Dr, I have pain all over my body!

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1 Dr, I have pain all over my body! Challenges to make the diagnosis in a common elderly complaint Inter-hospital Geriatrics Meeting Speaker: Cheng Jen Ngai Chairperson: Dr. Ip CY Caritas Medical Centre

2 Pain is a common symptom in the elderly 醫生, 我周身唔舒服周身都痛!!

3 Statistics on pain in the elderly 25 50% of community based elders have pain up to 85% of residents in long term care report pain, of which 45 80% is undertreated 20% of the older Americans are taking analgesic medications regularly 63%of those had taken pain medication for more than six months The American Geriatric Society (AGS) Panel on Chronic Pain in Older Persons 2002 Chronic Pain in Cognitively Impaired Elderly: Challenges in Assessment, Diagnosis, and Treatment, By Paula Siciliano

4 Challenges to make the correct diagnosis of pain symptoms Very often, no correct diagnosis could be made, because: We have perception that pain is a normal part of aging and we always assume pain is due to degenerative changes Elderly patient s complaints and history could be nonspecific Pain is a very personal and subjective experience affected by multiple factors, including psychological and social

5 In this presentation A case of an elderly lady who presented with generalized pain No definite diagnosis in the beginning After the diagnosis was made, the patient responded well to the treatment

6 F/ 82 years old Background history Cleansing worker, retired for more than 20 years On CSSA Lived alone Widow, with 2 children, supportive and always visited patient Non smoker, non drinker

7 Pre-morbid functional status Walk with stick Feeding/ Bathing/ Toileting independent Self went out to buy food Personal Emergency Link Service ( 一線通平安鐘服務 ) available at home

8 Past medical history Good past health Sometimes visited GOPD for URTI No regular medications or Chinese medicine taken No known drug allergy

9 Chief complaint Complained pain all over the body since 2/ neck pain 2. low back pain 3. knee pain 4. shoulder pain 5. Headache 6. Hand pain and numbness

10 Nature of the pain Bilateral knee pain after prolonged sitting Neck pain and the LBP, esp at the bilateral para spinal muscle, which increase on movement Bilateral shoulder pain, L>R, which increase on raising the shoulder Headache over bilateral frontal area and vertex, described as shooting pain, each time last for few hours to days Right palm pain and numbness

11 Other symptoms Noticed to have poor appetite Claim subjective weight loss Poor sleep and early morning wakening Deny recent stressful event or depressed mood Deny suicidal idea

12 Other symptoms No hip pain No joint stiffness No muscle weakness complained No rash / joint swelling No history of injury/ trauma

13 Other symptoms No facial pain/ eye pain No visual disturbance No nausea/ vomiting/ photophobia No fever No chest pain/ SOB

14 History of present illness Seek medical advice at GOPD for the headache and generalised pain in 3/2010 Voltaren SR was given, which partially reduces the pain Referred to medical for further management

15 History of present illness Attended medical clinic in 4/2010 Subsequently admitted to the ward on 17/4/2010 for further investigations

16 Physical examinations Afebrile BP:120/55, P:80 GCS:15/15, full orientation Cardiovascular system unremarkable Respiratory system unremarkable Abdominal system unremarkable

17 Physical examinations--cns Tone normal, no tremor Power of upper limbs: 4+/5 (R=L, P=D) Power of lower limbs: 4/5 (R=L, P=D) Reflex normal Sensation grossly normal Gait with stick stable

18 Neck soft Physical examinations : musculoskeletal Paraspinal muscle tenderness Right knee swollen, tender and bony crepitations heard on movement Passive range of movement of shoulder joint and hip joints full No shoulder joint swelling and no sign of subluxations

19 Blood test Hb:11.5, NcNc ALP:84, Cr:74, ca:2.22, PO4:1.06 TSH:1.38 ESR:74, CRP:33

20 Radiological investigations CT brain: No gross intracranial lesion Air fluid level noted at the left maxillary sinus, likely represent sinusitis changes

21 X-ray cervical spine: -Degenerative change with multi-level margical osteophytes formation -The disc spaces and vertebral body heights are preserved

$X-ray shoulder: -No definite fracture nor$ The subacromial space is not narrowed -There is

22 X-ray shoulder: -No definite fracture nor dislocation found. The subacromial space is not narrowed -There is no abnormal calcification seen in the soft tissue. No other specific bony lesion detected

23 X-ray knee: -Normal bone density and alignment. -There are degenerative change of both knees with marginal osteophytes. The bilateral patellofemoral joint spaces are narrowed

24 Problems list 1. Multiple joint pain 2. Headache 3.?mood disturbance 4. CT brain showed features of maxillary sinusitis, with increased inflammatory marker of ESR, CRP 5. X ray shows degenerative changes of the joints

25 Diagnosis 1. Cervical spondylosis 2. Osteoarthritis of knee 3. Maxillary sinusitis 4.?tension headache

26 Management Dologesics was given for pain relief SFI glucosamine started for OA knee Physiotherapist was referred for pain relief

27 Progress Bone pain and the headache partially improved after admission Patient discharged on 19/4/2010 Referred to GDH for pain relief and mobility training Referred to ENT for the sinusitis

28 GDH assessment First visit on 9/6/2010 Still complained of multiple joint pain, at the shoulder, neck and the knee On and off headache, but improving Running nose with clear discharge Physical examination unremarkable except degenerative changes at the knee noticed

29 ?depressive symptoms Express sadness about the pain symptoms Complain decreased appetite and weight loss Loss of interest in daily leisure activates No suicidal idea?? Depression/ adjustment disorder

30 Geriatric depression score: 8/15

31 Assessment by physiotherapist Bed mobility and transfer independent Standing under supervision Squatting failed due to the bilateral knee pain Walk with stick independent at ground floor Walk upstairs with rail and stick under supervision 6m walk : 13seconds

32 Assessment by physiotherapist EMS:16/20 BBS:28/56

33 Assessment by occupational therapist Satisfactory hand function Feeding, hygiene independent Toileting, bathing, dressing standby assistance

34 Assessment by occupational therapist Difficulty in stair climbing BI:81/100

35 Assessment by occupational therapist adapted Lawton IADL:38/56

36 Progress Repeated blood test : All normal, except ESR:69, CRP:82 What is the reason for the increase inflammatory marker??

37 What is the diagnosis??polymyalgia rheumatica (PMR) For: There was shoulder pain, neck pain There was systemic symptoms of decrease appetite, weight loss Inflammatory marker was increased Against: X There was no morning joint stiffness which was typical feature of inflammatory pain X The prominent knee pain was not typical feature of PMR

38 What is the diagnosis??degenerative changes in the multiple joints??polymyalgia rheumatica + Degenerative changes in the joints

39 Progress Patient was referred to rheumatology clinic on 11/8/2010 Diagnosis of polymyalgia rheumatica was made Prednisolone 15mg daily was prescribed

40 Progress of symptoms Patient has significant improvement of pain at the follow up 2 weeks later Appetite improved and there was subjective weight gain Mood also improved, she said she felt much happier

41 Progress of inflammatory markers ESR decreased

42 Progress of inflammatory markers CRP decreased

43 Progress of functional aspects EMS and BBS both improved!!

44 Progress of functional aspects Stair climbing improved BI improved significantly!!

45 Diagnosis The good steroid response also suggests the diagnosis of polymyalgia rheumatica!!

46 Progress In view of good rehabilitation outcome, patient was discharged from GDH on 29/9/2010 Patient now has regular follow up at the rheumatology clinic

47 Polymyalgia rheumatica (PMR) One of the most common: 1. inflammatory rheumatic disease of the elderly 2. indications for long term steroid use in the community Self limiting condition with excellent prognosis if diagnosed promptly Untreated patients often fell unwell and have an impaired quality of life

48 Epidemiology Prevalence increases with increasing age Almost never seen in people under the age of 50 average age of onset is just over 70 The incidence of the disease in patients over 50 is about 100 per % of patients are women Frequency varies by geographical region, highest rates occur in Northern Europe Incidence of PMR is often underestimated Cimmino MA, Zaccaria A. Epidemiology of polymyalgia rheumatica. Clin exp Rheumatol 2000; 18 (4 suppl.20):s9 11

49 Pathogenesis Exact mechanism unknown!! both genetic and environmental factors contribute to disease susceptibility and severity

50 Pathogenesis 1. Environmental factors: particularly infections with Chlamydia, Mycoplasma, parainfluenza virus or parvovirus B19 are believed to be the trigger of the disease 2. Genetic factors: the HLA DRB1 allele is linked to an increased susceptibility and severity of the disease

51 Pathogenesis Genetically predisposed patient Environmental factor, eg: a virus triggers monocyte activation Production of cytokines esp: interleukin 2 and interleukin 6 Induces manifestations of polymyalgia rheumatica

52 Pathogenesis Nonerosive synovitis and tenosynovitis are believed to be responsible for the symtpoms of the disease, and it is found that macrophages and CD4+ T lymphocytes are activated in synovial membranes from the involved joints Evidence of subclinical arterial inflammation can be detected in some patients, with the presence of activated dendritic cells, interleukin 1 and interleukin 4 Polymyalgia rheumatica and giant cell arteritis. Salvarani C; Cantini F; Hunder GG Lancet Jul 19;372(9634):

53 Symptoms and signs Morning stiffness typically lasts at least 30 minutes, with difficulty in activities related to the shoulder and hip, eg: trouble dressing, rising from or turning over in bed Symmetrical shoulder pain (70 to 95 %), hip and neck pain (50 to 70 %), which is worse with movement and may interfere with sleep Muscle tenderness Subjective weakness but the muscle strength is usually normal Decreased active, and sometimes passive, range of motion of the shoulders, neck, and hips Mild and non erosive synovitis and bursitis, especially appears to occur in more peripheral joints, such the knees, wrists, and metacarpophalangeal joints Swelling and pitting edema of the hands, wrists, ankles, and top of the feet, which represent tenosynovitis and synovitis in regional structures Systemic signs and symptoms including malaise, fatigue, depression, anorexia, weight loss, and fever

54 Diagnostic difficulties in polymyalgia rheumatica No gold standard diagnostic test Little sound evidence from randomized controlled trials on which to base diagnosis and management Diagnosis is often made on clinical grounds only, which can lead to diagnostic error It has many non specific features and a wide differential diagnosis Patients complaints could be varied

55 Diagnosis of Polymyalgia Rheumatica Safe Stepped diagnostic process supported by grade B evidence

56 Stepwise approach for management of polymyalgia rheumatica

57 Step I: diagnosis Core inclusion criteria Age >50 years, duration >2 years Bilateral shoulder or pelvic girdle aching, or both Morning stiffness duration of > 45mins Evidence of an acute phrase response **PMR can be diagnosed with normal inflammatory markers, if there is a classic clinical picture and response to steroids. These patients should be referred for specialist assessment

58 Step II: Core exclusion criteria Active infection Active cancer Active giant cell arteritis All 3 conditions could have increase inflammatory markers

59 Differential diagnosis Inflammatory rheumatic disease 1. Rheumatoid arithritis (predominant peripheral joint involved) 2. SLE, vasculitis (multisystem disease) 3. inflammatory myopathy (weakness of muscles with high CK)

60 Differential diagnosis Non inflammatory disease 1. Osteoarthritis 2. Adhesive capsulitis and rotator cuff lesions 3. Drug induced myalgia 4. Chronic pain syndromes/ fibromyalgia (longstanding history, with tender spots) 5. Hypothyroidisam (TSH level ) 6. Metabolic bone disease (PTH, vitamin D level)

61 Investigations Recommended laboratory investigations before commencement of steroid therapy: CBC TSH ESR/ CRP Creatine kinase L/RFT RF Bone profile Dipstick urinalysis Protein electrophioresis CXR

62 Investigations ESR is the most sensitive diagnostic study, but it is not specific CRP is often elevated and may parallel ESR Creatine kinase (CK) is normal and helps to differentiate from polymyositis and other primary myopathic disorders ANA and RF usually normal MRI shoulder joint is not necessary for the diagnosis, it will reveal subacromial and subdeltoid brusitis, glenohumeral joint synovitis

63 Early specialist referral suggested if: Younger patient < 60 years Chronic onset (>2 months) Lack of shoulder involvement Lack of inflammatory stiffness Prominent systemic features, weight loss, night pain, neurological signs Normal or extremely high acute phrase response Features of other rheumatic disease

64 Steps III: treatment Low dose steroids Initial standardized dose of oral prednisolone 15 20mg daily to reduce the inflammatory manifestations Patient reported global improvement of >70% within a week of commencing steroids Normalization of inflammatory markers in 4 weeks A lesser response should prompt the search for an alternative condition

65 Step IV: Follow up If no alternative diagnosis, follow 4 6 weeks was suggested

66 Step IV: Follow up Monitor laboratory investigations CBC ESR, CRP RFT glucose

67 Step IV: Follow up Monitor symptoms of proximal pain morning stiffness diability related to PMR adverse events osteoporotic risk symptoms that may suggest an alternative diagnosis

68 Treatment regime Suggested regime of oral prednisolone: Daily prednisolone 15mg for 3 weeks Then 12.5mg for 3 weeks Then 10mg for 4 6 weeks Then reduction by 1mg every 4 8 weeks or alternate day reductions Usually 1 2 years of treatment is needed, 50 75% of patient can discontinue corticosteroid therapy after 2 years of treatment Kyle V, Hazleman BL. Teatment of polymyalgia rheumatic and giant cell arteritis. II Relation between steroid dosing and steroid associated side effects. Ann Rheum Dis 1989;48:662 6

69 Treatment regime -- alternatives IM methylprednisolone (depomedrone) Used in milder case and can reduce the risk of steroid related complications Initial dose: 120mg every 3 4 weeks Reduce by 20mg every 2 3 months

70 Other considerations bone protection Individuals with high fracture risk: Bisphosphonate with calcium and vitamin D supplementation Other individuals: Calcium and vitamin D supplementation

71 Treatment regime No consistent evidence for an ideal steroid regime suitable for all patients Approach to treatment must be flexible and tailored to the individual Dose adjustment may be required for disease severity, co morbidity, side effects and patient wishes

72 Early specialist referral suggested IF: Incomplete, poorly sustained or nonresponse to corticosteroids Inability to reduce corticosteroids Contraindications to corticosteroid therapy The need for prolonged corticosteroid therapy (> 2 years)

73 Treatment for relapse Relapse is common, in up to 25% of patients, more likely to occur during the initial 18 months of therapy and within 1 year of corticosteroid withdrawal For the 1 st and 2 nd relapse, increase steroids to previous dosage For further relapse, consider immunosupressants e.g. Methotrexate (a dose of 10 mg/wk) Studies show that, Infliximab, a tumour necrosis factor has not shown impressive disease controlling or steroidsparing effects

74 Giant cell Arteritis (GCA) and poylmyalgia rheumatica (PCR) GCA is a common overlapping inflammatory rheumatic diseases with PCR 10% of patients with PMR have GCA 50% of patients with GCA have PMR PMR occurs 3 to 5 fold more frequently than GCA Dasgupta B, Kalke S. Polymyalgia rheumatic. In: Isenberg D, Maddison P, Woo P, Glass D, Breedveld F (eds), Oxford testbook of rheumatology, 3 rd edn. Oxford: Oxford University Press, 2004:977 82

75 Giant cell arteritis (GCA) Systemic, inflammatory, vascular syndrome predominantly affects the cranial branches of arteries arising from the arch of the aorta Major features are due to arterial inflammation and its consequences Chronic vasculitis of large and medium vessels, with granulomatous transmural inflammation histologically T lymphocytes in the vessels produce interferongamma and interleukin 2 Macrophages produce interleukin 1, 6 and transforming growth factor beta

76 Giant cell arteritis (GCA) Incidence is reported as 2.2/ patientyears in UK Mean onset at age of 70, rare before age of 50 Three times more common in females than in males

77 Typical features of GCA Abrupt onset headache (usually temporal) and temporal tenderness Visual disturbance, including diplopia or amaurosis fugax Jaw or tongue claudication Prominence, beading or diminished pulse on examination of the temporal artery Upper cranial nerve palsies Limb claudication or other evidence of largevessel involvement

78 The American College of Rheumatology classification criteria for GCA 1. Age at disease onset >50 years 2. New onset of or new type of localized pain in the head 3. Temporal artery abnormality: temporal artery tenderness to palpation or decreased pulsation, unrelated to arteriosclerosis of cervical arteries 4. Elevated ESR: >50 mm/h 5. Abnormal artery biopsy: vasculitis characterized by a predominance of mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells GCA if at least three of these five criteria are present (a sensitivity of 93.5% and a specificity of 91.2%)

79 Should we do temporal artery biopsy in all patients with PMR? PMR occurs 3 to 5 fold more frequently than GCA Patients with pure PMR lack the classic findings of GCA such as temporal artery tenderness, headache, jaw pain, visual loss, and evidence of ischemia such as cluadication are very unlikely to have a positive result after temporal biopsy Temporal biopsy is NOT recommended as a routine test Gabriel SE, O Fallon MW, Achkar AA, et al. The use of clinical characteristics to predict the results of temporal aretery biopst among patients with suspected giant cell arteritis. J rheumatol 1995;22:93 6

80 Temporal artery biopsy Always perform the biopsy on the symptomatic side of head If a specific part of the artery is tender, beaded or inflammed, include that area in the biopsy Take at least 2 3cm of the artery Better to include multiple sections because the lesion may be segmental Results of the temporal artery biopsies remain positive after as long as 4 weeks high doses of corticosteroid are administered

81 Duplex ultrasonography Detect the characteristic hypoechoic halo around the affected temporal arteries, representing vessel wall edema, arterial stenosis and occlusion The halo sign had a sensitivity of 69% and specificity of 82%when compared with the biopsy for the diagnosis of giant cell arteritis But it cannot be recommended as a replacement of temporal artery biopsy as it has no prognostic value and it requires high level of expertise

Hypoechoic area around the temporal artery trunk in

82 Halo sign Halo sign in colour duplex sonography examination in a patient with giant cell arteritis. Hypoechoic area around the temporal artery trunk in longitudinal (upper panel) and transverse (lower panel) views

83 Key point of treatment for giant cell arteritis The dose of prednisolone is much higher than that of PMR! Low dose corticosteroid used in polymyalgia rheumatica is ineffective in giant cell arteritis

84 Guidelines for the management of giant cell arteritis

85 Key point of treatment for giant cell arteritis I. ) Uncomplicated GCA (without visual symptoms): Prednisolone 40 60mg (at least 0.75 mg/kg) daily until resolution of symptoms and laboratory abnormalities

86 Key point of treatment for II. ) Complicated GCA giant cell arteritis 1. Evolving visual loss or history of amaurosis fugax: i.v. methylprednisolone 500mg to 1 g daily for 3 days 2. Established vision loss at least 60mg prednisolone daily to protect the other eye

87 Key point of treatment for In all patients: giant cell arteritis Low dose aspirin 75mg daily (if no contraindications) Bisphosphonates and calcium, vitamin D supplementation Proton pump inhibitor

88 Complications of giant cell arteritis Loss of vision which is often irreversible Scalp necrosis Cerebrovascular accidents Aortic aneurysm, dissection, or stenosis Coronary involvement So, making the diagnosis and have prompt treatment with steroid is important!

89 Bring home message Polymyalgia rheumatica is a frequent disorder in the elderly population that can cause severe pain, functional impairment and a reduction in overall quality of life Making the diagnosis of polymyalgia rheumatica and subsequently treating the patient results in rapid and dramatic improvement in the patient s complaints and a return to previous functional status Consider the diagnosis of polymyalgia rheumatica when our patients complain of symptoms of pain and stiffness, with increase in inflammatory marker Always think of giant cell arteritis as the treatment is different

9/11/11. Temporal Arteritis. Background. Background. Richard E. Castillo, OD, DO NORTHEASTERN STATE UNIVERSITY Director, Ophthalmic Surgery Service

9/11/11. Temporal Arteritis. Background. Background. Richard E. Castillo, OD, DO NORTHEASTERN STATE UNIVERSITY Director, Ophthalmic Surgery Service Temporal Arteritis Richard E. Castillo, OD, DO NORTHEASTERN STATE UNIVERSITY Director, Ophthalmic Surgery Service 1 Background Giant Cell Arteritis Temporal Arteritis Cranial Arteritis Granulomatous Arteritis