Despite advances in the diagnosis and treatment of neurosurgical diseases, spinal epidural abscesses (SEA) remain challenging. The diagnosis is complex, treatments are controversial, and the potential for adverse outcomes is significant. SEA accounts for 2 of every 10,000 of hospital admissions, an incidence which has doubled in the past twenty years. Reasons which may account for this include an aging population, increased IV drug use, and increase in number of vascular and spinal procedures. SEA can arise from an underlying medical condition, such as diabetes mellitus, alcoholism, chronic obstructive pulmonary disease (COPD), or HIV infection. Loci for SEA can be formed by other spinal abnormalities or by prior invasive spinal procedures, including epidurals, nerve blocks, or steroid injections. Sources for systemic infection may include vascular access catheters, IV drug use, or chronic UTI. 50% of spinal epidural infections have hematogenous origin, 30% arise from the skin or connective tissue, and 20% are unclassified. Common pathogens include S. aureus and P. aeruginosa. From 15% to 40% of SEA may be due to MRSA. In cases of spine trauma or spinal surgery, S. epidermidis may also be a pathogen. 79% of SEA appear dorsal to the spinal cord. A possible explanation for this finding is that the largest extent of the epidural space lies posterior to the nerve roots. The 21% that appear anterior are often associated with vertebral discitis and/ or osteomyelitis. Achieving correct diagnosis in cases of SEA may be challenging. 50% of epidural spinal abscesses are initially misdiagnosed. The most common presenting symptom is back pain, present in up to 85% of patients. Fever is present in up to 50%. Less common symptoms are paresthesias, sensory deficits, radicular pain, or motor deficits. SEA can occur spontaneously in patients with increased co-morbidi-ties. In post-operative patients, SEA may take days to weeks to appear. A dorsal SEA results from the spontaneous seeding of the dorsal epidural fat. As the abscess enlarges, neural compression may occur. Conversely, a ventral SEA may result from either spontaneous seed-ing of the ventral epidural fat or seeding of the disc space with secondary extension into the ventral epidural space. A ventral SEA is more likely to present with systemic symptoms (i.e., fevers, septicemia) prior to presentation of neurological deficits. The best way to diagnose SEA is to approach high-risk patients with suspicion. The neuro-logical exam may aid in localizing the level of spinal involvement in cases …
{"title":"Spinal Epidural Abscesses","authors":"Sonia Teufack","doi":"10.29046/jhnj.005.1.002","DOIUrl":"https://doi.org/10.29046/jhnj.005.1.002","url":null,"abstract":"Despite advances in the diagnosis and treatment of neurosurgical diseases, spinal epidural abscesses (SEA) remain challenging. The diagnosis is complex, treatments are controversial, and the potential for adverse outcomes is significant. SEA accounts for 2 of every 10,000 of hospital admissions, an incidence which has doubled in the past twenty years. Reasons which may account for this include an aging population, increased IV drug use, and increase in number of vascular and spinal procedures. SEA can arise from an underlying medical condition, such as diabetes mellitus, alcoholism, chronic obstructive pulmonary disease (COPD), or HIV infection. Loci for SEA can be formed by other spinal abnormalities or by prior invasive spinal procedures, including epidurals, nerve blocks, or steroid injections. Sources for systemic infection may include vascular access catheters, IV drug use, or chronic UTI. 50% of spinal epidural infections have hematogenous origin, 30% arise from the skin or connective tissue, and 20% are unclassified. Common pathogens include S. aureus and P. aeruginosa. From 15% to 40% of SEA may be due to MRSA. In cases of spine trauma or spinal surgery, S. epidermidis may also be a pathogen. 79% of SEA appear dorsal to the spinal cord. A possible explanation for this finding is that the largest extent of the epidural space lies posterior to the nerve roots. The 21% that appear anterior are often associated with vertebral discitis and/ or osteomyelitis. Achieving correct diagnosis in cases of SEA may be challenging. 50% of epidural spinal abscesses are initially misdiagnosed. The most common presenting symptom is back pain, present in up to 85% of patients. Fever is present in up to 50%. Less common symptoms are paresthesias, sensory deficits, radicular pain, or motor deficits. SEA can occur spontaneously in patients with increased co-morbidi-ties. In post-operative patients, SEA may take days to weeks to appear. A dorsal SEA results from the spontaneous seeding of the dorsal epidural fat. As the abscess enlarges, neural compression may occur. Conversely, a ventral SEA may result from either spontaneous seed-ing of the ventral epidural fat or seeding of the disc space with secondary extension into the ventral epidural space. A ventral SEA is more likely to present with systemic symptoms (i.e., fevers, septicemia) prior to presentation of neurological deficits. The best way to diagnose SEA is to approach high-risk patients with suspicion. The neuro-logical exam may aid in localizing the level of spinal involvement in cases …","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"229 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121107218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peter G. Campbell, L. Tartaglino, H. Dayoub, P. Jabbour, A. Dumont, L. Gonzalez, R. Rosenwasser, S. Tjoumakaris
Introduction Spinal arteriovenous malformations (SAVMs) are rare and under-diagnosed entities. If untreated, SAVMs can lead to progressive spinal cord myelopathy. The diversion of arterial blood through dorsal and/or medullary veins can lead to a vascular steal phenomena often accompanying highflow lesions, or venous hypertension and congestion which ultimately reduces intramedullary blood flow in lower flow malformations1. Therefore, timely diagnosis and a precise understanding of these lesions can determine surgical strategies and prevent delays in treatment.
{"title":"Emerging Clinical Imaging Techniques for Spinal Arteriovenous Malformations","authors":"Peter G. Campbell, L. Tartaglino, H. Dayoub, P. Jabbour, A. Dumont, L. Gonzalez, R. Rosenwasser, S. Tjoumakaris","doi":"10.29046/JHNJ.006.1.006","DOIUrl":"https://doi.org/10.29046/JHNJ.006.1.006","url":null,"abstract":"Introduction Spinal arteriovenous malformations (SAVMs) are rare and under-diagnosed entities. If untreated, SAVMs can lead to progressive spinal cord myelopathy. The diversion of arterial blood through dorsal and/or medullary veins can lead to a vascular steal phenomena often accompanying highflow lesions, or venous hypertension and congestion which ultimately reduces intramedullary blood flow in lower flow malformations1. Therefore, timely diagnosis and a precise understanding of these lesions can determine surgical strategies and prevent delays in treatment.","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114862586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Spinal Metastasis – Diagnosis, Management, and the Role of the Hospitalist","authors":"B. Ganesh, C. Harrop, J. Edwards","doi":"10.29046/jhnj.015.1.004","DOIUrl":"https://doi.org/10.29046/jhnj.015.1.004","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123635928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Tracy, Joseph I. Cn, G. Doucet, X. He, D. Pustina, K. Osipowicz
{"title":"Advances in Clinical Neuroimaging","authors":"A. Tracy, Joseph I. Cn, G. Doucet, X. He, D. Pustina, K. Osipowicz","doi":"10.29046/jhnj.011.2.009","DOIUrl":"https://doi.org/10.29046/jhnj.011.2.009","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"58 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123347369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Williams, E. Wuthrick, Hyun Kim, J. Palmer, S. Garg, H. Eldredge-Hindy, C. Daskalakis, K. Feeney, M. Mastrangelo, L. Kim, Takami Sato, T. Olencki, D. Liebner, C. Farrell, James J. Evans, K. Judy, D. Andrews, A. Dicker, M. Werner-Wasik, W. Shi, K. Kendra
{"title":"Phase I Study of Ipilimumab Combined with Whole Brain Radiation Therapy or Radiosurgery for Melanoma Patients with Brain Metastases","authors":"N. Williams, E. Wuthrick, Hyun Kim, J. Palmer, S. Garg, H. Eldredge-Hindy, C. Daskalakis, K. Feeney, M. Mastrangelo, L. Kim, Takami Sato, T. Olencki, D. Liebner, C. Farrell, James J. Evans, K. Judy, D. Andrews, A. Dicker, M. Werner-Wasik, W. Shi, K. Kendra","doi":"10.29046/jhnj.013.1.003","DOIUrl":"https://doi.org/10.29046/jhnj.013.1.003","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"13 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128913318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
William Flounders, J. Gates, Steven Heffner, Bs Rn Msn Fnp-Bc Mba Michael Lawler, J. Pardini, Rn Ba Ccrn Scrn Maureen DePrince, Md Mba Facs Faha Robert H. Rosenwasswer
{"title":"A Systems Thinking Approach to Redesigning the Patient Experience to Reduce 30 Day Hospital Readmission","authors":"William Flounders, J. Gates, Steven Heffner, Bs Rn Msn Fnp-Bc Mba Michael Lawler, J. Pardini, Rn Ba Ccrn Scrn Maureen DePrince, Md Mba Facs Faha Robert H. Rosenwasswer","doi":"10.29046/jhnj.013.2.001","DOIUrl":"https://doi.org/10.29046/jhnj.013.2.001","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"52 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130848904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Trigeminal Neuralgia: Case Report and Review","authors":"B. Zussman, Y. Moshel","doi":"10.29046/JHNJ.007.2.003","DOIUrl":"https://doi.org/10.29046/JHNJ.007.2.003","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128447404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction The vexing question of optimal glucose level in the intensive care unit has long perplexed intensivists. Hyperglycemia is a natural response to physiologic stress,1 and in the critically ill patient has been attributed to inflammatory processes, insulin counter-regulatory hormones, organ dysfunction, iatrogenic carbohydrate or medication related hyperglycemia, and insulin resistance as evidenced by concurrently elevated insulin levels.1 Hyperglycemia occurs in 50-75% of patients admitted to an ICU, and has been associated with various adverse outcomes including increased mortality, organ dysfunction, susceptibility to infections, and neurological complications.1,2 On the cellular level, tissue/organ damage is theorized to be mediated via the production of toxic polyol metabolites and reactive oxygen species,3 with compromise of mitochondrial/cellular function.1 At the opposite extreme, hypoglycemia is acutely detrimental and clearly mandates avoidance. Glucose variability has also been linked to adverse outcomes,4 and insulin administration itself has been associated with increased mortality.5 As such, it is believed that resolution of hypoglycemia, and not insulin administration, is the determinant of improved outcomes.5
{"title":"Glucose Control in the (Neuro) Intensive Care Unit","authors":"M. Moussouttas","doi":"10.29046/JHNJ.004.4.005","DOIUrl":"https://doi.org/10.29046/JHNJ.004.4.005","url":null,"abstract":"Introduction The vexing question of optimal glucose level in the intensive care unit has long perplexed intensivists. Hyperglycemia is a natural response to physiologic stress,1 and in the critically ill patient has been attributed to inflammatory processes, insulin counter-regulatory hormones, organ dysfunction, iatrogenic carbohydrate or medication related hyperglycemia, and insulin resistance as evidenced by concurrently elevated insulin levels.1 Hyperglycemia occurs in 50-75% of patients admitted to an ICU, and has been associated with various adverse outcomes including increased mortality, organ dysfunction, susceptibility to infections, and neurological complications.1,2 On the cellular level, tissue/organ damage is theorized to be mediated via the production of toxic polyol metabolites and reactive oxygen species,3 with compromise of mitochondrial/cellular function.1 At the opposite extreme, hypoglycemia is acutely detrimental and clearly mandates avoidance. Glucose variability has also been linked to adverse outcomes,4 and insulin administration itself has been associated with increased mortality.5 As such, it is believed that resolution of hypoglycemia, and not insulin administration, is the determinant of improved outcomes.5","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"252 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122861585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Clinical Guidelines Written by Residents","authors":"Andrews, W. David","doi":"10.29046/JHNJ.004.2.003","DOIUrl":"https://doi.org/10.29046/JHNJ.004.2.003","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"37 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122208659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Verma, T. Crothers, Brian J. Neuman, A. Vaccaro, J. Heller
{"title":"A Case of Intradural Extramedullary Spinal Tuberculosis Diagnosed 8 Years After Treatment of the Primary Infection","authors":"K. Verma, T. Crothers, Brian J. Neuman, A. Vaccaro, J. Heller","doi":"10.29046/JHNJ.008.1.005","DOIUrl":"https://doi.org/10.29046/JHNJ.008.1.005","url":null,"abstract":"","PeriodicalId":355574,"journal":{"name":"JHN Journal","volume":"49 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131401921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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