Temporal/Giant Cell Arteritis Follow-up

  • Author: Tarakad S Ramachandran, MBBS, FRCP(C), FACP; Chief Editor: B Mark Keegan, MD, FRCPC   more...
 
Updated: Feb 3, 2012
 

Further Outpatient Care

Giant cell arteritis (GCA) is treated primarily in an outpatient setting. The median duration of symptoms before diagnosis is 1 month.

  • Ongoing monitoring of symptoms and ESR are mandatory.
  • ESR often normalizes within days of instituting steroid therapy.
  • With tapering steroid doses, ischemic complications may occur at any time but tend to occur a median of 1 month after beginning therapy.
  • The typical patient with GCA remains on steroid therapy for roughly 2 years.
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Deterrence/Prevention

No effective prevention strategies are known.

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Complications

  • Complications of GCA result from ischemic complications of vasculitis and are discussed in Clinical.
  • Sequelae of steroid therapy include acute and chronic adverse effects and are discussed in Treatment and Medication.
    • Because of the high frequency of chronic adverse effects, TAB confirmation of diagnosis is highly desirable.
    • Patients with GCA suffer the following steroid-related complications during the course of their treatment: vertebral body compression fracture (26%), symptomatic steroid myopathy (11%), steroid psychosis (3%).
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Prognosis

  • With prompt, adequate therapy, full recovery is the rule.
    • The reduced rate of neuro-ophthalmologic complications in recent years reflects improved recognition and treatment.
    • Blindness is now a rare complication.
  • Untreated, the prognosis for the patient with GCA is extremely poor, with blindness or death resulting from myocardial infarction, stroke, or dissecting aortic aneurysm. Vision loss in the second eye may occur even after the initiation of treatment (possibly because those vessels have already been affected by arteritis) in 6-13% of patients.[30]
  • While morbidity and mortality have improved significantly with corticosteroid therapy, a higher mortality after treatment and definitely a higher morbidity caused by the corticosteroids have been reported.
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Patient Education

  • Symptomatic relapse: Patients must be instructed concerning the seriousness of symptomatic relapses so that prompt medical attention is sought.
  • Steroid use: Patients must know the importance of strictly adhering to their steroid dose schedule and, if necessary, must utilize ancillary interventions such as dietary restrictions that can reduce the incidence of steroid-related adverse effects.
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Contributor Information and Disclosures
Author

Tarakad S Ramachandran, MBBS, FRCP(C), FACP  Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine

Disclosure: Abbott Labs None None; Teva Marion None None; Boeringer-Ingelheim Honoraria Speaking and teaching

Coauthor(s)

Arun Ramachandran  State University of New York Upstate Medical University

Arun Ramachandran is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Jorge E Mendizabal, MD  Consulting Staff, Corpus Christi Neurology

Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed  Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

B Mark Keegan, MD, FRCPC  Assistant Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester

B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association

Disclosure: Novartis Consulting fee Consulting; Bionest Consulting fee Consulting

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Richard J. Caselli, MD to the development and writing of this article.

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Hematoxylin- and eosin-stained superficial temporal artery biopsy specimen, cross section. The hallmark histologic features of GCA shown here include intimal thickening with luminal stenosis, mononuclear inflammatory cell infiltrate with media invasion and necrosis, and giant cell formation in the media.
Lumbar angiogram showing stenosis and occlusion of femoral artery branches due to vasculitis.
Hematoxylin- and eosin-stained femoral artery branch, cross section, taken from a lower limb amputation specimen. Mononuclear cell invasion and necrosis in the media of this large artery can be observed. Extensive lower limb vasculitis from GCA resulted in ischemic necrosis of the lower limb, necessitating amputation.
 
 
 
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