MSK - Rheumatological red flags Flashcards
contrast the features on medical interview, physical examination and investigation of crystal and septic arthritis
Clinical features of septic arthritis
• Fever, “septic”
appearance
• Joint pain (no diurnal or activity variation)
• Joint swelling
• Heat over the affected joint
• Erythema overlying the joint
• Loss of function
• Pain on attempted joint motion (passive or active)
• Rapidly progressive joint destruction within days or
1-2 weeks (X-rays)
Clinical features of gout:
- Monoarticular involvement most commonly
- attacks begin abruptly & typically reach maximum intensity within 8-12 hours (c.f. insidious over several days in pseudogout)
- attacks can become more polyarticular, involving more proximal & upper extremity joints, more frequent & lasting longer without treatment
- Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa, olecranon)
- Eye involvement – Tophi, crystal-containing conjunctival nodules, band keratopathy, blurred vision, anterior uveitis (rare), scleritis
What are the common diagnostic pitfalls of septic arthritis?
- History of trauma may lead to mis-attribution
- Fever may be absent (eg: in immunosuppressed patients)
- Joint sepsis may co-exist with acute gout
- Staphylococcal joint sepsis may co-exist with endocarditis or deep abscess (eg: epidural space)
describe the initial management of gout and septic arthritis
Septic arthritis:
- adequate and timely drainage of the infected synovial fluid
- arthroscopic washout preferred
- administration of appropriate antimicrobial therapy (combination of penicillin and gentamicin or a later-generation cephalosporin)
- immobilization of the joint to control pain (opiates)
Gout:
- Colchicine (an acute gout med that is less commonly used now due to narrow TI) plus NSAIDs
- Oral corticosteroids plus colchicine
- Intra-articular steroids plus colchicine or NSAIDs
What are the features on the medical interview, physical examination and investigations that suggest a systemic inflammatory process?
• Fatigue (disproportionate to the patient’s usual tiredness) in the presence of adequate sleep
• Lethargy (not as productive as usual)
• eg. “I’m just not myself”, ”I feel washed out”
• Insidious Onset
Sometimes weight loss with or without anorexia or a low grade fever are associated
contrast the features on presentation of infection and inflammation in the context of a systemic inflammatory condition
• Infection of multiple joints contemporaneously is otherwise quite rare: think
immunosuppression or damaged joints.
What are the clinical spectrum of small vessel vasculitis
• Fevers, night sweats, malaise
• Myalgias, arthralgia and/ or arthritis
• Rashes: palpable purpura (more specific), non-palpable
purpura (less specific), urticaria
• Nail-fold or digital infarcts
• Mononeuropathy multiplex (eg: foot drop)
• Upper respiratory tract: sinusitis, epistaxis
• Lungs: haemoptysis, diffuse alveolar haemorrhage
• Haematuria (may look “smoky” in colour), microhaematuria or proteinuria on dipstick (glomerulonephritis)
Define vasculitis
- Conditions related to inflammation in the walls of blood vessels: arteries and veins of all sizes
- Clinical features are a mixture of inflammatory and ischaemic/infarction organ dysfunction +/- damage as the lumen of affected vessels become narrowed when the walls become thickened.
-Some vasculitis syndromes manifest in one organ only (eg
skin, kidney), but MOST involve multiple organs.
-Limb girdle ache/stiffness in the mornings (esp around the shoulders) is especially common in multiple organ syndromes.
What are the 3 main types of vasculitis?
- Large vessel: giant cell arteritis, Takayasu
- Medium vessel: Kawaaki, Polyarteritis nodosa
- Small vessel:
- ANCA associated: GPA (Wegener’s), MPA, EGPA (Churg-Strauss)
- Immune complex: Cryoglobulinaemic, IgA (HSP), HUV, anti-GBM
Variable vessel: Behcet, Cogan
A new headache
• 79 year old woman
• 4-week history of recurrent headaches, gradual
onset. No previous PHx headaches.
• Jaw pain when chewing and talking on the phone.
• Vision normal.
• 5kg weight loss, fatigued.
• Severe shoulder and hip stiffness, worse in the
morning.
DDx?
• Polymyalgia rheumatica(PMR)/ giant cell
arteritis
• Rheumatoid arthritis (but no arthritis)
• Polymyositis
• Hypo- or hyperthyroidism (may present with myopathy)
• Malignancy (may present with paraneoplastic syndrome)
• Infection
Describe giant cell arteritis
• New headache
• Jaw claudication
• Unexplained fever, ESR > 100 mm/hour
• PMR-type symptoms ie limb girdle stiffness
• In any patient with a diagnosis of PMR, especially when the ESR remains elevated despite treatment with low dose steroids
• Sudden monocular blindness (Anterior Ischaemic Optic
Neuropathy – AION. Can be transient initially.)
• Caucasian men and women (> 55 years)
Px of GCA (giant cell arteritis)
• Superficial headache, scalp tenderness (common), jaw and tongue claudication (common)
• Polymyalgia rheumatica with shoulder and hip girdle pain and morning stiffness (very common)
• Fever and fatigue (common)
• Weight loss (common)
• Anterior ischaemic optic neuropathy, retinal artery
occlusion (15%). Risk
What would a temporal artery biopsy show in giant cell arteritis?
Segmental destruction of internal elastic lamina,
granulomatous vessel inflammation with giant cells (small arrows).
Inflammatory
exudate extends into the intima, where there is fibrosis.
What vessels can GCA involve?
- Not only temporal arteries
- aorta
- aortic major branches
What are Cx of GCA by vessels involved?
- Ophthalmic/ long ciliary arteries (Blindness)
- Subclavian (arm claudication, absent pulses)
- Renal (renovascular hypertension, Angiotensin 2 mediated )
- Aorta (esp ascending and thoracic, Aortic Valve incompetance: late - aneurysm rupture)
- Coronary (angina pectoris, infarction)
- Internal carotid (TIA, stroke)
- Vertebral (TIA, stroke)
- Iliac (leg claudication)
- Mesenteric (bowel ischaemia)
Describe the relationship between polymyalgia rheumatica & giant cell arteritis
• Both are diseases of elderly caucasians
• PMR and GCA frequently occur synchronously or
sequentially in the same individual
• PMR is noted in > 50% of GCA patients
• 25% of PMR patients have co-existent GCA
• Histological temporal arteritis has been documented in patients with no headache and
clinically normal temporal arteries (Very tricky!)
• PET imaging shows increased aortic uptake in many
patients with PMR who have no headache
