F
Facial Muscle Wasting
BASIC INFORMATION 
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Detailed history to include inquiries regarding previous bouts of painful mastication or chronic corticosteroid use
PHYSICAL EXAM FINDINGS
▪ Full physical examination, paying particular attention to the head, the condition of other muscle groups, and the skin
▪ Bilateral atrophy of the temporal and masseter muscles; skull-like appearance of the head
○ Dogs with MM can show salivation, dysphagia, and difficulty in opening their mouths, progressing to trismus.
• Enophthalmos, with third eyelid protrusion and small palpebral fissure due to dramatic loss of retrobulbar muscular support
DIAGNOSIS 
TREATMENT 
CHRONIC TREATMENT
• Glucocorticoid therapy
○ Idiopathic polymyositis (prednisone, 1-2 mg/kg q 12 h for 14 days, then tapering over at least 4 weeks to 12 months or longer)
PEARLS & CONSIDERATIONS 
COMMENTS
• Facial muscle atrophy is a common feature of many emaciating conditions in which there is also accompanying generalized loss of lean body mass.
• Generalized muscle atrophy is often first noticed in the facial muscles, especially in long-haired breeds.
Facial Paralysis, Idiopathic 
BASIC INFORMATION 
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Dogs usually have an apparent ear droop and occasionally will have deviation of the nose away from the affected side. Food may collect in the affected commissure of the lips, and there may be associated halitosis.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Idiopathic facial paralysis must be differentiated from other conditions involving the peripheral aspect of the facial nerve (e.g., otitis media interna, hypothyroidism, ear polyps, and polyneuropathies).
TREATMENT 
ACUTE GENERAL TREATMENT
• Treatment is primarily supportive. Sterile lubricant ophthalmic ointment should be applied to the affected eye(s) at least q 6-8 h to prevent exposure keratitis and corneal ulceration.
Dewey CW. Encephalopathies: Disorders of the brain. In: Dewey CW, editor. A practical guide to canine and feline neurology. ed 2. Ames, IA: Wiley-Blackwell Publishing; 2008:160-162.
Varejao AS, et al. Magnetic resonance imaging of the intratemporal facial nerve in idiopathic facial paralysis in the dog. Vet Radiol Ultrasound. 2006;47:328.
Fanconi Syndrome 
BASIC INFORMATION 
EPIDEMIOLOGY
GENETICS & BREED PREDISPOSITION
• Inherited form in basenji; mode of inheritance unknown; affects 10%-30% of basenji dogs in United States
• Documented disease in other breeds (not necessarily inherited): border terriers, Norwegian elkhounds, single reports in a Yorkshire terrier, Labrador retriever, cocker spaniel, dachshund, whippet, Shetland sheepdog, and mixed breed
ETIOLOGY AND PATHOPHYSIOLOGY
• Defects are primarily proximal tubular resorptive defects.
○ Filtered glucose is normally completely reabsorbed in the proximal tubule, so long as tubular concentration (similar to plasma concentration) does not exceed the transport maximum (about 180 mg/dL). A defect in the transport mechanism can lead to renal glucosuria despite normoglycemia.
○ Aminoaciduria may be generalized or involve only certain groups of amino acids, because different carrier molecules are involved in transport of acidic, basic, and neutral amino acids. Some dogs have cystinuria with minor defects in resorption of methionine, glycine, and dibasic amino acids.
○ Phosphate is reabsorbed primarily in the proximal tubule, with very little reabsorbed in the distal tubule. Excessive phosphaturia due to tubular defects may lead to hypophosphatemia.
DIAGNOSIS 
INITIAL DATABASE
• Urinalysis: isosthenuria or minimally concentrated urine, glucosuria and proteinuria common, +/− ketonuria
• Serum biochemistry panel: normoglycemia; hyperchloremic metabolic acidosis, and azotemia occur late in disease process.
TREATMENT 
TREATMENT OVERVIEW
One treatment protocol (www.basenji.org/fanconi.pdf) replaces nutrients excreted in urine to maintain plasma concentrations. This protocol has not been compared to other (potentially simpler) protocols to determine whether it improves survival or quality of life, but it is used by many owners of basenji dogs with Fanconi syndrome.
ACUTE GENERAL TREATMENT
• If acute uremic crisis, hospitalize for intravenous fluid therapy and other management appropriate for decompensated chronic renal failure (see p. 207)
CHRONIC TREATMENT
• Acidosis: sodium bicarbonate titrated to keep venous pH normal. Doses may exceed 11 mEq/kg per day (650 mg = 10 grain = 7.8 mEq). Starting dose can be based on pH and Pco2 using a chart in the basenji club website protocol, or if immediate blood gas monitoring not available, 30 grains q 12 h.
• Hypokalemia: supplement 5-15 mEq per day, depending on severity of hypokalemia. Potassium gluconate has 8 mEq K+ per tsp. Potassium citrate provides 5 mEq K+ per 540 mg tablet; the citrate is metabolized to 5 mEq bicarbonate, which may help control acidosis.
NUTRITION/DIET
• Vitamin and mineral replacement: 1-2 canine multivitamins per day (e.g., Pet-Tab Plus), 1-2 Pet-Cal (calcium, phosphorus, and vitamin d supplement) per day, and 1 human multivitamin with trace minerals (i.e., Centrum) per week in dogs with polyuria and polydipsia. Do not give Pet-Cal if dog is in renal failure.
POSSIBLE COMPLICATIONS
• Neurologic signs (seizures, ataxia, dementia, or central blindness) of unknown cause are seen in up to 20% of dogs.
Fear Due to Veterinary Visits/Treatments
BASIC INFORMATION 
EPIDEMIOLOGY
SPECIES, AGE, SEX
• Dogs, which may have coevolved with humans, are least affected before 2 years of age but may worsen with exposure. Females > males.
RISK FACTORS
• Dogs/cats who appear developmentally delayed and/or overly fearful within their first few months of life may be more susceptible to this form of learned fear.
CLINICAL PRESENTATION
• Avoidance of stimulus or stimulus modality that triggers response (e.g., metal table, smell of alcohol, all flooring that is not nonslip)
ETIOLOGY AND PATHOPHYSIOLOGY
• The etiology is exposure to stimuli and environments animals feel are worrisome, threatening, or uncertain and from which they cannot escape in time or space, despite signaling their need to do so. Regardless of whether the humans feel the environment is not threatening, what matters is the animal’s perception and response.
• The pathophysiology is as for any condition involving behavioral stress, distress, and/or anxiety and appears to be rooted in neurochemical encoding of information in the amygdala.
DIAGNOSIS 
TREATMENT 
TREATMENT OVERVIEW
• Treatment should be focused on ameliorating any signs of stress, distress, or anxiety as they appear, and at preventing them from worsening by learning in the future. This means specific triggers must be identified and addressed for the patient population as a whole and for each animal as an individual.
ACUTE AND CHRONIC TREATMENT
• Cease exposure to or engagement in whatever environments or behaviors are provoking the animal (e.g., if animals are resistant to getting on the table, let them sit on the floor; if they slip on the table, give them a nonslip mat).
• If the animal continues to manifest distress, consider panicolytic medication to abort the distress while the animal is with the veterinarian. The first drug of choice is alprazolam (dogs, 0.01-0.1 mg/kg [likely most effective range: 0.02-0.04 mg/kg] PO q 4-6 h PRN; cats, 0.0125-0.025 mg/kg PO q 12-24 h PRN; some published sources mistakenly recommend a tenfold higher dose). May also be used as a preventive: 0.5-1 dose given 2 hours before the expected provocative event and repeated 30 minutes beforehand. Alternatively, clonidine (dogs: 0.01 mg/kg PO q 12-24 h increased stepwise up to 0.05 mg/kg PO q 12-24 h (maximum dose 0.9 mg/day) or gabapentin (dogs: 10-20 mg/kg PO q 8-12 h) may be useful.
• Integrate Certified Pet Dog Trainers (CPDTs) with extensive experience in behavior modification into the practice (www.ccpdt.org).
BEHAVIOR/EXERCISE
• Prophylactic veterinary visits should be fun. Interventional veterinary visits should be nonthreatening, calming, reassuring, and as stress free as possible.
• Animals learn fear as they age, so early appointments should involve treats, play, massage, and lots of fun activities before anything threatening (e.g., a vaccination) should be attempted. Therefore, puppy and kitten visits should be longer, and the animals should be allowed to interact with the staff and explore the hospital.
• Environments should be friendly to animals. This means that practices should attempt to do the following:
○ Modulate the noise environment by using acoustic tiles, plexiglass cage doors/walls when possible. Consider Muttmuffs (www.muttmuffs.com) for hospitalized/anesthetized animals.
○ Modulate the visual environment by the use of movable barriers and flexible and non-harsh lighting conditions. Consider calming caps (www.premier.com), Doggles (www.doggles.com), or eye shades as needed, especially when recovering from anesthesia.
○ Modulate the olfactory environment by allowing animals to have T-shirts or gloves worn by their humans with them in cages and during manipulations or anesthetic inductions. Rinse common areas with plain water. Spraying hands with pheromonal analog products (e.g., Feliway) has been anecdotally reported to decrease locomotor behavior/increase calm behaviors in cats.
○ Change tactile environments through nonskid flooring, yoga mats, and covering tables and scales with nonslip surfaces.
PEARLS & CONSIDERATIONS 
COMMENTS
• Iatrogenic fear conditioned by veterinary visits and care may trigger otherwise latent pathologic behavioral conditions.
• Because manifestations of fear are commonly cited as reasons for relinquishment, euthanasia, or avoidance of veterinary visits, the single most important welfare concern for pet animals may be how they react to veterinary care and visits.
• Everyone can recognize the signs associated with this condition. Only if we begin to find it unacceptable to scare animals will we stop doing it.
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