Ophthalmologic Manifestations of Giant Cell Arteritis 

  • Author: Manolette R Roque, MD, MBA; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jun 15, 2011
 

Background

Giant cell arteritis (GCA) is also called temporal arteritis (see image below), cranial arteritis, and granulomatous arteritis. GCA is a systemic inflammatory vasculitis of unknown etiology that affects medium- and large-sized arteries.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14] It is a disease of elderly persons and can result in a wide variety of systemic, neurologic, and ophthalmologic complications. Visual loss is one of the most significant causes of morbidity in GCA. Permanent visual impairment may occur in as many as 60% of patients. Newly recognized GCA should be considered a true neuro-ophthalmic emergency. Prompt treatment with steroids can prevent blindness and other vascular sequelae of GCA.[15]

Hematoxylin and eosin stain, low power. Temporal aHematoxylin and eosin stain, low power. Temporal artery. Note the thrombosis in the lumen, intimal hyperplasia, and infiltration of the arterial wall muscular layers with inflammatory cells. A multinucleated giant cell is seen internal to the muscularis at the area of the internal elastic lamina (upper right).

Relationship with polymyalgia rheumatica

A close relationship exists between GCA and polymyalgia rheumatica (PMR).[16, 17, 18, 19, 20, 21, 22, 23] Despite numerous reports associating these 2 disease entities, the precise nature for this association is poorly understood and currently unknown. However, it is evident that both conditions affect similar patient populations and frequently affect the same individual. Several authors have suggested that these 2 diseases are actually different stages of a single disease spectrum. See Special Concerns.

Criteria for diagnosis

The American College of Rheumatology criteria (1990) for the diagnosis of GCA are as follows[2, 24] :

  • Age at onset of 50 years
  • New headache
  • Abnormalities of the temporal arteries
  • Erythrocyte sedimentation rate (ESR) of 50 mm/h
  • Positive results of a temporal artery biopsy (vasculitis characterized by a predominance of mononuclear infiltrates or granulomas, usually with multinucleated giant cells)
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Pathophysiology

GCA typically involves inflammation of the aortic arch and its branches, but almost any artery of the body as well as some veins may be affected occasionally. The inflammation tends to involve the arteries in a segmental or patchy manner, although long portions of arteries may be involved.[25, 26, 27] The likely determinant of arterial susceptibility to GCA is the presence and/or quantity of internal elastic lamina within the vessel wall. For example, intracranial cerebral vasculature is not affected in GCA because these vessels lack an internal elastic lamina.

The extracranial vertebral arteries, superficial temporal arteries, posterior ciliary arteries, and ophthalmic arteries are the most commonly involved arteries. The internal carotid, external carotid, and central retinal arteries are affected somewhat less frequently. In some postmortem studies, lesions were found in the proximal and distal aorta, subclavian, brachial, and abdominal arteries. Intracranial arteries are involved infrequently.

Histopathology (see Histologic Findings) in GCA reveals inflammatory infiltrate surrounding a fragmented internal elastic lamina within the media of an arterial wall. The infiltrate consists predominantly of mononuclear cells with giant cell formation. The mechanism is believed to be related to dysfunction of cellular immunity, but the etiology is unknown (see Causes). See the image depicted below.

Hematoxylin and eosin stain, low power. Temporal aHematoxylin and eosin stain, low power. Temporal artery. Note the thrombosis in the lumen, intimal hyperplasia, and infiltration of the arterial wall muscular layers with inflammatory cells. A multinucleated giant cell is seen internal to the muscularis at the area of the internal elastic lamina (upper right).
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Epidemiology

Frequency

United States

The reported incidence of GCA varies from approximately 0.5-27 cases per 100,000 people aged 50 years or older. The annual incidence is higher in northern areas of the United States.

In Olmstead County, Minnesota, 125 cases were identified over a 42-year review representing an average annual incidence rate of 17.8 cases per 100,000 population aged 50 years and older and a prevalence of persons with active or remitted GCA of 200 cases per 100,000 population aged 50 years or older. A regular cyclical pattern in incidence over 20 years has been noted.

International

The annual incidence in northern European countries has been reported to be more than 20 cases per 100,000 people. Scandinavian countries have reported the highest incidence.

The annual incidence in southern European countries has been reported to be less than 12 cases per 100,000 people. In Lugo, Spain, the average annual incidence for the population aged 50 years and older was 10 cases per 100,000 people.

In Saskatoon, Saskatchewan (Canada) and the surrounding area, the estimated incidence of GCA for the population aged older than 50 years was 9.4 cases per 100,000 people.[28]

Ostberg reported that autopsy studies performed on 889 postmortem cases revealed arteritis (eg, temporal artery, aorta) in 1.6%, suggesting that GCA may be more common than is clinically apparent.[29]

The incidence of GCA in Saudi Arabia is probably less than in the United States and Western Europe. In 1998, Bosley and Riley reported only 4 positive biopsy results from 72 temporal artery biopsies performed over a 15-year period.[30]

Mortality/Morbidity

In the milder form of GCA, patients may complain only of generalized muscle aches and pains and unusual fatigue.[1, 2] These may be mistaken for symptoms of polymyalgia rheumatica. Intermittent claudication occurs in about 50% of patients. During chewing of firm foods such as meat, fatigue or discomfort of the jaw muscles is noted. In a small percentage of patients, claudication of the tongue or throat develops with eating and repeated swallowing. Nervous system alterations are found in as many as 30% of patients; 14% have either mononeuritis or polyneuropathy, and 7% have transient ischemic attacks or strokes.

  • Visual symptoms are present in about 33% of patients; 40-50% are transient (amaurosis fugax and diplopia) and 50-60% are permanent. Regarded as one of the more serious complications of GCA is the onset of blindness from involvement of the ophthalmic artery. Permanent visual loss may be partial or complete and may occur without warning; about 50% are unilateral and 50% are bilateral. Varied visual symptoms including blurring of vision, diplopia, and loss of vision occur in 36-60% of patients.
  • Rarely, the inflammatory process may weaken the aortic wall, leading to localized aneurysm formation, aortic annular dilatation, and aortic regurgitation. Narrowing or occlusion of the branch vessels of the thoracic aorta (clinically referred to as aortic arch syndrome) may be found in 9-14% of cases, producing symptoms similar to those of Takayasu arteritis (decreased upper extremity pulses and blood pressure, arm or leg claudication, Raynaud phenomenon, transient ischemic attacks, coronary ischemia, and abdominal angina).
  • Aortic aneurysms, aortic regurgitation, and aortic dissection occur less commonly. Evans and colleagues reported aortic aneurysms occurring in 15% of patients at a median of 6 years after the GCA initially was diagnosed. Two thirds were thoracic aortic aneurysms, with the majority located in the ascending aorta. Almost 33% developed symptomatic aortic regurgitation.
  • Involvement of major vessels (aorta) predisposes patients to higher risks for death. In Evans and colleagues' report, 50% of those with thoracic aortic aneurysms died suddenly from aortic dissection.

Race

Incidence rates appear to be higher in Caucasians of European descent. This condition is less common in African Americans and Asians.[31]

Sex

Women are 2-4 times more likely to have GCA than men.

Age

Age is the most important risk factor for GCA.

  • GCA occurs mostly in patients older than 50 years, with incidence increasing with age and peaking in the eighth decade. The disease is rare in patients younger than 50 years.
  • Although the increasing incidence of GCA after age 50 years implies a relationship to aging, the meaning of this observation is not fully understood.
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Contributor Information and Disclosures
Author

Manolette R Roque, MD, MBA  General Manager, Full Partner, Ophthalmic Consultants Philippines Co.; President and CEO, Chief Refractive Surgeon, EYE REPUBLIC Ophthalmology Clinic; Section Chief, Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief, Ocular Immunology and Uveitis, International Eye Institute, St Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic; Director, AMC Eye Center, Alabang Medical Center; President, Philippine Ocular Inflammation Society

Manolette R Roque, MD, MBA is a member of the following medical societies: American Academy of Ophthalmic Executives, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

Barbara L Roque, MD  Full Partner, Ophthalmic Consultants Philippines Co; Service Chief, Pediatric Ophthalmology and Strabismus, Department of Ophthalmology, Asian Hospital and Medical Center; Active Staff, International Eye Institute, St Luke's Medical Center Global City; Visiting Ophthalmologist, AMC Eye Center, Alabang Medical Center

Barbara L Roque, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Cataract and Refractive Surgery, Philippine Academy of Ophthalmology, Philippine Society of Cataract and Refractive Surgery, and Philippine Society of Pediatric Ophthalmolo

Disclosure: Nothing to disclose.

Elisabetta Miserocchi, MD  Fellow in Immunology and Uveitis Service, Department of Ophthalmology, Harvard Medical School

Disclosure: Nothing to disclose.

C Stephen Foster, MD, FACS, FACR, FAAO  Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution

C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Kilbourn Gordon III, MD, FACEP  Urgent Care Physician

Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society

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

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

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Hematoxylin and eosin stain, low power. Temporal artery. Note the thrombosis in the lumen, intimal hyperplasia, and infiltration of the arterial wall muscular layers with inflammatory cells. A multinucleated giant cell is seen internal to the muscularis at the area of the internal elastic lamina (upper right).
Anterior ischemic optic neuropathy. Image courtesy of Richard Kho, MD, Q.C. Eye Center, Quezon City, Philippines.
Branch retinal vein occlusion in a patient with giant cell arteritis. Image courtesy of Manolette Roque, MD, Ophthalmic Consultants Philippines Co., EYE REPUBLIC Ophthalmology Clinic, Web Atlas of Ophthalmology.
 
 
 
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