Giant Cell Arteritis: The Blood Vessel Inflammation That Can Cause Blindness
Giant Cell Arteritis, commonly called GCA, is a chronic autoimmune inflammatory disease affecting medium-sized and large arteries throughout the body. The disease is also called temporal arteritis because the temporal arteries, which supply blood to the scalp and eyes, are frequently involved. Giant Cell Arteritis is a serious medical condition because inflammation of arteries supplying the eyes can cause sudden vision loss and permanent blindness. Vision loss from Giant Cell Arteritis is irreversible. Once blindness occurs, vision cannot be restored. This makes Giant Cell Arteritis a medical emergency requiring urgent diagnosis and treatment. Giant Cell Arteritis exclusively affects older adults. The disease rarely develops in people under age fifty. The vast majority of cases occur in people over age sixty. The average age of onset is around seventy years. Giant Cell Arteritis is the most common vasculitis in older adults. The disease affects approximately fifteen to twenty people per one hundred thousand over age fifty. Giant Cell Arteritis affects both men and women, with women affected slightly more frequently. Giant Cell Arteritis is caused by abnormal immune activation targeting large and medium-sized arteries. The immune system produces antibodies against artery walls. T cells infiltrate artery walls. Inflammatory cytokines cause inflammation of artery tissue. The inflammation damages the artery wall. Artery narrowing or blockage occurs. If arteries supplying the eyes are blocked, blood flow to the retina stops. Retinal ischemia causes vision loss. Amaurosis fugax is transient vision loss warning of imminent retinal artery occlusion. Permanent vision loss follows if not urgently treated. Approximately half of untreated GCA patients develop vision loss. Early diagnosis and prompt treatment prevent blindness in most cases. The dramatic potential for vision loss makes rapid recognition and treatment essential. Understanding Giant Cell Arteritis helps with early recognition and urgent appropriate management to prevent permanent blindness and other serious complications. The association with Polymyalgia Rheumatica affects clinical presentation and diagnosis. Early diagnosis allows treatment before vision loss occurs.
How Does Immune Attack on Arteries Cause Giant Cell Arteritis?
To understand Giant Cell Arteritis, we need to learn about arteries and the immune system. Arteries are blood vessels that carry blood away from the heart. Large arteries like the aorta distribute blood to major body regions. Medium-sized arteries deliver blood to specific organs and tissues. Arteries have three layers. The intima is the innermost layer. The media is the muscular middle layer. The adventitia is the outer layer. In Giant Cell Arteritis, the immune system attacks artery walls. T cells infiltrate the artery wall. B cells produce antibodies against artery components. Inflammatory cytokines including interleukin-6 and TNF-alpha are produced. The inflammatory process damages the artery wall. The intima becomes inflamed. The media develops inflammation and necrosis. The adventitia develops inflammatory infiltrates. Giant cells, the large cells giving GCA its name, develop within the inflamed artery wall. These multinucleated giant cells are characteristic of GCA. The inflammatory process progressively damages the artery. The artery wall weakens and becomes fragile. The artery may rupture. Thrombosis, blood clot formation, may occur in the inflamed artery. The blood clot blocks blood flow. Ischemia, reduced blood flow, occurs downstream from the blockage. The organs supplied by the blocked artery become ischemic. If retinal arteries are blocked, retinal ischemia occurs. The retina requires constant oxygen and nutrients from blood flow. When blood flow stops, retinal cells die within minutes. Retinal cell death causes permanent vision loss. The vision loss is irreversible. No treatment can restore dead retinal cells. This makes prevention of retinal artery occlusion critical. The temporal arteries supply blood to the scalp, face, and eyes. Inflammation of temporal arteries causes headache. Inflammation can progress to occlusion. When temporal artery occlusion occurs, ischemia of the territory supplied develops. If the ophthalmic artery is occluded, vision loss occurs. Anterior ischemic optic neuropathy causes vision loss. The optic nerve loses blood supply. Optic nerve cell death occurs. Permanent vision loss results. Central retinal artery occlusion causes complete vision loss in the affected eye. The retina loses all blood supply. Complete retinal cell death. Permanent blindness in that eye. Other arteries affected by GCA include the vertebral arteries, carotid arteries, and axillary arteries. Vertebral artery occlusion causes stroke. Carotid artery occlusion causes stroke or transient ischemic attacks. Axillary artery occlusion affects arm blood flow. Aortic involvement causes aortitis. The aorta becomes weakened and aneurysmal. Aortic rupture is life-threatening. The systemic nature of GCA means many organs can be affected. Understanding the arterial pathology explains the urgency of treating GCA before vascular occlusion occurs.
What Are the Main Symptoms and Signs of Giant Cell Arteritis?
Giant Cell Arteritis causes variable symptoms depending on which arteries are involved. The most common and distinctive symptoms relate to temporal artery involvement. Headache is the most common symptom. Severe headache affecting the temples and scalp. The headache is often described as throbbing. The pain is often on one side more than the other. Headache is often the first symptom. The person may seek medical care for this new-onset severe headache. Headache is present in about ninety percent of GCA patients. The headache may be the only symptom initially. However, other symptoms usually develop. Temporal artery tenderness is common. Palpation of the temporal arteries causes pain. The arteries may feel thick or nodular. The temporal arteries may be swollen and prominent. Tender temporal arteries are highly suggestive of GCA. Jaw claudication is distinctive. Pain in the jaw with chewing. The pain develops after chewing a few bites. The person must stop eating. The jaw pain results from ischemia of jaw muscles from temporal artery narrowing. Jaw claudication is highly specific for GCA. The presence of jaw claudication should prompt urgent evaluation. Tongue claudication occurs in some. Pain of the tongue with chewing. Numbness of the tongue. Tongue ulceration and necrosis in severe cases. Tongue necrosis is rare but indicates severe arterial disease. Scalp pain and tenderness. Pain of the scalp. Tenderness to touch or hair combing. The pain results from temporal artery inflammation. Vision symptoms are the most serious. Amaurosis fugax is transient vision loss. Sudden vision loss lasting minutes to an hour. Vision returns completely. However, amaurosis fugax is a warning sign. Permanent vision loss often follows within days if not treated. Amaurosis fugax is a medical emergency. Immediate ophthalmology evaluation and GCA treatment necessary. Permanent vision loss from retinal artery occlusion. Sudden complete vision loss in one eye. Central retinal artery occlusion. Permanent blindness in that eye. No pain with vision loss. The person suddenly cannot see in that eye. Anterior ischemic optic neuropathy. Altitudinal visual field loss. Vision loss in upper or lower half of visual field. Gradual peripheral vision loss. Diplopia, or double vision, may occur. Diplopia results from cranial nerve ischemia. Oculomotor nerve involvement. Abducens nerve involvement. Eye pain may occur. Pain with eye movements. Photophobia, light sensitivity. These indicate eye ischemia. Polymyalgia Rheumatica symptoms. About fifty percent of GCA patients have PMR. Bilateral shoulder pain and stiffness. Bilateral hip pain and stiffness. Severe morning stiffness. Joint pain and swelling. These PMR symptoms may be the initial presentation. Fever may occur. Low-grade fever. Fever accompanying active disease. Fever resolves with appropriate treatment. Weight loss may develop. Loss of appetite from systemic inflammation. Reduced food intake. Weight loss results. Unexplained weight loss may prompt evaluation. Fatigue is prominent. Profound exhaustion. Systemic inflammation causes fatigue. Depression and mood changes. New onset depression. Anxiety about vision loss. Grief about symptoms. Cognitive changes. Difficulty concentrating. Mental slowness. Confusion in severe disease. Stroke symptoms may develop. Weakness or numbness from stroke. Speech difficulties. Facial droop. Arm weakness. Leg weakness. Stroke indicates large artery involvement. These are medical emergencies. The sudden onset of vision symptoms or stroke in an older adult with headache and temporal artery tenderness suggests GCA. Prompt evaluation is essential. Vision-threatening symptoms require emergency evaluation.
How is Giant Cell Arteritis Detected and Diagnosed?
Giant Cell Arteritis is diagnosed through a combination of clinical findings and specific diagnostic tests. Vision-threatening symptoms require emergency evaluation. Prompt diagnosis is critical for preventing blindness. Clinical history is important. Older adult over age fifty. New onset severe headache. Temporal artery tenderness. Jaw claudication. Vision symptoms. Polymyalgia Rheumatica symptoms. These clinical features strongly suggest GCA. Physical examination reveals characteristic findings. Prominent temporal arteries. Tender temporal arteries on palpation. Pulseless temporal arteries in severe cases. The artery may feel thick or have a cord-like texture. Scalp tenderness. Limited jaw opening from pain. Evaluation of visual acuity. Visual field testing. Evaluation of ocular movements. Assessment for eye involvement. Fundoscopic examination. Examination of the retina. Pale optic disc if optic nerve ischemia. Retinal whitening if central retinal artery occlusion. Erythrocyte sedimentation rate, or ESR, is markedly elevated. ESR elevation is nearly universal in GCA. Normal ESR is less than twenty. GCA usually causes ESR greater than fifty. Often greater than one hundred. Marked ESR elevation supports diagnosis. ESR correlates with disease activity. C-reactive protein, or CRP, is elevated. CRP indicates acute inflammation. CRP elevations in GCA are prominent. The combination of markedly elevated ESR and CRP is highly suggestive of GCA. Hemoglobin may be reduced. Anemia from chronic disease. Mild to moderate anemia. Hemoglobin improves with treatment. Platelet count may be elevated. Thrombocytosis accompanying inflammation. Platelet elevation resolves with treatment. Alkaline phosphatase may be elevated. Liver enzymes may be mildly elevated. Albumin may be low. These abnormalities reflect systemic inflammation. Temporal artery biopsy confirms diagnosis. Biopsy shows giant cell arteritis. Intimal hyperplasia. Inflammatory infiltrates. Giant cells in the media. The pathological findings confirm GCA. Biopsy is the gold standard for diagnosis. However, clinical suspicion of GCA with vision-threatening symptoms warrants immediate treatment. Biopsy should not delay treatment. Treatment can be started while awaiting biopsy. Color duplex ultrasonography of temporal arteries. Noninvasive imaging. Can show artery wall thickening. Can show occlusion. Can guide biopsy location. Increasingly used for diagnosis. Does not replace biopsy. PET scan may show aortitis. Large vessel involvement. Assessment of aortic disease. Not routine for diagnosis. Used when aortitis suspected. MRI of arteries assesses large vessel involvement. Carotid and vertebral artery assessment. Aortic involvement assessment. Helps evaluate extent of disease. Ophthalmology consultation if vision symptoms. Assessment for eye involvement. Evaluation of optic nerve and retina. Assessment for arterial occlusion. Urgent evaluation of vision-threatening symptoms. The combination of clinical presentation with markedly elevated inflammatory markers and temporal artery biopsy findings confirms diagnosis. Vision-threatening symptoms warrant emergency treatment without delay for biopsy.
What Vision-Threatening Complications Can Giant Cell Arteritis Cause?
Giant Cell Arteritis can cause serious complications affecting vision and other organs. Vision loss is the most serious complication. Permanent blindness is irreversible and devastating. Understanding complications emphasizes urgency of treatment. Amaurosis fugax, transient vision loss, is a warning sign. Sudden temporary vision loss. Vision returns completely within minutes to an hour. However, amaurosis fugax indicates imminent arterial occlusion. Permanent vision loss usually follows within days if untreated. Amaurosis fugax is a medical emergency. Urgent treatment necessary. Treatment initiates immediately. Central retinal artery occlusion causes permanent vision loss. The central retinal artery supplies the retina. Occlusion blocks blood flow completely. Retinal cells die within minutes. Permanent blindness in that eye. The vision loss is sudden and complete. No treatment restores vision. Prevention through early GCA treatment is crucial. Anterior ischemic optic neuropathy causes vision loss. The optic nerve loses blood supply. Optic nerve cells die. Vision loss is sudden. Visual field defect in upper or lower half. Altitudinal vision loss. No treatment restores lost vision. Prevention through early treatment crucial. Branch retinal artery occlusion causes partial vision loss. One branch of central retinal artery occluded. Partial retinal ischemia. Visual field defect corresponding to occluded branch. The vision loss is permanent. Posterior ischemic optic neuropathy causes gradual vision loss. Progressive optic nerve ischemia. Progressive vision loss over weeks. By the time diagnosed, significant vision loss present. Prevention crucial. Diplopia from cranial nerve ischemia. Oculomotor nerve ischemia. Abducens nerve ischemia. Double vision results. Eye movements painful. However, diplopia often resolves. Vision loss from ischemia is permanent. The distinction is important. Vision loss is irreversible. Stroke from large artery occlusion. Carotid artery occlusion. Vertebral artery occlusion. Cerebral ischemia. Stroke causes neurological deficit. Permanent neurological disability. Hemiparesis. Speech difficulties. Cognitive decline. Stroke prevention through early treatment crucial. Aortic aneurysm from aortitis. Aortic wall inflammation and weakening. Aortic dilation. Aneurysmal aorta at risk for rupture. Aortic rupture is catastrophic. Sudden massive hemorrhage. Death within minutes. Early aortic disease detection allows treatment. Regular aortic imaging for aortic disease surveillance. Myocardial ischemia from coronary artery involvement. Coronary artery inflammation. Acute coronary syndrome. Heart attack. Myocardial infarction. Coronary artery involvement less common than large vessel disease. However, serious when occurs. Polymyalgia Rheumatica symptoms. Severe muscle pain and stiffness. Disability from pain. Functional limitation. However, PMR responds to corticosteroids. PMR not vision-threatening. But PMR indicates GCA risk. Depression from vision loss. Permanent blindness causes severe depression. Grief about vision loss. Anxiety about future. Depression and psychological distress. Mental health support important. Without urgent treatment, complications are serious and irreversible. With prompt diagnosis and treatment, complications are prevented.
What Treatments Help People with Giant Cell Arteritis?
Treatment for Giant Cell Arteritis focuses on suppressing inflammation rapidly to prevent vision loss and other serious complications. Treatment is a medical emergency. Immediate high-dose corticosteroids are necessary. Corticosteroids suppress inflammation rapidly. Prednisone is the standard corticosteroid. Initial dose typically forty to sixty milligrams daily. Higher doses, sometimes up to eighty milligrams daily, for vision-threatening symptoms. The high initial dose suppresses inflammation rapidly. Inflammation decreases within days. Vision-threatening symptoms resolve quickly. Headache improves. Jaw claudication resolves. Vision loss prevented in most cases. Once vision loss occurs, treatment does not restore it. This emphasizes the critical importance of early treatment before vision loss. The initial high-dose corticosteroid phase lasts weeks. Then gradual tapering over months to years. The tapering schedule depends on inflammatory marker response. ESR and CRP guide tapering. If inflammatory markers increase during tapering, the taper is slowed. If markers remain normal, taper continues. Typical tapering takes six months to one year or longer. Some patients require prolonged therapy. Long-term low-dose corticosteroids may be necessary. Side effects from prolonged corticosteroid therapy. Osteoporosis. Infection risk. Diabetes. Hypertension. Weight gain. Mood changes. Eye problems. These side effects require management. Bone-protective therapy. Calcium and vitamin D. Bisphosphonates. Weight-bearing exercise. Infection monitoring. Diabetes screening. Blood pressure monitoring. Eye monitoring. Methotrexate may reduce corticosteroid requirement. Immunosuppressive agent. Allows lower corticosteroid doses. Reduces long-term corticosteroid side effects. Benefits not universal. Some benefit. Others do not tolerate methotrexate. Methotrexate toxicity monitoring necessary. IL-6 inhibitors are newer therapy. Tocilizumab blocks interleukin-6. FDA approved for GCA. May allow corticosteroid dose reduction. Alternative for patients with high steroid intolerance. Shows promise for disease control. TNF inhibitors less effective than TNF inhibitors used for other vasculitis. Some benefit reported. Not first-line therapy. Aspirin is often used. Low-dose aspirin. May reduce stroke and vision loss risk. Prevents thrombosis. Commonly used alongside corticosteroids. Antiplatelet effect helps prevent arterial occlusion. Temporal artery biopsy confirms diagnosis. Biopsy should not delay treatment. Immediate treatment initiated on clinical suspicion. Biopsy obtained later. Ophthalmology evaluation urgent if vision symptoms. Emergency evaluation and treatment. Prevent vision loss. Hospitalization often needed. IV corticosteroids for severe disease. IV methylprednisolone for rapid inflammation suppression. Hospitalization allows monitoring. IV therapy for vision-threatening disease. Aortic imaging if aortitis suspected. CT or MRI of aorta. Assess aortic involvement. Monitor for aneurysm. Regular aortic monitoring in GCA patients. Anticoagulation may be considered. Risk of thrombosis high. Anticoagulation in addition to antiplatelet therapy. Reduces stroke and vision loss risk. Not routine but considered in high-risk cases. With appropriate high-dose corticosteroid therapy, most GCA patients avoid vision loss. Treatment is urgent and lifesaving. Early diagnosis and immediate treatment prevent catastrophic complications.
Living with Giant Cell Arteritis
Living with Giant Cell Arteritis requires urgent treatment, ongoing medical management, careful monitoring for complications, and psychological adjustment to a serious disease threatening vision. For people newly diagnosed with GCA, the diagnosis brings both fear and relief. Fear of vision loss. Fear of blindness. Anxiety about complications. However, relief that the cause of severe headache is known. Effective treatment exists. Treatment can prevent vision loss. Patient education about GCA is critical. Understanding that GCA is a medical emergency. Understanding that treatment must begin immediately. Understanding that vision loss is irreversible but preventable. Understanding that prompt treatment saves vision. Medication compliance is absolutely essential. Taking high-dose corticosteroids as prescribed. Never skipping doses. Never reducing dose without physician guidance. Compliance is literally lifesaving for vision. Gradual corticosteroid tapering under physician supervision. Slow tapering prevents flare. Too-rapid tapering causes disease reactivation. Individual variation in tapering tolerance. Shared decision-making on tapering schedule. Some taper successfully. Others experience flares. Reinitiation of higher dose. Re-tapering more slowly. Vision monitoring is essential. Regular ophthalmology follow-up. Visual acuity checks. Visual field testing. Ocular imaging. Early detection of vision changes allows prompt treatment. However, sudden vision loss is medical emergency. Seek immediate emergency care for sudden vision loss. Temporal artery monitoring. Palpation of temporal arteries. Assessing for recurrence of tenderness. Palpable pulseless arteries. Change in temporal artery status prompts evaluation. Inflammatory marker monitoring. Regular ESR and CRP testing. Guides treatment and tapering decisions. Elevation prompts taper slowing or dose increase. Aortic monitoring if aortitis. Regular aortic imaging. CT or MRI of aorta. Monitors for aortic aneurysm development. Detects progressive aortic disease. Aortic aneurysm surveillance critical. Bone health monitoring. DEXA scans assess bone density. Corticosteroids cause rapid bone loss. Bone-protective therapy essential. Calcium and vitamin D supplementation. Bisphosphonates for significant bone loss. Weight-bearing exercise. Adequate protein intake. Monitoring for infections. Corticosteroids increase infection risk. Early recognition and treatment of infections. Fever monitoring. Infection screening. Blood culture if fever. Antibiotic therapy as needed. Cardiovascular risk management. Blood pressure monitoring. Lipid monitoring. Diabetes screening. Exercise within tolerance. Heart-healthy diet. Aspirin therapy. Stroke prevention important. Mental health support. Anxiety about vision loss. Fear of blindness. Depression from serious disease. Counseling helps. Support groups help. Antidepressants may help. Coping with uncertainty. The disease activity fluctuates. Inflammatory markers guide treatment. But individual symptoms variable. Uncertainty about whether vision loss will occur despite treatment. Most avoid vision loss with appropriate treatment. However, psychological toll of knowing vision loss is possible. Support groups connecting people with GCA. Share experiences. Learn coping strategies. Reduce isolation. Activity management. Most people with GCA can maintain relatively normal activity. Appropriate exercise within tolerance. Regular activity maintained. However, during acute flares, activity limitations may be necessary. Rest when needed. Gradual return to activity as disease controlled. Work and retirement. Most with appropriate treatment can continue working. Some may need modified duties or flexible schedules. Some may retire due to disease severity. Disability support available. Social support from family and friends. Family understanding of GCA. Explanation of vision loss risk. Support with activity limitations. Emotional support. Recognizing early vision warning signs. Amaurosis fugax is warning sign. Sudden vision loss warrants emergency evaluation. Seek emergency care immediately. Do not wait. Vision is too precious to delay treatment. With appropriate urgent high-dose corticosteroid therapy, careful monitoring for vision loss, gradual tapering of medications, bone and cardiovascular risk management, mental health support, family and social support, and vigilant monitoring for complications, most people with Giant Cell Arteritis prevent blindness and maintain good quality of life despite the serious nature of this vision-threatening disease.
Frequently Asked Questions About Giant Cell Arteritis
FAQ 1: Is Giant Cell Arteritis the same as Polymyalgia Rheumatica? No, Giant Cell Arteritis and Polymyalgia Rheumatica are different diseases. However, they are related. About fifty percent of GCA patients have PMR symptoms. About fifteen percent of PMR patients develop GCA. Both occur in similar age groups. Both respond to corticosteroids. However, GCA is vision-threatening. PMR is not. GCA affects arteries. PMR affects muscles and soft tissues. Distinguishing them is important for treatment decisions. Vigilant monitoring for GCA in PMR patients. GCA is much more serious due to vision loss risk.
FAQ 2: Can vision loss from Giant Cell Arteritis be reversed? No, vision loss from Giant Cell Arteritis cannot be reversed. Retinal cell death from ischemia is permanent. Optic nerve cell death is permanent. Dead cells cannot be regenerated. Once vision is lost, it is gone forever. This makes prevention of vision loss critical. Early diagnosis and immediate treatment prevent vision loss in most cases. If vision loss occurs, treatment cannot restore vision. This is why GCA is a medical emergency.
FAQ 3: How quickly must Giant Cell Arteritis be treated? Giant Cell Arteritis must be treated as a medical emergency. If vision-threatening symptoms present, treatment begins immediately. Do not delay for biopsy. Treatment is lifesaving for vision. If vision loss already occurred, treatment does not restore vision. However, further vision loss in the other eye is prevented. Treatment can be started within hours of symptom recognition. Earlier treatment better. Rapid biopsy after treatment started. However, treatment is urgent. Do not delay.
FAQ 4: What is the risk of vision loss in Giant Cell Arteritis? Without treatment, approximately fifty percent of GCA patients develop vision loss. Vision loss is catastrophic. Permanent blindness in one or both eyes. However, with appropriate treatment, vision loss is prevented in most cases. If treated before vision loss, prognosis for vision excellent. If amaurosis fugax occurs, urgent treatment started. Permanent vision loss usually prevented. The key is early recognition and immediate treatment.
FAQ 5: Can Giant Cell Arteritis affect the other eye if vision is lost in one eye? Yes, GCA can affect both eyes. If retinal artery occlusion occurs in one eye, the other eye is at risk. Immediate treatment prevents vision loss in the other eye. Aggressive treatment with high-dose corticosteroids suppresses inflammation throughout the body. Both eyes protected. However, once one eye is blind, preventing blindness in the other eye is crucial. Urgent treatment is essential if vision loss occurs in one eye.
References and Further Reading
For more information about Giant Cell Arteritis, you can visit several trusted and authoritative sources providing detailed information for patients and families dealing with this serious vision-threatening disease. The World Health Organization at WHO.int provides comprehensive information about Giant Cell Arteritis and vasculitic diseases. The American College of Rheumatology at Rheumatology.org provides patient education, clinical resources, and guidelines for Giant Cell Arteritis. The National Institute of Arthritis and Musculoskeletal and Skin Diseases at NIAMS.NIH.gov offers patient education and research information about GCA. The American Academy of Ophthalmology at AAO.org provides information about vision-threatening aspects of GCA and eye disease. MedlinePlus, a service of the National Library of Medicine at MedlinePlus.gov, has detailed medical information about Giant Cell Arteritis written in language that patients and families can easily understand without specialized medical knowledge. The five main reference links are: 1) WHO.int – Giant Cell Arteritis, 2) American College of Rheumatology, 3) NIAMS – National Institute of Arthritis, 4) American Academy of Ophthalmology, and 5) MedlinePlus – Giant Cell Arteritis.
Disclaimer
This article adapts publicly available information from WHO’s Giant Cell Arteritis and vasculitic disease information pages. This content is for informational and educational purposes only and does not constitute medical advice. ObserverVoice.com is a news and information platform — not a healthcare provider. If you or someone you know is an older adult showing signs of Giant Cell Arteritis including new onset severe headache, temporal artery tenderness, jaw claudication, vision loss including amaurosis fugax, scalp tenderness, fever, weight loss, or other symptoms, please seek immediate emergency medical evaluation with qualified healthcare professionals, ophthalmologists, and rheumatologists for urgent diagnostic evaluation and immediate treatment initiation with high-dose corticosteroids if GCA suspected. Vision loss from GCA is irreversible and is a medical emergency. Early diagnosis and immediate treatment prevent permanent blindness. For more information, visit WHO.int and ObserverVoice.com.
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