Low Back Pain and Spondyloarthropathies Flashcards
What causes the majority of low back pain and what are the mechanical causes of low back pain?
Majority is caused by mechanical forces and will respond spontaneously - 90%
Nonmechanical causes:
- Spondylarthropathy
- Cancer / malignancy
- Spinal infection
- Referred visceral pain (i.e. pancreatitis)
What are the warning signs of a nonmechanical lower back pain?
Constitutional symptoms
No improvement of pain over weeks
Pain is worse at night or has been increasing
Prolonged morning back stiffness with pain onset before age 40
What are the shared features of the spondyloarthropathies?
- No rheumatoid factor (anti-IgG antibody)
- Associated with HLA-B27
- Insidious onset beginning before age 40
- Inflammatory back pain -> associated with morning stiffness >1 hour, improves with exercise
- Peripheral arthritis is also associated
- Enthesitis - shared pathology of inflammation where ligaments / tendons insert onto bone
- Dactylitis
- Uveitis
What diseases fall under the umbrella of seronegative spondyloarthropathies?
- Ankylosing spondylitis - most prototypical
- Reactive arthritis
- Psoriatic arthritis
- Spondyloarthropathies associated with IBD’s
- Juvenile and undifferentiated SpA’s.
PAIR = Psoriatic, Ankylosing, Inflammatory Bowel, Reactive
What is the most common spondyloarthropathy and if you have HLA-B27 do you get it? Who tends to get it and what worsens it?
Ankylosing spondylitis (AS) is the most prevalent one.
No. Only 1% of those with HLA-B27 have it, but 90% of patients with ankylosing spondylitis will have HLA-B27.
Most common in males in their 20s-40s, worsened by smoking like RA. May happen as frequently in females, but subclinically.
What is the progression of symptoms in AS?
Diffuse nonspecific radiation of pain into both buttocks, starting in the sacroiliac joints, and slowly progressing up the spine from the lumbosacral region.
Inflammation of the annulus fibrosus with granulation tissue around the entheses results in the formation of new bone -> gradual progression to bamboo spine.
What peripheral joints are commonly involved in AS and what problems can this cause? How does this tie into why the patients should quit smoking?
Commonly involves hips, shoulders, and joints of the chest wall: i.e. AC or sternoclavicular joints
Involvement of costochondral and costovertebral joints can contribute to the development of restrictive lung disease -> loss of chest expansion is common in late-stage disease
Apical pulmonary fibrosis and mechanical restrictive lung disease are very common -> another reason why these patients are advised to quit smoking
What are the eye and cardiovascular complications common in AS?
Eye -> acute anterior uveitis is common, which is marked by painful eye redness and blurred vision.
Cardiovascular -> Aortitis of ascending aorta leads to distortion of aortic ring -> aortic regurgitation is relatively common.
Is AS associated with osteopenia / osteoporosis?
Although it is associated with new bone formation at sites of enthesitis, chronic inflammatory state can lead to osteoporosis in unaffected areas -> increasing fracture risk
Give three musculoskeletal tests which can be used to assess the severity of ankylosing spondylitis?
- Schober’s Test - test of lumbar spinal flexion
- Cervical flexion test - test of cervical extension
- Eliciting sacroiliac tenderness by direct or indirect compression
How does Schober’s test work?
Mark a point on the PSIS (back dimples) and then 10cm above it. Have the patient bend down as far as they can. If the distance measured is not at least 15cm now, they have limited lumbar flexion and pathology is likely.
How does the cervical flexion test work?
Have the patient stand with their but against the wall. Try to extend the neck to touch their occiput to the wall. Measure the distance to see the degree of cervical overflexion defect.
How will the posture of patients progress in AS?
Starts from normal, but overtime there will be progressive loss of lumbar lordosis and accentuated thoracic kyphosis (hunched over)
How is the diagnosis of AS made?
Via the presence of a radiological criterion in conjunction with at least one clinical criterion
Radiologic criteria range from grades 1-4 grading the progression of sacroilitis.
How does sacroilitis progress?
Starts with widening and blurring of the subchondral bone, then progresses to erosions and partial bridging of bone.
Ankylosis starts with the synovial portion of the sacroiliac joint (anterior/inferior) and then progresses to the ligamentous portion (posterior/superior). Endstage is fusion of the sacroiliac joint forming a very rigid structure.
How does the involvement of the vertebrae progression in AS?
Starts with sclerosis of superior / inferior margins of vertebral bodies - “Shiny corners”
Then marginal syndesmophytes begin to form at the intervetebral joints until they fuse and become continous -> bamboo spine.
How can AS be confused with OA?
There will be joint-space narrowing, cystic / erosive changes, and subchondral sclerosis.
Note however: involvement of shoulders which can occur in AS would not happen in osteoarthritis unless it was secondary.
What is the most sensitive test for early sacroilitis in AS?
MRI of the sacroiliac joint with contrast -> would show prominent edema
What is the treatment for AS?
Same as rheumatoid arthritis pretty much. For biologics, in addition to anti-TNFa agents, IL-17 inhibitor Secukinumab is approved for treatment
What is dactylitis and which of the spondyloarthropathies is it most common in?
“Sausage fingers” - inflammation of all the tendons and joints within a finger or toe leads to massive swelling.
Most common in psoriatic arthritis, but could theoretically happen in any of them
Who gets reactive arthritis? What role does HLA-B27 have?
Occurs a few days to 6 weeks after a GI or GU infection.
50% of people will have HLA-B27, and this allele is required for sacroilial involvement.
Post-GU infection most common in males (chlamydial)
GI infections has equal prevalence between sexes
Are bacteria viable in reactive arthritis? Why does it happen
We believe not -> joint culture results are usually negative, perhaps with the exception of chlamydia, implying the inflammation is caused by nonviable bacterial components
-> defective Th1 response
What bacteria are implicated in reactive arthritis?
GI:
Shigella, Salmonella, Campylobacter, Yersinia -> all cause infectious diarrhea
GU: Chlamydia
What are the symptoms of reactive arthritis?
Can’t see - Conjunctivitis -> transient and often asymptomatic
Can’t pee - urethritis
Can’t bend my knee - asymmetric oligoarthritis. Associated with back pain if B27.
Also:
- Enthesopathy -> Achilles tendinitis
- Mucocutaneous lesions: Oral ulcerations - tongue and other mucous membranes. Keratoderma - thickening of palms and soles.
