Giant Cell Arteritis Clinical Presentation

  • Author: Mythili Seetharaman, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: May 23, 2012
 

History

The following are criteria for giant cell arteritis (GCA) issued by the American College of Rheumatology in 1990 (the presence of ≥3 yields a diagnostic sensitivity of 93.5% and specificity of 91.2%):[14]

  • Age 50 years or older
  • Newly onset localized headache
  • Temporal artery tenderness or decreased temporal artery pulse
  • ESR of at least 50 mm/h
  • Abnormal artery biopsy specimen characterized by mononuclear infiltration or granulomatous inflammation

Giant cell arteritis is a strikingly heterogeneous systemic inflammatory disorder. Presentation varies from fever of unknown origin to visual loss and limb claudication. Arterial lesions may be widespread; therefore, the varied expression of giant cell arteritis can be analyzed according to the anatomical pattern of the arteries affected. Polymyalgia rheumatica and giant cell arteritis may represent two parts of a single disease spectrum, with giant cell arteritis at the more severe end. They share certain constitutional symptoms, eg, fatigue, weight loss, and fever. Approximately 50% of patients with giant cell arteritis have features of polymyalgia rheumatica, ie, proximal stiffness, soreness, and pain. Earlier descriptions of giant cell arteritis emphasize manifestations that were attributable to involvement of the ophthalmic artery and branches of the external carotid system, but arterial lesions may be widespread.

Constitutional symptoms

Patients with giant cell arteritis or polymyalgia rheumatica frequently report malaise and fatigue. They are usually mildly febrile. The fever associated with giant cell arteritis may reach 102°F in some cases. Night sweats may occur. Thus, the presentation of fever of unknown origin is much more common with giant cell arteritis than polymyalgia rheumatica.

Anorexia and weight loss may be prominent features, suggesting a malignancy, in which case an age-appropriate malignancy evaluation is recommended.

Proximal myalgias and stiffness

Polymyalgia rheumatica is characterized by symmetric proximal joint and muscle aching, soreness, and stiffness. These symptoms are most prominent in the shoulder, neck, and pelvic girdles and may involve the distal joints and muscle groups. The onset of symptoms may be abrupt or insidious over weeks to months.

Aching and stiffness are worse in the morning and with exertion, and they may be severe and incapacitating. Muscles may be tender, disuse may lead to atrophy, and contractures may develop. Muscle strength (usually normal) is often difficult to evaluate because of pain.

Polymyalgia rheumatica often coexists with giant cell arteritis. In some series, 10-15% of patients with pure polymyalgia rheumatica had associated giant cell arteritis based on findings from biopsy of the temporal artery. Conversely, 50-70% of patients with giant cell arteritis had associated polymyalgia rheumatica.

Even when treating patients for isolated polymyalgia rheumatica, instruct the patient to report the development of headache or visual symptoms that could be caused by occult giant cell arteritis.

Joint symptoms

Most patients have poorly localized tenderness over the joints, especially the shoulders and hips.

Synovitis was once excluded as a feature of giant cell arteritis, but moderate bland effusions can develop in the knees and occasionally other joints (eg, shoulders, wrists).

Carpal tunnel syndrome and peripheral synovitis may be present in patients with polymyalgia rheumatica, potentially causing diagnostic confusion.

Symptoms related to vasculitis involving branches of the external carotid artery

Headache and scalp pain are probably the most common symptoms of giant cell arteritis, occurring in 50-75% of patients. Headache is often the first manifestation and is described as extracranial, dull, boring, and burning. Persistent and prominent temporal headaches represent a typical symptom. Patients with occipital artery involvement may have occipital pain and difficulty combing their hair or discomfort from the pressure of a pillow on the head.

Involvement of the posterior auricular artery may manifest as pain in the ear canal, pinna, or parotid gland.

Jaw claudication and pain (predominantly in the masseter muscles with chewing) are highly specific symptoms of giant cell arteritis and occur in nearly 50% of patients. Patients with involvement of the maxillary or lingual arteries may have jaw or tongue pain when chewing or talking, and tongue gangrene has been reported.

Unilateral and bilateral scalp necrosis has been reported in patients with giant cell arteritis and is associated with an increased likelihood of visual complications.[15, 16]

Rare cases of tongue necrosis have been reported in patients with giant cell arteritis.[17]

Symptoms related to vasculitic involvement of the ophthalmic artery and its branches

In patients with giant cell arteritis, decreased vision secondary to arteritis is the most common serious consequence. This occurs in 20-50% of patients who present to ophthalmologists and is the presenting symptom at diagnosis in 60% of patients with giant cell arteritis who develop visual loss.

A careful history from most patients who present with sudden visual loss reveals that headache, constitutional symptoms, and polymyalgia rheumatica (usually specific enough to suggest diagnosis) precede blindness in approximately 40% of patients. Even the evolution of the visual loss is often staggered, with a partial field defect progressing to complete blindness over days. If giant cell arteritis remains untreated, the second eye may become affected within 1-2 weeks.

Ocular manifestations vary according to the pattern of arterial branch involvement.

The posterior ciliary arteries are the arteries most frequently involved in giant cell arteritis; thus, ischemic optic neuritis is the most common lesion.

The central retinal artery supplies the retina, which is the terminal branch of the ophthalmic artery. Occlusion of the central retinal artery or its branches occurs in fewer than 10% of patients with eye involvement; therefore, retinal changes (eg, exudates, hemorrhages, vasculitis) are uncommon.

Amaurosis fugax occurs in approximately 10% of patients with giant cell arteritis, and, if not treated, 80% of those patients develop permanent visual loss.

The posterior ciliary arteries that supply the optic nerve and the muscular branches that supply the extraocular muscles also derive from the ophthalmic artery. Thus, diplopia or ptosis, observed in 5% of patients with giant cell arteritis, may precede visual loss.

Note that the visual abnormality that occurs can be a composite of many ischemic events occurring together in the optic nerve, extraocular muscles, chiasm, and the brain itself.

Symptoms related to large artery involvement

These symptoms are related to involvement of the aortic arch and thoracic aorta. Limited pathologic studies show giant cell arteritis in vessels with bruits; however, the frequency of aortic and aortic root involvement in giant cell arteritis, based on clinical evidence, varies between 9% and 18%.[18]

Certain clinical characteristics distinguish large vessel from cranial giant cell arteritis. Approximately 88% of large vessel involvement occurs in women. Patients typically have a younger age at onset, fewer constitutional symptoms, and a longer interval until diagnosis. Thoracic aneurysms with giant cells in the tissue can develop as late as 15 years after the diagnosis and successful treatment of giant cell arteritis. These patients are less likely to have positive temporal artery biopsy findings, headache, jaw claudication, or visual changes and are more likely to have arm claudication at disease onset.

The major symptoms are arm or leg claudication. Occasionally, symptoms related to intermittent or persistent brain ischemia develop and are related to a subclavian steal syndrome or narrowing of other aortic arch vessels or, rarely, even intracerebral vascular disease.

Abdominal aortic aneurysms can occur. Giant cell arteritis can manifest as symptoms of aortic aneurysms and intestinal infarction. For unknown reasons, renal involvement is rare.

Radiographic data suggests vasculitic involvement of lower extremity vessels in patients with giant cell arteritis.[19] Giant cell arteritis and Takayasu arteritis have overlapping symptoms in varying frequencies, suggesting a spectrum of presentation for large vessel arteritis rather than distinct disease entities.[20]

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Physical

In polymyalgia rheumatica, a striking paucity of findings is encountered during the physical examination relative to the severity of the symptoms. The same may be true for giant cell arteritis, although ocular and funduscopic evidence of ischemic disease is present in symptomatic patients.

  • Patients may present with fever.
  • Muscles may be tender.
  • Joints are tender, especially over the shoulder and pelvic girdles. Mild peripheral synovitis may be present in patients with polymyalgia rheumatica.
  • Temporal arteries are prominent, beaded, tender, and pulseless; however, a totally normal appearance of these vessels in no way excludes a diagnosis of giant cell arteritis.
  • Funduscopic examination findings are typically normal, although optic atrophy or ischemic optic neuropathy may be observed in patients with symptoms of visual loss.
  • Bruits may be heard over the carotid, axillary, or brachial arteries.
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Causes

The cause of polymyalgia rheumatica and giant cell arteritis is unknown. Environmental and genetic factors likely play a significant role.

Genetic factors

Polymyalgia rheumatica and giant cell arteritis may aggregate in families.[21]

Polymyalgia rheumatica and giant cell arteritis are more common among individuals of European descent and less common among African Americans.

In polymyalgia rheumatica and giant cell arteritis, the frequency of the human leukocyte antigen DR4 is approximately twice that of normal controls in some series and may be an important susceptibility factor.

An infectious etiology has been speculated to trigger giant cell arteritis.[22]

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Contributor Information and Disclosures
Author

Mythili Seetharaman, MD  Consultant Rheumatologist, OAA, Allentown, PA; Clinical Assistant Professor, Thomas Jefferson University Hospital; Consulting Staff, Einstein Arthritis Center, Albert Einstein Medical Center, St Christopher's Hospital for Children

Mythili Seetharaman, MD is a member of the following medical societies: American College of Rheumatology and American Medical Association

Disclosure: Abbott pharmaceuticals Honoraria Speaking and teaching

Coauthor(s)

Stephen A Paget  MD, Physician in Chief Emeritus, Joseph P Routh Professor of Medicine, New York Hospital Weill Cornell Medical College; Program Director, Cornell Arthritis and Multipurpose Arthritis and Musculoskeletal Diseases Center (MAMDC), Hospital for Special Surgery

Stephen A Paget is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, and New York Academy of Sciences

Disclosure: Crescendo bioscience Consulting fee Consulting

Evan Leibowitz, MD  Fellow, Department of Internal Medicine, Division of Rheumatology, Valley Hospital

Evan Leibowitz, MD is a member of the following medical societies: Alpha Omega Alpha and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

John Varga, MD  Professor, Department of Internal Medicine, Division of Rheumatology, Northwestern University

John Varga, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Central Society for Clinical Research, and Society for Investigative Dermatology

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

Lawrence H Brent, MD  Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

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