N
Narcolepsy
BASIC INFORMATION 
DEFINITION
• A syndrome in which abnormalities in the sleep/wake cycle are manifested as excessive sleepiness and cataplexy.
• Excessive sleepiness is characterized by waxing and waning drowsiness and abrupt onsets of falling asleep.
• Cataplexy is a brief episode of flaccid paralysis without altered consciousness, usually elicited by excitement or emotion.
EPIDEMIOLOGY
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Cataplexy is the most common clinical sign and is manifested by partial to complete paralysis that may involve all muscles or may be restricted to certain limbs or the head and trunk.
○ Consciousness is maintained at the onset of the attack; however, prolonged episodes may lead to rapid eye movement (REM) sleep.
○ There is an abrupt onset as well as termination of the attack, and the attack may be disrupted by a loud noise or stimulation of the animal.
• Excessive sleepiness is characterized by prolonged periods of sleep, difficulty arousing the dog during sleep, and apparent drowsiness throughout the day.
DIAGNOSIS 
ADVANCED OR CONFIRMATORY TESTING
• Cerebrospinal fluid may contain a decreased hypocretin-1 concentration (<80 pg/mL; the normal range is 250-350 pg/mL).
• The food-elicited cataplexy test (FECT) is performed by placing pieces of food at set intervals apart and timing the animal while it consumes the food.
• Mildly affected animals may need pharmacologic testing to confirm a cataplectic attack.
○ Physostigmine salicylate, a cholinesterase inhibitor that crosses the blood-brain barrier, is given (0.025-0.1 mg/kg IV). Physostigmine increases the chances of spontaneous or elicited cataplectic attacks within 5-15 min in susceptible animals. The side effects of this drug are excessive salivation and diarrhea.
TREATMENT 
CHRONIC TREATMENT
• Cataplexy is treated with tricyclic antidepressants that act by blocking cellular norepinephrine reuptake in the central nervous system (CNS).
○ Imipramine (1 mg/kg PO q 8 h) has been used successfully in the long-term treatment of cataplexy. Imipramine also blocks serotonin reuptake.
• Excessive sleepiness is treated with stimulant sympathomimetics such as methylphenidate (0.1 mg/kg PO q 24 h) or dextroamphetamine.
PROGNOSIS AND OUTCOME 
• Cataplectic attacks are generally not life threatening, and although there is no cure, the clinical signs are usually successfully minimized with treatment.
Nasal Cutaneous Disorders
BASIC INFORMATION 
EPIDEMIOLOGY
SPECIES, AGE, SEX
• Diseases more likely to appear in dogs <1 year of age: demodicosis, dermatophytosis, dermatomyositis, hereditary nasal parakeratosis, juvenile cellulitis
GENETICS & BREED PREDISPOSITION
• Systemic lupus erythematosus (SLE) and cutaneous (discoid) lupus erythematosus (DLE): collies, Shetland sheepdogs, German shepherds
RISK FACTORS
• Sun exposure can cause or aggravate canine and feline solar dermatitis, DLE, SLE, and pemphigus erythematosus.
• Susceptible dogs fed diets high in phytates (high-cereal) or in minerals such as calcium can develop zinc-responsive dermatosis.
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT: Presentation depends on the underlying disease:
• Nonpruritic hair loss confined to the bridge of the nose (e.g., localized demodicosis, localized dermatophytosis) or with a generalized dermatopathy (e.g., generalized demodicosis, dermatophytosis, endocrinopathies)
• Pruritus and facial rubbing, with secondary nasal alopecia in cases of allergic disease or intranasal foreign bodies (usually accompanied by sneezing and/or nasal discharge)
• Erosions and ulcers in cases of immune-mediated diseases or nodules and plaques (e.g., neoplastic, cutaneous histiocytosis, fungal diseases)
• Signs of systemic illness may be reported concurrently with generalized disorders (e.g., systemic mycoses, SLE, systemic histiocytosis).
PHYSICAL EXAM FINDINGS: Any of the following are possible, depending on etiology and severity:
ETIOLOGY AND PATHOPHYSIOLOGY
Nasal lesions arise following various pathomechanisms, including:
• Infectious agents, which induce an immune response from the host, resulting in tissue inflammatory cell infiltrates (folliculitis, furunculosis, granulomatous lesions, etc.)
• Altered cornification process (proliferation, differentiation, or desquamation), resulting in hyperkeratosis
• Development of antibodies or activated lymphocytes against normal body constituents (autoimmune diseases) or against inciting antigens (drugs, bacteria, viruses), which leads to tissue damage
• Defective melanin production or destruction of melanocytes, leading to pigment disorders; a disturbance at the basal epidermal cell level can cause hypopigmentation.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Immune-mediated: pemphigus foliaceus and erythematosus, SLE, DLE, uveodermatologic syndrome, nasal arteritis, canine eosinophilic furunculosis of the face, feline mosquito bite hypersensitivity
• Pigmentary: nasal depigmentation (“Dudley nose”), seasonal nasal hypopigmentation (“snow nose”), vitiligo, alopecia and melanoderma, lentigo simplex
• Metabolic/endocrine: superficial necrolytic dermatitis (hepatocutaneous syndrome), canine hypothyroidism
• Neoplastic: squamous cell carcinoma (SCC), basal cell carcinoma, epitheliotropic lymphoma, fibroma, feline “sarcoid,” and other such conditions
• Miscellaneous: idiopathic sterile granulomas and pyogranulomas, cutaneous and systemic histiocytosis, idiopathic nasal hyperkeratosis
(Courtesy Dr. Nadia Pagé.)
INITIAL DATABASE
• Skin cytologic examination: phagocytized bacteria, inflammatory cells, acantholytic keratinocytes (pemphigus), fungal organisms
• CBC/serum biochemistry profile/urinalysis (if concurrent systemic disease is suspected): results depend on underlying cause and are often normal or with nonspecific changes when cause is not systemic.
• Ocular examination (if vision loss or visible ocular lesions): uveitis (uveodermatologic syndrome). See p. 1313.
ADVANCED OR CONFIRMATORY TESTING
• Skin biopsies for histopathologic evaluation and possible immunofluorescence or irnmunohistochemical staining. Indicated when initial database is inconclusive and nasal lesions persist. Using general anesthesia, nasal planum lesions can be biopsied with a 3- or 4-mm biopsy punch. The lesion should be centered in the specimen. If possible, multiple specimens should be taken of primary lesions (e.g., pustules, papules, bullae). Crusted lesions or depigmented lesions can also be useful.
• Culture: bacterial, fungal (if evidence of bacterial/fungal infection, and if resistance to prior treatment)
TREATMENT 
TREATMENT OVERVIEW
• The goal of treatment is to achieve permanent cure or control of the disease. Topical treatment may be sufficient for localized and/or superficial skin disorders, whereas systemic therapy (ranging from simple to ongoing and intensive) may be needed when nasal cutaneous disorders are the first expression of a serious medical condition.
ACUTE AND CHRONIC GENERAL TREATMENT
• Treatment depends on the etiology of the lesions. Specific treatment is selected based on results of tests described above.
• If the animal has undergone prior recent treatment and a drug reaction is suspected, the animal should avoid contact with the offending medication.
Ferguson E. An approach to facial dermatoses. In: Foster AP, Foil CS, editors. BSAVA manual of small animal dermatology. ed 2. British Small Animal Veterinary Association; 2003:94.
Medleau L, Hnilica KA. Small animal dermatology: a color atlas and therapeutic guide, ed 2. Philadelphia: Saunders Elsevier, 2006.
Scott DW, Miller WH, Griffin CE. Muller and Kirk’s small animal dermatology, ed 6. Philadelphia: WB Saunders, 2001.
Nasal Discharge
BASIC INFORMATION 
DEFINITION
• Although usually obvious, the discharge can sometimes be missed due to licking or caudal drainage.
EPIDEMIOLOGY
SPECIES, AGE, SEX
• Younger cats may have viral upper respiratory infections (see p. 1127) or nasopharyngeal polyps (see p. 751).
CLINICAL PRESENTATION
DISEASE FORMS/SUBTYPES: Types of nasal discharge:
• Acute versus chronic onset (acute onset more likely to be caused by foreign bodies and early viral infection)
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Feline viral upper respiratory tract infections (feline rhinotracheitis, feline calicivirus, Chlamydia psittaci)
• Neoplasia (adenocarcinoma, lymphosarcoma, undifferentiated carcinoma, osteosarcoma, chondrosarcoma, fibro-sarcoma, transmissible venereal tumor)
• Canine viral infections (canine distemper virus, canine parainfluenza virus, canine herpesvirus, canine adenovirus, types 1 and 2)
INITIAL DATABASE
• Physical assessment for unilateral versus bilateral nasal disease performed by holding a glass microscope slide close to the external nares while holding the animal’s mouth closed. When the animal exhales through the nose, steam will be present asymmetrically or unilaterally (one naris obstructed) or not at all (both nares obstructed). Neoplasia, foreign bodies, and dental disease are often causes of unilateral nasal disease and discharge, whereas other local and systemic conditions often result in bilateral disease.
• Fundic examination to look for evidence of neoplasia, fungal disease, hypertension, and associated retinal hemorrhage
TREATMENT 
ACUTE GENERAL TREATMENT
• Treatment for underlying coagulopathy (e.g., vitamin K1; 0.25–2.5 mg/kg for first-generation rodenticide intoxication or 2.5 mg/kg for second-generation rodenticide intoxication, SQ or PO q 12 h × 7–28 days, and fresh frozen plasma transfusion)
• Broad-spectrum antibiotics if secondary nasal/dental infection (bacteria are rarely the primary cause of nasal disease, but secondary infection with normal nasal flora is common) or pneumonia (culture and sensitivity [C&S] test for the lower airways is essential if pneumonia is present). Bartonella spp. have been recently implicated as a cause of chronic rhinitis and epistaxis; azithromycin appears to be the drug of choice (5–10 mg/kg PO q 24 h; start at 5 mg/kg and, if tolerated, increase by 2.5 mg/kg each day. After 1 week, reduce to q 48 h).
• Analgesics if painful (e.g., opiates such as buprenorphine, 0.006–0.01 mg/kg IV/IM q 6-8 h; nonsteroidal antiinflammatory drugs [NSAIDs] such as deracoxib, 1–2 mg/kg PO q 24 h, can also be used). Use NSAID analgesics with caution if the animal has a history of concurrent renal, liver, gastrointestinal, or hemostatic disorders.
• Clinicians should remove the animal from environmental agents (e.g., smoke, dust); if not possible, the clinician should introduce measures to reduce exposure (e.g., air filtration systems).
• Clinicians should consider recommending surgery for treating dental disease, neoplasia, nasopharyngeal polyps, cleft palate, foreign bodies, or traumatic causes.
• Chemoembolization of nasal tumors may be considered when surgery, radiation, or chemotherapy is associated with excessive morbidity, cost, or a poor outcome.
CHRONIC TREATMENT
• Nutrition: cats especially may not eat if unable to smell food. Consider feeding tube (e.g., esophagostomy; see p. 1267) for nutritional support.
PROGNOSIS AND OUTCOME 
• Good if the underlying problem is canine viral upper respiratory tract infection or foreign body or if the animal has undergone a successful surgery or tooth extraction
• Guarded for feline chronic viral upper respiratory tract infections; low-grade nasal congestion and discharge, with periodic flare-ups, may become persistent or lifelong.
Nasal Mites
BASIC INFORMATION 
EPIDEMIOLOGY
GENETICS & BREED PREDISPOSITION: There are no known breed, sex, or age predilections.
RISK FACTORS: Contact with an infected animal.
GEOGRAPHY AND SEASONALITY: Nasal mites appear to have a worldwide distribution with no seasonality.
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Other reported clinical signs include nasal discharge (typically serous), facial pruritus, head shaking, and hyposmia.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
