Temporal Arteritis in Emergency Medicine Follow-up

  • Author: Christopher H Lee, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Apr 15, 2011
 

Further Inpatient Care

  • Hospital admission for temporal arteritis is unusual but may be indicated depending upon the severity of symptoms and the ability of the patient to provide self-care at home.
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Further Outpatient Care

  • Most patients can be treated on an outpatient basis.
  • An adequate quantity of corticosteroids should be prescribed.
  • Follow-up care should be arranged within 72 hours.
  • Symptoms typically improve within 1-3 days.
  • Corticosteroid therapy may last for 1-2 years, depending on the patient’s response.
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Inpatient & Outpatient Medications

  • Nonsteroidal anti-inflammatory drugs can provide pain relief.
  • Methotrexate[6] and azathioprine have been used as both adjuncts and steroid-sparing agents for temporal arteritis, but conclusive evidence regarding their efficacy remains uncertain. These medications should not be prescribed from the emergency department, but they may be added at a later time upon rheumatology follow-up.
  • Long-term steroid use (greater than 3 wk) may require the addition of calcium, vitamin D, and bisphosphonate therapy to prevent steroid-induced osteoporosis.
  • Retrospective data shows that low-dose aspirin has been associated with a lower risk for developing acute vision loss and stroke in patients with temporal arteritis. In the absence of contraindications, low-dose (81 mg) aspirin should be considered along with corticosteroids.[7]
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Transfer

  • Hospital transfer is indicated only if visual disturbance is severe and cannot be adequately evaluated and managed at the current facility.
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Complications

  • Permanent vision loss is the most feared complication of untreated temporal arteritis and can even progress in some cases despite the initiation of corticosteroid therapy. This will tend to occur within the first 5 days of treatment if therapy is going to fail. As an outpatient, corticosteroid doses should be increased until symptoms improve.
  • Approximately 50% of patients with temporal arteritis experience at least one flare-up that requires prolonged corticosteroid therapy.
  • Patients with temporal arteritis are at increased risk for thoracic and abdominal aortic aneurysms compared to age-matched controls.
  • Uncommon complications include CVA, memory loss, myocardial infarction, and peripheral neuropathy.
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Prognosis

  • Generally, temporal arteritis is a self-limiting condition lasting up to 2 years.
  • Treatment with corticosteroids has proven to be effective in most cases, but the lengthy duration of treatment can lead to corticosteroid-induced complications.
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Patient Education

  • Timely follow-up care from the emergency department is critical to accurately diagnose temporal arteritis.
  • Medication compliance and instructions to return to the emergency department if the condition worsens should be emphasized.
  • Patients should be counseled that existing visual loss prior to arrival at the emergency department may not be regained despite initiation of therapy.
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Contributor Information and Disclosures
Author

Christopher H Lee, MD  Clinical Instructor, Section of EMS, Department of Emergency Medicine, Yale University School of Medicine

Christopher H Lee, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jean Marie Hammel, MD  Assistant Professor, Associate Residency Director of Emergency Medicine Residency Program, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine

Jean Marie Hammel, MD is a member of the following medical societies: Alpha Omega Alpha and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard S Krause, MD  Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

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: eMedicine Salary Employment

Gino A Farina, MD, FACEP, FAAEM  Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD 

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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Hematoxylin and eosin stained superficial temporal artery biopsy specimen, cross section. The hallmark histologic features of giant cell arteritis 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 in the same patient whose temporal artery biopsy specimen is shown in the previous image.
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 giant cell arteritis resulted in ischemic necrosis of the lower limb, necessitating amputation.
 
 
 
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