WSAVA Nov 2021 Proceedings - Flipbook - Page 31
years of age and, therefore, a dog meeting these criteria is presumptively
diagnosed with idiopathic epilepsy and advanced diagnostics are often
not necessary. Because such typical guidelines are not available for the
feline idiopathic epileptic, advanced diagnostics are usually recommended for the seizuring cat, even when idiopathic epilepsy is suspected. Such
diagnostics include advanced imaging such as MRI or CT and potentially
a CSF tap. Abnormalities on CSF are very sensitive to intracranial disease,
but often not specific. However, when evaluated in conjunction with the
MRI/CT imaging, it can be a helpful diagnostic tool. Cultures and infectious disease titers (Cryptococcus, toxoplasmosis and FIP) may also be
useful tests to be performed on CSF.
MAINTENANCE THERAPY
The aim of any anti-epileptic treatment is to “control” the seizures by
reducing their frequency, intensity and severity with minimum side effects.
Decision to start anti-epileptic treatment is still a subject of controversy.
Cats with a single seizure or isolated seizures separated by longs period
of time do not require treatment. Treatment is indicated when: the first
seizure is life-threatening (status epilepticus or severe clusters), multiple
seizures are observed in a short period of time, seizures occur more than
once a month and/or owners objects to their frequency, the seizures
are becoming more frequent or more severe, an underlying progressive
disorder has been identified as the cause of the seizures. Commonly
used anti-epileptics in cats are: phenobarbitone (3 mg/kg q12hrs orally),
levetiracetam (20 mg/kg q8hrs orally), zonizamide (5 to 10 mg/kg q24hrs
orally) and pregabalin (2 to 4 mg/kg q8 to 12 hrs orally). Phenobarbitone
is the first choice of many clinicians for cats with seizures. Compared to
dogs steady state serum level tends to drop with time, elimination half-life
in cats is stable at around 34 to 43 hours and therefore drug concentration
of phenobarbitone are not expected to decrease in cats receiving longterm therapy without changing the oral dosage. Monitoring of serum level
is only justified shortly after the onset of treatment (when steady state
level is reached after 10 to 15 days) due to the differences in elimination
kinetics of phenobarbitone between population of cats or when drugs
that might interfere with phenobarbitone’s pharmacokinetic are added.
Recommended therapeutic ranges have not been properly defined in cats
but are considered similar to the recommended one in dogs [20 to 35 ug/
ml]. Cats should not be considered as refractory to treatment until serum
concentrations reach 35 ug/ml unless unacceptable side effects persist.
Side effects of phenobarbitone in cats include: sedation, ataxia, polyphagia, weight gain, neutropenia, thrombocytopenia, coagulopathy, severe
cutaneous eruptions and marked lymphadenopathy (idiosyncratic delayed
hypersensitivity). The author does not recommend the use of oral bromide
in cats due to the high incidence of side effect in this species and in
particular clinical and radiographic signs similar to feline asthma such as
coughing and/or difficulty breathing.
0011
BRACHYCEPHALIC OBSTRUCTIVE AIRWAY
SYNDROME: PATHO-PHYSIOLOGY AND
RECOGNITION
J. Ladlow1,2, N. Liu3
High Wycombe/United Kingdom, 2Cambridge/United Kingdom, 3ES/United Kingdom
1
Qualifications:
Jane Frances Ladlow
MA VetMB Cert VR, CertSAS FHEA DipECVS MRCVS
jfladlow1001@cam.ac.uk
BOAS: Pathophysiology and Recognition
Pathophysiology
Brachycephalic Obstructed Airway Syndrome (BOAS) is clinical signs
resulting from upper airway obstruction related to the restricted length of
the skull, particularly the nasal cavity.
Work by the Royal Veterinary College (RVC) suggested that the craniofacial ratio (CFR), which is muzzle length over cranial length, is correlated
with BOAS status1. The tissue proportions in the upper airway seem breed
specific however, reflecting the different types of skull morphology seen in
breeds which are labelled as brachycephalic.
The prevalence of BOAS within the extreme breeds is not yet clear. In
our study population in the UK (excluding clinical cases) we classified
approximately 40% of Bulldogs, 46% of French Bulldogs and 60% of Pugs
with clinically significant disease.2
Disease Syndrome-Pathophysiology
Brachycephalic dogs have a widened and shortened skull and muzzle.
Although the skull is shortened, the soft tissues are not always reduced in
a proportionate manner.
The upper airway disease may present as respiratory noise, exercise intolerance, heat sensitivity, sleep disorders, dyspnoea, cyanosis or collapse3.
Gastro-intestinal signs include regurgitation and vomiting with oesophagitis from increased gastro-oesophageal reflux4. Some dogs, particularly
with nasal or nasopharyngeal obstruction also have sleeping disorders.
Lesion sites
In BOAS there are primary congenital abnormalities (stenotic nares,
hyperplastic soft palate, hypoplastic trachea, macroglossia, enlargednasal
turbinates, nasopharyngeal constriction) that result in restriction to airflow, tissue swelling and hypertrophy and excessive inspiratory pressures
in the upper airway. These lesions can cause secondary areas of collapse
and inflammation, notably laryngeal collapse. The increased thoracic pressures may result in gastrointestinal signs of reflux and hiatal hernia with
the accompanying risk of aspiration pneumonia or bronchial collapse. It is
not always clear which lesions are primary and which are secondary and
these may alter between breeds.
In the early papers on BOAS, the stenotic nares were thought to be of
paramount importance, and we have found similar results in the French
Bulldog in particular, with a marked increased risk of BOAS if the nostrils
are moderately or severely stenosed.
We have modified a nostril grading system5 (Figure 5). Grade 0 and 1
are not associated with a greater risk of airway disease whereas grade 3
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