Acute Monoarthritis: Diagnosis in Adults

 

Am Fam Physician. 2016 Nov 15;94(10):810-816.

Author disclosure: No relevant financial affiliations.

Acute monoarthritis can be the initial manifestation of many joint disorders. The most common diagnoses in the primary care setting are osteoarthritis, gout, and trauma. It is important to understand the prevalence of specific etiologies and to use the appropriate diagnostic modalities. A delay in diagnosis and treatment, particularly in septic arthritis, can have catastrophic results including sepsis, bacteremia, joint destruction, or death. The history and physical examination can help guide the use of laboratory and imaging studies. The presence of focal bone pain or recent trauma requires radiography of the affected joint to rule out metabolic bone disease, tumor, or fracture. If there is a joint effusion in the absence of trauma or recent surgery, and signs of infection (e.g., fever, erythema, warmth) are present, subsequent arthrocentesis should be performed. Inflammatory synovial fluid containing monosodium urate crystals indicates a high probability of gout. Noninflammatory synovial fluid suggests osteoarthritis or internal derangement. Pitfalls in the diagnosis and early treatment of acute monoarthritis include failure to perform arthrocentesis, administering antibiotics before aspirating the joint when septic arthritis is suspected (or failing to start antibiotics after aspiration), and starting treatment based solely on laboratory data, such as an elevated uric acid level.

Monoarthritis refers to the clinical presentation of pain or swelling in a single joint.1 The diagnosis can pose a considerable challenge in the primary care setting because the pain may be limited to the joint, or it may represent early manifestation of a systemic disease.2 Understanding the clinical clues associated with potential diagnoses and using an evidence-based, systematic clinical approach are of utmost importance.3 A delay in diagnosis and treatment, particularly with septic arthritis, can have catastrophic results including sepsis, bacteremia, joint destruction, or death.35 Pitfalls in the diagnosis and early treatment of acute monoarthritis include failure to perform arthrocentesis, administering antibiotics before aspirating the joint when septic arthritis is suspected (or failing to start antibiotics after aspiration), and starting treatment based solely on laboratory data, such as an elevated uric acid level.35

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SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Radiography is not necessary for an accurate diagnosis of monoarthritis in the absence of trauma or focal bone pain.

C

3, 4

Analysis of synovial fluid distinguishes infectious and inflammatory causes of acute monoarthritis from noninflammatory causes.

C

3, 4, 11, 14

Gouty arthritis may be diagnosed without synovial fluid analysis using a diagnostic rule.

C

24

Disseminated gonococcal infections may not result in septicemia or positive synovial fluid cultures; therefore, cultures should be obtained from the potentially infected mucosal site.

C

31, 32

Inflammatory synovial fluid containing monosodium urate crystals, particularly in the presence of podagra, is highly suggestive of gout.

C

23, 24

Erythrocyte sedimentation rate and C-reactive protein level are more useful for following a disease course than discriminating the presence or absence of the disease in patients with monoarthritis.

C

19, 33


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Radiography is not necessary for an accurate diagnosis of monoarthritis in the absence of trauma or focal bone pain.

C

3, 4

Analysis of synovial fluid distinguishes infectious and inflammatory causes of acute monoarthritis from noninflammatory causes.

C

3, 4, 11, 14

Gouty arthritis may be diagnosed without synovial fluid analysis using a diagnostic rule.

C

24

Disseminated gonococcal infections may not result in septicemia or positive synovial fluid cultures; therefore, cultures should be obtained from the potentially infected mucosal site.

C

31, 32

Inflammatory synovial fluid containing monosodium urate crystals, particularly in the presence of podagra, is highly suggestive of gout.

C

23, 24

Erythrocyte sedimentation rate and C-reactive protein level are more useful for following a disease course than discriminating the presence or absence of the disease in patients with monoarthritis.

C

19, 33


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.

Etiology of Acute Monoarthritis

Any condition that may cause joint pathology can initially present as monoarthritis, resulting in a broad differential diagnosis1  (Table 16). Because of this, monoarthritis has no unifying etiology. The most common diagnoses in the primary care setting are osteoarthritis, gout, and trauma.3

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Table 1.

Causes of Acute Monoarthritis

Common

Avascular necrosis

Crystals

Calcium oxalate

Calcium pyrophosphate dihydrate (pseudogout)

Hydroxyapatite

Monosodium urate (gout)

Hemarthrosis

Infectious arthritis

Bacteria

Fungi

Lyme disease

Mycobacteria

Virus

Internal derangement

Osteoarthritis

Osteomyelitis

Overuse

Trauma

Less common

Ankylosing spondylitis

Bone malignancies

Bowel disease–associated arthritis

Hemoglobinopathies

Juvenile rheumatoid arthritis

Loose body

Psoriatic arthritis

Reactive arthritis

Rheumatoid arthritis

Sarcoidosis

Systemic lupus erythematosus

Rare

Amyloidosis

Behçet syndrome

Familial Mediterranean fever

Foreign-body synovitis

Hypertrophic pulmonary osteoarthropathy

Intermittent hydrarthrosis

Pigmented villonodular synovitis

Relapsing polychondritis

Synovial metastasis

Synovioma

Systemic onset juvenile idiopathic arthritis (Still disease)

Vasculitic syndromes


Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):85.

Table 1.

Causes of Acute Monoarthritis

Common

Avascular necrosis

Crystals

Calcium oxalate

Calcium pyrophosphate dihydrate (pseudogout)

Hydroxyapatite

Monosodium urate (gout)

Hemarthrosis

Infectious arthritis

Bacteria

Fungi

Lyme disease

Mycobacteria

Virus

Internal derangement

Osteoarthritis

Osteomyelitis

Overuse

Trauma

Less common

Ankylosing spondylitis

Bone malignancies

Bowel disease–associated arthritis

Hemoglobinopathies

Juvenile rheumatoid arthritis

Loose body

Psoriatic arthritis

Reactive arthritis

Rheumatoid arthritis

Sarcoidosis

Systemic lupus erythematosus

Rare

Amyloidosis

Behçet syndrome

Familial Mediterranean fever

Foreign-body synovitis

Hypertrophic pulmonary osteoarthropathy

Intermittent hydrarthrosis

Pigmented villonodular synovitis

Relapsing polychondritis

Synovial metastasis

Synovioma

Systemic onset juvenile idiopathic arthritis (Still disease)

Vasculitic syndromes


Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):85.

Symptoms consistent with osteoarthritis include pain that tends to worsen with activity, morning stiffness lasting less than 30 minutes, and asymmetric joint pain.7 The most commonly affected joints are the hands, knees, hips, and spine.7 Although osteoarthritis often follows an insidious course, acute flare-ups are common and can be mistaken for other etiologies. The presence of focal bone pain or recent trauma requires radiography of the affected joint to rule out metabolic bone disease, tumor, or fracture.3,4

Gout is a common disorder with a 3% prevalence worldwide. It accounts for more than 7 million ambulatory visits in the United States annually.8,9 Crystal-induced arthritis presents as a rapidly developing monoarthritis with swelling and erythema, and most commonly involves the first metatarsophalangeal joint.8 Over time, the joint space can be irreversibly damaged with tophi formation.8,10 The presence of monosodium urate crystals indicates gout; these crystals are identified by their needle-like appearance and strong negative birefringence3,8 (Figure 16). Calcium pyrophosphate dihydrate crystals are polymorphic, weakly positive under birefringent microscopy, and their presence indicates pseudogout.3 Other crystal-induced arthritis etiologies include calcium oxalate and hydroxyapatite.1

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Figure 1.

Needle-shaped monosodium urate crystals visible with light microscopy of synovial fluid in a patient with gout.

Reprinted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):89.


Figure 1.

Needle-shaped monosodium urate crystals visible with light microscopy of synovial fluid in a patient with gout.

Reprinted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):89.

Infection is a common etiology of joint pain. When infection is suspected in the presence of a joint effusion or inflammation, arthrocentesis should be performed, in addition to further laboratory testing as indicated (Figure 2 6). (A video of arthrocentesis of the knee is available at https://www.youtube.com/watch?v=fZ2dcZhoGP8.) Gonococcal arthritis is the most common type of nontraumatic acute monoarthritis in young, sexually active persons in the United States.11

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Diagnosis of Acute Monoarthritis

Figure 2.

Algorithm for diagnosing acute monoarthritis. (MRI = magnetic resonance imaging; WBC = white blood cell.)

Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):84.

Diagnosis of Acute Monoarthritis


Figure 2.

Algorithm for diagnosing acute monoarthritis. (MRI = magnetic resonance imaging; WBC = white blood cell.)

Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):84.

Septic arthritis is a key consideration in adults presenting with acute monoarthritis, particularly in the presence of joint pain, erythema, warmth, and immobility.12 The most important risk factors for septic arthritis are a prosthetic joint, skin infection, joint surgery, rheumatoid arthritis, age older than 80 years, diabetes mellitus, and renal disease.11 One study found that among persons presenting with acute joint pain and a predisposing condition, 10% had septic arthritis.4 When septic arthritis is suspected, it is important to begin empiric antibiotics immediately following arthrocentesis, because failure to initiate prompt antibiotic therapy can lead to subchondral bone loss and permanent joint dysfunction.5,11,12 The most common route of entry into the joint is hematogenous spread during bacteremia4,1216; therefore, isolation of the causative agent through synovial fluid culture is essential for the diagnosis and guidance of antibiotic therapy.12

Less common causes of monoarthritis include systemic diseases such as spondyloarthropathies (e.g., psoriatic arthritis, reactive arthritis, ankylosing spondylitis), sarcoidosis, Behçet syndrome, systemic lupus erythematosus, and rheumatoid arthritis.1 Rheumatic diseases and corticosteroid use can cause avascular necrosis of the bone.1

Diagnosing Acute Monoarthritis

The diagnosis of acute monoarthritis begins with a comprehensive history and physical examination to reveal potential diagnostic clues3,6,17  (Table 2 1,3,6,12,18,19). Key elements of the patient history include a review of systems, age, previous joint disease, recent trauma, medication use, family history of gout, concurrent illness, sexual history, diet, travel history, tick bites, alcohol use, intravenous drug use, and an occupational assessment.3,6,17

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Table 2.

Diagnostic Clues in Patients Presenting with Monoarthritis

Clues from history and physical examinationDiagnoses to considerEvaluation

Active range of motion restricted more than passive range of motion

Periarticular pathology

Radiography and/or MRI if indicated

Back pain, eye inflammation

Ankylosing spondylitis

HLA-B27 testing, radiography

Coagulopathy, use of anticoagulants

Hemarthrosis

CBC, ESR, arthrocentesis to confirm diagnosis and rule out infection

Diuretic medication, presence of tophi, renal stones

Gout

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Hilar adenopathy, erythema nodosum

Sarcoidosis

CBC, ESR, ACE level, chest radiography, pulmonary referral

Immunosuppression and/or intravenous drug abuse

Septic arthritis

CBC, ESR, arthrocentesis for cell count and cultures

Insidious onset of pain and swelling over days to weeks

Indolent infection, osteoarthritis, infiltrative disease, tumor

CBC, ESR, arthrocentesis for cell count and cultures, radiography and possible MRI if tumor is a consideration

Maximum pain at limits of range of motion (i.e., stress pain)

Osteoarthritis

Radiography

Normal joint examination

Referred pain

Consider alternative diagnosis

Onset of pain and swelling over several hours or one to two days

Infection, crystal deposition disease, other inflammatory arthritic condition

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Pain elicited by joint movements against resistance only

Tendinitis, bursitis

MRI or ultrasonography if diagnosis in question

Previous acute attacks in any joint with spontaneous resolution

Crystal deposition disease, other inflammatory arthritic condition

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Prolonged course of corticosteroid therapy

Infection, avascular necrosis

CBC, ESR, arthrocentesis for cell count and cultures if concern for infection, radiography and possible MRI if considering avascular necrosis

Psoriatic skin plaques, nail pitting, dactylitis

Psoriatic arthritis

CBC, ESR, arthrocentesis, HLA-B27 testing, ANA testing; none of these tests are diagnostic but can exclude other conditions

Restricted active and passive range of motion

Intra-articular pathology

Radiography and/or MRI if indicated

Sudden onset of pain in seconds or minutes

Fracture, internal derangement, trauma, loose body

Radiography

Urethritis, conjunctivitis, diarrhea, rash, sacroiliitis

Reactive arthritis

CBC; ESR; arthrocentesis; HLA-B27 testing; urine PCR testing for Chlamydia trachomatis; stool cultures for Salmonella, Shigella, and Campylobacter

Young adult, migratory polyarthralgias, tendons inflamed

Gonococcal arthritis

Urine PCR testing, blood culture, and synovial fluid analysis for Neisseria gonorrhoeae


ACE = angiotensin-converting enzyme; ANA = antinuclear antibodies; CBC = complete blood count; ESR = erythrocyte sedimentation rate; MRI = magnetic resonance imaging; PCR = polymerase chain reaction.

Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):86, with additional information from references 1, 3, 12, 18, and 19.

Table 2.

Diagnostic Clues in Patients Presenting with Monoarthritis

Clues from history and physical examinationDiagnoses to considerEvaluation

Active range of motion restricted more than passive range of motion

Periarticular pathology

Radiography and/or MRI if indicated

Back pain, eye inflammation

Ankylosing spondylitis

HLA-B27 testing, radiography

Coagulopathy, use of anticoagulants

Hemarthrosis

CBC, ESR, arthrocentesis to confirm diagnosis and rule out infection

Diuretic medication, presence of tophi, renal stones

Gout

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Hilar adenopathy, erythema nodosum

Sarcoidosis

CBC, ESR, ACE level, chest radiography, pulmonary referral

Immunosuppression and/or intravenous drug abuse

Septic arthritis

CBC, ESR, arthrocentesis for cell count and cultures

Insidious onset of pain and swelling over days to weeks

Indolent infection, osteoarthritis, infiltrative disease, tumor

CBC, ESR, arthrocentesis for cell count and cultures, radiography and possible MRI if tumor is a consideration

Maximum pain at limits of range of motion (i.e., stress pain)

Osteoarthritis

Radiography

Normal joint examination

Referred pain

Consider alternative diagnosis

Onset of pain and swelling over several hours or one to two days

Infection, crystal deposition disease, other inflammatory arthritic condition

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Pain elicited by joint movements against resistance only

Tendinitis, bursitis

MRI or ultrasonography if diagnosis in question

Previous acute attacks in any joint with spontaneous resolution

Crystal deposition disease, other inflammatory arthritic condition

CBC, ESR, uric acid level, arthrocentesis with evaluation for crystals

Prolonged course of corticosteroid therapy

Infection, avascular necrosis

CBC, ESR, arthrocentesis for cell count and cultures if concern for infection, radiography and possible MRI if considering avascular necrosis

Psoriatic skin plaques, nail pitting, dactylitis

Psoriatic arthritis

CBC, ESR, arthrocentesis, HLA-B27 testing, ANA testing; none of these tests are diagnostic but can exclude other conditions

Restricted active and passive range of motion

Intra-articular pathology

Radiography and/or MRI if indicated

Sudden onset of pain in seconds or minutes

Fracture, internal derangement, trauma, loose body

Radiography

Urethritis, conjunctivitis, diarrhea, rash, sacroiliitis

Reactive arthritis

CBC; ESR; arthrocentesis; HLA-B27 testing; urine PCR testing for Chlamydia trachomatis; stool cultures for Salmonella, Shigella, and Campylobacter

Young adult, migratory polyarthralgias, tendons inflamed

Gonococcal arthritis

Urine PCR testing, blood culture, and synovial fluid analysis for Neisseria gonorrhoeae


ACE = angiotensin-converting enzyme; ANA = antinuclear antibodies; CBC = complete blood count; ESR = erythrocyte sedimentation rate; MRI = magnetic resonance imaging; PCR = polymerase chain reaction.

Adapted with permission from Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):86, with additional information from references 1, 3, 12, 18, and 19.

Symptoms that worsen with activity and improve with rest suggest a mechanical process, whereas symptoms with an inflammatory process often worsen with rest and present with morning stiffness.1 Osteoarthritis often starts as mild joint inflammation that may initially arouse suspicion for new-onset inflammatory diseases, such as rheumatoid arthritis.20 Morning stiffness and its duration in the affected joint, pain with activity or rest, recent history of trauma, history of previous joint symptoms, and family history of joint inflammation are all important factors that can help differentiate etiologies.12 Osteoarthritis typically worsens with activity, particularly after a period of rest (gelling phenomenon).18 Morning stiffness from osteoarthritis usually lasts for a shorter duration than that of rheumatoid arthritis, which typically lasts 45 minutes or more.7

A gout attack typically begins at night and peaks within 24 hours, causing pain, swelling, and erythema.20 Common clues from the patient history include obesity, a high-calorie diet, alcohol intake, and the use of loop and thiazide diuretics.8 Trauma may also precipitate an acute gout flare-up,8,21 and the presentation can closely resemble septic arthritis.20

Determining whether a condition is truly monoarticular can prove beneficial, because prodromal arthralgias can suggest infection.1 Gonococcal arthritis is often preceded by migratory arthritis and tenosynovitis before settling in a primary joint.1 Conducting a sexual history is imperative, as is documenting any urinary problems, purulent discharge from the urethra, or other signs of infection, such as pharyngitis.11,12 Risk factors such as intravenous drug use, tick bites, and travel history can lead to a diagnosis of infectious or reactive arthritis.1

Axial skeleton inflammatory arthritis (e.g., sacroiliitis) in addition to symptoms in a single peripheral joint suggest a spondyloarthropathy.1 Spondyloarthropathies can often present as monoarthritis and progress from joint to joint in a migratory or additive pattern.20 It is important to ask patients about other symptoms, such as enthesopathy (tenderness at the muscle or fascia attachment sites) and dactylitis (sausage-like swelling of fingers or toes), because these are common.20 Some patients also present with ocular inflammation (uveitis) and urethritis (Reiter syndrome).20 A history of skin conditions and a positive family history of inflammatory arthritis suggest psoriatic arthritis, which can present as monoarthritis in the early stages.20

Physical Examination

The physical examination should focus on the involved and contralateral joints, the surrounding area, possible systemic manifestations, or polyarticular involvement.3,6,17 The first step is to confirm that the joint pain is truly localized and not a periarticular process, such as tendinitis, bursitis, or cellulitis.1 The presence of a joint effusion signifies intra-articular pathology, with patients typically reporting painful limitation of active and passive joint motion.1

A diagnosis of osteoarthritis can often be based on the history and physical examination.3 The characteristic presentation includes painful and limited range of motion, crepitus, effusions, instability, or deformities.18 Heberden and Bouchard nodes are pathognomonic for osteoarthritis. They result from hard, bony thickening that gradually forms around the distal and proximal interphalangeal joints of the fingers, respectively.20 The first carpometacarpal joint is one of the most common sites of osteoarthritis.20

Inflammatory arthritis elicits painful range of motion and erythema that is typically confined to the affected joint. Gout can present with intense erythema of the skin. It is often confused with cellulitis because this finding may extend past the joint margin.1,8

There are many superficial examination findings that can suggest specific diagnoses. Subcutaneous nodules (tophi) and podagra (gouty arthritis of the first metatarsophalangeal joint) are highly specific for gout.20 Erythema nodosum may be a manifestation of sarcoidosis or inflammatory bowel disease; psoriatic skin plaques are associated with psoriatic arthritis; and oral ulcers can indicate reactive arthritis or Behçet syndrome.1

Septic arthritis is most likely to seed within a larger joint,1,22 and to be accompanied by erythema, warmth, and immobility.12 Although clinical manifestations have low sensitivity,12 acute monoarthritis with fever should be considered to have a bacterial etiology until proven otherwise because of the potential consequences of inadequate treatment.20 For example, morbidity associated with septic arthritis includes functional deterioration, arthrodesis, and amputation11,12; the mortality rate is 10% to 20%.12

Diagnostic Tests

Because the causes of acute monoarthritis vary widely, a stepwise approach to diagnosis can aid decision making (Figure 2 6). In the setting of trauma, radiography of the affected joint is required to rule out dislocation or fracture before performing active physical examination maneuvers.1 Radiography can also show signs of osteoarthritis, such as joint space narrowing, osteophytes, and subchondral sclerosis.1 If a joint effusion is present in the absence of traumatic injury, arthrocentesis should be performed, particularly when other inflammatory signs are present and there is a reasonable concern for infection (e.g., fever, erythema, warmth).1

Analysis of synovial fluid distinguishes infectious and inflammatory causes of acute monoarthritis (e.g., rheumatoid, septic, and crystal-induced arthritis) from non-inflammatory causes (e.g., trauma, osteoarthritis).3,4,11,14 Analysis should include cell count and differential, white blood cell count, Gram stain, cultures, and crystal evaluation.1,4

Many cases of acute gouty arthritis are diagnosed without synovial fluid analysis.23 To improve the predictive value of clinical diagnosis, a gout calculator has been developed24,25  (Table 3 24). Seven predictive variables are included in this rule, and a scoring system has been developed to guide the decision to treat the patient for gout, pursue synovial fluid analysis, or search for other causes.24,25 A complete blood count and uric acid level can also aid in the diagnosis, especially if synovial fluid cannot be successfully obtained.3,19

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Table 3.

Diagnostic Rule for Gout When Synovial Fluid Analysis Is Unavailable

Patient with monoarthritis


Male sex

2 points

Previous patient-reported arthritis attack

2 points

Onset within 1 day

0.5 point

Joint redness

1 point

Involvement of first metatarsophalangeal joint

2.5 points

Hypertension or ≥ 1 cardiovascular diseases*

1.5 points

Serum uric acid > 5.88 mg per dL (350 μmol per L)

3.5 points

Total score:

________


≤ 4 points

> 4 and < 8 points

≥ 8 points


Non-gout in 95%

Uncertain diagnosis

Gout in 87%

Consider alternative diagnosis, such as CPPD arthritis, reactive arthritis, septic arthritis, rheumatoid arthritis, osteoarthritis, or psoriatic arthritis

Perform arthrocentesis and analysis with polarization microscopy for the presence of crystals; if not possible or available, then extensive follow-up of the patient

Manage the patient as having gout, including care for cardiovascular risk


CPPD = calcium pyrophosphate dihydrate deposition disease.

*—Indicates angina pectoris, myocardial infarction, heart failure, cerebrovascular accident, transient ischemic attack, or peripheral vascular disease.

Adapted with permission from Kienhorst LB, Janssens HJ, Fransen J, Janssen M; British Society for Rheumatology. The validation of a diagnostic rule for gout without joint fluid analysis: a prospective study. Rheumatology (Oxford). 2015;54(4):612.

Table 3.

Diagnostic Rule for Gout When Synovial Fluid Analysis Is Unavailable

Patient with monoarthritis


Male sex

2 points

Previous patient-reported arthritis attack

2 points

Onset within 1 day

0.5 point

Joint redness

1 point

Involvement of first metatarsophalangeal joint

2.5 points

Hypertension or ≥ 1 cardiovascular diseases*

1.5 points

Serum uric acid > 5.88 mg per dL (350 μmol per L)

3.5 points

Total score:

________


≤ 4 points

> 4 and < 8 points

≥ 8 points


Non-gout in 95%

Uncertain diagnosis

Gout in 87%

Consider alternative diagnosis, such as CPPD arthritis, reactive arthritis, septic arthritis, rheumatoid arthritis, osteoarthritis, or psoriatic arthritis

Perform arthrocentesis and analysis with polarization microscopy for the presence of crystals; if not possible or available, then extensive follow-up of the patient

Manage the patient as having gout, including care for cardiovascular risk


CPPD = calcium pyrophosphate dihydrate deposition disease.

*—Indicates angina pectoris, myocardial infarction, heart failure, cerebrovascular accident, transient ischemic attack, or peripheral vascular disease.

Adapted with permission from Kienhorst LB, Janssens HJ, Fransen J, Janssen M; British Society for Rheumatology. The validation of a diagnostic rule for gout without joint fluid analysis: a prospective study. Rheumatology (Oxford). 2015;54(4):612.

A synovial fluid white blood cell count greater than 50,000 per mm3 (50.0 × 109 per L) with at least 90% neutrophils is the most useful laboratory finding for making an early diagnosis of septic arthritis.3 This traditional cutoff lacks sensitivity because there can be wide overlap with inflammatory conditions, but higher white blood cell counts in the synovial fluid have a greater association with septic arthritis.1,26 Staphylococci and streptococci are the most common bacterial causes at 40% and 28%, respectively, and their presence may suggest drug abuse. These organisms are also associated with cellulitis, endocarditis, and chronic osteomyelitis.12,27,28

Gram-stain results should guide initial antibiotic choice. Gram-negative organisms account for 10% to 21% of cases of septic arthritis.1,12,29 Mycobacterial and fungal arthritis typically present in immunocompromised patients, and Lyme arthritis often presents as a late manifestation of Lyme disease.1,12,30 Special consideration should be given to patients with prosthetic joint infection because the cutoff values for infection may be as low as 1,100 white blood cells per mm3 (1.1 × 109 per L), with a neutrophil differentiation greater than 65%.3 Gonococci are cultured from joints in fewer than 50% of cases of gonococcal arthritis1,31,32; therefore, it is often necessary to obtain cultures from appropriate mucosal sites of infection.1,31,32 Noninflammatory synovial fluid (less than 2,000 cells per mm3 [2.0 × 109 per L]) is suggestive of osteoarthritis or internal derangement.1 Inflammatory synovial fluid containing monosodium urate crystals is highly suggestive of gout, particularly in the presence of podagra; however, the absence of crystals does not exclude crystal-induced arthritis, such as pseudogout.23,24

Erythrocyte sedimentation rate and C-reactive protein level are often elevated in inflammatory conditions.19,33 Literature comparing these two values is limited; however, it has been determined that these tests are more useful for following a disease course than discriminating the presence or absence of the disease.19,33

Data Sources: PubMed and Medline searches were performed using the key terms arthritis, crystal, gonorrhea, gout, infectious, inflammatory, and synovial fluid. The search included reviews, clinical trials, and meta-analyses. Also searched were the Cochrane Database of Systematic Reviews and Essential Evidence Plus. Search dates: September through November 2015, and September 2016.

The Authors

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JONATHAN A. BECKER, MD, is an associate professor in the Department of Family and Geriatric Medicine and program director for the Family Medicine Residency at the University of Louisville (Ky.) School of Medicine....

JENNIFER P. DAILY, MD, is an assistant professor in the Department of Family and Geriatric Medicine and associate director of the University of Louisville and Kentucky One Health Primary Care Sports Medicine Fellowship at the University of Louisville.

KATHERINE M. POHLGEERS, MD, MS, is a primary care sports medicine fellow at the University of Louisville School of Medicine. At the time the article was submitted, Dr. Pohlgeers was a third-year family medicine resident at the University of Louisville School of Medicine.

Address correspondence to Jonathan A. Becker, MD, University of Louisville, 201 Abraham Flexner Way, Ste. 690, Louisville, KY 40204 (e-mail: jon.becker@louisville.edu). Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations.

REFERENCES

show all references

1. Gorn AH, Brahn E. Monoarticular arthritis (diagnostic approach). Essential Evidence Plus; 2015. http://www.essentialevidenceplus.com/content/eee/702 [login required]. Accessed July 11, 2016....

2. Jeong H, Kim AY, Yoon HJ, et al. Clinical courses and predictors of outcomes in patients with monoarthritis: a retrospective study of 171 cases. Int J Rheum Dis. 2014;17(5):502–510.

3. Ma L, Cranney A, Holroyd-Leduc JM. Acute monoarthritis: what is the cause of my patient's painful swollen joint? CMAJ. 2009;180(1):59–65.

4. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA. 2007;297(13):1478–1488.

5. Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet. 2010;375(9717):846–855.

6. Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003;68(1):83–90.

7. Manek NJ, Lane NE. Osteoarthritis: current concepts in diagnosis and management. Am Fam Physician. 2000;61(6):1795–1804.

8. Hainer BL, Matheson E, Wilkes RT. Diagnosis, treatment, and prevention of gout. Am Fam Physician. 2014;90(12):831–836.

9. Smith E, Hoy D, Cross M, et al. The global burden of gout: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(8):1470–1476.

10. Schlesinger N, Thiele RG. The pathogenesis of bone erosions in gouty arthritis. Ann Rheum Dis. 2010;69(11):1907–1912.

11. Goldenberg DL. Septic arthritis. Lancet. 1998;351(9097):197–202.

12. Horowitz DL, Katzap E, Horowitz S, Barilla-LaBarca ML. Approach to septic arthritis. Am Fam Physician. 2011;84(6):653–660.

13. Cooper C, Cawley MI. Bacterial arthritis in an English health district: a 10 year review. Ann Rheum Dis. 1986;45(6):458–463.

14. McCarthy DJ. Joint sepsis: a chance for cure. JAMA. 1982;247(6):835.

15. Ross JJ, Saltzman CL, Carling P, Shapiro DS. Pneumococcal septic arthritis: review of 190 cases. Clin Infect Dis. 2003;36(3):319–327.

16. Smith JW, Piercy EA. Infectious arthritis. Clin Infect Dis. 1995;20(2):225–230.

17. Baker DG, Schumacher HR Jr. Acute monoarthritis. N Engl J Med. 1993;329(14):1013–1020.

18. Sinusas K. Osteoarthritis: diagnosis and treatment [published correction appears in Am Fam Physician. 2012;86(10):893]. Am Fam Physician. 2012;85(1):49–56.

19. Waits JB. Rational use of laboratory testing in the initial evaluation of soft tissue and joint complaints. Prim Care. 2010;37(4):673–689, v.

20. Luosujärvi R. Disease-specific signs and symptoms in patients with inflammatory joint diseases. Essential Evidence Plus; 2013. http://www.essentialevidenceplus.com/content/ebmg_ebm/440 [login required]. Accessed July 11, 2016.

21. Pittman JR, Bross MH. Diagnosis and management of gout. Am Fam Physician. 1999;59(7):1799–1806,1810.

22. Morgan DS, Fisher D, Merianos A, Currie BJ. An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect. 1996;117(3):423–428.

23. Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M. A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Arch Intern Med. 2010;170(13):1120–1126.

24. Kienhorst LB, Janssens HJ, Fransen J, Janssen M; British Society for Rheumatology. The validation of a diagnostic rule for gout without joint fluid analysis: a prospective study. Rheumatology (Oxford). 2015;54(4):609–614.

25. Krishnan E, Svendsen K, Neaton JD, Grandits G, Kuller LH; MRFIT Research Group. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. 2008;168(10):1104–1110.

26. Li SF, Henderson J, Dickman E, Darzynkiewicz R. Laboratory tests in adults with monoarticular arthritis: can they rule out a septic joint? Acad Emerg Med. 2004;11(3):276–280.

27. Ryan MJ, Kavanagh R, Wall PG, Hazleman BL. Bacterial joint infections in England and Wales: analysis of bacterial isolates over a four year period. Br J Rheumatol. 1997;36(3):370–373.

28. Deesomchok U, Tumrasvin T. Clinical study of culture-proven cases of non-gonococcal arthritis. J Med Assoc Thai. 1990;73(11):615–623.

29. Dubost JJ, Soubrier M, De Champs C, Ristori JM, Bussiére JL, Sauvezie B. No changes in the distribution of organisms responsible for septic arthritis over a 20 year period. Ann Rheum Dis. 2002;61(3):267–269.

30. Steere AC, Schoen RT, Taylor E. The clinical evolution of Lyme arthritis. Ann Intern Med. 1987;107(5):725–731.

31. Wise CM, Morris CR, Wasilauskas BL, Salzer WL. Gonococcal arthritis in an era of increasing penicillin resistance. Presentations and outcomes in 41 recent cases (1985–1991). Arch Intern Med. 1994;154(23):2690–2695.

32. Bardin T. Gonococcal arthritis. Best Pract Res Clin Rheumatol. 2003;17(2):201–208.

33. Guidelines for the initial evaluation of the adult patient with acute musculoskeletal symptoms. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Arthritis Rheum. 1996;39(1):1–8.

 

 

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