Transcript Hot red joint

Septic and crystal arthritis
Jaya Ravindran
Rheumatologist
Case 1
• 82 year old
• Admitted 2.6.08 acute on chronic knee pain 3-4
days
• Recent excision of shin BCC with skin graft
complicated by cellulitis
• Ex Not unwell afebrile MEWS O
• Warm, slightly tender knee effusion, tolerating 90
flexion
• ? Wound infection started on antibiotics
• CRP 187
Case 1
• Radiological
abnormality?
• Differential
diagnosis?
• Further
investigations?
• Management?
Case 1
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No organisms, scanty WBC
Pyrophosphate crystals
Low dose colchicine
CRP 42
Case 2
• DS 42 year old lady
• PMH Crohns
• Admitted 12.5.08 with onset of feeling hot and
cold, D & V, headache 10 days ago
• 3 days ago developed painful swelling left wrist,
right knee and left ankle
• SH Roadie, smoker – 10 roll-ups/day, lives with
husband and son
Case 2
• Ex unwell,T38.5, p117/min, BP
116/64, RR20/min, satn 91%
air, urine nad
• Tender swollen and red wrist,
knee and ankle
• CXR ‘clear’
• IMP septic
• Plan BC, analgesia, iv
antibiotics, IVI
• Systolic dropped to 90 systolic
• Na 122 CRP 285, Blood gas
P02 7, PCO2 7 PH 7.4
• Transferred to WGH
Case 2
• Seen by rheumatologist joints aspirated
• 13.5 blood cultures group A Strep, aspirate no
growth, WBC
• 15.5 vasculitic rash, low complement ?post Strep
• 16.5 ECHO normal, CRP and joints settling
• 17.5 Right pleuritic chest pain with rub
Case 2
• P02 8 treat for PE as well
• 21.5 CTPA cavitating consolidation right lower
lobe, hilar nodes, no PE
• Still spiking ?empyema – nil aspirated,, no AFB in
sputum, HIV negative, awaiting WBC scan
Case 3
• DB 45 year old man
• PMH RA on
sulphasalazine
• 4 day history painful
hot swollen red right
big toe
• Differential?
• Investigations?
Case 4
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82 year old man
PMH LVF,AF, TIA, BPH
DH Aspirin, bumetanide, ramipril, digoxin, statin
Referred with acute on chronic wrist pain
needing MST
• Pain was so severe that he asked next door’s
dog to stop barking!
• WBC 13, CRP 155, Cr 143, XR OA changes
Case 4
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Ex Well afebrile MEWS 0
Tender warm swollen right wrist
Dry tap
Imp ? Crystal
Oral prednisolone
Good response but then confused, t 37.5,
p116/min, 3+ blood & 1+ prot urine dip,
increasing painful swelling in left wrist and toe
• Diagnosis and plan?
Case 4
• WBC 20, Cr 261
• MSU, BC and joint aspirated
• IVI and antibiotics, MST and ramipril
stopped
• Uric acid crystals, no growth in aspirate
• Wrists injected once presumed UTI treated
• Wrists better, CRP 3, Cr 124
What are other differentials for
monoarticular pain?
Monoarthritis - differential
• Monoarticular sero-ve spondyloarthritis eg
psoriatic and reactive arthritis
• Monoarticular RA
Monoarthritis - differential
• Haemarthroses
(warfarin, bleeding
disorders)
• Trauma – fracture, internal
derangement,
haemarthroses
Others to think about
• Osteonecrosis/AVN
(steroids/alcohol/SLE)
• Prosthetic joint loosening, # or infection
Others to think about
• Periarticular pathology
• Cellulitis
Septic arthritis
• 15-30 per 100,000 population
• Fatal in 11% of cases in UK
• Delayed or inadequate treatment leads to
irreversible joint damage
How do you get septic arthritis?
Pathogenesis
Who gets septic arthritis ?
Who gets septic arthritis?
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pre-existing joint disease
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prosthetic joints
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low SE status, IV drug abuse, alcoholism
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diabetes, steroids, immunosuppression
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Skin lesions e.g. ulcers, particularly in context
RA often source of infection
• Which organisms cause septic arthritis?
Which organisms?
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common organisms Staphylococci or
Streptococcus
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Elderly & immunocompromised gram -ve
organisms
Which organisms?
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Anaerobes more common with
penetrating trauma
Pseudomonas - IV drug abusers
young adults - significant incidence
gonococcal arthritis
Who gets septic arthritis?
• poor prognostic features:
older
pre-existing joint disease & presence of synthetic
material within joint
What are the signs and
symptoms of septic
arthritis?
Symptoms & signs of septic arthritis
• Symptoms usually
present for < 2/52
• Typically hot, swollen, red
tender joint with reduced
range of movement,
difficulty weight bearing
• Night and rest pain
• Large joints more
commonly affected than
small
• majority of joint sepsis in
hip or knee
• Systemic upset (MEWS)
Symptoms & signs of septic arthritis
• In pre-existing inflammatory joint disease
symptoms in affected joint(s), out of proportion
to disease activity in other joints.
• 10% of cases > one joint
• presence of fever not reliable indicator
• Features of gonococcal arthritis ?
Gonococcal arthritis
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Women>men
Menses, pregnancy
1-3% arthritis
1day- weeks after sexual
encounter
• Migratory (70%),
Tenosynovitis (70%),
monoarthritis (32%),
polyarthritis (10%)
• Fever, Dermatitis
(pustules, vesicular,
haemorrhagic bullae,
mac.papular)
What investigations are useful
in septic arthritis?
Investigations
• Synovial fluid aspiration
– gram stain/m,c,s
– Absence of organism does
not exclude septic arthritis
– polarised light microscopy
(crystals)
– NB suspected prosthetic
joint sepsis should
ALWAYS be referred to
orthopaedics
Investigations
• Blood cultures
• Significant proportion blood cultures + ve
in absence of + ve synovial fluid cultures
• FBC ESR & CRP
• Absence of raised WBC, ESR or CRP
does not exclude diagnosis of sepsis
Other investigations
• CRP useful for monitoring response to
treatment
• Urate may be normal in acute gout
• U+E & LFT – prognosis and influence
antibiotic regime
Other tests?
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Gonococcal - skin pustule - skin swab,
urethral/cervical /rectal/throat swab,
blood culture, joint aspirate
genitourinary or respiratory tract infection
then culture sputum and CXR & MSU
If periarticular sepsis – appropriate
swabs and cultures
• Radiology ?
Imaging
• Plain X rays no benefit in diagnosis but form
baseline for any future joint damage. May
show chondrocalcinosis (pyrophosphate
arthritis).
• MRI sensitive for osteomyelitis and spinal
involvement
Imaging
• Ultrasound useful in guiding needle
aspiration eg hip
• White cell scanning helpful in diagnosing
prosthetic sepsis
• What are the radiological features
of infected prosthesis?
Prosthetic infection
Spinal infection
• Discitis – with destruction end plates
• Management?
• MEWS score?
• Shock?
• Multi-organ failure?
• RESUSCITATION
Antibiotic treatment of septic arthritis
• Local and national guidelines
• Liaise with micro. guided by gram stain
• Conventionally given iv for 2 weeks or until
signs improve, then orally for around 4
weeks
Joint drainage & surgical options
• medical aspiration, surgical aspiration via
arthroscopy or open arthrotomy
• Suspected hip sepsis – early orthopaedic
referral – may need urgent open
debridement
Recommendations specific to 1o care &
emergency department
• commonest hot joint to present in 1o care is 1st MTP
gout
• diagnosed on clinical grounds without needle
aspiration or referral to hospital. (Make referral if
inadequate recovery)
• Some GPs aspirate & inject joints for inflammatory
arthritis or osteoarthritis. If withdraw
pus/unexpected cloudy fluid should send sample
with patient to local emergency department
Recommendations specific to 1o care &
emergency department
• GPs & doctors in EAU should refer patients
with suspected septic arthritis to specialist
with expertise to aspirate joint.
• May be orthopaedic surgeon or
rheumatologist
• Admit if sepsis is suspected or confirmed.
Summary
• with a short history of a hot, swollen,
tender joint (or joints) plus restriction of
movement; septic arthritis until proven
otherwise
• If clinical suspicion high investigate &
treat as septic arthritis even in absence of
fever – always joint aspiration and blood
cultures
GOUT
• Definition and metabolism?
Gout
• An inflammatory arthritis caused by
hyperuricaemia
• Uric acid is formed from the
breakdown of purines (DNA)
• Excreted in the urine
• Characterised by the deposition of
urate crystals in the joints and soft
tissues
Gout Epidemiology
• Prevalence 1-2%
• Most common cause of inflammatory
arthritis in men 3-5:1 and postmenopausal women
• Usually presents between 40-60 years
• Diagnosis of gout ?
Polarized microscopy - negatively
birefringent needle shaped crystals
Clinical - usually self-limiting
monoarthritis
• Usually resolves 7-10
days
Diagnostic criteria for gout – ACR
criteria
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> 1 attack of acute arthritis
Maximum inflammation within 1 day
Attack of monoarthritis
Redness over joints
Painful or swollen 1st MTP
Unilateral attack 1st MTP
Unilateral attack tarsal joint
Tophus
Hyperuricaemia
Asymmetric swelling within joint on x-ray
Subcortical cysts without erosions on x-ray
Joint fluid culture –ve for organisms
6 or more criteria
Chronic gout
• Up to 10 years to
develop
• Less painful
• Older age
• Tophi – hands, feet,
elbows, ears
• Erosions
• Poly/oligoarticular
Erosive gout
• Causes of gout ?
Classification of Gout
1. Primary Gout: Majority
• Causes either over-production (10%) or underexcretion of uric acid (90%).
2. Secondary Gout:
• increased formation of uric acid
• reduced excretion of uric acid
• drugs / toxins
• miscellaneous
Increased Production of Uric
Acid
High alcohol esp beer or dietary intake
esp high seafood and meat
Increased Production of Uric
Acid
Increased purine turnover:
• Lympho/myeloproliferative disorders
• Tumours
• Muscle necrosis
• Chronic Haemolysis
• Severe psoriasis
Reduced Excretion of Uric
Acid
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Chronic renal disease
Hypertension
Hypothyroidism
Hyperparathyroidism
Drugs
Drug induced hyperuricaemia
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Diuretics esp.thiazides
Low dose aspirin
Cytotoxics
Cyclosporin
Ethambutol and pyrazinamide
• Associated diseases and triggers gout?
Associations
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Hypertension
Obesity
Hypercholesterolaemia
Diabetes
Triggers of gout
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Minor trauma
Operations
Unaccustomed exercise
Dietary excess
Alcohol
Dehydration
Starting diuretics
Useful investigations
• U+E, glu, BP, urate at 4 weeks
• Pyrophosphate arthritis features ?
Clinical
• Acute monoarthritis in elderly esp in
hospital
• Chronic polyarthritis with hypertrophic OA
changes
Chondrocalcinosis
• Polarized microscopy features?
• Metabolic Causes?
• Triggers?
Pyrophosphate Crystals
Metabolic Causes of
pyrophosphate arthritis
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Haemochromatosis
Hyperparathyroidism
Hypophosphatasia
Hypomagnasaemia
Triggers of pyrophosphate arthritis
• Management of gout?
Management of acute gout
• Affected joints should be rested (C) and analgesic, anti-inflammatory
drug therapy commenced immediately, and continued for 1–2 weeks
(A).
• Fast-acting oral NSAIDs at maximum doses are the drugs of choice
when there are no contraindications (A).
• In patients with increased risk of peptic ulcers, bleeds or
perforations, co-prescription of gastro-protective agents should
follow standard guidelines for the use of NSAIDs and Coxibs (A).
• Colchicine can be an effective alternative but is slower to work than
NSAIDs (A). In order to diminish the risks of adverse effects
(especially diarrhoea) it should be used in doses of 500 µg bd–qds
(C).
Management of acute gout
• Allopurinol should not be commenced during an acute attack (B) but
in patients already established on allopurinol, it should be continued
and the acute attack should be treated conventionally (A).
• Opiate analgesics can be used as adjuncts (C).
• Intra-articular corticosteroids are highly effective in acute gouty
monoarthritis (B) and i.a, oral, i.m or i.v corticosteroids can be
effective in patients unable to tolerate NSAIDs, and in patients
refractory to other treatments (A).
• If diuretic drugs are being used to treat hypertension, an alternative
antihypertensive agent should be considered, but in patients with
heart failure, diuretic therapy should not be discontinued (C).
Recommendations for diet, lifestyle modification and
non-pharmacological modalities of therapy
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In overweight patients dietary modification to achieve ideal body
weight should be attempted (B), but ‘crash dieting’ (B) and high
protein/low carbohydrate (Atkins-type) diets (C) should be avoided.
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Inclusion of skimmed milk and/or low fat yoghurt, soy beans and
vegetable sources of protein and cherries, in the diet should be
encouraged (B).
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Intake of high purine foods and red meat should be restricted (B).
Liver, kidneys, shellfish and yeast extracts should be avoided (B),
and overall protein intake should be restricted (C).
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Patients with gout and a history of urolithiasis should be
encouraged to drink >2 l of water daily (B) and avoid dehydration
(C). Alkalinization of the urine with potassium citrate (60 mEq/day)
should be considered in recurrent stone formers (B).
Recommendations for diet, lifestyle modification and
non-pharmacological modalities of therapy
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Alcohol consumption should be restricted to <21
units/week (men) and 14 units/week (women) (B),
and patients should be encouraged to have at least
3 alcohol-free days per week (C). Beer, stout, port
and similar fortified wines are best avoided (C).
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Affected joints should be elevated and exposed in
a cool environment (C). ‘Bed cages’ (C) and ice
packs (B) can be effective adjuncts to therapy.
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Trauma to joints (B) and intense physical exercise
(B) should be avoided but moderate physical
exercise encouraged (B).
Management of recurrent, intercritical and chronic gout
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The plasma urate should be maintained below, 300 µmol/l (C).
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In uncomplicated gout uric acid lowering drug therapy should be started if a second
attack, or further attacks occur within 1 yr (B).
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Uric acid lowering drug therapy should also be offered to patients with tophi (C),
patients with renal insufficiency (B) patients with uric acid stones and gout (B) and to
patients who need to continue treatment with diuretics (B).
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Commencement of uric acid-lowering drug therapy should be delayed until 1–2
weeks after inflammation has settled (C).
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Initial long-term treatment of recurrent uncomplicated gout normally should be with
allopurinol starting in a dose of 50–100 mg/day and increasing by 50–100 mg
increments every few weeks, adjusted if necessary for renal function, until the
therapeutic target (SUA <300 µmol/l) is reached (maximum dose 900 mg) (B).
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NB renal impairment, elderly, azathioprine
Management of recurrent, intercritical and chronic gout
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Uricosuric agents can be used as second-line drugs in patients who are
under-excretors of uric acid and in those resistant to, or intolerant of,
allopurinol (B). The preferred drugs are sulphinpyrazone (200–800 mg/day)
in patients with normal renal function or benzbromarone (50–200 mg/day) in
patients with mild/moderate renal insufficiency (B).
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Colchicine 0.5 mg bd should be co-prescribed following initiation of
treatment with allopurinol or uricosuric drugs, and continued for up to 6
months (A). In patients who cannot tolerate colchicine, an NSAID or Coxib
can be substituted provided that there are no contraindications, but the
duration of NSAID or Coxib cover should be limited to 6 weeks (C).
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Aspirin in low doses (75–150 mg/day) has insignificant effects on the
plasma urate, and should be used as required for cardiovascular
prophylaxis (B). However, aspirin in analgesic doses (600–2400 mg/day)
interferes with uric acid excretion and should be avoided (B).
Other drugs and diseases
• consider losartan and fibrate if
hypertensive and hyperlipidaemia
(uricosuric)
• Screen for and treat metabolic syndrome
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