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Gout, Pseudo Gout and Septic Dr Ruth Sy

Gout, Pseudo Gout and Septic Dr Ruth Sy

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Published by: Doc Jen Kwan on Feb 12, 2012
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Page 1 of 3 Medicine II Rheumatology Gout, Pseudogout and Septic Arthritis Dr.

Ruth Sy July 18, 2007 Gout Definition  Gout is a syndrome caused by an inflammatory response to the formation of monosodium urate monohydrate (MSUM) crystals which develop secondary to hyperuricemia  Acute and chronic forms are recognized. Hyperuricemia may be due to environmental and/or genetic factors Clinical Features  Most commonly affects middle-aged males  Acute and usually relapsing, self-limiting arthropathy  Chronic form associated with tophus formation and bone and joint destruction  Commonly associated with obesity, heavy alcohol intake, hypertension, renal impairment and diuretic use  Target areas ± 1st metatarsophalangeal joints (insteps, heels, ankles and knees) Crystals Found in Synovial Fluid Monosodium urate Acute Gout monohydrate (MSUM) Tophaceous Gout Asymtomatic Calcium Pyrophosphate Acute Dihydrate (CPPD) Pseudogout Destructive Arthropathy Asymptomatic Basic Calcium Phosphate Acute Calcific Periarthritis Acute Arthritis Asymptomatic Lipid Acute Arthritis Cholesterol Asymptomatic Acute Gouty Arthritis  Abrupt onset of severe joint inflammation often at night  Subsides completely over 3 to 10 days st  75% in the 1 MTP joint  Urate crystals in synovial fluid  May have hyperuricemia  Usually monoarticular, may be polyarticular Hyperuricemia  Overproduction (10%) o Ethanol o Deficiency of HGRPT or G6PD o Superactive PRPP synthetase o Myeloproliferative disorders o Psoriasis  Underexcretion (90%) o Dehydration, Starvation, Ketosis o Renal Abnormality o Drugs: Diuretics, Low dose aspirin o Toxins, Ethanol, Lead o Hypothyroidism Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease Associations -Hyperparathyroidism -Hypomagnesemia -Familial Hypocalciuric -Hypothyroidism -Hypercalcemia -Gout -Hemochromatosis -Neuropathic Joint -Hemosiderosis -Aging -Hypophosphatasia -Amyloidosis -Trauma

Jen Kwan

Prolonged PR interval Plus evidence of recent Strep infection: Elevated ASO titer. Allopurinol) Continue prophylactic doses of colchicines for at least 9 months after normalization of the plasma urate concentration Routes By Which Bacteria Can Reach the Joints 1. General Principles in the Management of Gout Acute Gout NSAIDs Colchicine Do not attempt to modify plasma urate concentration Recurrent Gout or Reverse factors Chronic Gout promoting hyperuricemia Maintain urine output >1400 ml/day when asymptomatic. Erythema Maginatum. (+) CRP. start with very low doses and look out for serious toxicity. renal function and blood count Further investigations usually unnecessary  Remove any avoidable factors contributing to hyperuricemia.g. Chorea. influenzae <1 Gram negative bacilli E. Spread from an adjacent soft tissue infection 4. Fever > 38°C. gonorrhea & 50 meningitidis H. Diagnostic or therapeutic measures 5. Probenecid. Nodules Minor Prior ARFor RHD. recent scarlet fever *Diagnosis with two major or 1 major + 2 criteria and evidence of recent Strep infection Jen Kwan .Page 2 of 3 Medicine II Rheumatology Approach to the Management of Tophaceous Gout in the Elderly  Confirm diagnosis by crystal identification Beware coexistent infection. Antistreptococcal bodies. Dissemination from osteomyelitis 3. Arthralgias. coli. ESR > 120. Leukocytosis. add agent to lower plasma urate concentration (e. diuretics and high risk of gastrointestinal problems  Beware of Allopurinol If it has to be used. Group A Strep on throat culture. Avoid uricosuric drugs. such as unnecessary diuretics  Consider the need for specific therapy (this is often unnecessary)  Use low dose colchicine as the drug of 1st choice for painful inflammatory problems  Beware of non-steroidal antiinflammatory disease (NSAIDs) Consider renal disease. Mycobacterium & <1 Fungi Children (%) 27 16 8 40 9 <1 Revised Jones Criteria for the Diagnosis of Rheumatic Fever Major Arthritis. Carditis. Hematogenous route 2.  Check serum uric acid. Penetrating damage by puncture or cutting Septic Arthritis Organisms in Septic Arthritis Adults (%) Gram positive cocci Staph aureus 35 Strep pyogenes 10 Strep pneumonia Strep viridans Gram negative cocci N. Salmonella 5 & Pseudomonas sp.

myalgia. stiff neck Stage II ± Early Disseminated  Multiple or recurrent erythema migrans  Borrelia lymphocytoma  Migratory arthralgia/arthritis  Meningoencephalitis  Peripheral neuropathy (Bell¶s Palsy)  Carditis (Conduction Defects) Stage III ± Late  Acrodermatitis chronic atrophicans  Intermittent/Chronic oligoarthritis  Chronic meningoencephalitis or encephalitis  Sensorimotor neuropathies Typical Patterns of Joint Involvement in Lyme Disease Pattern Incidence Mild Migratory 20% arthralgia Midcourse Intermittent 60% oligoarthritis Late Chronic 10% oligoarthritis Musculoskeletal Syndromes Associated with HIV Infection  Arthralgia  Infectious arthritis o Opportunistic infections o Pyogenic infections  Reiter¶s syndrome  Psoriatic arthritis  Myositis  Sjörgen¶s syndrome  Undifferentiated spondyloarthropathy  AIDS-associated arthritis  Painful articular syndrome  Avascular necrosis of bone Jen Kwan . arthralgia.Page 3 of 3 Medicine II Rheumatology Lyme Disease Major Clinical Features of Lyme Disease Stage I . headache.Early  Erythema migrans  Flu-like syndrome ± malaise. fever.

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