Reducing Prenazone and Feeling Stifness Again
CMAJ. 2001 Jan 23; 164(2): 223–227.
Clinical nuts
Rheumatology: 11. Evaluation of the patient with pain all over
Series Editor: Dr. John Chiliad. Esdaile
The instance
Over the last calendar month, Mrs. S, an 80-yr-erstwhile woman with a history of generalized osteoarthritis and osteoporotic fractures, has been experiencing increased pain and stiffness in her hands, wrists, upper arms, shoulders and calves and has had transient swelling at the wrists. She is oftentimes roused from sleep by hurting. Morning stiffness lasts 3 hours, and she complains of marked fatigue. She denies having fevers, headache, jaw claudication or scalp tenderness. Investigations have shown mild normocytic anemia, a white blood jail cell count of 3.5 х xnine/50 (polymorphonuclear leukocytes 1.8 х 109/L, lymphocytes 1.iii х x9/L) and a platelet count of 67 х ten9/Fifty. Her erythrocyte sedimentation rate was 75 mm/h. The results of tests for rheumatoid factor and antinuclear antibodies were negative. Her symptoms are non relieved past acetaminophen, and her tolerance of nonsteroidal anti-inflammatory drugs is poor because of breadbasket upset. Her response to prednisone, ten mg/solar day, was prompt and marked but, because the dose could not be reduced below 5 mg/24-hour interval without a flare-upwards of symptoms, she was referred for rheumatologic assessment.
Patients with widespread musculoskeletal pain are ofttimes encountered in clinical practice, just their assessment can exist a formidable challenge because of the broad range of possible diagnoses: rheumatologic, endocrine/metabolic, neurologic, infectious, malignant or psychiatric disorders (Table 1). The most mutual crusade is probably cocky-limited viral infection. A specific diagnosis is necessary before effective treatment tin can exist recommended.
Table 1
In well-nigh cases, a differential diagnosis can be established by clinical assessment (history and physical test) and a few simple investigations (Tabular array 2). The latter are recommended when symptoms are severe or have lasted longer than 1 or two weeks. Nearly patients volition not require every test listed in Tabular array ii; for example, younger patients with symptoms of fibromyalgia volition probably need simply the first 5. Extensive investigations should be reserved for situations when the clinical diagnosis is unclear.
Table 2
Rheumatologic causes of widespread pain
Fibromyalgia
Fibromyalgia affects up to 2% of the population and can showtime at whatsoever age; information technology is at least 7 times more common in women than in men.1 Past the time the diagnosis is made, patients have frequently had symptoms for many years. Patients with fibromyalgia complain of pain all over and, by definition, accept pain on both sides of the body, above and below the waist, and in both the trunk and extremities.2
Patients describe the hurting in many dissimilar ways, frequently very emotionally. Muscular stiffness is a prominent complaint. Associated features include nonrestorative sleep, irritable bowel syndrome, headaches, paresthesias and a sensation of swelling of the hands and anxiety. Fibromyalgia is frequently associated with depression, retention and concentration difficulties, and anxiety, and it ofttimes accompanies other chronic painful disorders.
A diagnosis of fibromyalgia is made when there is widespread hurting lasting for at least 3 months accompanied by tenderness at detached locations (Fig. 1). Tender points are palpated with the thumb, using sufficient force to cause blanching of the nailbed. To exist eligible for enquiry studies, patients must have at least 11 tender points of a possible 18 only, in exercise, the diagnosis can exist fabricated in patients with fewer tender points if there is widespread hurting and many of the other characteristic symptoms.3 Patients with fibromyalgia are oftentimes tender all over; the presence of tenderness other than at the classic locations does non exclude the diagnosis.
Fig. 1: Tender points in fibromyalgia are found at the following bilateral locations: suboccipital muscle insertion points; anterior aspects of the intertransverse spaces at C5–7; midpoint of the upper border of the trapezius; origin of the supraspinatus; second costochondral junction, superolateral aspect; lateral epicondyle, 2 cm distal; buttock, upper outer quadrant; greater trochanter, posterior attribute; medial fat pad of the knee. Reproduced with permission of Arthritis Rheum 1990;33:169,2 Lippincott Williams & Wilkins.
A diagnosis of fibromyalgia does non preclude the need to investigate the presence of other weather condition. The physician should make this diagnosis with reluctance in an older patient without a long history of musculoskeletal symptoms. The cause of fibromyalgia is unknown, and its relation to preceding trauma, such as motor vehicle accidents, is controversial.3 Some recent reports4 , 5 suggest an association with prior physical or sexual corruption.
Current approaches to handling are ofttimes unsatisfactory (Table 3). When fibromyalgia is associated with another rheumatic disorder, handling for the second disorder typically does not improve the fibromyalgia. Many patients tin can be helped by encouragement and reassurance, regular aerobic exercise and improvement of sleep. Notwithstanding, patients with fibromyalgia tend to remain symptomatic at unchanged levels for many years. Nearly, if non all, should be encouraged to continue working and to maintain regular social activities despite their symptoms. Whether inability benefits should exist granted for a diagnosis of fibromyalgia is an unresolved issue.3
Table 3
Myopathies
Idiopathic inflammatory myopathies, such as dermatomyositis and polymyositis, typically crusade proximal muscle weakness rather than pain, although pain is sometimes prominent, particularly if there is associated joint inflammation. A careful history and test will usually let the practitioner to distinguish between true muscle weakness and weakness due to hurting. Muscle pain may be significant in myopathies secondary to toxins or drugs such as cholesterol-lowering agents or colchicine. Hypothyroidism sometimes presents as a myopathy, with proximal muscle weakness and an elevated creatine phosphokinase level, or every bit generalized myalgia with normal muscle enzymes.
Connective tissue diseases and rheumatoid arthritis
These atmospheric condition are discussed more fully in a previously published commodity in this series by Alice Klinkhoff.6 In the elderly, rheumatoid arthritis may start with typical polymyalgia rheumatica symptoms (come across later on). Symmetrical synovial swelling may so appear weeks or months later on.
Polymyalgia rheumatica
Polymyalgia rheumatica (PMR) is an idiopathic disorder affecting people over the historic period of 50 years. It is characterized by the presence of inflammation in joints7 and other synovial structures.8 Patients with PMR have widespread pain and stiffness (every bit was the example for Mrs. S), which is near severe at the limb girdles, neck and low back. Constitutional symptoms such as fatigue, malaise, fevers and weight loss are often prominent and may occasionally obscure the musculoskeletal complaints. Fatigue and angst may atomic number 82 to a diagnosis of depression. Physical findings include hurting at the extremes of motion of the shoulders, hips and knees; some patients cannot heighten their artillery over their head considering of the pain. At that place may be synovial swelling or effusions at fingers, wrists and knees and, occasionally, pitting edema of the hands or feet.
Laboratory tests will reveal normocytic anemia, an elevated platelet count, an erythrocyte sedimentation rate (ESR) of over twoscore mm/h, an elevated level of α2 globulins and elevated liver enzymes in up to i-tertiary of patients. Results volition exist negative for rheumatoid factor and antinuclear antibodies (Tabular array 4). Although most patients will accept a markedly elevated ESR, depending on the duration of symptoms, in a recent retrospective study,9 22% of patients had a pretreatment ESR of 30 mm/h or lower.
Table 4
Giant jail cell arteritis
Giant cell arteritis (GCA) is a vasculitis of medium and big vessels that typically involves arteries of the caput and neck, although its distribution may exist more full general.10 GCA and PMR are related disorders that may develop together, or ane may precede the other.11 In addition to the constitutional symptoms associated with PMR, symptoms of GCA include headache, swelling of the temporal artery, scalp tenderness, jaw claudication, natural language or throat pain and visual disturbances.
Physical findings are variable for this condition. The medico should examine the patient for thickening, nodularity or tenderness of the temporal arteries12 and scotomata (areas of lost or reduced vision within the visual field), should listen for bruits at the temporal and occipital arteries, and should inquire near pain associated with brushing hair, difficulty in chewing meat and pain when swallowing.
When this diagnosis is suspected, the patient should be started on high doses of corticosteroids (i mg/kg per day) immediately because of the gamble of sudden blindness associated with untreated GCA.13 Controversy exists about whether a biopsy is needed in all patients with suspected GCA.11 , 14 In my do, patients with typical symptoms and findings, an elevated ESR and a prompt response to high doses of corticosteroids are non subjected to biopsy. A biopsy is carried out for all other patients with suspected GCA. It is sometimes necessary to do bilateral temporal avenue biopsies to prove the diagnosis. A temporal artery biopsy tin can be performed inside 7–14 days of starting treatment without compromising the histopathologic findings.15
Management of polymyalgia rheumatica and giant cell arteritis
Occasionally, a patient with balmy symptoms of PMR may be successfully treated with nonsteroidal anti-inflammatory drugs (NSAIDs). However, a patient's rapid, substantial response to low doses of corticosteroids (10–20 mg/day) is included in some sets of criteria for the diagnosis of PMR (Table 4). Patients with PMR often describe their response to corticosteroids equally "magic" or "miraculous."
A usual course of therapy for PMR begins with prednisone, v mg, twice daily. If the response is insufficient afterward two or 3 days, the dose is increased to 10 mg twice daily. Almost all patients reply to prednisone, 5 mg, twice a day, or their dose can exist tapered off to this level inside a month or then.16 Patients with PMR usually require treatment with corticosteroids for extended periods, often for at least 18 months. For example, they may be maintained on a stable dose of prednisone for several months, before the dose is gradually reduced by 1 mg every month or two, depending on changes in symptoms and ESR. Attempts to reduce prednisone doses more quickly may lead to a flare-up of symptoms, if the diagnosis is correct; thus, it is best to taper it off at a rate that will take patients off the drug in no less than 1 year. Alternate-mean solar day corticosteroids are usually poorly tolerated, and symptoms increase on the "off" day.
In many patients, tapering off prednisone is hard or impossible, and rheumatologic consultation may exist helpful. Sometimes the use of NSAIDs will facilitate tapering off the steroid, merely the combination of prednisone and NSAIDs is associated with an increased gamble of gastrointestinal toxicity. Use of rubber misoprostol or proton pump inhibitors should be considered. The efficacy of steroid-sparing agents such as methotrexate and hydroxychloroquine has non been well established.
The handling of GCA commonly requires higher initial doses of prednisone, unremarkably twoscore–60 mg daily in divided doses, to reduce the risk of sudden blindness.xiii A response is by and large obtained within a few days when patients are treated with prednisone, 25 mg, twice daily (or 20 mg twice daily for fragile elderly patients or patients with multiple medical problems). If symptoms are not controlled, the daily prednisone dose is increased by ten–25 mg. The starting dose is maintained for 4–6 weeks so, if symptoms are controlled and the ESR has fallen, tapering off is started.
Schedules for tapering off corticosteroids are empirical, but, in general, rapid or large dose reductions should be avoided. The post-obit schedule has proven effective; each number represents the total daily prednisone dose expressed in milligrams and is given for a month: 50, xl, xxx, 25, xx, fifteen, 10, 7.5, 5, two.5. Thereafter, the patient takes 2.5 mg every other day for a month, then ii.5 mg every third day for a month, and and so the drug is discontinued. In this schedule, prednisone is taken in one case daily later the first 3–4 months. Some practitioners similar to convert patients to an alternate-mean solar day regimen, but this alter should not be made until disease symptoms are well controlled and the ESR is stable.
As with PMR, patient symptoms and changes in the ESR are used to guide tapering off. The ESR commonly rises gradually as the prednisone dose is reduced. A sudden rise in the ESR should prompt an evaluation for the recurrence of disease signs and symptoms, too as for alternative causes, such every bit infection. An asymptomatic rise in the ESR is not an indication for increasing the dose of corticosteroid, just may necessitate delaying farther dose reductions. Articulate evidence of disease flare-ups should prompt an increase in the prednisone dose by well-nigh 50% or sufficient to suppress symptoms and reduce the ESR. Corticosteroid treatment is usually continued for at least 1 year. Steroid-sparing agents such as azathioprine or methotrexate are occasionally helpful in patients who are unable to tolerate reductions in prednisone.
The prolonged utilise of corticosteroids is typically associated with multiple side effects, including weight proceeds, hypertension and glaucoma. Osteoporosis is a detail problem in the elderly, predominantly female population affected by PMR and GCA. (Its management is discussed in an upcoming commodity in this series by John P. Wade.) Effective interventions for the prevention of corticosteroid-induced osteoporosis are available and should exist initiated at the onset of corticosteroid handling.17 , 18 , 19
Handling for Mrs. Southward
At the fourth dimension of the initial rheumatologic cess, 4 months after the onset of symptoms, the results of the physical examination were notable only for osteoarthritic changes in Mrs. S's fingers and knees. The differential diagnosis was believed to include PMR, rheumatoid arthritis and systemic lupus erythematosus (SLE). On further investigation, the patient'due south consummate blood count and ESR were plant to be normal. Specific serology for SLE (levels of complement, anti-DNA antibodies and antibodies to extractable nuclear antigens) was negative. Mrs. Southward was started on vitamin D, calcium and cyclic etidronate for osteoporosis, and slow tapering off the dose of prednisone was begun.
Four months afterward, when this dose was 2 mg daily, the patient visited her medico complaining of scalp hurting and tenderness, swollen scalp "veins" and pain in her throat, cervix and clavicles. Physical examination revealed marked thickening and tenderness of the temporal arteries. The ESR was 55 mm/h. A temporal artery biopsy showed changes attributable to GCA. The prednisone dose was increased to 20 mg twice daily, resulting in prompt resolution of all symptoms. It has since been tapered off over the concluding year to 2.5 mg daily. The course of Mrs. Southward's handling has been complicated by an episode of herpes zoster, but she has remained gratuitous of farther osteoporotic fractures and the temporal arteritis has been well controlled. The cytopenias accept non recurred and remain unexplained.
Footnotes
This series has been reviewed and endorsed by the Canadian Rheumatology Association.
The Arthritis Order salutes CMAJ for its extensive series of manufactures on arthritis. The Society believes that this kind of information is crucial to educating physicians most this devastating disease.
This commodity has been peer reviewed.
Acknowledgements: The writer thanks Drs. John Esdaile, Andrew Chalmers and Howard B. Stein for their helpful suggestions for this newspaper and thanks Jennifer Lewis for manuscript preparation.
Competing interests: None alleged.
Reprint requests to: Dr. Michael P.E. Puttick, 1875 Abbott St., Kelowna BC V1Y 1B6; gro.rhso@mtup
References
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Articles from CMAJ : Canadian Medical Clan Journal are provided here courtesy of Canadian Medical Clan
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC80687/
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