Page 832 - Clinical Small Animal Internal Medicine

800 Section 8 Neurologic Disease

Treatment of the “sterile” meningoencephalitides although they must be monitored closely for relapse of
VetBooks.ir focuses on the control of inflammation and suppression clinical signs. Conversely, many patients require long‐
term and often life‐long therapy.
of the immune system with glucocorticoids and in
Some conditions, such as SRMA, generalized tremor
some cases additional immunosuppressive medications.
Prednisone or dexamethasone is often started at antiin- syndrome and idiopathic eosinophilic meningoencepha-
flammatory doses after imaging studies and CSF collec- litis, can typically be managed with glucocorticoids
tion, pending the results of infectious disease testing. alone. This strategy can also work for patients with
Antimicrobial drugs are usually indicated while awaiting GME, NME or NLE although anecdotal evidence sug-
these results. When the clinician has ruled out infectious gests that these dogs do not respond as well, and may
causes, the patient is reassessed and their response to benefit from additional immunosuppressive therapy. This
therapy is evaluated. Some animals will respond fully to benefit may occur due to additional mechanisms of
antiinflammatory glucocorticoids. However, those with immunosuppression (typically interference with lym-
an absent or partial response will often benefit from phocyte proliferation) or by allowing a decreased gluco-
escalation to an immunosuppressive dose (Table 73.4). corticoid dose, which reduces adverse effects and
If remission is achieved, this dose is continued for an improves overall management. Several different immu-
extended period and then the dose is slowly reduced over nosuppressive drugs have been utilized in this scenario
a period of weeks to months. Some animals are eventually (see Table 73.4), and choice is based primarily on clini-
able to have their glucocorticoid therapy discontinued, cian preference, as rigorous studies demonstrating a

Table 73.4 Antiinflammatory and immunosuppressive medications for meningoencephalitis and meningomyelitis

Medication Dosing Mechanism of action Adverse effects Additional considerations

Prednisone or 0.5–1.0 mg/kg q12–24h Regulation of Polyuria, polydipsia, Prednisolone preferred in
prednisolone (antiinflammatory); inflammatory gene polyphagia, cats
2.2–6.6 mg/kg/day expression, impaired gastrointestinal ulceration,
(immunosuppressive) leukocyte migration, hypercoagulability,
interference with hepatopathy
arachidonic acid cascade
and cytokine production
Dexamethasone 0.07–0.15 mg/kg As for prednisone As for prednisone
q12–24h
(antiinflammatory);
0.3–1.0 mg/kg/day
(immunosuppressive)
2
Cytosine 200 mg/m IV over Interferes with pyrimidine Nausea, vomiting, bone
2
arabinoside 8–24 hours or 50 mg/m (DNA) synthesis marrow suppression,
SC twice daily for 2 days hepatic toxicosis
Leflunomide 3–4 mg/kg/day Interferes with pyrimidine Nausea, diarrhea, lethargy,
(DNA) synthesis bone marrow suppression
(rare)
Azathioprine 2 mg/kg q24h initially Interferes with purine Vomiting, diarrhea, bone Clinical effect may be
(5–14 days) then (DNA) synthesis marrow suppression, delayed up to 4–6 weeks
0.5–1.0 mg/kg q48h hepatic toxicosis
Mycophenolate 10 mg/kg q8h or Interferes with purine Vomiting, diarrhea
mofetil 20 mg/kg q12h (dogs) (DNA) synthesis
Ciclosporin A 5 mg/kg q12–24h Calcineurin inhibitor Inappetence, vomiting, May adjust according to
(inhibits T cell diarrhea, gingival response or blood
proliferation) hyperplasia, papillomatosis, concentrations; concurrent
hepatic or renal toxicosis ketoconazole administration
(rare) may allow lower dose
2
Lomustine 60–90 mg/m q4 weeks Alkylating agent Bone marrow suppression,
(CCNU) hepatic toxicosis
2
Procarbazine 25–50 mg/m q24h Alkylating agent Nausea, vomiting, bone
(suspected) marrow suppression,
hepatic toxicosis