Temporal Arteritis (Giant Cell Arteritis)

 

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Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Kiersten Young, Savannah Lane, Lucinda hampton, Elaine Lonnemann, 127.0.0.1, WikiSysop, Kim Jackson and Sehriban Ozmen  

Definition/Description

Giant cell arteritis (GCA), also known as temporal arteritis or granulomatous arteritis, is a systemic inflammatory vasculitis that affects medium-sized to large arteries . The primary arteries involved are the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery . GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes . GCA and PMR usually occur together in the same patient .

Prevalence

GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50. 95% of cases occur in patients older than 55 years. Women are 2-6 times more likely to be affected than men. Giant cell arteritis occurs in 25% of all cases of polymyalgia rheumatica (PR). GCA is more frequent among people of Scandinavian and Northern European descent.

Characteristics/Clinical Presentation

Headaches/ generalized head pain, decreased visual acuity, diplopia, decreased color vision, visual field defect, aching/ stiffness of joints, conjunctival hyperanemia, cough, corneal oedema, iritis, Cranial symptoms such as jaw claudication, temporal artery tenderness, amaurosis fugax, decreased temporal pulse, and scalp pain present in the majority of cases.

Associated Co-morbidities

• Polymyalgia Rheumatica (PMR)
• Visual Disturbances
• Facial pain
• Osteoporosis
• Hypokalemia
• Various infections such as oral/esophageal thrush
• Herpes Zoster
  
  

Medications

High dose corticosteroids (4).

Diagnostic Tests/Lab Tests/Lab Values

Gold standard is a temporal artery biopsy (4).

Increased ESR (erythrocyte sedimentation rate) >50 mm/h is one of the five American College of Rheumatology criteria for the diagnosis of GCA. 4
CRP C-reactive protein is said to be increased in patients with GCA. It has been reported that CRP has a 100% sensitivity and when CRP is elevated in combination with ESR there is a 97% specificity (4).
Thrombocytosis also serves as an important diagnostic tool for GCA. It has been shown that an elevated platelet may have a higher positive predictive value than ESR. In the setting of clinical suspicion and a raised ESR, thrombocytosis has a relatively high specificity for distinguishing GCA from other diseases (4).
Plasma fibrinogen 
Newer diagnostic modalities, including ultrasound, magnetic resonance imaging, and positron emission tomography can play an important role in directing treatment in cases with negative TAB 
 

Etiology/Causes

It has been postulated that the basis for the disease lies within abnormalities of the arterial elasticum, with disintegration of the inner elastic membrane of affected arteries, resulting in a giant cell reaction in proximity to this elasticum.

An alternative theory is that the initial lesion is a degeneration of the muscular layers of the artery’s tunica media caused by ischemia, which leads to fragmentation of the elasticum with formation of giant cells occurring secondarily.

Systemic Involvement

Less common symptoms affecting only about eight percent of those with the condition include: pleural effusion, coronary vasculitis, pericarditis, myocarditis, peripheral neuropathy, hearing loss, renal arteritis, lymph node hyperplasia, and abnormal liver function, mesenteric ischemia, sore throat, choking sensation.

Constitutional symptoms may include weight loss, malaise, fever, depression,polymyalgia rheumatica, and night sweats

Medical Management (current best evidence)

Initial steps:

Prednisone 40 mg to 60 mg daily;
intravenous methylprednisolone
500 mg – 1 g × 3 days if visual
compromise or neurologic symptoms.
Treatment should not be withheld
pending TAB results.

Next Steps:

Gradually taper of prednisone by 10 mg
every 2 weeks to 20 mg, then 2.5 mg
every 2 weeks to 10 mg, then 1 mg
every month

Physical Therapy Management (current best evidence)

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Differential Diagnosis

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Case Reports/ Case Studies

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Recent Related Research (from Pubmed)

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References

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1. Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268

2. Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.

3. Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.

5. Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.

6. Petri H, Nevitt A, Sarsour K, Napalkov P, Collinson N. Incidence of Giant Cell Arteritis and Characteristics of Patients: Data-Driven Analysis of Comorbidities. Arthritis Care & Research. 2015;67(3):390-395.