2.2 Approach to Joint Disease Flashcards
What is true about arthritis and inflammation?
all forms of arthritis are inflammatory, but some are more so than others
- the forms are split between “inflammatory” and “non-inflammatory” to help from a diagnostic point of view
- in reality there is a lot of overlap in terms of pathogenesis and end-stage pathways
osteoarthritis is by far the most common form that is seen in GP
What are the “inflammatory” and “non-inflammatory” forms of arthritis?
inflammatory:
- Immune Mediated (erosive + non-erosive IMPA)
- infective (e.g., bacterial)
- crystal induced (e.g., gout)
non-inflammatory:
- osteoarthritis
- traumatic arthritis
- coagulopathic arthritis
IMPA can be erosive or non-erosive, and can have many possible subtype variations. How are these differentiated?
the classification of various types of IMPA is driven by:
- the presence or absence of extra-articular disease in addition to polyarthritis
- radiographically observed erosive changes in affected joints
- any identifiable primary initiating
disease process
What is non-erosive immune-mediated polyarthritis (IMPA)
“typically defined by a synovial accumulation of immune complexes (type III hypersensitivity), which starts a cascade reaction that draws neutrophils into the joint. Some erosive forms of IMPA may also include a T cell-mediated response (type IV hypersensitivity) directed against articular cartilage”
- an immune-mediated inflammation of the joint spaces triggered by abnormal B and T cell interaction
- may initially be a normal response to antigenic stimulation, which does not down regulate appropriately
- large amounts of antibody/antigen complexes deposit on the synovium, leading to the formation of inflammatory products, as well as neutrophil and macrophage chemotaxis
What are risk factors for autoimmune diease?
- genetics (beagles, nova scotia duck tolling retrievers)
- certain infections (bacterial endocarditis, discospondylitis)
- immune-mediated bowel disease
- neoplasia
- chronic hepatitis
What are the subtypes of non-erosive IMPA?
Type I: uncomplicated idiopathic- most common type (50%)- diagnosis by exclusion
Type II: infection-associated; e.g. endocarditis(reactive arthritis) (25%)
Type III: Gl disease-associated (most commonly IBD)/hepatic (15%)- usually see signs of Gl disease
Type IV: neoplasia-associated (< 10%) - many neoplasias have been associated with it
Other types: Systemic Lupus Erythematous, drug reactions (e.g. Dobermans & sulphonamides), breed associated IMPA, vaccine induced (Calciviral in kittens, Distemper), Lyme disease (Borrelia burgdorferi)
What are the clinical signs associated with non-erosive IMPA?
- acute or chronic lameness: stilted, crouched gait, may present as ataxia
- multiple painful, swollen joints (ROM decrease, pain, heat, crepitus)
- often systemic signs: pyrexic, lethargic, inappetent
- ligamentous laxity
- distal joints more commonly affected
note: stiffness is typically more severe and longer-lasting than OA
What can a travel history tell out about non-erosive IMPA?
possible exposure to infectious agents
- Ehrlichia, heartworm, and leishmania (abroad)
- Borrelia and Lyme disease (UK)
each of these can lead to IMPA
How do you investigate arthralgia?
arthralgia is pain within the joint:
- arthrocentesis and cytological evaluation of the joint fluid is the best place to start: protein and cell counts
- synovial biopsy
- radiographs are often unnecessary, but may help to rule out erosive disease and joint laxity
once a diagnosis of IMPA is reached, subtype can be identified via:
- CBC/biochem
- ultrasound of abdomen
- thoracic radiographs
- echocardiology
these evaluate is any underlying disease is triggering the IMPA (e.g., neoplasia, bowel disease)
What may be seen on cytological analysis of arthrocentesis in IMPA?
What is erosive IMPA?
Also a type III hypersentitivity reaction(+/- Tpe IV)
cellular or humoral immunopathogenic factors → chronic synovitis → chemotaxis of inflammatory cells (e.g., neutrophils), to the site of inflammation
- end-stage erosive IMPA is the formation of synovial pannus: leads to the destruction of cartilage, bone, tendons, ligaments, and blood vessels
What is pannus?
pannus is an abnormal layer of fibrovascular tissue or granulation tissue
- common sites for pannus formation include over the cornea, over a joint surface (as seen in erosive IMPA), or on a prosthetic heart valve
- pannus may grow in a tumor-like fashion, as in joints where it may erode articular cartilage and bone
- pannus tissue is composed of aggressive inflammatory cells that release collagenolytic enzymes
What are the subtypes of erosive IMPA?
can further subtype into the following, but won’t change treatment plan or outcome:
(1) Rheumatoid arthritis
- most common, hard to diagnose in small animals
- +ve for rheumatoid fracture (but this is unspecific)
(2) Periosteal proliferative polyarthritis
- in cats (v. rare)
- affects young, male cats
- often have FeLV (no association shown) & are negative for rheumatoid fracture
(3) Polyarthritis of Greyhounds (Felty’s Syndrome)
- controversial & only reported in Australia & America
What is the traditional diagnosis of rheumatoid arthritis?
Radiographic erosion: most clinically relevant factor
- BUT must have 7 of the 10 below
How do you treat erosive and non-erosive IMPA?
(1) identify inciting factor
- remove/treat
(2) modify lifestyle to decrease joint stress
- controlled exercise
- weight loss
- physiotherapy
(3) supress the immune system or control inflammation
- prednisolone: mainstay (immunosuppressive doses)
- +/- cyclosporin, cyclophosphamide, azathioprine (not cats)
- leflunomide (disease modifying antifheumatic drugs)
(4) analgesia
- difficut as cannot use NSAIDs with prednisolone
in areas where tick-borne diseases are prevalent, empirical treatment may be necessary
(5) monitor
- clinical improvement should be seen within 7 days
- not very necessary to resample synovial fluid but can
- significant decrease in WBC and neutrophils is a good prognostic indicator
(6) surgery
- uncommon, expensive, morbidity
- e.g, arthrodesis, joint replacement
How do you recognize and treat septic arthritis?
(1) clinical signs:
- very lame (usually non-weight-bearing)
- hot swollen joint
- +/- systemic signs: pyrexia
(2) diagnosis:
- arthrocentesis for culture and sensitivity
- NOTE: must send samples for culture, HOWEVER ~50% of cases are negative for infection. Do not put too much stock into a negative culture if the clinical picture is indicative of septic arthritis
- If culture is positive, you may recheck for a negative culture before ending antibiotic therapy. Obviously, if negative from the start, re-testing will have no diagnostic/therapeutic value
(3) management (after treatment):
- rest in early stages
- physio/hydrotherapy to reduce adhesions
