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Flashcards in MSK - Rheumatological red flags Deck (31):

contrast the features on medical interview, physical examination and investigation of crystal and septic arthritis

Clinical features of septic arthritis
• Fever, “septic”
• 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)

- 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?

1. Large vessel: giant cell arteritis, Takayasu
2. Medium vessel: Kawaaki, Polyarteritis nodosa
3. 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


• Polymyalgia rheumatica(PMR)/ giant cell
• 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).

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


How do you Rx a suspected GCA?

Emergency (high risk of sudden blindness)
• Commence prednisolone 40 – 60 mg daily immediately and arrange temporal artery biopsy
• Decide what to do if the biopsy is negative – usually steroids are rapidly tapered and stopped unless the pre-test probability of GCA is very high
• Taper corticosteroids according to the ESR or CRP
• Provide fracture prevention therapy
• Be alert to early (infection) and late (fractures and aortic aneurysm) complications


A very painful left knee
• 63-year-old woman , history of knee osteoarthritis
• 2 days of severe right knee pain, swelling and redness.
• Unable to sleep, walk due to pain.
• Febrile (38.5o C), resists passive movement of the right knee.
• Tense effusion of the right knee.


1. Bacterial septic arthritis (not to be missed)
2. Crystal arthritis (eg: gout, pseudogout)
3. Subchondral bone lesion (eg: fracture, osteonecrosis, osteomyelitis)
4. Haemarthrosis (eg: trauma, haemophillia, anticoag therapy)
5. Palindromic rheumatism (very rare)


What Ix should you do in an acute monoarthritis?


Yellow: inflammatory serum coloured synovial fluid

Purple/dark red: haemarthrosis

Purulent: in chronic monoarthritis (e.g. bacterial septic arthritis Ix late)


What are the risk factors for joint sepsis?

• Very young or advanced age
• Recent joint aspirate/injection, penetrating injury
• Portals for bacteraemia (eg: skin ulcers, bowel inflammation eg diverticulitis, colonic biopsy, dental work, UTI and lower urinary tract instrumentation)
• Previous joint damage (eg: rheumatoid or osteoarthritis)
• Corticosteroid therapy
• Diabetes mellitus, chronic renal or liver disease
• Immunodeficiency (eg: hypogammaglobulinaemia, CLL, any cancer)
• Prosthetic joints


What causative organisms typically affect single and usually large joints?

Staph. Aureus

N. Gonorrhoea

E.Coli and other Gram-negative cocci and Strep. species


What typical symptoms suggest an immune complex response to a systemic infection?

Polyarticular arthralgia +/- tenosynovitis


Who are at a higher risk of disseminated Neiserria Gonorrhoea?

Sick young adult (20 – 35), multiple joints infected, casual sexual activity and


How would you Ix a septic arthritis?

• Always obtain synovial fluid for analysis ASAP. A low synovial WCC does not exclude infection, esp immunosuppressed
• Plain radiographs: baseline and repeated at 1 week if no diagnosis. Demineralisation and rapid articular cartilage loss are diagnostic of untreated septic arthritis. This is critical data if cultures are negative.
• MRI scan: sensitive and relatively specific
• FBE: Neutrophillia is not specific
• Blood cultures: Useful. 50% of patients with non-gonococcal
septic arthritis have positive cultures
• CRP: Non-specific but useful if elevated


What are the common causative organisms in septic arthritis?

• Staphylococcus aureus (60%)
• Beta-haemolytic Streptococci (15%)
• Gram negative bacilli (15%)
• Streptococcus pneumoniae (


DDx of confluent palpable purpura

• Infection most likely (very short history).
• Drug reaction eg OCP or antibiotics are common causes.
• Another type of vasculitis (eg Henoch Schonlein Purpura)


What are the (2) classifications of small vessel vasculitis? What are some of their examples?

1. Anti Neutrophil Cytoplasmic Antibody (ANCA)-negative SVV:
- Hypersensitivity vasculitis (many causes, eg: drug reactions)
- Henoch Schönlein Purpura (HSP)
- Rheumatic disorders: SLE, RA, Sjogren’s disease
- Mixed cryoglobulinaemia (Hepatitis C, rarely HIV or cancer)
- Infections: Hepatitis C, Hepatitis B
- Malignancy: Leukaemia, lymphoma, myelodysplastic syndromes

2. ANCA-associated SVV (AAV):
- Microscopic polyangiitis (MPA)
- Granulomatosis with polyangiitis (Wegener’s, GPA)
- Churg Strauss syndrome (CSS)


In a suspected small vessel vasculitis presenting with palpable purpura, what should you be careful not to miss?


• Meningococcal infection: meningococcaemia may present with purpuric rash in absence of
fever or symptoms and signs of meningitis
• Staphylococcal bacteraemia: palpable purpura may occur in Staphylococcal septicaemia, usu
associated with deep infection: eg. endocarditis, septic arthritis, vetebral osteomyelitis, epidural
abscess etc.
• Subacute bacterial endocarditis: may present
with palpable purpura, splinter haemorrhages.


Why is it important to consider vasculitis mimics?

• Misdiagnosis or failure to diagnose infection or embolus may lead to permanent organ damage or death
• Treatment of mimics is often specific and potentially life saving (eg: antibiotics for infective endocarditis or meningococcal infection)
• Corticosteroid treatment may be futile (eg: cholesterol
embolisation, calciphylaxis) or masks progressive infection
(eg: endocarditis)


What Ix would you order in suspected small vessel vasculitis?

• Full blood examination: Normocytic anaemia and/ or
thrombocytosis support a chronic inflammatory process.
Thrombocytopenia suggests ITP .• Blood film: looking for fragmented red cells, high RDW, suggesting intravascular haemolysis
• Acute Phase Reactants : ESR and CRP
• Albumin – a negative acute phase reactant. Call fall quickly.
• Renal Function Tests: Creatinine, urea
• Septic workup: Blood cultures, MSU, Chest X-ray, Multiplex PCR for meningococcus, pneumococcus
• MSU microscopy: “Glomerular” or dysmorphic red cell count, red cell casts suggest glomerulonephritis (consider
renal biopsy)
• MSU culture: Urinary sepsis
• Echocardiogram: Essential for any febrile patients with heart murmur, prosthetic valves or pacemakers
• Skin (punch) biopsy: Select fresh lesions for Gram stain,
culture and H&E/immunostaining . Usual pattern is Leucocytoclastic vasculitis. IgA deposits in HSP. Immune
complexes absent in AAV


How do you Ix for systemic involvement?

Based on likelihood of organ involvement
• Tissue biopsy : direct evidence. Choose biopsy site based on clinical involvement and lowest risk of complications. Common sites skin, kidney, liver.
• Angiography: useful if clinical suspicion of medium vessel
vasculitis (eg. PAN)
• Lung: CT scan, pulmonary function tests
• Neuropathy: nerve conduction tests


Mx of septic arthritis

• Maintain high index of suspicion
• Choose effective antibiotics based on age, clinical
situation, Gram stain.
• Joint Drainage is critical – closed needle drainage is
rarely adequate. Arthroscopic washout preferred. (mandatory for hip and shoulder joints, prosthetic joints and damaged
joints in RA)
• Analgesia (opiates usually required)
• Initial rest followed by joint mobilisation
• Consider associated infection (eg: endocarditis)

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