Imj225.dalbeth.fm

Internal Medicine Journal 2002; 32: 315–319 Audit of the management of suspected giant cell arteritis in a large teaching hospital N. DALBETH,1 N. LYNCH,1 L. McLEAN,2 F. McQUEEN1,2 and J. ZWI1 1Auckland Healthcare and 2Department of Molecular Medicine, University of Auckland, Auckland, New Zealand Abstract
Results: The mean waiting time for biopsy for all Background: The diagnosis of giant cell arteritis patients was 5.6 days (range 0–42 days). This time (GCA) is often confirmed by an early temporal artery varied from 9.3 days for rheumatology patients to (TA) biopsy of adequate length. Treatment of this days for ophthalmology patients (P = 0.003).
condition with high-dose corticosteroids may be asso- Only 44/117 (37.6%) specimens measured more than ciated with significant morbidity, including osteo- 10 mm. For GCA patients, the median initial oral prednisone dose was 60 mg/day. Osteoporosis proph-ylaxis was prescribed in 24/37 (65%) GCA patients, Aim: To audit current management of patients with suspected GCA at Auckland Healthcare, a largeteaching hospital.
Conclusions: There is significant variation in the man-agement of GCA within our institution. This audit Methods: We performed a retrospective chart review has highlighted several areas where improvement of all TA biopsies from January 1996 to June 2000. A could be made, particularly in streamlining the total of 117 biopsies from 111 patients was audited.
process of obtaining TA biopsy and in promoting the Of these patients, 37/111 (33%) had a final clinical use of osteoporosis prophylaxis. (Intern Med J 2002; diagnosis of GCA (GCA patients). The areas of inter- est for audit were waiting time for TA biopsy, lengthof sample, initial corticosteroid therapy and osteo- Key words: audit, corticosteroids, giant cell arteritis,
osteoporosis, temporal artery biopsy.
temporal arteries. Although clinical findings areintegral to the diagnosis of GCA, temporal artery Giant cell arteritis (GCA) is a common form of vas- (TA) biopsy remains an important confirmatory test.2 culitis affecting elderly patients. Clinical features Typical histological findings of active GCA include include arteritic symptoms such as headache, scalp transmural inflammation, disruption of the internal tenderness, jaw claudication and visual disturbance, elastic lamina, intimal fibrosis and oedema, and giant and systemic symptoms including malaise, weight loss cells.3 The risk of false-negative biopsy owing to ‘skip and fatigue. Symptoms of polymyalgia rheumatica lesions’ is well recognized.4 Management with high- (PMR) may occur concurrently.1 Clinical examina- dose corticosteroids reduces complications of disease, tion may demonstrate tender, thickened or pulseless particularly loss of vision.5 However, side-effectsrelated to therapy can be significant.6 Although thereis controversy about some aspects of GCA manage-ment, good clinical practice includes a waiting time Correspondence: Nicola Dalbeth, MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, for biopsy of less than 2 weeks, specimen length of Oxford OX3 9DU, UK. Email: nicola.dalbeth@imm.ox.ac.uk more than 10 mm and osteoporosis prophylaxis for all Received 14 May 2001; accepted 9 November 2001. This retrospective study audited the management of five had findings consistent with healed GCA, and suspected GCA at a large teaching hospital facility. In seven had ‘age-related changes’ or normal biopsies.
particular, we assessed the waiting times for biopsy, The seven patients with negative biopsies had other- length of biopsy specimen, initial corticosteroid dose wise typical clinical features of GCA.
and use of routine osteoporosis prophylaxis.
Of the 11 patients with TA biopsies reported as consistent with healed GCA, only five patients wereconsidered by the clinical team as having a final diag- We audited all TA biopsies taken at Auckland nosis of GCA. The remaining six patients were Healthcare (Auckland Hospital and Greenlane treated for conditions other than GCA (including Hospital) over a 4.5-year period between January polymyalgia rheumatica alone, non-specific poly- 1996 and June 2000. This institution is a 1036-bed arthritis, atherosclerotic stroke, cluster headache, teaching hospital associated with the University of migraine and chronic pain syndrome).
Auckland, and has a population catchment of386 000 people. The biopsies were identified from a computerized database in the Department ofPathology, and confirmed by cross-referencing data- Patients with a final diagnosis of GCA had a mean age bases in the Departments of Rheumatology and of 73.2 years (range 54–89 years). The majority of General Surgery. A retrospective patient chart review these patients were female (70%) and 95% were of was performed for each procedure. Results were European descent (the remaining 5% was of Samoan analysed using Student t-tests and contingency tables descent). There were only 7/37 (19%) patients who on Prism 3.0 (Graph Pad, San Diego, CA, USA).
had symptoms for less than 1 week before presenta-tion. The most common symptoms were headache During this time, 122 biopsies were taken from 116 (89%) and visual disturbance (64%). Associated patients (mean 27 biopsies/year). Bilateral biopsies PMR symptoms (either at the time of diagnosis or were performed in six patients (three sequential and previously) were reported in 63%, and symptoms of three simultaneous). Medical records were not avail- jaw claudication occurred in 43%. The mean erythro- able for five patients, so that a total of 117 biopsies cyte sedimentation rate (ESR) for this group was (114 episodes) in 111 patients was audited.
77.3 mm/h (range 19–133 mm/h). There were 3/37(8.1%) GCA patients with ESR less than 30 mm/h.
A number of different specialties requested TA biop- Information regarding waiting time was available for sies, most commonly Rheumatology and Ophthal- 104/114 procedures. There were 11/104 (10.6%) mology. There were 82/114 (71.9%) procedures done patients who waited for 2 weeks or more for biopsy.
by the General Surgery service, 30/114 (26.3%) by The mean waiting time for TA biopsy was 5.6 days.
the Ophthalmology service, and 2/114 (1.8%) by the Rheumatology patients had a mean waiting time of Neurosurgery service. Most of the biopsies requested 9.3 days (range 0–42 days). This compares with a by Rheumatology and other medical services were mean waiting time of 2.6 days (range 0–9 days) for taken by the General Surgical service, while all biopsies requested by Ophthalmology were taken by 0–23 days) for General Medical patients (P = 0.003 for Ophthalmology vs Rheumatology). (Fig. 1) Of the TA biopsies taken, histopathologists reported Waiting times also varied depending on the surgical 25/117 (21.4%) as being consistent with active GCA, service performing the TA biopsy, with a mean time 11/117 (9.4%) as being consistent with healed GCA, of 2.9 days (range 0–10 days) for Ophthalmology and 81/117 (69.2%) as normal or ‘age-related changes’ (including arteriosclerosis).
There were 37/111 (33%) patients termed ‘GCA Mean waiting times for biopsy varied from 2.8 days patients’ for the purposes of this analysis. This group for those with positive biopsy results, 6.4 days for was defined as having a clinical diagnosis of GCA and those with negative biopsy results, and 12.36 days for was treated long term for this condition. Of these 37 those with healed GCA on biopsy (P = 0.03, positive patients, 25 had active GCA reported on TA biopsy, Internal Medicine Journal 2002; 32: 315–319 Management of giant cell arteritis Waiting time for temporal artery biopsy for referring specialties. P = 0.003, Ophthalmology vs Osteoporosis prophylaxis use depending on treating specialty. Other physicians include General Physicians, Neurologists and Geriatricians. P = 0.023, Ophthalmology vs Rheumatology. GCA, giant cell arteritis.
We assessed the length of TA biopsy measured by the Oral prednisone doses were not significantly higher in histopathologist after formalin fixation (which may be GCA patients with visual symptoms compared with associated with some shrinkage). Very few biopsy measurements were recorded in the clinical recordsby the surgical team.
Follow-up information regarding complications ofcorticosteroids was available for 32/37 GCA patients.
Pathology measurements showed that 44/117 There were 10/32 patients (31.2%) who had at least (37.6%) specimens measured more than 10 mm. The one complication that could be attributed to high- median biopsy length was 10 mm. There were 15/117 dose corticosteroids (including newly diagnosed (12.8%) biopsies that measured 5 mm or less, and diabetes mellitus, or worsening diabetic control, only 6/117 (5.1%) biopsies measured more than osteoporotic fractures, proximal myopathy and 20 mm. There was no difference in length between positive and negative TA biopsy samples.
For GCA patients, the use of osteoporosis prophy- Information regarding initial prednisone dosage was laxis (other than calcium supplementation) was also available for 36/37 GCA patients. For these patients, variable, with only 24/37 (65%) receiving osteo- the median initial prednisone dose was 60 mg/day porosis prophylaxis. For patients treated with (range 10–80 mg/day). Only 10/36 (27.8%) patients osteoporosis prophylaxis, 20/24 (83.3%) received were treated with less than 60 mg/day prednisone.
Pulsed intravenous methylprednisolone was used in4/36 (11.1%) GCA patients (two patients treated by The use of osteoporosis prophylaxis other than the Neurology service, two patients treated by the calcium supplementation in GCA patients varied Ophthalmology service, all with new onset of visual depending on treating specialty, with 12/15 (80%) symptoms). One patient was prescribed steroid- Rheumatology-treated patients and 2/8 (25%) sparing medication (methotrexate) during the follow- Ophthalmology-treated patients receiving such therapy (P = 0.023) (Fig. 2).
Initial prednisone doses varied depending on the treating specialty. The mean initial dose for Rheum-atology GCA patients was 50 There is significant variation in some aspects of the initial management of suspected GCA within our large teaching hospital. This study has raised partic- ular issues of interest, including excessive waiting Internal Medicine Journal 2002; 32: 315–319 times for some biopsies, short specimen length and Patients with GCA are at high risk of corticosteroid- inadequate osteoporosis prophylaxis.
induced osteoporosis, due to advanced age and alsoto high prednisone doses administered for long The importance of an early TA biopsy of adequate periods. It has been demonstrated that significant length is generally accepted, although the minimum bone loss occurs in the first year of corticosteroid acceptable length remains controversial. The use12 and that prophylactic bisphosphonates13,14 can presence of the patchy distribution of pathological prevent treatment-related osteoporotic fractures.
lesions has led to a recognition that longer specimens Our study reinforces the need for an education should be taken.4 It has been suggested that it is best programme to promote greater awareness of early to sample an area where clinical disease is suspected, but, failing this, at least 1 cm and preferably 2 cm ofartery should be taken.7 Almost two-thirds of the In summary, this audit has demonstrated shortfalls in biopsies taken from the patients in our study ideal clinical care and the need for a more coordi- measured 1 cm or less, suggesting that we may be nated approach to the management of suspected GCA at Auckland Healthcare. Such variations in themanagement of GCA may well occur in other large The upper limit of acceptable waiting time is also teaching hospitals. Development of evidence-based disputed. An early study8 showed that positive biopsy clinical guidelines and closer liaison between rates fell from 82 to 20% after 1 week of therapy. In subspecialty services are likely to improve the care of this study, the mean biopsy length was short, with a mean of 7 mm (similar to our mean sample length).
More recently, a study from the Mayo clinic9 showed no difference in positive biopsy rates after 2 weeks ofcorticosteroid therapy. However, the mean biopsy The authors would like to thank Professor Charles length in this study was much greater at 36 mm (with McGhee, Department of Ophthalmology, University one biopsy measuring 12.5 cm) and, arguably, this of Auckland, and Dr Peter Gow, Rheumatologist, may have offset the longer waiting time. Our study Middlemore Hospital, Auckland for their useful did not show that specimen length had a significant effect on biopsy results, although the sample size maybe insufficient to detect such a difference. The findingof shorter waiting times in those with positive biop-sies is interesting and may suggest the importance of obtaining early biopsies to avoid false-negativeresults. However, a possible confounding factor may 1 Hazleman B. Polymyalgia rheumatica and giant cell arteritis. have greater perceived urgency for those patients with In: Klippel JH, Dieppe PA (eds). Rheumatology. London: more classical features of disease. The variations in 2 Hall S, Lie JT, Kurland LT et al. The therapeutic impact of waiting time between services at our institution may temporal artery biopsy. Lancet 1983; 2: 1217–20.
in part be explained by the prompt action of the 3 Ashton-Key M, Gallagher PJ. Surgical pathology of cranial Ophthalmology service in taking biopsies on their arteritis and polymyalgia rheumatica. Baillieres Clin 4 Klein RG, Campbell RJ, Hunder GG, Carney JA. Skip lesions in temporal arteritis. Mayo Clin Proc 1976; 51: 504–10.
Generally, higher doses of corticosteroids were used 5 Kyle V. Treatment of polymyalgia rheumatica/giant cell as initial therapy in our group of GCA patients, with arteritis. Baillieres Clin Rheumatol 1991; 5: 485–92.
considerable variation in dosage. A dose of 40 mg/day 6 Kyle V, Hazleman BL. Treatment of polymyalgia rheumatica and giant cell arteritis. II. Relation between steroid dose and quate.10 Higher corticosteroid doses may be indicated steroid associated side effects. Ann Rheum Dis 1989; 48: 662–6.
for patients with visual symptoms. Prescribing differ- 7 Anon. Temporal artery biopsy [editorial]. Lancet 1983; 1: 396.
ences between ophthalmologists and rheumatologists 8 Allison MC, Gallagher PJ. Temporal artery biopsy and are well recognized.11 The high rate of corticosteroid- corticosteroid treatment. Ann Rheum Dis 1984; 43: 416–17.
associated side-effects in our patients is similar to 9 Achbar AA, Lie JT, Hunder GG et al. How does previous previous reported rates for GCA and PMR patients.6 corticosteroid treatment affect the biopsy findings in giant cell (temporal) arteritis? Ann Intern Med 1994; 120: 987–92.
A retrospective chart review such as our study may 10 Kyle V, Hazleman BL. Treatment of polymyalgia rheumatica underestimate the true incidence of therapy-related and giant cell arteritis. I. Steroid regimens in the first two months. Ann Rheum Dis 1989; 48: 658–61.
Internal Medicine Journal 2002; 32: 315–319 Management of giant cell arteritis 11 Swannell AJ. Polymyalgia rheumatica and temporal 13 Adachi JD, Benson WG, Brown J et al. Intermittent etidronate arteritis: diagnosis and management. Br Med J 1997; 314: therapy to prevent corticosteroid-induced osteoporosis. N Engl 12 Reid IR, Heap SW. Determinants of vertebral mineral density 14 Saag KG, Emkey R, Schnitzer TJ et al. Alendronate for the in patients receiving long-term glucocorticoid therapy. Arch prevention and treatment of glucocorticoid-induced osteoporosis. N Engl J Med 1998; 339: 292–9.
Internal Medicine Journal 2002; 32: 315–319

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