Monoarthritis

Acute Monoarthritis
Introduction:
 Acute monoarthritis = a single joint that has been inflamed for less than 6 weeks
 Causes:
1. Septic arthritis
2. Acute gout
3. Acute pseudogout
 What should you do to investigate?
o Aspirate the joint (take a small sample of fluid from the joint) → if the joint is red, aspirate it!
o Send the fluid for the 3 Cs:
i. Cell count → takes a couple of hours
ii. Culture → take 24-48 hours
iii. Crystals → takes a couple of hours
i. Also send for a gram stain
1) Septic Arthritis:
Patient Case:
 Mr. Williams is a 62 year old man presents with a left ankle that has recently become much more painful, warm, and red
 He has diabetes (and is on metformin and glyburide) and has had his right knee replaced due to osteoarthritis
 He recently had a pedicure for diabetes
 Physical exam:
o Temperate = 38.6oC
o He is flushed and in pain
o Left ankle is warm, red, and extremely painful
o Cannot put much weight on the ankle
 He is sent urgently to the emergency department with a diagnosis of “suspected left ankle infection”
 Orthopedic surgery is consulted and they aspirate the joint:
i. Cell count = 59 x 109 cells/L (inflammatory!)
ii. Crystals = negative
iii. Gram Stain = gram positive cocci in clusters
iv. Culture = pending
 Acute Bacterial Arthritis = A Medical Emergency! 
 Without rapid detection and appropriate treatment, it can quickly lead to fulminant joint damage
 This can happen in just days
Risk Factors:
Systemic Risk Factors: Local Risk Factors:
 Immunosuppressed Individuals:  Presence of a prosthetic joint
o Diabetics  Recent joint surgery
o Cancer  Underlying joint abnormality (ex. arthritis)
o Certain medications (ex. methotrexate, leflunomide,  Direct penetrating trauma
prednisone, Anti-TNF alpha drugs, other biologics)  Skin infection
 Age → very young or old
 Lifestyle → alcohol excess, IV drugs
 Recent infection

How Does the Infection Get to The Joint?

1. #1 cause = hematogenous spread from a remote site
2. Direct inoculation (ex. penetrating trauma, recent surgery, etc.)
3. Spread from contiguous site (infected bone)
Management:
 Initial management:
i. Admit to Hospital
ii. Take to the OR for urgent incision and drainage (I&D)
 Infected joint is actually an infection in a closed space and usually requires drainage!
iii. Start on empiric IV Cefotaxime
iv. Analgesia for pain control
v. Rest
  Continued management:
o Repeat I&D until surgeon is confident the joint is clean (may require several returns to the OR ☹)
o IV antibiotics for 4-6 weeks
Organisms:
1. Gram positive cocci (80%):
o Staphylococcus (60+%)
o Streptococcus (20%)
2. Gram negative (15%):
o Immune compromised, elderly, neonates, IV drug users
3. Anaerobic organisms
2) Acute Gout:
Patient Case:
 Mike is a 48 year old married man who works at Labatts and has hypertension (he is on 25 mg hydrochlorothiazide)
 Two days post cholecystectomy, he presents with severe pain, swelling, and redness 1st MTP joint
 A similar episode occurred on a trip to Mexico 2 years ago but he just took OTC medication, which helped
 His big toe is aspirated and the fluid is analyzed:
o Cell count = 15 x 109 cells/L (inflammatory but on the low side for infection)
o Culture = no growth at 24 hours
o Crystals = needle shaped, negatively bi-refringent crystals
Acute Gout:
 An acute inflammatory arthritis caused by uric acid crystal deposition in the joint
 Uric acid is a product of the metabolic breakdown of purines and is usually excreted by the kidneys in urine
 Hyperuricemia can be caused by either:
o Increased intake/production of uric acid (ex. from diet and alcohol)
o Decreased excretion of uric acid (more common) → frequently occurs in renal failure
 The excess uric acid can crystallize and the crystals deposit in joints, tendons, and
surrounding tissues, resulting in an attack of gout
o HOWEVER:
 Many people are walking around with hyperuricemia and many of these
people will not get gout
 Therefore, hyperuricemia alone CANNOT be used to make a diagnosis of
gout – must have symptoms!
 There is no good evidence for treating isolated hyperuricemia
 Clinical features of an acute gout attack:
o Starts quickly and very intensely, can develop over a few hours!  It can look just
o Very painful (ex. patients will commonly say they can’t stand the bed sheets touching it) like an infected
o Joint is swollen, warm, and red joint! 
o Patient may feel unwell and have an associated fever
 Usually affects a single joint in the lower extremity → first metatarsophalangeal (MTP) joint (i.e. the big toe) is affected in 50% of cases
 Untreated attacks typically take about seven to ten days to resolve
Who Gets Gout?
 First attack in men is usually between the ages of 35 and 50
 In women, it starts after menopause as estrogen has a protective effect on the excretion of uric acid
Common Risk Factors:
 Impaired renal function
 Diuretics (Lasix and hydrochlorothiazide)
 Excessive alcohol intake (beer being the worst culprit)
 Family history
 Male sex
 Age
 Other disease associations:
o Obesity
o Hypertension (high blood pressure)
o Diabetes
o Hyperlipidemia (high lipids)
Triggers:
 Surgery
 Mechanical Injury
 Alcohol
 Recent Illness
 Travel/dehydration
 Start/Stop Allopurinol
How to Confirm the Diagnosis:
 Must aspirate the joint and find urate crystals to prove the diagnosis
o Urate crystals are needle shaped and negatively birefringent in polarized light
 Blood tests to order:
1. CBC:
 May see elevated WBC
 May see reactive thrombocytosis (increased platelets)
2. Creatinine (to measure renal function, may be the cause of the gout)
3. Uric acid:
 Levels may be normal during an acute attack as all the crystals are in
the joint!
 If they are low, measure again later on
4. Fasting glucose
5. Fasting lipid levels (triglycerides and cholesterol)
Treatment:
 Treatment philosophy = treat the acute attack, then worry about working to the lower the levels of uric acid in the body
 Non-pharmacologic treatments:
1. Rest, ice, and elevate the joint
2. Dietary modification
 Meat and seafood (particularly shellfish) are bad
 Vegetables and low-fat dairy are good
3. Reduce alcohol intake
4. Good hydration
 Pharmacologic treatments:
1. Intra-articular corticosteroids injected into the affected joint:
 Works fast and effectively to treat the joint without systemic effects
 However, very painful in the big toe so patients may refuse ☹
2. Oral NSAIDs or COXIBs → indomethacin 50 mg PO TID
3. Oral colchicine (older non-NSAID anti-inflammatory)
4. Oral prednisone (particularly if the gout is in multiple joints)
5. Allopurinol:
 Works by inhibiting the conversion of xanthine to uric acid by xanthine oxidase
 Once you are on it, you are on it for life as stopping the medication can cause an
acute attack (therefore not a good option for patients with poor compliance)
 Want to reduce the uric acid levels to the lower limit of laboratory reference range Mechanism of Action of Allopurinol
 DO NOT start during an acute attack as it can worsen the attack
 When to Consider:
 Recurrent acute episodes of gout affecting lifestyle
 Patients at risk from complications of treatments required for acute attacks (ex.
frequent courses of steroids)
 Patient acceptance of the need for lifelong medication compliance
 Presence of uric acid tophaceous deposit:
o When hyperuricemia is present for years, solid blobs of uric acid may
become deposited in the skin and bone Tophi from chronic
o These deposits are called tophi gout
Risk of Recurrence:
 First year = 60% recurrence
 Two years = 80% recurrence
 Five years = 90% recurrence
 Bottom Line = if you have an attack you are very likely to get another one!
3) Acute Pseudogout:
Patient Case:
 Mary, a 68 year old woman, developed a severe right sided knee pain and significant swelling after a recent brisk walk
 She has diabetes (she is on metformin) and hypercholesterolemia
 She has had mild chronic bilateral knee pain which has been worse with activity (OA?)
 On examination:
o The right knee is very swollen and noticeably warm
o She has difficulty flexing the right knee past 100 degrees
o The left knee has a small effusion, is cool, and has slightly reduced flexion (likely OA)
o She has early changes of osteoarthritis (degenerative arthritis) in the hands
 Her knee joint is aspirated and the fluid is analyzed:
o Cell count = 18 x 109 cells/L (inflammatory)
o Culture = no growth at 24 hours
o Crystals = rhomboid shaped, intracellular, positively bi-refringent crystals
Acute Pseudogout:
 Acute inflammatory arthritis caused by calcium pyrophosphate (CPP) crystals
 Clinical features of the attack:
o Starts quickly and very intensely
o Tends to be less intense than gout and takes longer to reach peak than acute gout  It can look just
o Very painful like an infected
o Joint is swollen, warm, and red joint! 
o Patient may feel unwell and have an associated fever
 Usually affects a single joint in the lower extremity → knee is the most common
 Untreated attacks can last several days to a few weeks
 Those who get pseudogout are generally older individuals, often have associated osteoarthritis
Pseudogout vs. Chondrocalcinosis:
 Pseudogout = an acute inflammatory arthritis caused by calcium pyrophosphate crystal deposition in the joint
 Chondrocalcinosis = a radiographic finding of calcium pyrophosphate deposition in the cartilage (not treated unless there are clinical signs!)
How to Confirm the Diagnosis:
 Must aspirate the joint and find intracellular calcium pyrophosphate crystals to prove diagnosis
 CPP crystals are rhomboid shaped and positively birefringent in polarized light
Treatment:
 Non-pharmacologic treatment:
1. Rest, ice, and elevate the joint
2. Good hydration
 Pharmacologic treatment:
1. Intra-articular corticosteroids injected into the affected joint
2. Oral NSAIDs or COXIBs → indomethacin 50 mg PO TID
3. Oral prednisone
 No chronic treatments to prevent recurrences
Summary:
 Acute, red, hot monoarthritis = a result of an intense inflammatory response to a foreign organism/substance in a joint
 Must rule out infection!
 Must aspirate the joint and send for cell count, culture, and crystals (the 3 C’s)
 Chronic Monoarthritis (Osteoarthritis)
Patient Case:
 Diane is a 68 year old woman who has had on-going bilateral knee pain for the past 3 years that flares up and down and tends to be worse
when she is active
 At times, she has difficulty sleeping because of knee pain
 She manages to walk every morning when her knees are “feeling good”
 She joined Weight Watchers and lost 28 lbs and has kept it off for the last 5 years
 She is otherwise healthy and takes no other medications with the exception of occasional acetaminophen for her knees
 X-rays of her knees show joint space narrowing and subchondral sclerosis, x-rays of her hands show osteophytes and sparring of the MCPs:

Definition of Osteoarthritis:
 Osteoarthritis is the most common form of chronic monoarthritis
 It is a joint disease characterized clinically by:
o Pain that typically worsens with weight bearing and activity and improves with rest
o Morning stiffness and gelling of the involved joint after periods of inactivity
o Tenderness on palpation, bony enlargement, crepitus on motion, and/or limitation of joint motion
 Epidemiology:
o Affects 1 in 10 Canadians
o OA is associated with significant costs:
 Direct = drugs, healthcare resource use
 Indirect = lost employment time, costs of informal caregiving
 Under treatment leads to significant pain and loss of quality of life ☹
 Clinical characteristics:
o Insidious over months to years
o Associated with morning stiffness for 15-30 minutes
o Usually occurs in those of older age, and in women more than men
o Causes pain with activity
o Boney enlargements
o Distribution of joints:
i. Hands = DIP, PIP, 1st CMC joints
ii. Hip
iii. Knee
iv. Feet = first MTP
v. Spine = cervical, lumbar
Osteoarthritis Vs. Rheumatoid Arthritis:

Osteoarthritis: Rheumatoid Arthritis:

 PIPs and DIPs affected  PIPs affected and DIPs spared
 MCPs and wrist usually spared  MCPs and wrist affected
 First CMC affected
Pathophysiology:
 Osteoarthritis is a degenerative disease that involves the breakdown of
articular cartilage, which results in bone rubbing on bone
 The pathogenesis also involves inflammation and biomechanical factors
 This process results in joint pain and stiffness, swelling, and decreased
range of motion, as well as changes that can be seen on x-ray:
1. Loss of joint space
2. Subchondral sclerosis
3. Osteophyte formation
4. Subchondral cysts (fluid pressed in)
5. Malalignment of joint

 There may or may not be a participating cause:

o Secondary osteoarthritis = the degeneration is secondary to an injury to the cartilage, occurs faster than primary
o Primary osteoarthritis = no obvious cartilage injury, changes are due to aging over time
 All laboratory investigations should be normal in osteoarthritis
Risk Factors:
1. Genetics (tends to run in the family)
2. Advanced age
3. Female gender
4. Obesity (maybe due to increased weight on joints)
5. Muscle weakness (don’t have good strength = increased pressure on joints)
6. Occupation (repetitive actions)
7. Trauma and injuries
Management:
Goals of Treatment:
 Pain reduction
 Improved function
 Changes the disease outcome
 Low cost
 Low side effects
Non-Pharmacologic Options:
1. Exercise and weight loss
2. PT → strength training for surrounding muscles
3. Proper footwear
4. Assistive devices
Pharmacologic Options:
A) Oral Medications:
1. Acetaminophen:
 Useful in mild to moderate osteoarthritis
 Acetaminophen is recommended as first line therapy for the
treatment of pain due to osteoarthritis
 Pros = cheap, safe, proven benefit
 Cons = small effect
 Maximum of 3 grams per da y
3. Opioid Analgesics:
 It is rare for patients with OA to show addictive behaviour
 Side effects (a real concern in the elderly):
o Sedation
o Confusion
o Constipation
o Risk for falls and other accidents
 Efficacy:
o Codeine does have some evidence for efficacy; however, also
has a high incidence of side-effects
o Oxycodone, morphine, and hydromorphone = better choices
 Start with low prn doses (night time and prior to activity)
 If one opiate doesn’t work, try another instead of increasing the dose
B) Topical Medications:
1. Capsaicin:
 A substance derived from the chili pepper
 Depletes nerve endings of chemicals needed for
the transmission of pain
 Results in “analgesia”
 Touch and temperature sensation are not affected
 Limited use:
o Messy
o Takes 3-7 days to work
o May have burning/stinging for first 7-10 days
o Do not get in the eyes!!!!!!!
C) Injectable Medications:
1. Corticosteroids:
 Pros:
o Cheap
o Relatively safe (low risk of infections)
 Cons:
o Short term benefit at 4-8 weeks but negative at 12-24 weeks
(however, for some it may work for months!)
o Predictors of response are unclear
o No more than 3-5 injections in a single joint per year
2. NSAIDs:
 Options = traditional NSAIDs or COX-2 selective NSAIDs (COXIBs)
 Inhibit production of prostaglandins
 NSAIDs consistently outperform acetaminophen
HOWEVER they increase the risk of GI, cardiac, and
renal issues
o Ulcers
o Decreased GFR → decreased kidney function
o May increase the risk of MI
 Need to balance risks vs. benefits
 Use the lowest possible dose for the shortest duration of time
4. Glucosamine:
 Glucosamine is a component of cartilage that is reduced in
osteoarthritic cartilage
 Replacing glucosamine may have beneficial
effects but research so far has not really found
glucosamine to be efficacious
 Dose = 500 mg three times daily
 If no effect after 3 months, stop
 DONA brand is the only one with positive
evidence
2. Topical NSAIDs:
 Options:
o Pennsaid → prescription topical diclofenac 1.5% with a
DMSO carrier
o Voltaren → Emulgel available over the counter
o Other formulations available at compounding pharmacies
 Limited use for osteoarthritis:
o Small effects in clinical trials
o Need to apply 4 times per day
o Expensive
o Messy
 Benefits = little systemic absorption
2. Viscosupplementation:
 Joints typically contain a small amount of
lubricating fluid called synovial fluid, of
which hyaluronic acid is a component
 Synovial fluid hyaluronic acid is
decreased in patients with osteoarthritis
 Viscosupplements are synthetically or
biologically derived hyaluronic acid given by a series of either 3
injections once a week or by a single injection
 Only approved for osteoarthritis of the knee (not found to be
effective in other joints)
 Pros = if it works, may have a significant benefit
 Cons:
o Expensive (~ $300 per course, not covered by OHIP!)
o The effects are variable, lasting months in some people and
not working at all in others
o Post-injection arthralgia
Surgery:
 Who is appropriate:
o Most people with arthritis, including older individuals, should be
referred for surgical treatment when other treatment is ineffective
and function is impaired.
o Surgery should not be used as a last resort
o There is no “magic age” for surgery – doesn’t matter how old they
are, if they are generally in good health, this option should be
considered
 Consider surgery before:
o Advanced muscle weakness
o Joint deformities
o Significant loss of function with further deconditioning
 Decision for referral for surgery is based on:
o Pain and stiffness, function, and deformity
o Other medical risk factors
o Patient goals and preferences
o Prior non-surgical treatment
o X-ray changes