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568.e2 Juvenile Polyarteritis

Juvenile Polyarteritis Client Education
Sheet
VetBooks.ir Etiology and Pathophysiology

BASIC INFORMATION
• Immunoglobulin A (IgA) and IgM are often • Systemic and intrathecal (CSF) immuno-
globulin A concentrations are often increased.
Definition increased in the circulation, and IgA is often • Blood C-reactive protein and serum amyloid-
Systemic necrotizing vasculitis of small and increased in the cerebrospinal fluid (CSF). A are often increased.
medium-sized arteries of the heart, mediastinum, • Systemic necrotizing vasculitis with severe • Brain/spinal MRI, CT (p. 1132): usually
and cervical spinal cord. This condition is most subarachnoid hemorrhages throughout spinal normal
often reported in colonies of research beagles. cord and brainstem • Histopathologic evaluation of tissues: severe
Steroid-responsive meningitis-arteritis is a • Immunoglobulin deposited in the walls of necrotizing vasculitis (especially medium-
related or likely the same disease. arteries stimulate an inflammatory cascade sized arteries of the heart, mediastinum,
leading to necrosis and marked perivascular and cervical spinal cord), necrosis, destruc-
Synonyms accumulation of neutrophils, macrophages, tion of elastic layers, severe perivascular
Steroid-responsive meningitis-arteritis (SRMA), and lymphocytes. accumulation of neutrophils, macrophages,
beagle pain syndrome, canine juvenile polyar- • The thickening and necrosis of small to and lymphocytes
teritis syndrome, necrotizing vasculitis medium-sized arteries result in occlusion and
thrombosis that may cause neural ischemia TREATMENT
Epidemiology and pain.
SPECIES, AGE, SEX • Vessels of the cervical spinal cord, media- Treatment Overview
• Most often in young beagles (<12 months stinum, and coronary arteries may be involved. Signs should resolve within 24-48 hours of
old) • The underlying trigger is unknown. starting glucocorticoid therapy. To avoid relapse,
• Also affects young dogs of other breeds (6-18 treatment should not be stopped abruptly or
months old) DIAGNOSIS tapered too quickly. Some animals relapse
• No sex predisposition during treatment.
Diagnostic Overview
GENETICS, BREED PREDISPOSITION Clinicians should give careful consideration to Acute General Treatment
• The occurrence in research beagles suggests the list of differential diagnoses (below). Initial • The mainstay of treatment is prednisone/
an underlying genetic component. laboratory testing typically suggests systemic prednisolone therapy: start at 1.5-2 mg/
• Beagle, Bernese mountain dog, boxer, inflammation. Advanced imaging helps rule kg, PO, IM, or SQ q 12h for 3-5 days,
German shorthaired pointer, Nova Scotia out other neurologic disorders. Arthrocentesis then 1 mg/kg, PO q 12h for 14 days. Begin
duck tolling retriever and/or a CSF collection help to confirm the gradual taper after 14 days.
diagnosis. • Restrict activity until signs resolve (typically
RISK FACTORS 24-48 hours).
Age and breeds described above. Differential Diagnosis • Azathioprine 1-2 mg/kg PO q 24h for
• Cervical disk herniation: diagnostic imaging patients who do not respond to or tolerate
CONTAGION AND ZOONOSIS (spinal radiographs, CT, MRI) glucocorticoids. There is a delay of efficacy
Unlikely contagious or zoonotic • Spinal cord trauma: history, diagnostic for azathioprine of 2-4 weeks.
imaging (spinal radiographs, CT, MRI)
Clinical Presentation • Polyarthritis and/or polymyositis Chronic Treatment
DISEASE FORMS/SUBTYPES • Granulomatous meningoencephalomyelitis: • Taper glucocorticoids to the minimum dose
• Acute form CSF analysis that controls clinical signs (usually 0.25-0.5 mg/
• Chronic, episodic • Infectious meningoencephalitis: CSF analysis kg PO q 48h) over 2-6 months. Eventually,
• Discospondylitis: diagnostic imaging (spinal drugs may be withdrawn altogether.
HISTORY, CHIEF COMPLAINT radiographs, CT, MRI) • Reduce azathioprine dosage and interval after
• Reluctance to eat and drink is commonly • Bacterial meningitis: CSF analysis and culture approximately 14 days (1-2 mg/kg PO q
reported; this is likely caused by neck pain • Protozoal infection: muscle biopsy, serologic 48h), and discontinue azathioprine as soon
and reluctance to bend down to the food titers as practical, based upon clinical assessment.
and water bowl.
• Reluctance to move; inactivity Initial Database Drug Interactions
• Paresis occurs rarely. • CBC: neutrophilia Nonsteroidal antiinflammatory drugs (NSAIDs)
• Clinical signs can be episodic, lasting a few • Serum biochemistry profile: increased acute should not be used with glucocorticoids.
days, and then resolve. phase proteins
• With multiple, untreated episodes, patients • Urinalysis: proteinuria (sometimes) Possible Complications
can exhibit signs consistent with neurologic • Thoracic, abdominal, cervical radiographs: • Polyuria/polydipsia/polyphagia associated
dysfunction (paresis, rarely cranial nerve normal with glucocorticoid administration
deficits). • Gastrointestinal upset and ulceration associ-
Advanced or Confirmatory Testing ated with glucocorticoid administration
PHYSICAL EXAM FINDINGS • Synovial fluid analysis (p. 1059): reduced • Infections secondary to chronic immunosup-
• Fever viscosity, neutrophil infiltration, negative pression
• Cervical pain bacterial culture • Bone marrow toxicity and hepatic failure
• Generalized hyperesthesia • CSF analysis (pp. 1080 and 1323): neutro- from azathioprine therapy
• Reluctance to move philic pleocytosis, increased protein, with
• Anorexia, lethargy, malaise a negative bacterial culture. In the chronic Recommended Monitoring
• Atypical/chronic form: proprioceptive deficits, or episodic form, the CSF changes may be • CBC, serum chemistry profile, urinalysis
ataxia, paresis, cranial nerve deficits (rarely) milder. every 1-2 weeks when on high dosages of

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