CRACKCast E116 – Arthritis

In CRACKCast, Podcast by Adam Thomas1 Comment

This episode of CRACKCast covers Rosen’s Ch 106, Arthritis. When a patient rolls in with an active joint, we need to know how to rule out those can’t-miss diagnoses.

Shownotes: PDF HERE

Rosens In Perspective:

What are the types of joints?

“As opposed to synarthrotic suture joints of the skull and amphiarthrotic fibrocartilage unions like the pubic symphysis, the joints of concern in acute arthritis are the synovial or diarthrotic (moving) joints.

These synovial joints are composed of two ends of subchondral bone covered by articular cartilage, surrounded by a capsule that is lined with a thin synovial membrane and supported by ligaments, tendons, and muscle (Fig. 106.1A).

Articular cartilage is an avascular, aneural tissue composed of a matrix of collagen fibers and proteoglycans synthesized by chondrocytes. The properties of articular cartilage allow tremendous load bearing. Together with the viscous lubricating synovial fluid, an ultrafiltrate of blood supplemented with hyaluronic acid and low-molecular-weight proteins, the cartilage that articulates joint movement is nearly frictionless.”

The big emergency this episode will cover again and again is our approach to the potentially septic joint.

Septic arthritis is most commonly instigated by hematogenous seeding of a diarthrotic joint. The bacteria can then proliferate in the joint, before causing a severe inflammatory reaction. Contiguous spread can also occur through direct trauma.

[1] List a differential diagnosis (4 for each) for monoarticular, polyarticular symmetrical, and polyarticular asymmetrical arthritis. 

If the site of the patient’s pain is articular, classifying whether the arthritis is monoarticular (eg, septic arthritis or gout) or polyarticular may aid in diagnosis. Polyarticular arthritis may be symmetrical (eg, rheumatoid or drug-induced) or asymmetrical (eg, rubella, acute rheumatic fever [ARF], Lyme disease, or gonococcal arthritis). In addition, it may also be migratory (eg, gonococcal or rubella), subsiding in one area before presenting in another, or additive, remaining in the first joint and progressing to additional joints.

TABLE 106.1: Differential Diagnosis of Arthritis in the Emergency Department, Based on Typical Distributions

MONOARTICULAR POLYARTICULAR:

SYMMETRICAL

POLYARTICULAR:

ASSYMMETRICAL

Septic arthritis

Gout

CPPD/pseudogout

Osteoarthritis

Trauma, hemarthrosis

Rheumatoid arthritis flare

Psoriatic arthritis

Polymyalgia rheumatica

Enteric arthritis

Ankylosing spondylitis

Hep B/C induced arthritis

Gonococcal arthritis

Lyme arthritis

ARF

Reactive arthritis

Viral arthritides

ARF, Acute rheumatic fever; CPPD, calcium pyrophosphate dihydrate deposition Disease.

[2] What are systemic signs of arthritis? List extraarticular manifestations of RA.  

TABLE 106.2: Systemic Signs of Arthritis Diseases*

Organ System Findings Diseases
Airway Airway Obstruction RA, relapsing polychondritis
Cardiac Pericarditis RA, ARF
Murmurs ARF, relapsing polychondritis, ankylosing spondylitis
Eyes Iritis, uveitis Spondyloarthropathies
Conjunctivitis Reactive arthritis
GI IBD Spondyloarthropathies
Dysentery Reactive Arthritis
Genitalia Lesions, Urethral Discharge Reactive arthritis, gonococcemia
Hematologic Aplastic anemia Parvovirus
Neurologic Cauda equina syndrome Ankylosing spondylitis
Cervical spine instability Ankylosing spondylitis, RA, OA
Oral mucosa Ulcerations Reactive arthritis
Pulmonary Pleuritis, nodules RA
Renal Renal crisis, ARF Scleroderma
Skin Plaques on elbows, knees Psoriasis
Sclerodactyly, calcinosis Scleroderma
Erythema chronicum migrans Lyme disease
Tophi Gout
Erythema Marginatum Rheumatic fever
Subcutaneous nodules RA

*Excludes rheumatic vasculitis diseases.

ARF, Acute rheumatic fever; IBD, inflammatory bowel disease; RA, Rheumatoid Arthritis

Extraarticular manifestations of RA: 

  • Osteoporosis, atlantoaxial subluxation
  • Muscle weakness, synovitis, myositis, myopathies
  • Sarcopenia, obesity
  • Rheumatoid nodules**
  • ocular/oral dryness (sjogren’s syndrome)*
  • Episcleritis, scleritis, uveitis
  • Interstitial fibrosis*, pneumonias, pulmonary hemorrhage
  • Pericarditis, myocarditis, CAD
  • Mesenteric vasculitis
  • Glomerulonephritis
  • Carpal tunnel syndrome; mononeuritis multiplex
  • Anemia*

[3] What are two presentations of gonococcal arthritis?

  1. Mono-oligoarticular arthritis
  2. True disseminated gonococcal infection (sometimes termed arthritis-dermatitis syndrome: bacteremia, diffuse migratory arthralgias, characteristic skin lesions, and tenosynovitis)

Cervical, urethral, rectal, and pharyngeal cultures are positive in up to 75% of cases, so all mucosal orifices of the patient (and partner, if possible) should be cultured appropriately

In disseminated gonococcal infection, the skin lesions often contain the gram-negative diplococcus.

[4] What are common radiologic findings in arthritis? 

Anyone with an acutely problematic joint(s) should have a normal x ray. If the x-ray is abnormal, the disease has likely been present for longer than 1 week.

TABLE 106.3: Common Radiologic Findings in Arthritis

Arthritis Findings
Acute arthritis (gout, pseudogout, septic arthritis)

 

Soft tissue swelling

 

Late septic arthritis (need at least 8 to 10 days for changes to be seen)

 

Subchondral bone destruction

Periosteal new bone

Loss of joint space

Osteoporosis

Late joint space narrowing

 

Late pseudogout (knee, hip; radiocarpal, midcarpal, all MCP joints)

 

Linear calcification in cartilage

Asymmetrical joint space narrowing

MCP “hook spurs” in HHC

Osteophyte formation

Subchondral cyst formation

Lack of osteoporosis

 

Degenerative arthritis (acromioclavicular, first carpometacarpal, first MTP, DIP joints; knee, hip, cervical spine, lumbosacral spine)

 

Asymmetrical joint space narrowing

Sclerosis of juxta-articular bone

Bone spurs and cysts—adjacent to

Severe cartilage degeneration

No osteoporosis

 

 

Tuberculous arthritis (knee, hip, shoulder)

 

Soft tissue swelling

Marked demineralization

Bone rarefaction

Little reactive sclerosis

Late bone destruction

Joint space preserved

 

Late rheumatoid arthritis (wrist, MCP, PIP, MTP, first IP joints; foot, atlantoaxial joint, glenohumeral joint)

 

 

Symmetrical joint space narrowing

Osteoporosis of periarticular bone

Marginal erosions (no overhanging margins as in gout)

Little reactive bone formation

DIP, Distal interphalangeal; HHC, hereditary hemochromatosis; IP, interphalangeal;

MCP, metacarpophalangeal; MTP, metatarsophalangeal; PIP, proximal interphalangeal.

 

[5] List 2 indications, 2 contraindications, 2 complications of arthrocentesis

This is the only way to definitively make the dx of septic arthritis or a crystal arthropathy!

Indications:

  • Obtain joint fluid for analysis
  • To drain tense hemarthrosis (trauma or hemophilia)
  • Assess for blood – determining whether a laceration communicates with the joint space
  • Intra-articular injection of analgesics and anti-inflammatories in the setting of acute/chronic arthritis

These are “relative” CI

  • Overlying cellulitis where a joint would be aspirated
  • Coagulopathy (elevated INR) or severe bleeding disorder
  • Prosthetic joint

The primary complications of arthrocentesis are:

  • bleeding or
  • infection in the joint space,
  • reaction to anesthetic agents, and
  • long-term corticosteroid-related complications.

[6] Describe arthrocentesis techniques for common joints. (box)

Box 106.1 (9th Ed): Arthrocentesis Techniques for Common Joints

Wrist: Radiocarpal Joint (Dorsal Approach)

  1. Identify landmarks by palpating the Lister tubercle (distal end of dorsal radius)
  2. Palpate the extensor pollicis longus tendon, which passes over the radial side of the Lister tubercle (best palpated while the wrist is in extension). You will insert the needle on the ulnar side of the extensor pollicis longus tendon, just distal to the Lister tubercle.
  3. Lay the wrist on a cushion so that it is flexed 20 to 30 degrees.
  4. Apply traction from the fingers and mild ulnar deviation, and insert a 22-gauge needle dorsally.

Elbow: Radiohumeral Joint (Lateral Approach)  

  1. Identify landmarks by extending the elbow and then palpating the depression between the lateral epicondyle of the humerus and the head of the radius.
  2. Keeping your finger on the radial head, flex the patient’s elbow, pronate the forearm, and lay the palm on a flat surface.
  3. Insert a 20-gauge needle just distal to the lateral epicondyle, directed medially.

Shoulder: Glenohumeral Joint (Posterior Approach)

  1. Lay the patient’s arm, internally rotated, across the waist.
  2. Identify the posterolateral comer of the acromion.
  3. Insert a 20-gauge needle 2 to 3 cm inferior to this point, directed anteriorly and medially (and slightly superiorly) toward the coracoid process.

Hip: Acetabulofemoral Joint (Lateral Approach)

  1. Lay the patient supine and internally rotate the affected leg.
  2. Palpate the greater trochanter.
  3. Insert a 3.5-inch 18-gauge needle superiorly to the trochanter, horizontal and parallel to the stretcher. If the femoral neck is encountered, withdraw 2 mm to 4 mm and redirect slightly cephalad until synovium is aspirated.

Knee: Patellofemoral Joint (Medial Approach)

  1. Flex the knee 15 to 20 degrees (often achieved with a rolled towel under the knee). The foot should be perpendicular to the floor.
  2. Palpate the anteromedial patellar edge at the patellar midpoint or superior portion.
  3. Insert an 18-gauge needle 1 cm medial to this point, directed toward the posterior surface of the patella.

Ankle: Tibiotalar Joint (Anteromedial Approach)

  1. With the patient supine, have the patient plantarflex the foot.
  2. Identify the anterior tibial tendon.
  3. Insert a 3.5-inch 20- or 22-gauge needle medial to this tendon in the depression at the anterior edge of the medial malleolus.

Metatarsophalangeal Joint (Dorsomedial Approach)

  1. Identify the distal metatarsal head and the proximal base of the first phalanx.
  2. Identify the extensor tendon by asking the patient to extend the great toe.
  3. While the patient is supine, flex the toe 15 to 20 degrees, and then apply traction.
  4. Insert a 22-gauge needle dorsally just medial to the extensor tendon.

[7] Describe typical synovial fluid findings by arthritis type: Describe the testing of synovial fluid and how you would interpret the results. (table)

 

“no guidelines or studies exist supporting the use of blood testing (ESR, CRP, WBC, uric acid) as a general screen of acute undifferentiated arthritis in the ED.” – so we can’t really use these tests to exclude specific causes of an acutely swollen joint. Therefore, aspiration is a must!

 

Table 106.4: Typical Synovial Fluid Findings by Arthritis Type

 

NON-INFLAMMATORY INFLAMMATORY SEPTIC HEMORRHAGIC
Color Clear/yellow Yellow/white Cloudy/opaque Opaque, may contain fat droplets
Viscosity Thick, stringy Variable Thin, watery Variable
Synovial white blood cells 200 to 2000/mm3
<25,000/mm3
+LR for SA = 0.32
2000 to 50,000/mm3
<50,000/mm3
+LR for SA = 0.42
>25,000/mm3
+LR for SA = 2.9
>50,000/mm3
+LR for SA = 7.7
>100,000/mm3
+LR for SA = 28
<2000/mm3
Synovial polymorphonuclear cells Variable Variable >90%
+LR for SA = 2.7
<25%
Gram stain Negative Negative 29% to 65% positive Negative
Leading diagnosis Osteoarthritis Gout, reactive arthritis Bacterial arthritis Trauma, hemophilia

 

[8] How is gout managed? List 4 therapies for acute gout.

Without treatment, the attack is self-limited, peaking during 24 to 48 hours and lasting about a week.

Table: Acute Treatment 

ED pharmacologic mainstays for acute gout are nonsteroidal antiinflammatory drugs (NSAIDs; including cyclooxygenase 2–selective agents), corticosteroids (including ACTH), and colchicine.

 

NSAIDS
  • Ibuprofen
  • Naproxen 500 mg BID
  • Indomethacin 50 mg TID
  • Little evidence to say that one type of NSAID is superior to another
  • Treat 24 hrs post symptoms relief (usually 2-6 days)
Colchicine (impedes the inflammatory response to crystals in fluid)
  • 1.2 mg PO, then 0.6 mg PO one hour later
  • Then 0.6 mg po TID
Colchicine is contraindicated in patients with hematologic, renal, and hepatic insufficiency; its low therapeutic index makes it readily lethal in overdose.
Steroids Intra-articular injection (rule out SA first!)

  • Triamcinolone acetonide
    • 20 to 40 mg for the knee
    • 5 to 10 mg for smaller joints is
  • Systemic steroids, such as oral prednisone (40 mg/day for 3 to 5 days, with or without a taper),
A Cochrane review of three trials of various steroids against other agents failed to demonstrate evidence of efficacy for systemic steroids.
Adrenocorticotropic Hormone (Corticotropin). 25–40 IU ACTH subcutaneously not commonly used (or studied) because of its expense and lack of general availability, synthetic ACTH is a desirable alternative to the preceding agents because of its rapid onset of action and decreased toxicity in older patients.

American College of Rheumatology (ACR) Guidelines for gout management now endorse 25–40 IU ACTH subcutaneously as an appropriate alternative for nil per os (NPO) patients.

Others
  • Rest, ICE, elevation
  • Narcotics
  • local/regional anesthetic blocks

Long Term Prophylaxis

New guidelines for gout recommended that prophylactic agents (such as, allopurinol), or newer agents (such as, febuxostat and probenecid) should neither be stopped nor initiated during an acute attack.

[9] What are the risk factors for gout?

Risk factors include:

  • chronic obesity,
  • hypertension,
  • diabetes,
  • thiazide diuretics
  • cyclosporine use,
  • lead or radiocontrast exposure.
  • Purine-rich diets (meat; seafood, especially anchovies and shellfish; beer; and legumes) predispose at-risk individuals to attacks;
  • high-fructose corn syrup and soft drinks are also implicated.

High dairy and coffee consumption have been shown to decrease risk.

[10] List the microbiology of bacterial septic arthritis related to patient groups.

Table 106.5: Microbiology of Bacterial Septic Arthritis Related to Patient

PATIENTS ORGANISMS
Neonates and infants Staphylococcus aureus, group B streptococcus, GNR bacteria
Children Haemophilus influenzae, S. aureus
Adolescents and young adults Neisseria gonorrhoeae, Chlamydia trachomatis
Older adults S. aureus, Streptococcus, GNR bacteria
Sickle cell anemia Salmonella
Injection drug abusers Pseudomonas, S. aureus, GNR bacteria

* GNR = Gram Negative Rod

Acute nongonococcal septic arthritis in adults is caused most often by gram-positive organisms (75% to 90%),

[11] Describe treatment for septic arthritis.

Once the diagnosis is made, hospitalization is indicated for administration of intravenous (IV) antibiotics and needle, arthroscopic, or open drainage of the affected joint. Antibiotic selection is initially based on Gram stain results and then adjusted on the basis of final culture results and sensitivities.

For gram-positive organisms, the initial drug of choice is vancomycin 30 mg/kg daily in two divided doses, as MRSA is frequently causative.

For gram-negative bacilli, use a third-generation cephalosporin, such as ceftriaxone 2 g IV once daily, cefotaxime 2 g IV three times a day, or ceftazidime with gentamicin (especially if Pseudomonas infection is suspected).

Although no trials of antibiotic duration have been reported, antibiotic therapy is generally continued parenterally for 2 to 4 weeks, depending on the response, and followed with 2 to 6 weeks of oral antibiotic therapy.

[12] Name 6 viral arthritides. 

  • Hepatitis B (mimic RA presentation, but followed by jaundice)
  • Hepatitis C (mimics rheumatoid arthritis)
  • HIV (usually monoarticular)
  • Parvovirus B19 (cause of fifths disease in children)
  • Rubella virus; Rubella vaccine virus (look for maculopapular rash and lymph nodes)
  • Alphaviruses (ross river, chikungunya) – all mosquito borne

WiseCRACKS

[1] What is the normal WBC count in a joint aspiration?

200-2000 WBC/mm3

Joint aspiration is the only way to definitively investigate a swollen joint.

Systematic reviews show insufficient evidence for a normal CRP level, ESR, WBC count, or procalcitonin level to take septic arthritis below the threshold for further evaluation in adults. Serum blood cultures reveal the causative organism less than half of the time. Similarly, a WBC > 10k and ESR > 30 only minimally increase the likelihood of septic arthritis.

Important points for emphasis:

  • A positive Gram stain is diagnostic, but a negative result for bacteria does not rule out septic arthritis;
  • Significant overlap exists between inflammatory and septic causes of acute arthritis, with very high fluid cell count or polymorphonuclear (PMN) cell pleocytosis suggesting infection, but more modest cell counts failing to exclude it.
  • High cell counts (>50,000/mm3) can occur in rheumatoid arthritis, gout, and pseudogout. Most of the cells in both septic and severe inflammatory arthritis are PMN cells.
  • Monosodium urate crystals are needle shaped and strongly negatively birefringent (yellow when parallel to the compensator and blue when perpendicular), ranging in size from 2 to 10 μm. Calcium pyrophosphate crystals, in contrast, are polymorphic, rhomboid, and positively (although weakly) birefringent.
  • Remember that septic arthritis CAN coexist with a crystal arthropathy!
  • A synovial WBC count of more than 1100/mm3 or a pleocytosis of greater than 64% PMN cells is sensitive and specific for infection in the setting of prosthetic joints.
  • Don’t forget to think about periarticular causes of an irritated joint!
  • lactate dehydrogenase (LDH) levels above 250 U/L are sensitive for septic arthritis, and LDH levels below this threshold seem to exclude septic arthritis, according to one study. Low synovial glucose and high protein concentrations are neither sensitive nor specific for septic arthritis.

[2] List 6 RFs for septic arthritis

  • Bimodal age distribution peaks for young children and adults older than 55 years old
  • age over 80,
  • low socioeconomic status,
  • injection drug abuse (in which joint infections typically involve the axial skeleton but can involve extremities),
  • alcoholism, diabetes, skin infections,
  • advanced human immunodeficiency virus (HIV) infection or
  • other immunocompromised states,
  • Chronic arthritis (particularly rheumatoid, crystalline, and degenerative osteoarthritis),
  • recent intra-articular corticosteroid injections or prosthetic implants.

[3] What is Calcium Pyrophosphate Dihydrate Deposition Disease (Pseudogout)

This occurs when calcium complex crystals form across articular surfaces. CPPD is manifested on radiographs as chondrocalcinosis.

When precipitating crystals trigger an inflammatory synovitis, it is termed pseudogout.

[4] List 5 characteristics of Seronegative spondyloarthropathies. List 4 causes. 

  • sacroiliac involvement, (chronic low back pain)
  • peripheral inflammatory arthropathy (oligoarthritis)
  • absence of rheumatoid factor,
  • pathologic changes around the enthesis (ligamentous and tendinous insertion into bone) – heel enthesitis, dactylitis
  • A genetic component related to the HLA-B27 marker (50-90% of these patients have a positive marker)
    • however, a positive HLA-B27 by itself is not diagnostic of SpA, since a significant proportion of subjects in the general population are also positive

The most important of these chronic polyarthritic inflammatory diseases are:

  • ankylosing spondylitis,
  • reactive arthritis,
  • the arthropathy of inflammatory bowel disease (enteropathic arthritis),
  • Psoriatic arthritis.

[5] List 5 pathogens responsible for reactive arthritis (aka Reiter’s Syndrome)

Reactive arthritis is generally a disease of patients from 20 to 40 years old, in whom arthritis develops 2 to 6 weeks after an episode of urethritis, cervicitis, or dysentery. The syndrome is predominantly polyarticular, asymmetrical, and often additive.

  • Chlamydia trachomatis
  • Salmonella
  • Shigella
  • Yersinia
  • Campylobacter

[6] Describe the Jones Criteria. 

This is what we use to diagnose acute rheumatic fever (ARF). ARF is a systemic disease triggered by a complex hyperimmune response in the weeks after group A streptococcal pharyngitis

The Jones Criteria:

  • Lab evidence of prior group A strep infection**
  • Major (need 2 or more)
    • Polyarthritis
    • Carditis
    • Chorea
    • Erythema marginatum
    • Subcutaneous nodules
  • Minor (need 1 major and 2 minor)
    • Arthralgia
    • Fever
    • Elevated ESR/CRP
    • Long PR on ECG

[7] What is erythema marginatum?

See Figure 106.6.

This is the pathognomonic rash found in acute rheumatic fever.

An “evanescent, pink or faintly red, nonpruritic rash involving the trunk and sometimes the limbs but not the face…The lesion extends centrifugally, with return of the skin in the center to a normal appearance. The outer edge of the lesion is sharp; the inner edge is diffuse. The lesion is also known as “erythema annulare” since the margin of the lesion is usually continuous, making a ring. Individual lesions may appear, disappear, and reappear in a matter of hours. A hot bath or shower may make them more evident.” – UpToDate

[8] Describe your approach to the anticoagulated patient with a swollen joint. 

Literature supports the safety of joint aspiration on therapeutic levels of DOAC’s and Warfarin. The risk of causing major hemorrhage is low (<0.2%).

So, we can’t really use anticoagulation as an excuse not to tap a joint, especially if they may have a septic joint!

The only change suggested is using a 22 gauge needle!

A recent retrospective review of >1000 pts. taking DOACs: There were no bleeding complications in any of the 1050 procedures. (avg. age 75 yrs, concomitant ASA and clopidogrel use as well!). 87% had 5 day follow-up.

Link: https://www.ncbi.nlm.nih.gov/pubmed/?term=joint+aspiration+direct+oral+anticoagulants

[9] Differentiate between articular vs. periarticular inflammation. 

True arthritis produces generalized joint pain, warmth, swelling, and tenderness. Often pain at REST. Discomfort increases with both passive and active motion of the joint because the inflamed synovium is exquisitely sensitive to stretching, and because all parts of the joint are involved in the inflammatory process.

By contrast, periarticular inflammation (bursitis, tendinitis, or localized cellulitis) tends to be more focal, weight bearing and passive ROM are tolerated.

This post was uploaded and copyedited by Owen Scheirer (@OwenGregg1)

Adam Thomas

Adam Thomas

Adam Thomas is a MedEd re-purpose-r. He cofounded the CrackCast project to fill the obvious gap in current FOAMed. He is a true podcasting supporter, and finds it to be the best way he learns. Currently a resident in the FRCP program at the University of British Columbia.
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Chris Lipp
Chris Lipp is one of the founding Fathers for CrackCast and an EM Resident in Victoria, BC. His interests are in sports, exercise, and wilderness medicine. When he isn’t out on one of his accidental 20km trail runs, you can find him jamming with friends, or outdoors, and reading Rosen’s…..
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