Case Presentation

Jane Klaes, DO November 29, 2006

Mr. GS

c/c: right knee pain Hx c/c: Mr. GS is a 45-year old man with a 3-day history of right knee pain. The pain began the morning after attending an auto show. No history of trauma. Due to pain limiting ambulation, pt went to ER where he was given Duricef and Naprosyn. Swelling decreased but pt presented to office due to pain on ambulation. No F/C, eye pain, cough, SOB, mouth pain or sores, urethral discharge, other joint pain. PMHx: none PSHx: none All: NKDA Meds: Duricef and Naprosyn from ER x 3 days FHx: no arthritis, no CAD, no DM, no CA Soc Hx: no tobacco, 4-5 beers per day for >10 years, no illicits, married, auto worker ROS: negative except for above

Mr. GS

PE

VS BP 140/90, R 14, P 90, T 99.5 HEENT: WNL H: RRR no murmur L: CTAB A: soft, NT, ND Ext: right knee erythematous, edematous, warm, small effusion, flexion limited to 90 degrees (passive and active), no instability

Mr. GS

Labs:

Na 141, K 4.2, Cl 102, CO2 23, BUN 20, Cr 1.2 WBC 11.9, normal diff

Mr. GS

D/Dx:

D/Dx of monoarticular arthritis

Infectious

Crystalline

Gonococcal Non-gonoccocal Fungal Lymes Gout Pseudogout

Trauma Avascular necrosis Hemarthrosis Internal derangement Osteomyelitis OA Malignancy RA Psoriatic Sarcoidosis Reactive arthritis

Clues to Diagnosis
Clues from H&P
Onset seconds to minutes Onset hours to days Onset days to weeks IVDA, immunocompromised Previous attacks Prolonged steroid rx Anticoagulants Urethritis, conjunctivitis, diarrhea, rash Psoriatic patches Diuretics, tophi, alcoholic binges Eye inflammation, LBP Young adult, dermatitis, migratory polyarthralgias

Diagnosis

Hilar adenopathy, erythema nodosum

Clues to Diagnosis
Clues from H&P
Onset seconds to minutes Onset hours to days Onset days to weeks IVDA, immunocompromised Previous attacks

Diagnosis
Fracture, internal derangement Infection, crystals, inflammatory arthritis OA, tumor, infiltrative dz, indolent inf Septic arthritis Crystals, inflammatory arthritis

Prolonged steroid rx, chronic EtOH

Avascular necrosis
Hemarthrosis Psoriatic arthritis

Urethritis, conjunctivitis, diarrhea, rash Reactive arthritis

Diuretics, tophi, alcoholic binges

Gout
Ankylosing spondylitis Gonoccocal arthritis Sarcoidosis

Workup

Xray if trauma or sx > 2 weeks CBC, ESR, uric acid Arhtrocentesis (diagnostic) BC in pts with suspected septic arthritis Pharyngeal, urethral, cervical swabs for suspected gonoccocal arthritis

Arthrocentesis

Mandatory if suspect infection Relative contraindication: cellulitis May be performed if pt taking coumadin Often provides symptomatic relief Send fluid for WBC with diff, crystal analysis, gram stain, cx

Arthrocentesis

Knee extended (or flexed 90 degrees) 1cm lateral and 1 cm cephalad to superiorlateral edge of patella 45 degree angle directed into knee joint

Synovial analysis
Crystals
WBC <2000

WBC >2000
WBC >100,000

Bloody
Fat droplets

Synovial analysis
Crystals WBC <2000 WBC >2000 WBC >100,000 Bloody Fat droplets Gout, pseudogout OA Inflammatory arthritis Septic arthritis Fracture, tumor, internal derangement Fracture

Pearls

CBC and temperature can be normal in early septic arthritis but may be elevated in gout or pseudogout Risk factors for septic joint:

Septic arthritis requires immediate IV Abx to prevent joint destruction Gonoccocal arthritis is most common cause of monoarthritis in young sexually active person (F>M) If crystals are found in synovial fluid, infection cannot be ruled out automatically. Serum uric acid is often normal in acute gout, and may be elevated in conditions other than gout. Intra-articular problems cause restriction in passive and active ROM; periarticular problems cause restriction in active>passive ROM Bulge sign can be elicited to detect small knee effusion

Prosthetic joint, skin infection, joint sx, RA, age>80, DM

Results of arthrocentesis

Gout

Etiology: deposition of monosodium urate crystals in synovial fluid or tissues

Occurs in middle age (women after menopause) Genetic predisposition Association with diabetes and hypertrigliceridemia Frequency: 2.7/1000 in US M:F 9:1 Pathogenesis

Lysis of PMNs with ingested crystals triggers inflammatory response

Uric acid precipitates as monosodium urate 7mg/dl is limit of solubility for monosodium urate Hyperuricemia (>7mg/dl) is risk factor

Gout can occur with normal serum uric acid Hyperuricemia can exist without gout

Hyperuricemia

Uric acid is the end product of purine metabolism Humans lack uricase, the enzyme that breaks uric acid into water-soluble product Most gout is caused by underexcretion of uric acic

Hyperuricemia
Overproduction Primary idiopathic Underexcretion Primary idiopathic

Enzyme deficiency
Enzyme overactivity Lymphoproliferative dz Myeloproliferative dz Polycythemia vera Psoriasis Pagets disease Rhabdomyolysis Exercise Alcohol Obesity, hypertriglyceridemia Purine-rich diet

Renal insufficiency
Polycystic kidney dz Drug ingestion (salicylates, diuretics, alcohol, sinemet, niacin) HTN Acidosis Diabetes insipidis Down syndrome Starvation ketosis Hypothyroidism Lead intoxication Hyperparathyroidism Sarcoidosis

Hyperuricemia

Overproduction

600 mg/day is normal production Dx by 24-hour uric acid collection

If >800 mg excreted - overproducer

Underexcretion

Uric acid is excreted by kidneys and GI tract Renal excretion is defective in most patients with gout (98%)

Acute gouty arthritis

Usually monoarticular 75% in LE Modifiable risk factors for attacks:

Abrupt change in uric acid or trauma may precede attack Presents as pain with swelling, erythema, warmth, tenderness, +/- fever

Alcohol Obesity Hypertension Lead exposure Binging on protein- and purine-rich foods Thiazide and loop diuretics

Pain usually begins in night

Attacks last 7-10 days if untreated

Water resorbed from joint spaces

Complications

Tophaceous gout

Monosodium urate depositions in soft tissue

Renal

Occur ave. 12 years from initial attack

Great toe, fingers, wrist, hand, olecranon bursae, Achilles tendon

Gouty tophi involving the proximal interphalangeal joint with erythema of the overlying skin.

From deposition of crystals

Diagnosis

Negatively birefringent crystals from on polarized light microscopy PMNs and intracellular monosodium urate crystals in joint aspirate

Treatment

Acute

NSAIDs (Indomethacin) Colchicine

Preferred treatment for pts who do not have contraindication Start at maximal dose immediately after onset of attack Inhibits phagocytosis of urate crystals and release of chemotactic factor (decreases inflammation) Works best if started immediately after onset of attack GI side effects not well tolerated Used in patients with contraindications to NSAIDs

Corticosteroids intraarticular, systemic

Prevention

General

Use preventive tx for patients with recurrent attacks or complications (not first attack) Start uric acid-lowering drugs after acute attack ends because they mobilize uric acid stores Treat to serum uric acid = 6mg/dL
Weight loss, decreased EtOH, decreased consumption of purine-rich foods, control of HTN

Non-pharm

Purine-rich foods: liver, kidney, anchovies, sardines, herring, mussels, bacon, codfish, scallops, trout, haddock, veal, venison, turkey, alcohol

Prevention

Low dose NSAID or colchicine

Uricosuric drugs (probenecid, sulfinpyrazone)

Use with urate-lowering drugs Discontinue after stable uric acid level and free from acute attacks 3-6 months

Allopurinol

Increase renal excretion Used for under-excreters Do not use if CrCl < 50 Inhibited by aspirin

Xanthine oxidase inhibitor Decreases production of uric acid Drug of choice with impaired renal function (CrCl <50)

References

AAFP: Diagnosis and Management of Gout, April 1999 AAFP: Gout and Hyperuricemia, February 1999 AAFP: Diagnosing Acute Monoarthritis in Adults, July 2003 E-Medicine: Monoarthritis, Gout and Pseudogout Up to Date: Gout