Temporal Arteritis (Giant Cell Arteritis): Difference between revisions
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<div class="noeditbox">Welcome to [[Pathophysiology of Complex Patient Problems|PT 635 Pathophysiology of Complex Patient Problems]] This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!</div><div class="editorbox"> | | ||
<div class="noeditbox">Welcome to [[Pathophysiology of Complex Patient Problems|PT 635 Pathophysiology of Complex Patient Problems]] This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!</div><div class="editorbox"> | |||
'''Original Editors '''- [[Pathophysiology of Complex Patient Problems|Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.]] | '''Original Editors '''- [[Pathophysiology of Complex Patient Problems|Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.]] | ||
'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} | '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} | ||
</div> | </div> | ||
== Definition/Description == | == Definition/Description == | ||
Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref> The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery. This condition is known as a condition of the elderly and is a significant cause of secondary headahe in older adults. GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>. GCA and PMR usually occur together in the same patient<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.[[Image: | Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref> The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery. This condition is known as a condition of the elderly and is a significant cause of secondary headahe in older adults. GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>. GCA and PMR usually occur together in the same patient<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.[[Image:Deep temporal arteries.png|left|500x300px]] | ||
[[Image:Deep temporal arteries.png|right|3x5px]] | [[Image:Deep temporal arteries.png|right|3x5px]] | ||
== Prevalence<br> == | == Prevalence<br> == | ||
GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>. 95% of cases occur in patients older than 55 years (2) Women are 2-6 times more likely to be affected than men<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>. Giant cell arteritis occurs in 25% of all cases of polymyalgia rheumatica (PR)<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>. GCA is more frequent among people of Scandinavian and Northern European descent<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.<br><br> | GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>. 95% of cases occur in patients older than 55 years (2) Women are 2-6 times more likely to be affected than men<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>. Giant cell arteritis occurs in 25% of all cases of polymyalgia rheumatica (PR)<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>. GCA is more frequent among people of Scandinavian and Northern European descent<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.<br><br> | ||
== Characteristics/Clinical Presentation == | == 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<ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref><ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref><ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br><br><br> | 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<ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref><ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref><ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br><br><br> | ||
== Associated Co-morbidities == | == Associated Co-morbidities == | ||
| Line 26: | Line 27: | ||
*Hypokalemia | *Hypokalemia | ||
*Various infections such as oral/esophageal thrush | *Various infections such as oral/esophageal thrush | ||
*Herpes Zoster<ref name="data">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</ref><br><br> | *Herpes Zoster<ref name="data">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 &amp; Research. 2015;67(3):390-395</ref><br><br> | ||
== Medications == | == Medications == | ||
High dose corticosteroids<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.<br> | High dose corticosteroids<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>.<br> | ||
== Diagnostic Tests/Lab Tests/Lab Values == | == Diagnostic Tests/Lab Tests/Lab Values == | ||
| Line 42: | Line 43: | ||
*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<ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br> | *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<ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br> | ||
[[Image:Giant cell arteritis -- very low mag.jpg]]<br> | [[Image:Giant cell arteritis -- very low mag.jpg]]<br> | ||
== Etiology/Causes == | == 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. | 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<ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>.<br> | 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<ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>.<br> | ||
== Systemic Involvement == | == 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. | 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, and polymyalgia rheumatica, night sweats<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref><ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br> | Constitutional symptoms may include weight loss, malaise, fever, depression, and polymyalgia rheumatica, night sweats<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref><ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>.<br> | ||
== Medical Management (current best evidence) == | == Medical Management (current best evidence) == | ||
| Line 75: | Line 76: | ||
<br> | <br> | ||
<div><br></div> | <div><br></div> | ||
== Physical Therapy Management (current best evidence) == | == Physical Therapy Management (current best evidence) == | ||
| Line 82: | Line 82: | ||
<br> | <br> | ||
== Differential Diagnosis == | |||
<br> | <br> | ||
== Case Reports/ Case Studies == | == Case Reports/ Case Studies == | ||
| Line 99: | Line 99: | ||
http://pubs.rsna.org/doi/pdf/10.1148/radiol.2272010487 | http://pubs.rsna.org/doi/pdf/10.1148/radiol.2272010487 | ||
<br> | |||
3. De Hertogh W, Vaes P, Versijpt J. Diagnostic work-up of an elderly patient with unilateral head and neck pain. A case report. Manual Therapy. 2013;18(6):598-601. | |||
https://www.researchgate.net/profile/Willem_De_Hertogh/publication/232086111_Diagnostic_work-up_of_an_elderly_patient_with_unilateral_head_and_neck_pain_A_case_report/links/0deec527d1346ac25a000000.pdf | |||
https://www.researchgate.net/profile/Willem_De_Hertogh/publication/232086111_Diagnostic_work-up_of_an_elderly_patient_with_unilateral_head_and_neck_pain_A_case_report/links/0deec527d1346ac25a000000.pdf | |||
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) == | == Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) == | ||
<div class="researchbox"> | <div class="researchbox"> | ||
<rss>http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1TUbR4JfRTvSrbbAM3hVX4olPV5UgCMCMh8k-36-4I7JL0BggL|charset=UTF-8|short|max=10</rss> | <rss>http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1TUbR4JfRTvSrbbAM3hVX4olPV5UgCMCMh8k-36-4I7JL0BggL|charset=UTF-8|short|max=10</rss> | ||
</div> | </div> | ||
== References == | == References == | ||
Revision as of 02:26, 11 April 2016
Welcome to PT 635 Pathophysiology of Complex Patient Problems This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!
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[edit | edit source]
Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.[1] The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery. This condition is known as a condition of the elderly and is a significant cause of secondary headahe in older adults. GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes[2]. GCA and PMR usually occur together in the same patient[1].
Prevalence
[edit | edit source]
GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50[1]. 95% of cases occur in patients older than 55 years (2) Women are 2-6 times more likely to be affected than men[1][3]. Giant cell arteritis occurs in 25% of all cases of polymyalgia rheumatica (PR)[2]. GCA is more frequent among people of Scandinavian and Northern European descent[1].
Characteristics/Clinical Presentation[edit | edit source]
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[3][2][4].
Associated Co-morbidities[edit | edit source]
- Polymyalgia Rheumatica (PMR)
- Visual Disturbances
- Facial pain
- Osteoporosis
- Hypokalemia
- Various infections such as oral/esophageal thrush
- Herpes Zoster[5]
Medications[edit | edit source]
High dose corticosteroids[1].
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
- The gold standard diagnostic test for GCA is a temporal artery biopsy[3].
- Increased ESR (erythrocyte sedimentation rate) >50 mm/h is one of the five American College of Rheumatology criteria for the diagnosis of GCA[3][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[3].
- 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.
- Plasma fibrinogen[3]
- 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[4].
Etiology/Causes[edit | edit source]
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[3].
Systemic Involvement[edit | edit source]
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, and polymyalgia rheumatica, night sweats[1][3][4].
Medical Management (current best evidence)[edit | edit source]
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:
Gradual 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[4]
Physical Therapy Management (current best evidence)[edit | edit source]
Physical Therapists should be aware of associated signs and symptoms and refer patients accordingly. Prompt initiation of treatment may prevent blindness and other ischemic consequences.There are no current physical therapy treatment options for temporal arteritis and best management described in literature involves use of corticosteroids.
Differential Diagnosis[edit | edit source]
Case Reports/ Case Studies[edit | edit source]
1. Colin G, Dupont M. Giant cell arteritis. Journal of the Belgian Society of Radiology. 2013;96(5):290.
http://br.ubiquitypress.com/articles/10.5334/jbr-btr.406/galley/403/download/
2. Lockhart M, Robbin M. Case 58: Giant Cell Arteritis1. Radiology. 2003;227(2):512-515.
http://pubs.rsna.org/doi/pdf/10.1148/radiol.2272010487
3. De Hertogh W, Vaes P, Versijpt J. Diagnostic work-up of an elderly patient with unilateral head and neck pain. A case report. Manual Therapy. 2013;18(6):598-601.
Recent Related Research (from Pubmed)[edit | edit source]
Failed to load RSS feed from http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1TUbR4JfRTvSrbbAM3hVX4olPV5UgCMCMh8k-36-4I7JL0BggL|charset=UTF-8|short|max=10: Error parsing XML for RSS
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268
- ↑ 2.0 2.1 2.2 Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.
- ↑ 4.0 4.1 4.2 4.3 4.4 Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.
- ↑ 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
