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Clinical Approach to Acute Monoarthritis Mohammad Hasan Jokar Acute Arthritis • The sudden onset of inflammation of the joint, causing severe pain, swelling, and redness. • Structural changes in the joint itself may result from persistence of this condition. Signs of Inflammation • Swelling • Warmth • Erythema • Tenderness • Loss of function Key Points • Distinguish arthritis from soft tissue non articular • • • syndromes (discrepancy between “active” and “passive” ROM suggests periarticular/soft tissue) If the problem is articular distinguish single joint from multiple joint involvement Inflammatory or non-inflammatory disease Always consider septic arthritis! Articular Vs. Periarticular Clinical feature Anatomic structure Painful site Pain on movement Swelling Articular Synovium, cartilage, capsule Diffuse, deep Active/passive, all planes Common Periarticular Tendon, bursa, ligament, muscle, bone Focal “point” Active, in few planes Uncommon Inflammatory Vs. Noninflammatory Feature Inflammatory Noninflammatory Pain (when?) Swelling Erythema Warmth AM stiffness Systemic features î ESR, CRP Synovial fluid WBC Examples Yes (AM) Soft tissue Sometimes Sometimes Prominent Sometimes Frequent WBC >2000 Septic, RA, SLE, Gout Yes (PM) Bony Absent Absent Minor (< 30 ‘) Absent Uncommon WBC < 2000 OA, AVN Acute Monoarthritis • Inflammation (swelling, tenderness, warmth) in one joint • Occasionally polyarticular diseases can present with monoarticular onset: (RA, JRA,Reactive and enteropathic arthritis, Sarcoid arthritis, Viral arthritis, Psoriatic arthritis) Acute Monoarthritis - Etiology • THE MOST CRITICAL DIAGNOSIS TO CONSIDER: INFECTION ! • Septic • Crystal deposition (gout, pseudogout) • Traumatic (fracture, internal derangement) • Other (hemarthrosis, osteonecrosis, presentation of polyarticular disorders) Questions to Ask – History Helps in DD • Pain come suddenly, minutes? – fracture. • 0ver several hours or 1-2 days? –infectious, • • • crystals, inflammatory arthropathy. History of IV drug abuse or a recent infection? – septic joint. Previous similar attacks? – crystals or inflammatory arthritis. Prolonged courses of steroids? – infection or osteonecrosis of the bone. Acute Monoarthritis Indications for Arthrocentesis • The single most useful diagnostic study in initial evaluation of monoarthritis: SYNOVIAL FLUID ANALYSIS • 1. Suspicion of infection • 2. Suspicion of crystal-induced arthritis • 3. Suspicion of hemarthrosis • 4. Differentiating inflammatory from noninflammatory arthritis Tests to Perform on Synovial Fluid • Total leukocyte count/differential: inflammatory vs. non-inflammatory. • Polarized microscopy to look for crystals. • Gram stain and cultures • Not necessary routinely: Chemistry (glucose, total protein, LDH) unlikely to yield helpful information beyond the previous tests. Case 1 • 52 yo wm presents to the Emergency Department with a 2 day history of excrutiating pain, with swelling, of the left knee. He denies a history of trauma. He reports fever of 39 degrees and chills. Physical Exam: T= 39.5 BP=150/92 P=105 RR=18 The physical exam is notable only for the musculoskeletal exam which reveals: Left knee with erythema, warmth, and swelling. There is exquisite tenderness and pain with any motion. There is reduced range of motion due to pain. Other joints are normal. • The presentation of monoarticular arthritis *****Aspiration of the joint***** Lab tests • CBC • Joint fluid study • Blood culture • Synovial fluid WBC 92,000 97 % PMNs Gram Stain Septic Arthritis • Key Features: – Monoarticular (almost always) – Dolor, rubor, calor – Swelling – Exquisite pain – Synovial fluid >50K WBCs and >95% PMNs – Aggressive disease warranting aggressive management Septic Arthritis • Management of the patient with septic arthritis – Arthrocentesis – Hospital admission – Orthopedic consult – IV antibiotics • Broad spectrum antibiotics until culture and sensitivity available Septic arthritis ******Drainage of the pus****** ******IV antibiotics are essential****** Septic Arthritis • Staphylococcus aureus - most aggressive – Rapid evolution to joint destruction – Importance of rapid diagnostic studies – Rapid initiation of therapy • Surgical drainage • Intravenous antibiotics Epidemiology • 1:1 M:F • Mean Age=55 • 85%=Monoarticular • Patients with Damaged Joints are at Increased Risk • Most are hematogenously spread • Fever present in only 60% of non-GC septic arthritis • Crystalline arthritis is 4x as common as septic arthritis; fevers/rigors non-specific Specific Infectious Agents • Causative agents identified in 2/3 of patients in • • • whom suspected 50% have known portal of entry 25% are iatrogenic 75% have extra-articular source: Look for skin, respiratory, or GU sources Groups at risk for septic arthritis • Rheumatoid Arthritis: Account for up to 50% of cases • Immunosuppressed Host, especially Organ • • • • • Transplant Patients Advanced Age: Greater than 60, especially with Prosthetic Joints: May result in Osteomyelitis Diabetes Neoplasm IV Drug Use: Repetitive transitory Bacteremia: Staphylococci (MRSA)>Enterobacter, Serratia, and Pseudomonas Hemodialysis: Recurrent Vascular Infections, especially Staphylococci Right wrist destruction by Staphylococcus aureus Antibiotics and Supportive Therapy • Guided by local antibiotic sensitivity patterns • Intra-articular antibiotics are not required and may cause a chemical synovitis • Usually administered for 4 to 6 weeks • NSAID’s avoided until the diagnosis is secure • Joint Immobilization for 1 to 3 days • ROM as soon as possible Case 2 • 22 yo wf presents to the Emergency Department with c/o left wrist pain of 2 days’ duration. She reports 2 weeks ago, the onset of left ankle pain and swelling which subsequently resolved in 3 days. She then developed 3 days of swelling and pain in the left knee, followed by 3 days of swelling and pain in the right knee. Physical Exam – Temp 39 – Normal examination of HEENT, Lungs, CV, and Abdomen – Skin: Pustular lesions right 3rd and 4th fingers – Musculoskeletal: Left wrist warm, swollen (arthritis) with erythema extending along the extensor tendons of the hand (tenosynovitis) Gonorrhea: rash, vesicle, and pustule Gonorrhea: rash, pustule, and bulla Gonorrhea: pustule Gonococcal Arthritis • Key Features – Migratory arthritis (immune mediated or reactive) – Tenosynovitis – Rash – Sexually active patient (though this may not be disclosed on history) Gonococcal Arthritis • Evaluation – Aspiration of affected joint • Inflammatory joint fluid (>2000 WBC’s) • Rarely WBC count in the “septic” range (>50,000 WBC’s) • Cultures usually negative – Culture • Oropharynx, anus, cervix/urethra, skin lesions Gonococcal Arthritis • Migratory • • • • Polyarthralgias/Polyarthritis/Tenosynovitis = 66%; Knee>hand>wrist Dermatitis=sparse peripheral necrotic pustules in 40% 83%=female, mean age=23, GU involvement in 63%, often asymptomatic Check VDRL and HIV and Co-treat Chlamydia DGI-like arthritis-dermatitis can also occur with H. influenzae, N. meningitidis, and S. moniliformis Management • Antibiotics – Ceftriaxone – Doxycycline added (to cover likely concomittant Chlamydia infection) – Surgical drainage of the joint rarely necessary Case3 • 32 y/o WM admitted to the hospital with 2 days • • of acute onset of arthritis in his right knee that progressed to the left knee. The day previous to the admission, he was evaluated in the ER, and an arthrocenthesis was attempted. The patient was discharged on ceohalexin 500 mg QID. ROS: 3 weeks previous to admission he had an episode of diarrhea that lasted for 10 days and improved after treatment with Cipro. Family History: Sister with recurrent uveitis. Physical Examination • PE: fever 38.5. Otherwise within normal limits. • Joint exam: tenderness, redness and effusions in both knees. • Labs: ESR 60, Synovial fluid showed no crystals and • Gram stain revealed no organisms. HLA B-27 positive. Patient was started on indomethacin 50 mg PO QID with significant improvement of his symptoms. Reactive Arthritis • “Reactive Arthritis (ReA) is an infectious induced systemic illness characterized by an aseptic inflammatory joint involvement occurring in a genetically predisposed patient with a bacterial infection localized in a distant organ/system”. Reactive Arthritis • Epidemiology • ReA is an acute and insidious polyarthritis after an • • enteric and urogenital infections. Incidence varies widely (1% to 20%). Frequency varies from 0 to 15% after infection with Salmonella, Shigella, Campylobacter or Yersinia. • HLA-B27 can be present in 72% to 84% of the cases. • Incidence after Chlamydia trachomatis is not well known. Reactive Arthritis • ReA can occurs in the absence of HLAB27, this play a very important role. Reactive Arthritis • Causative organisms • Frequent association: • • • • • • • • • Chlamydial trachomatis Ureaplasma urealyticum Salmonella enteritidis Salmonella typhimurium Shigella flexneri Shigella dysenteriae Campylobacter jejuni Yersinia enterocolitica Streptococcus SP Reactive Arthritis • Less common association: • • • • • • • • • • • Chlamydia pneumoniae Neisseria meningitidis serogroup B Bacillus cereus Pseudomonas Clostridium difficile Borrelia burgdorferi Escherichia coli Helicobacter pillory Lactobacillus Brucella abortus Hafnia alvei Reactive Arthritis • • • • Clinical Manifestations: Postenteric ReA is described equally in men an women. Postchlamydial is most common in men. In patients with postenteric ReA, the episode of diarrhea is usually prolonged. • Arthritis presents usually 2 to 3 weeks after the episode of diarrhea. • Arthritis usually resolves within 6 months, but a few patients had recurrences an a minority develops a chronic arthritis. Reactive Arthritis • In patients with postchlamydial disease, urethritis is • • • usually mild, painless and nonpurulent. Conjunctivitis is usually observed very early, before the onset of arthritis, uveitis is less common but occurs in 15% of patients with chronic persistent disease. Skin manifestations include: Keratoderma blenorrhagica, Circinate balanitis and oral ulcers. Less common patients can develop valvulitis, rhythm disturbances. Reactive Arthritis • Treatment: • NSAIDS are the first line of treatment. • In patient with frequent recurrences or chronic arthritis • • • benefit from DMARDS such us sulfasalazine or methotrexate. If there is axial involvement they will benefit from TNFalpha blockers. Topical steroids are indicated in conjunctivitis and uveitis. In monoarthritis steroid injections could be beneficial. Case 4 – 24 yo wm treated for gonococcal urethritis 2 weeks prior to presentation has complaint of low back pain, left ankle and right knee pain and swelling. He has noted “pink eye” in his left eye. Physical exam – Afebrile – HEENT- Left eye with conjunctival injection – Musculoskeletal- Tender right SI joint Effusion with warmth and tenderness of left ankle and right knee Evaluation – CBC, CMP- normal – ESR- 62 – U/A- neg protein, 2 WBCs, 5 RBCs • Culture and sensitivity negative – Xrays- SI joints, knees, ankles- normal Reiter’s Syndrome (Reactive Arthritis) • Triad: Conjunctivitis, urethritis, arthritis • Other features: Sausage digits, oral erosions, keratoderma blenorrhagicum, circinate balanitis • Triggered by a recent GI/GU(STD) infection Keratoderma Blennorrhagicum Reiter’s Syndrome • Key Features: – Preceding GI/GU infection • The GU infection may have been asymptomatic (especially in women), or not yet detected – Triad: Conjunctivitis, urethritis, arthritis (lower extremity>upper, asymmetric, oligoarticular) – Usually self-limited (3-12 month course) – 15% develop chronic, destructive arthritis Reiter’s Syndrome • Radiographic features • Xrays may be normal acutely, however changes develop over time – Periostitis – Sacroiliitis • Unilateral Reiter’s Syndrome • Management – Detection of underlying infection – Treatment of underlying infection – NSAID’s – DMARD’s- mixed results – Best evidence supports use of sulfasalazine Case 5 • 45 yo m presents to the Emergency Department with a 12 h history of excrutiating pain, with swelling, of the left foot Physical Exam: T= 39 BP=150/92 P=105 RR=18 The physical exam is notable only for the musculoskeletal exam which reveals: Left foot with erythema, warmth, and swelling. There is exquisite tenderness and pain with any motion. There is reduced range of motion due to pain. Other joints are normal. Lab tests • CBC: WBC 13000 PMN 85% • Creatinine:1 • Uric acid :6.5 • Synovial fluid :40000 90% PMNs Management of gouty arthritis • Asymptomatic hyperuricemia • Acute gouty arthritis • Chronic or tophaceous gout Purine nucleotides hypoxanthine Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion Tissue deposition in excess Urate crystal Phagocytosis with acute inflammation and arthritis microtophi Management of gouty arthritis • Asymptomatic hyperuricemia • Acute gouty arthritis • Chronic or tophaceous gout Management of gouty arthritis Treatment of asymptomatic hyperuricemia usually in not necessary Preventive measures • Avoiding excess weight gain • Reducing risks for hypertension • Avoiding diuretic therapy • Control alcohol intake Management of gouty arthritis • Asymptomatic hyperuricemia • Acute gouty arthritis • Chronic or tophaceous gout Purine nucleotides hypoxanthine Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion colchicine Tissue deposition in excess Urate crystal microtophi Phagocytosis with acute inflammation and arthritis NSAID Management of acute gout Do not attempt to modify plasma urate concentrations • NSAID • Colchicine • steroids Management of acute gout • NSAID Shorter half life – Indomethacin (50mg qid-50mg tid-25mg tid) – Ibuprofen 800mg q6h Contraindications – Renal insufficiency, peptic ulcer, warfarin therapy, liver disease, chronic heart failure Management of acute gout Colchicine Effective within the 24 hours of an attack Mechanism of colchicine • Inhibit phagocytosis (microtubular system) • Affect chemotaxis • Affect motility and adhesion of neutrophil • Reduce release PGE2 and LTB4 Management of acute gout Colchicine • Side effect – GI disturbance, blood dyscrasias, myoneuropathy • Contraindications – Renal dysfunction, liver disease, sepsis, bone marrow dysfunction Management of acute gout Corticosteroids • NSAID and colchicine are contraindicated Prednisone 20-50mg oral 3-20days • Intra-articular steroids Prophylactic therapy • Indications – Recurrent attacks – Tophi – Renal disease – Uric acid urolithiasis – Inherited metabolic disorders – Degree of hyperuricemia (11.8 mg/dl) Prophylactic therapy • Colchicine • NSAID • Urate-lowering therapy – Allopurinol – Uricosuric agents Induce a flare up Concurrent colchicine prophylaxis Purine nucleotides hypoxanthine allopurinol Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion Tissue deposition in excess Urate crystal microtophi Phagocytosis with acute inflammation and arthritis NSAID uricosurics colchicine Prophylactic therapy • Dietary restriction of purines rarely causes a fall in the plasma urate concentration more than 1.0 gm/dl • Flares occure during a fall in serum urate level Purine nucleotides hypoxanthine allopurinol Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion Tissue deposition in excess Urate crystal Phagocytosis with acute inflammation and arthritis microtophi Prophylactic therapy • Allopurinol Xanthine oxidase inhibitor Indications – Renal insufficiency – Nephrolithiasis – Tophi – Tumor lysis syndrome – Primary metabolic defects Prophylactic therapy • Allopurinol – 300mg-900mg – Side effect (<2%) • Potentiating imuran marrow suppressive effect • Hypersensitivity syndrome • Hepatitis • Interstitial nephritis Purine nucleotides hypoxanthine Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion Tissue deposition in excess Urate crystal uricosurics Phagocytosis with acute inflammation and arthritis microtophi Prophylactic therapy • Uricosuric agents – Probenecid – Sulphinpyrazone – Benzbromarone Mechanism – Inhibit renal tubular reabsorption Prophylactic therapy • Uricosuric agents Side effects – – – – Uric acid crystalluria GI disturbance Allergy Hepatic impairment Contraindications – Renal insufficiency – nephrolithiasis Prophylactic therapy • When instituting uricosuric therapy – Concurrent colchicine prophylaxis – Initial low dose, increase dose gradually – Maintain alkaline diuresis – Not use in urine volume less than 1400ml/24 hours Purine nucleotides hypoxanthine allopurinol Xanthine oxidase xanthine Uric acid Urinary excretion Alimentary excretion Tissue deposition in excess Urate crystal microtophi Phagocytosis with acute inflammation and arthritis NSAID uricosurics colchicine