APPROACH TO MONOARTHRITIS
DR CB NEL
“Inflammation of a single joint”
• Acute
• Chronic
WHERE IS THE INFLAMMATION?
• ARTICULAR
• pain all planes
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•
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•
PERI-ARTICULAR
pain in plane of
tendon
active = passive
active > passive
capsular swelling/effusion linear swelling
joint line tenderness
localised tenderness
diffuse erythema/heat
localised
erythema/heat
ACUTE MONOARTHRITIS
 Septic arthritis
 Crystal synovitis
 Trauma
 Haemarthrosis
 Foreign body reaction
 Monoarticular
presentation of oligo- /
polyarthritis
o RA
o Erythema nodosum
o Juvenile idiopathic
arthritis
o Reactive, Psoriatic or
other Seronegative
spondiloarthropathy
CHRONIC MONOARTHRITS
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Foreign body
Infection-Tuberculosis
Ch. Sarcoidosis
Enteropathic Arthritis (mainly Crohn’s)
Amyloidosis
Pigmented villonodular synovitis
Synovial pathology (sarcoma, chondromatosis)
Monoarticular presentation of oligo- / poly
articular disease
CRYSTRAL ARTHROPATHIES
Crystal-induced Arthritis
• Gout (monosodium urate crystals) most common
- First MTP, ankle, midfoot, knee (can be any joint though)
- Most initial attacks affect a single joint
- Fever (more common with polyarticular) can raise
suspicion for infection
- Presence of crystal does not exclude infection
- May see desquamation of overlying skin
- Thiazide diuretics can put at risk
- Needle shaped, negatively birefringent crystals
• Calcium pyrophosphate dihydrate/pseudogout
- Clinically not able to distinguish from gout
- Most common in knee and wrists
- Evolves over several days (less acute than gout)
- Rhomboid shaped, positively birefringent crystals
• Other crystals: apatite, calcium oxalate, liquid lipid
GOUT
URIC ACID POOL
Endogenous
Exogenous
Excretion
Kidneys (2/3)
Intestines (1/3)
Serum urate: 0,12 - 0,55mmol/l
Urine urate excretion: 1,5 - 4,4mmol/24 hours
MECHANISM OF HYPERURICAEMIA
• Underexcretion (Most common)
• Overproduction
HYPERURICAEMIA AND GOUT
• Disorder of purine metabolism
• Characterised
– hyperuricaemia
– deposition of uric acid or urate crystals in the tissues
•
Manifestations
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acute attacks of gouty arthritis
tophi
kidney stones
urate-nephropathy
PATHOGENESIS
• Hyperuricaemia causes gout, but is not
synonomous with gout
• Factors promoting crystallisation
(0.55mmol/l)
– the level of saturation
– solubility
– pH and temperature of the limb(colder areas)
PATHOGENESIS
Crystallisation in joint
Crystal absorbed by PMN
Secretion lysozyme enzymes
Severe synovitis
ACUTE GOUTY ARTHRITIS
• INCIDENCE
– Mostly men > 40yrs
– Association with Metabolic syndrome
– Sometimes postmenopausal women
(Often on Diuretics)
PRECIPITATING CAUSES IN ACUTE
GOUTY ARTHRITIS
• Trauma and surgery
• Medication
• Alcohol
• Diet
CLINIAL PICTURE
ACUTE GOUTY ARTHRITIS
• Goes to bed healthy
• Wakes up sudden monoarthritis ( 85% Podagra)
(heel, instep, knee, wrist and hands and elbow -olecranon
bursitis)
• Rigors with severe pain
• Night spent in torture
• Joint is red (“ripe tomato”),warm and very tender.
• After attack skin around the joint often peels off
• Acute attacks usually pass completely until the next attack
Uncontrolled hyperuricaemia may lead to
polyarticular gout
ACUTE GOUTY ARTHRITIS
DIAGNOSIS OF GOUT
• Family history, as well as a typical history of
attacks
• Typical clinical picture and tophi
• Elevated serum urate - (may be normal
during attacks)
• Urate crystals in aspiration fluid (as well as
tophi)
• X rays: Punched-out erosions (Rat bitten)
URATE CRYSTALS
TREATMENT
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Exclude precipitating causes
Increased water intake 2-3l/day
A low purine diet and avoidance of alcohol are recommended
Foods with a very high purine content: anchovy, sardines, liver and
kidneys. Most meats, fish and chicken products also have a high
purine content.
• Treatment of associated conditions such as
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obesity
Hypertension
Diabetes mellitus
hyperlipaemia
kidney failure
RX ACUTE ATTACK
• Avoid prescribing prophylactics (uric acid
lowering drugs)
• NSAIDS ( not used in kidney failure)
• Colchicine
• Corticosteroids (in resistant cases)
Progression in the disease
• Asymptomatic hyperuricaemia
– continues until possible first attack
• Acute gouty arthritis
• Interval hyperuricaemia
– periods between attcks
• Chronic tophaceous gout
• Complications
– kidney stones and nephropathy
CHRONIC TOPHACEOUS GOUT
• Deposition of uric acid crystals in the tissues
(tophi)
• After repeated attacks after 11 - 12 years
• The tophi occur in
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The auricles - helix
Tendons (hands, achilles tendon and feet)
Bursae - especially olecranon bursa
The tophi may ulcerate with secretion of pasty
material
INDICATIONS FOR LONG-TERM
PROPHYLACTIC THERAPY
 If conservative measures do not have the desired
effect and the levels still remain high (> 0.55 - 0.6
mmol/l) with repeated attacks
 (If less than 1 attack per year is experienced,
treatment is not necessary)
 Positive family history of gout and kidney stones
with very high urate levels
 Chronic tophaceous gout
 Kidney stones or nephropathy
MEDICINES FOR LONG-TERM
PROPHYLAXIS
• Allopurinol 300mg-900mg/day
• Uricosurics medicines
– Probenecid 250mg bd
– Must not be used if there is kidney failure or kidney stones
– To avoid kidney stones a high fluid intake (2l/day) must be
maintained and in addition the urine can be alkalised with
something like “citrosoda”
• Colchicine 0.5mg should be added once or twice daily
for the first few months in order to prevent recurrent
attacks
SEPTIC ARTHRITIS
CAUSES
Bacterial
Gonococcal
Non-gonococcal(Staphylococcus aureus , nongroup-A
beta-hemolytic streptococci, gram-negative bacteria, and
Streptococcus pneumoniae)
Viral – HBV, Rubella, Mumps, I.M, Parvovirus,
Enterovirus, Adenovirus
 Fungal
CAUSES
• Most serious cause of monoarthritis, can destroy cartilage in one to two
days
• Non-gonococcal are most serious
- most common in knees and hips
- sternoclavicular joints in IV drug users
- most febrile but do not appear especially ill
- 90% monoarticular, hematogenous spread
- 80% Gram(+) anaerobes
* 60% S. Aureus (most PCN, some meth resistant)
* 15% Non-group A, beta-hemolytic strep
* 3% Strep pneumo
- 18% Gram(-)
- Anearobes on rise in IV drug users/immunocompromised/HIV
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•
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•
common organisms Staphylococci or Streptococcus
young adults, significant incidence gonococcal
arthritis
Elderly & immunocompromised gram -ve
organisms
Anaerobes more common with penetrating trauma
ROUTES OF INFECTION
Risk factors
•
Pre-existing joint disease
•
Prosthetic joints
•
Low SE status, IV drug abuse, alcoholism
•
Diabetes, steroids, immunosuppression/HIV
•
Previous intra-articular steroid injection
DIAGNOSIS
• Synovial fluid aspiration
– Volume/viscosity/cellularity/a
ppearance
– Gram stain/culture
– Absence of organism does
not exclude septic arthritis
– Polarised light microscopy
(crystals). Crystals don’t
exclude septic arthritis.
– NB suspected prosthetic joint
sepsis should ALWAYS be
referred to orthopaedics
DIAGNOSIS
• Always blood cultures
• Significant proportion blood cultures + ve in
absence of + ve synovial fluid cultures
• FBC ESR & CRP
• BUT absence of raised WBC, ESR or CRP not
exclude diagnosis of sepsis - if clinical
suspicion high always treat
Antibiotic treatment of septic arthritis
• Local and national guidelines
• Liaise with micro. guided by gram stain
• Don’t wait for cultures to start empiric antibiotic
treatment
• 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
QUESTIONS?