saccular aneurysm In addition to the neurologic consequences of SAH, in- accounts for approximately 85%.1 Other causes of sponta- tense activation of the sympathetic nervous system occurs, neous SAH include bleeding from arteriovenous malforma- which can produce a variety of extracranial consequences tions, moyamoya syndrome, bleeding disorders, cocaine and including hypertension, stunned myocardium,7 neurogenic stimulant abuse, and extension of intracerebral hematomas. pulmonary edema,8 abnormal renal function, and systemic In up to one-fifth of cases, no source of bleeding is identified.2 inflammatory response syndrome (SIRS).9 This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. Acute aneurysmal SAH results from the sudden extrusion of blood from a defect in the wall of an arterial aneurysm. The Risk Factors duration of the bleeding event determines the impact of the primary injury, and ranges from a severe headache to syn- Several risk factors for SAH have been identified, although it cope to sudden death in about a quarter of patients.3 The is not clear whether these factors identify risk of developing amount of blood in the subarachnoid space sets the stage an aneurysm or risk of rupture of an aneurysm that already for secondary injury from hydrocephalus,4 vasospasm, and exists. Modifiable risk factors include hypertension, cigarette Issue Theme Advancements in Copyright © 2017 by Thieme Medical DOI https://doi.org/ Neurocritical Care and Emergency Publishers, Inc., 333 Seventh Avenue, 10.1055/s-0037-1607990. Neurology; Guest Editors: David Y. New York, NY 10001, USA. ISSN 1069-3424. Hwang, MD, FNCS, and David M. Greer, Tel: +1(212) 584-4662. MD, MA, FCCM, FAHA, FNCS, FAAN, FANA Aneurysmal Subarachnoid Hemorrhage Diringer, Zazulia 761 smoking,10 and heavy alcohol consumption.11 Genetic fac- Table 1 Hunt–Hess scale tors also play an important role in SAH.12 The odds ratio of SAH for individuals with one affected first-degree relative is Grade Symptoms 2; this increases to 51 for individuals with two affected first- 1 Asymptomatic or mild headache 13 degree relatives. Aneurysm development is more common 2 Moderatetosevereheadache,nuchalrigidity, in patients with connective tissue disease and polycystic with or without cranial nerve deficits kidney disease, and identifying other genetic markers is an – 3 Confusion, lethargy, or mild focal symptoms active area of investigation.14 17 4 Stupor and/or hemiparesis 5 Deep coma, decerebrate rigidity Pathophysiology Most aneurysms are located near the circle of Willis at the Table 2 World Federation of Neurologic Surgeons base of the brain and near arterial bifurcations (aneurysms secondary to bacterial endocarditis [mycotic Grade Glasgow Coma Scale Motor deficits aneurysms] tend to form more distally). About 85% of aneurysms occur in the carotid circulation, with the most I15 Absent common sites being the origin of the posterior communicat- II 13–14 Absent ing artery from the internal carotid artery (41%), anterior III 13–14 Present communicating artery/anterior cerebral artery complex IV 7–12 Present or absent (34%), and middle cerebral artery (20%).1 Up to 20% of – patients have multiple aneurysms.18 V36 Present or absent Presentation located in the posterior fossa, or if the hematocrit is extre- The typical presentation of acute SAH is the sudden onset of a mely low. Traditional teaching has been that if the CT is severe headache, nausea, vomiting, and syncope. Presenting normal and suspicion of SAH remains strong, a lumbar with focal neurologic deficits is very unusual, but may be puncture (LP) should be performed. More recent studies seen due to mass effect from a giant aneurysm, parenchymal suggest that the yield of LP in this setting is quite low.23 hemorrhage, subdural hematoma, or a large localized sub- Conventional catheter angiography is the gold standard arachnoid clot. In addition, third cranial nerve palsies (di- for the detection of intracranial aneurysms. CT angiography lated pupil, ptosis, and limited eye movements) may be has recently improved to the point where some centers present due to aneurysmal compression of the nerve, parti- perform it routinely.24,25 Magnetic resonance angiography cularly with posterior communicating artery aneurysms. techniques are rapidly advancing, but there can be some Seizures at onset may be reported by family, but it is not limitations of its use in the acute care setting. clear how many of these episodes represent true epileptic In 15 to 20% of cases, angiography fails to demonstrate the events versus abnormal posturing.19 cause of SAH.26 If a high-quality complete angiography does not identify a source of bleeding, patients have a very low Initial Management incidence of rebleeding, especially if the blood is limited to the perimesencephalic and ambient cisterns.27 The initial steps in managing a patient who is suspected of If the patient is lethargic or agitated, consideration should having a SAH focus on airway evaluation, early computed be given to elective intubation to facilitate performing safe tomographic (CT) imaging, blood pressure control, serial as- and rapid angiography. sessment of neurological function, and stabilization to un- This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. dergo additional diagnostic studies (CT angiography, catheter Medical Complications angiography). Clinical status is usually described using the method proposed by Hunt and Hess20 and World Federation of Blood pressure is typically elevated following SAH due to Neurological Surgeons (WFNS) Scales21 (►Table 1 and 2). pain and anxiety and sympathetic activation. Left untreated, hypertension is thought to increase the risk of aneurysmal 28 Diagnosis rerupture; however, few data exist to support this notion. Still, most recommend normalization of blood pressure.29 A noncontrast CTscan remains the diagnostic test of choice to Analgesics alone may be effective; otherwise, rapidly acting detect SAH. Current CT scanners have a sensitivity of 98.7% antihypertensive agents are employed. Preferred agents in- when performed within 6 hours of onset in patients pre- clude labetalol, hydralazine, and nicardipine.30,31 An impor- senting with thunderclap headache and a normal neurolo- tant exception to treatment of hypertension is when gical examination.22 Blood appears as a hyperdense signal in hydrocephalus is present. In that situation, blood pressure the cisterns surrounding the brainstem. CT may be falsely should be addressed only after the hydrocephalus is treated. negative if the volume of blood is very small, if the hemor- Cardiovascular abnormalities are common in SAH. Elec- rhage occurred several days prior, if the blood is primarily trocardiographic changes include sinus arrhythmia, tall Seminars in Respiratory and Critical Care Medicine Vol. 38 No. 6/2017 762 Aneurysmal Subarachnoid Hemorrhage Diringer, Zazulia peaked “cerebral” T-waves, ST segment depression, and without vasospasm will be referred to as delayed neurologic prolonged QT segments.32 Cardiac enzymes are often mildly ischemia (DCI). elevated. Arrhythmias occur frequently, but are most com- The relationship between SAH and arterial narrowing monly benign unless associated with electrolyte abnormal- seen on cerebral angiography was first described by Ecker ities; however, some patients may
Load more

Recommended publications
  • The Evolution of Invasive Cerebral Vasospasm Treatment in Patients
    Neurosurgical Review (2019) 42:463–469 https://doi.org/10.1007/s10143-018-0986-5 ORIGINAL ARTICLE The evolution of invasive cerebral vasospasm treatment in patients with spontaneous subarachnoid hemorrhage and delayed cerebral ischemia—continuous selective intracarotid nimodipine therapy in awake patients without sedation Andrej Paľa1 & Max Schneider1 & Christine Brand 1 & Maria Teresa Pedro1 & Yigit Özpeynirci2 & Bernd Schmitz2 & Christian Rainer Wirtz1 & Thomas Kapapa1 & Ralph König1 & Michael Braun2 Received: 16 February 2018 /Revised: 1 May 2018 /Accepted: 17 May 2018 /Published online: 26 May 2018 # Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Cerebral vasospasm (CV) and delayed cerebral ischemia (DCI) are major factors that limit good outcome in patients with spontaneous subarachnoid hemorrhage (SAH). Continuous therapy with intra-arterial calcium channel blockers has been intro- duced as a new step in the invasive treatment cascade of CV and DCI. Sedation is routinely necessary for this procedure. We report about the feasibility to apply this therapy in awake compliant patients without intubation and sedation. Out of 67 patients with invasive endovascular treatment of cerebral vasospasm due to spontaneous SAH, 5 patients underwent continuous superselective intracarotid nimodipine therapy without intubation and sedation. Complications, neurological improvement, and outcome at discharge were summarized. Very good outcome was achieved in all 5 patients. The Barthel scale was 100 and the modified Rankin scale 0–1 in all cases at discharge. We found no severe complications and excellent neurological monitoring was possible in all cases due to patients’ alert status. Symptoms of DCI resolved within 24 h in all 5 cases. We could demonstrate the feasibility and safety of selective intracarotid arterial nimodipine treatment in awake, compliant patients with spontaneous SAH and symptomatic CVand DCI.
    [Show full text]
  • PERIPHERAL ARTERIAL DISEASES Postgrad Med J: First Published As 10.1136/Pgmj.22.243.22 on 1 January 1946
    PERIPHERAL ARTERIAL DISEASES Postgrad Med J: first published as 10.1136/pgmj.22.243.22 on 1 January 1946. Downloaded from By SAUL S. SAMUELS, A.M., M.D. New York, N.Y. Arterial Diseases arteries that might be mentioned, but clinical Peripheral evidence of which is difficult to determine. They This new specialty has evolved within the past are encountered so infrequently that it hardly twenty years into a separate and distinct branch of seems important to devote much time to them. medicine and surgery. In its infancy it was rele- Among these may be mentioned syphilitic arteritis, gated to the internist who had some special interest tuberculosis of the peripheral arteries and certain in this work, just as in the early days of urology an non-specific forms of peripheral arteritis, which acquaintance with venereal diseases was sufficient have as yet been incompletely studied. for the designation of specialist in this field. In the field of functional disturbances of the peripheral arterial system, we consider two main General sub-groups. The first, and more important of Considerations these is Raynaud's Disease. This is a disturbance The peripheral arterial diseases may be separated of the control mechanism of the peripheral arteri- into two definite groups. The first and more oles which causes frequent attacks of vasospasm important is that of the changes in the arterial in the extremities and in the various acral parts of walls. These two groups may be again sub- the body, such as the tip of the nose, tongue and divided so that in the organic field we recognise ears.
    [Show full text]
  • Calcium Channel Blockers Yaser Alahamd, Hisham Ab Ib Swehli, Alaa Rahhal, Sundus Sardar, Mawahib Ali Mohammed Elhassan, Salma Alsamel and Osama Ali Ibrahim
    Chapter Calcium Channel Blockers Yaser Alahamd, Hisham Ab Ib Swehli, Alaa Rahhal, Sundus Sardar, Mawahib Ali Mohammed Elhassan, Salma Alsamel and Osama Ali Ibrahim Abstract Vasospasm refers to a condition in which an arterial spasm leads to vasoconstric- tion. This can lead to tissue ischemia and necrosis. Coronary vasospasm can lead to significant cardiac ischemia associated with symptomatic ischemia or cardiac arrhythmia. Cerebral vasospasm is an essential source of morbidity and mortality in subarachnoid hemorrhage patients. It can happen within 3–15 days with a peak incidence at 7 days after aneurysmal subarachnoid hemorrhage (SAH). Calcium channel blockers are widely used in the treatment of hypertension, angina pectoris, cardiac arrhythmias, and other disorders like SAH vasospasm related and Migraine. The specific treatment of cerebral vasospasm helps improving cerebral blood flow to avoid delayed ischemic neurologic deficit by reducing ICP, optimizing the rate of cerebral oxygen demand, and enhancing cerebral blood flow with one of the following approaches: indirect pharmacological protection of brain tissue or direct mechanical dilation of the vasospastic vessel. Nimodipine is the standard of care in aneurysmal SAH patients. Nimodipine 60 mg every 4 hours can be used for all patients with aneurysmal SAH once the diagnosis is made for 21 days. Keywords: coronary vasospasm, cerebral vasospasm, calcium channel blockers, cerebral blood flow, nimodipine 1. Introduction Vasospasm is a condition which is associated with an arterial spasm and vasocon- striction, which may lead to tissue ischemia and necrosis. Coronary vasospasm can lead to significant cardiac ischemia associated with symptomatic ischemia or cardiac arrhythmia. Cerebral vasospasm may arise as a complication of subarachnoid hem- orrhage (SAH).
    [Show full text]
  • Traumatic Brain Injury and Intracranial Hemorrhage–Induced Cerebral Vasospasm:A Systematic Review
    NEUROSURGICAL FOCUS Neurosurg Focus 43 (5):E14, 2017 Traumatic brain injury and intracranial hemorrhage–induced cerebral vasospasm: a systematic review Fawaz Al-Mufti, MD,1,2 Krishna Amuluru, MD,2 Abhinav Changa, BA,2 Megan Lander, BA,2 Neil Patel, BA,2 Ethan Wajswol, BS,2 Sarmad Al-Marsoummi, MBChB,5 Basim Alzubaidi, MD,1 I. Paul Singh, MD, MPH,2,4 Rolla Nuoman, MD,3 and Chirag Gandhi, MD2–4 1Department of Neurology, Rutgers Robert Wood Johnson Medical School, New Brunswick; Departments of 2Neurosurgery, 3Neurology, and 4Radiology, Rutgers University, New Jersey Medical School, Newark, New Jersey; and 5University of North Dakota, Grand Forks, North Dakota OBJECTIVE Little is known regarding the natural history of posttraumatic vasospasm. The authors review the patho- physiology of posttraumatic vasospasm (PTV), its associated risk factors, the efficacy of the technologies used to detect PTV, and the management/treatment options available today. METHODS The authors performed a systematic review in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines using the following databases: PubMed, Google Scholar, and CENTRAL (the Cochrane Central Register of Controlled Trials). Outcome variables extracted from each study included epidemiology, pathophysiology, time course, predictors of PTV and delayed cerebral ischemia (DCI), optimal means of surveillance and evaluation of PTV, application of multimodality monitoring, modern management and treatment op- tions, and patient outcomes after PTV. Study types were limited to retrospective chart reviews, database reviews, and prospective studies. RESULTS A total of 40 articles were included in the systematic review. In many cases of mild or moderate traumatic brain injury (TBI), imaging or ultrasonographic studies are not performed.
    [Show full text]
  • Variant Angina
    maco har log P y: r O la u p c e n s a A Fumimaro Takatsu, Cardiol Pharmacol 2015, 4:3 v c o c i e d r s Open Access a s Cardiovascular Pharmacology: DOI: 10.4172/2329-6607.1000143 C ISSN: 2329-6607 Letter to Editor OpenOpen Access Access Variant Angina: Why do you Ignore Spasm of Coronary Arteries? Fumimaro Takatsu MD* Department of Cardiology, Takatsu Naika Junkankika, 2-4-7 Mikawaanjo-Hommachi, Anjo, Aichi, Japan Introduction perform provocation of spasm; if possible (once the patient returned to a ward, I explain on the vasospasm and get written informed consent), Many authors reported on variant (form of) angina (Prinzmetal’s before the patient and families leave the hospital because almost all Variant Angina, vasospastic angina) till 1990s on the various aspects of of patients and families cannot realize electrocardiographic findings this disease. However, in this century, articles on this very important and would not have medications. Moreover, although not so frequent, disease have become very few. One reason of this apparent ignorance some patients with chest discomfort only on effort have no significant of vasospastic angina may be caused by a report by Cianflone et al. in coronary narrowing have vasospasm. 2000 [1], in which they studied only 34 patients and concluded that vasospasm is much less in Caucasian peoples. A scientific research, Complications especially in clinical medicine, at least more than several hundred Coronary vasospasm, of course, if prolonged, can cause acute patients must be studied for some conclusion. Thus, I feel, their result myocardial infarction by itself or by causing intraluminal thrombus or is very questionable and responsibility of American Heart Association rupture of minor atherosclerotic plaque.
    [Show full text]
  • Calcium Channel Blockers Cannot Prevent Pure Vasospastic Myocardial Infarction
    Postgrad Med J: first published as 10.1136/pgmj.63.735.41 on 1 January 1987. Downloaded from Postgraduate Medical Journal (1987) 63, 41-44 Calcium channel blockers cannot prevent pure vasospastic myocardial infarction P. Depelchin and S. Degre Department ofMedical Cardiology, H6pital Academique Erasme, Universite Libre de Bruxelles, 808 route de Lennik, 1070 Bruxelles, Belgium. Summary: Coronary artery spasm is a recognized cause of myocardial infarction. This report describes a case of myocardial infarction attributed to pure coronary spasm which was halted by a double perfusion with streptokinase and nitroglycerin. Further coronary artery spasm leading to a myocardial infarction could not be avoided several weeks later, although the patient was left on calcium channel blocker therapy. The two attacks were not preceded by warning angina pectoris, contrary to accepted belief. The best objective ofend-point drug therapy and its assessment in vasospastic angina are discussed. Introduction Coronary artery spasm alone or superimposed on an atheromatous lesion is now recognized as a cause of myocardial infarction.' Our therapeutic approach has therefore been directed not only towards treating by copyright. factors which increase myocardial oxygen demand but also to modulating smooth-muscle contraction res- ponsible for the coronary artery spasm. Calcium channel blockers and nitroglycerin compounds are potent smooth-muscle relaxing drugs and are effective in suppressing spasm-induced angina. However, nitroglycerin, even intracoronary administered after induced coronary spasms, has sometimes been unable to reverse the spasm.2 We present a patient free from http://pmj.bmj.com/ arteriosclerotic coronary artery disease who de- veloped pure vasospastic myocardial infarction in spite of calcium channel blocking therapy.
    [Show full text]
  • Coronary Vasospasm Associated with Hyperthyroidism
    Case Report Coronary Spasm Associated with Hyperthyroidism Acta Cardiol Sin 2010;26:48-51 Coronary Vasospasm Associated with Hyperthyroidism Jiunn-Wen Lin,1 Wei-Cheng Lian2 and Tin-Kwang Lin1 Acute myocardial ischemia is a rare and possibly life-threatening manifestation of hyperthyroidism. We describe a 48-year-old woman with severe coronary vasospasm associated with hyperthyroidism. The patient presented with chest pain and increasing shortness of breath for several days. Acute non-ST elevation myocardial infarction was diagnosed. Coronary angiography revealed diffuse vasoconstriction which was relieved by intracoronary nitroglycerin. Subsequently, she was diagnosed with hyperthyroidism and treated with antithyroid therapy and an oral calcium channel blocker. After restoration of euthyroidism, she remained free of chest pain. Our report reminds readers that severe coronary spasm might be sometimes associated with simultaneous hyperthyroidism, especially in patients without risk factors of atherosclerosis. Key Words: Acute myocardial infarction · Coronary vasospasm · Hyperthyroidism INTRODUCTION department with a two-day history of chest pain and in- creasing shortness of breath. The episodes of pain varied The cardiovascular system is very sensitive to thyroid in length and were aggravated by exercise. On direct hormone, and a wide spectrum of cardiac changes has questioning, she did not have palpitation, body weight been recognized in hyperthyroidism.1 Acute myocardial loss, heat intolerance, or resting tremor. She denied any ischemia is a rare and possibly life-threatening manifesta- history of cardiovascular disease and was premeno- tion of hyperthyroidism. However, in the absence of fixed pausal. She denied smoking, drinking alcohol or illicit coronary artery disease, hyperthyroidism is rarely associ- drug use.
    [Show full text]
  • Peripheral Artery Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic)
    ACCF/AHA Pocket Guideline November 2011 Management of Patients With Peripheral Artery Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic) Adapted from the 2005 ACCF/AHA Guideline and the 2011 ACCF/AHA Focused Update Developed in Collaboration With the Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society for Vascular Medicine, and Society for Vascular Surgery © 2011 by the American College of Cardiology Foundation and the American Heart Association, Inc. The following material was adapted from the 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease J Am Coll Cardiol 2011; 58:2020-2045 and the 2005 ACC/AHA guidelines for the management of the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic) J Am Coll Cardiol 2006;47:1239-312. This pocket guideline is available on the World Wide Web sites of the American College of Cardiology (cardiosource.org) and the American Heart Association (my.americanheart.org). For copies of this document, please contact Elsevier Inc. Reprint Department, e-mail: [email protected]; phone: 212-633-3813; fax: 212-633-3820. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American College of Cardiology Foundation. Please contact Elsevier’s permission department at [email protected]. B Contents 1. Introduction
    [Show full text]
  • Prinzmetal Variant Angina Associated with Multiple Sclerosis
    J Am Board Fam Pract: first published as 10.3122/jabfm.17.1.71 on 10 March 2004. Downloaded from Prinzmetal Variant Angina Associated with Multiple Sclerosis Scott Joing, MD, Robyn Casey, MD, and Les Forgosh, MD We report the case of a young woman with an acute coronary syndrome in the setting of a multiple scle- rosis exacerbation. A connection between the 2, possibly caused by spinal cord pathology, is suggested. (J Am Board Fam Pract 2004;17:71–3.) Prinzmetal variant angina is characterized by an- ages, suggesting a more acute process of demyeli- gina secondary to coronary artery vasospasm,1 typ- nation. The patient denied any previous episodes of ically at rest, associated with transient ST-segment chest pain as well as any cardiac history, hyperten- deviations.2 Further diagnostic workup using an- sion, hypercholesterolemia, or respiratory prob- giography may reveal coronary arteries with or lems. Past medical history included MS, depres- without atherosclerotic narrowings.1 Multiple scle- sion, possible seizure disorder, tonsillectomy, and rosis (MS) is typically a relapsing-remitting neuro- appendectomy. She was adopted, and her family logic disorder involving demyelinated plaques, history is unknown. Her usual medications include 3 which slow or block conduction along nerves. Lit- 150 mg of ranitidine twice daily, 50 mg of sertraline erature search reveals one case report indicating a twice daily, 100 mg of amantadine twice daily, 100 4 causal relationship between these 2 diseases. We mg of carbamazepine twice daily, norethindrone present an additional case involving a 38-year-old and ethinyl estradiol, propoxyphene napsylate as patient who experienced Prinzmetal variant angina needed, and interferon ␤1a once per week.
    [Show full text]
  • Safety and Efficacy of Sildenafil Citrate in Reversal of Cerebral Vasospasm: a Feasibility Study Kanchan K
    OPEN ACCESS Editor-in-Chief: Surgical Neurology International James I. Ausman, MD, PhD For entire Editorial Board visit : University of California, Los http://www.surgicalneurologyint.com Angeles, CA, USA Original Article Safety and efficacy of sildenafil citrate in reversal of cerebral vasospasm: A feasibility study Kanchan K. Mukherjee, Shrawan K. Singh1, Virender K. Khosla, Sandeep Mohindra, Pravin Salunke Departments of Neurosurgery and 1Urology, PGIMER, Chandigarh, India E-mail: Kanchan K. Mukherjee- [email protected]; Shrawan K. Singh- [email protected]; Virender K Khosla- [email protected]; Sandeep Mohindra- [email protected]; *Pravin Salunke - [email protected] *Corresponding author Received: 1 November 11 Accepted: 13 December 11 Published: 21 January 12 This article may be cited as: Mukherjee KK, Singh SK, Khosla VK, Mohindra S, Salunke P. Safety and efficacy of sildenafil citrate in reversal of cerebral vasospasm: A feasibility study. Surg Neurol Int 2012;3:3. Available FREE in open access from: http://www.surgicalneurologyint.com/text.asp?2012/3/1/3/92164 Copyright: © 2012 Mukherjee KK. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Objective: Cerebral vasospasm is the commonest cause for mortality and morbidity in patients following clipping of a ruptured aneurysm. Selective phosphodiesterase (PDE) inhibitor like sildenafil acts as a vasodilator. The objective of this study was to evaluate the safety and feasibility of oral sildenafil citrate in patients with symptomatic refractory vasospasm. Methods: A total of 832 patients with aneurysmal subarachnoid bleed were operated in 4 years.
    [Show full text]
  • Medical Management of Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage: a Review of Current and Emerging Therapeutic Interventions
    Hindawi Publishing Corporation Neurology Research International Volume 2013, Article ID 462491, 10 pages http://dx.doi.org/10.1155/2013/462491 Review Article Medical Management of Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage: A Review of Current and Emerging Therapeutic Interventions Peter Adamczyk, Shuhan He, Arun Paul Amar, and William J. Mack Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA Correspondence should be addressed to Peter Adamczyk; [email protected] Received 26 November 2012; Accepted 23 March 2013 Academic Editor: Jay Mocco Copyright © 2013 Peter Adamczyk et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cerebral vasospasm is a major source of morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (aSAH). Evidence suggests a multifactorial etiology and this concept remains supported by the assortment of therapeutic modalities under investigation. The authors provide an updated review of the literature for previous and recent clinical trials evaluating medical treatments in patients with cerebral vasospasm secondary to aSAH. Currently, the strongest evidence supports use of prophylactic oral nimodipine and initiation of triple-H therapy for patients in cerebral vasospasm. Other agents presented in this report include magnesium, statins, endothelin receptor antagonists, nitric oxide promoters, free radical scavengers, thromboxane inhibitors, thrombolysis, anti-inflammatory agents and neuroprotectants. Although promising data is beginning to emerge for several treatments, few prospective randomized clinical trials are presently available. Additionally, future investigational efforts will need to resolve discrepant definitions and outcome measures for cerebral vasospasm in order to permit adequate study comparisons.
    [Show full text]
  • High Susceptibility of Atherosclerotic Coronary Arteries to the Onset Of
    maco har log P y: r O la u p c e n s a A Koike et al., Cardiol Pharmacol 2015, 4:1 v c o c i e d r s a s Open Access DOI: 10.4172/2329-6607.1000131 C Cardiovascular Pharmacology: ISSN: 2329-6607 Research Article OpenOpen Access Access High Susceptibility of Atherosclerotic Coronary Arteries to the Onset of Vasospasm and Angina Pectoris-like Symptoms due to Coronary Spasm in WHHLMI Rabbits Tomonari Koike1*, Tatsuro Ishida2, Shiori Tamura3, Nobue Kuniyoshi1, Ying Yu1, Satoshi Yamada1, Ken-ichi Hirata2 and Masashi Shiomi1,3 1Institute for Experimental Animals, Kobe University Graduate School of Medicine, Kobe, Japan 2Division of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan 3Division of Comparative Pathophysiology, Kobe University Graduate School of Medicine, Kobe, Japan Abstract Objectives: We examined the relationship between atherosclerosis and provocation of coronary spasm as well as influence of coronary spasm on the onset of acute ischemic myocardial disease. Methods and Results: Coronary spasm was provoked in anesthetized normal Japanese white (JW) rabbits and WHHLMI rabbits, an animal model for coronary atherosclerosis and myocardial infarction, by injecting ergonovine during the infusion of norepinephrine through a marginal ear vein. A decrease in contrast flow in the left circumflex artery was observed on coronary angiograms. Ischemic changes were observed on the electrocardiogram of 29% (2/7) of JW and 79% (27/34) of WHHLMI rabbits. The frequency of coronary spasm was significantly high in rabbits with severe coronary plaques showing diffuse lesions. In addition, the degree of contraction of coronary strips with atherosclerotic plaques was higher than that of normal coronary strips excised from JW rabbits stimulated by a combination of ergonovine and norepinephrine.
    [Show full text]