Ophthalmologic Manifestations of Giant Cell Arteritis Workup

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

Laboratory Studies

  • ESR elevation (moderate to >100 mm/h) is common and is rarely (approximately 3%) normal. Highly elevated ESR results are characteristic of a GCA process rather than other vasculitic or rheumatologic entities. This acute phase reactant may be followed serially and may assist in monitoring for treatment dosing and response. The absence of this marker cannot completely exclude the diagnosis.[81, 25, 82, 83, 84]
  • C-reactive protein (CRP) is elevated and reflects the underlying inflammatory process. In the largest population-based giant cell arteritis study to date in the United States (3001 patients), CRP level greater than 2.45 mg/dL and elevated platelet count values are associated with a positive temporal artery biopsy while erythrocyte sedimentation rates were not as specific a predictor.[85] This acute phase reactant may be followed serially and may assist in monitoring for treatment dosing and response. Sensitivity for the detection of GCA is believed to be equal to or higher in CRP than in ESR. The absence of this marker cannot completely exclude the diagnosis.
  • Fibrinogen is increased along with other acute phase reactants.
  • Most patients are mildly anemic (normochromic, normocytic) during the active phases. Leukocyte and differential counts are generally normal. Platelet counts often are increased.[86]
  • In GCA, hepatic enzymes, such as alkaline phosphatase and aspartate aminotransferase (formerly called serum glutamic oxaloacetic transaminase [SGOT]), are elevated in 20-30% and 15% of cases, respectively. Prolonged prothrombin time also may be found.
  • Immunoglobulin levels are normal, and immune complexes are absent. Results of tests for antinuclear antibodies and rheumatoid factor are generally negative.
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Imaging Studies

  • Occasionally, imaging studies may be used to assist in the diagnosis of GCA. Aortic arch and cerebral angiography may show occlusion or alternating stenotic areas. Arteriography is sensitive but nonspecific and is deemed unreliable diagnostically. However, it is noted to be helpful when an area must be chosen to sample after the initial biopsy result has been negative.
  • Computerized tomography and magnetic resonance imaging of the brain are not first-line diagnostic procedures for GCA; however, they may be useful in patients with multi-infarct state secondary to cervicocephalic arteritis.[87, 88, 89, 90]
  • Color duplex ultrasonography of the temporal arteries has been used as a promising alternative or complement to superficial temporal artery biopsy.[91, 92]
    • Its sensitivity for GCA is 73%, and its specificity is 100% when a dark halo (classical halo sign) is seen about the vessel. This key diagnostic feature is believed to represent vessel wall edema.
    • Prospective study is necessary to validate the utility of the test, but a possible application includes confirming the diagnosis of GCA without performing a biopsy in persons with clinically evident disease.
    • Color duplex ultrasonography is user dependent and is not yet sufficiently sensitive to replace temporal artery biopsy, which is the criterion standard.
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Other Tests

  • Automated visual field testing typically reveals an inferior altitudinal defect, inferior nasal sectorial defect, or central scotoma.
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Procedures

  • Superficial temporal artery biopsy (TAB) shows focal granulomatous arteritis, often with giant cells and skip areas of normal arterial wall. The technique for superficial TAB has been reported.[93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111]
    • Perform a biopsy on the most symptomatic side initially. In a patient with suggestive symptoms and a negative initial biopsy result on the symptomatic side, performing a superficial TAB on the other side may confirm the diagnosis.
    • Perform the superficial TAB in the appropriate patient. Therapy should not be withheld pending the performance or results of the superficial TAB in patients with acute visual loss and high clinical suspicion for GCA.
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Histologic Findings

Early cases or regions with minimal involvement

Collections of lymphocytes are confined to the region of the internal or external elastic lamina or adventitia in early cases or regions of arteries with minimal involvement. Intimal thickening, with prominent cellular infiltration, is typically present.

Late cases or regions with marked involvement

All layers are affected in late cases or regions of arteries with marked involvement. There are widespread areas of necrosis of portions of the arterial wall. The elastic laminae usually are involved, and granulomas containing multinucleated histiocytic and foreign body giant cells, histiocytes, predominantly helper T-cell lymphocytes, and some plasma cells and fibroblasts are usually present.[112] See image shown below.

Anterior ischemic optic neuropathy. Image courtesyAnterior ischemic optic neuropathy. Image courtesy of Richard Kho, MD, Q.C. Eye Center, Quezon City, Philippines.

Weyand and colleagues have extensively described the distribution and function of inflammatory cells in the artery wall.[76, 113, 77, 27, 78] Eosinophils may be seen in the specimen section, but polymorphonuclear (PMN) leukocytes are rare. Thrombosis may develop at the sites of active inflammation. These areas with thrombosis may recanalize later. It has been observed that the inflammatory process is usually most marked in the inner portion of the media adjacent to the internal elastic lamina. This has led to the belief that the internal elastic lamina plays a central role in the initiation of the inflammatory process. Fragmentation and disintegration of elastic fibers occur. This is closely associated with an accumulation of giant cells. Note that giant cells are not seen in all sections; therefore, it is not required for the establishment of the diagnosis if other features are present. Fibrinoid necrosis is seen less commonly in necrotizing arteritis.

The more sections that are examined in the area of arteritis, the more likely it is that giant cells will be found. What is needed is transmural acute and chronic inflammation for acute diagnosis or evidence of previous repair. Healed or subacute phase shows fibrosis, fragmented internal elastic lamina, chronic inflammatory cells in the intima or media, and ideally neovascularization. Skip lesions or steroids can lead to false-negative biopsy results. Long breaks in internal elastic lamina favor healed arteritis over atherosclerosis.

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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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