- Congenital Disorders
- CLEFT PALATE
- STENOTIC NARES
- THE BRACHYCEPHALIC AIRWAY SYNDROME
- AIRWAY DISEASE IN THE CHINESE SHAR-PEI
- LARYNGEAL PARALYSIS
- LARYNGEAL HYPOPLASIA
- SUBGLOTTIC STENOSIS
- Infectious/Inflammatory Disorders
Sneezing and nasal discharge are the most common clinical signs of nasal cavity disease. Owners of puppies or kittens that are quickly cleaned by their mother or that are fastidious about licking any appearing discharge may overlook a nasal discharge. Viral disease or environmental irritants usually cause a serous or mucoid discharge; bacterial disease causes a purulent or mucopurulent discharge. Sneezing is usually prominent in acute disease but wanes with chronicity. Acute viral diseases sometimes cause enough destruction of the nasal epithelium to obliterate the sneeze reflex, despite the presence of nasal discharge and other upper respiratory signs. Less common signs of nasal disease include stertorous breathing, pawing or rubbing at the nose or mouth, facial pain, facial deformity, ocular discharge, exophthalmos, or fetid breath.
Because clinical signs related to the nose and sinuses can be manifestations of oral, pharyngeal, airway, and pulmonary disease, these areas should be carefully inspected. Evaluation of the nasal cavity should include oral and dental examination, radiographs of the nasal cavity, rhinoscopy, and visual examination of the nasopharynx and internal nares (). Pharyngeal and laryngeal disease is suggested by obstruction of airflow during inspiration, resulting in stridor, inspiratory dyspnea, loss or change of voice, exercise intolerance, or coughing. The combined signs of inspiratory dyspnea and stridor should lead the veterinarian to suspect laryngeal and/or pharyngeal disease. Diagnostic evaluation should include a thorough physical examination followed by sedation and visual inspection of the airways.
Congenital incomplete closure of the primary (lip and premaxilla) and secondary (hard and soft) palate occurs in both the puppy and kitten (). Affected animals may demonstrate signs of poor growth; drainage of milk from the nares during and after nursing; and nasal discharge, sneezing, coughing, and gagging while eating. Affected animals are also predisposed to secondary bacterial rhinitis, laryngotracheitis, and aspiration pneumonia.
Stenotic nares occur as a congenital disorder primarily in brachycephalic breeds of dogs and cats (). This condition is included in the characteristics of brachycephalic airway syndrome (along with elongated soft palate, eversion of laryngeal sacculi, and laryngeal collapse). The wings of affected nostrils fill most of the external nares, narrowing the transverse diameter and resulting in reduced passage of air through the nasal cavity (). Stertor, stridor, coughing, and gagging may be seen in affected animals. The primary treatment of stenotic nares is surgical resection of portions of the stenosed wings. The stenotic nares should be corrected as soon as possible, even in puppies 3 months old ().
THE BRACHYCEPHALIC AIRWAY SYNDROME
The brachycephalic airway syndrome may manifest as respiratory distress, stridor, reduced exercise and stress tolerance, and, in advanced cases, cyanosis, hyperthermia, and collapse (). Even in “normal” brachycephalic animals (English bulldog, Boston terrier), PaO2 decreases significantly during sleep; sleep-disordered breathing occurs in every English bulldog older than 2 weeks (). The syndrome occurs infrequently in brachycephalic breeds of cats. Anatomic narrowing of the upper airway results in negative intraairway pressure during inspiration and dynamic airway collapse. Prolonged increased negative pressure leads to progressive lengthening of the soft palate, redundancy/ swelling of pharyngeal tissue, eversion of laryngeal sacculi, and eventually laryngeal collapse. Secondary problems that may complicate the brachycephalic airway syndrome include laryngeal and pharyngeal edema, cor pulmonale, pulmonary edema, hyperthermia, and vagally induced arrhythmias.
Diagnosis of elongated soft palate is made by visual examination — the soft palate should just overlap the open epiglottis. Early resection of the soft palate improves the long-term prognosis (). Everted laryngeal saccuks appear as small, whitish swellings or balls of tissue resting in the ventral aspect of the glottic opening. Surgical removal is usually simple and rapid (). Laryngeal collapse is the most severe change associated with the brachycephalic airway syndrome — characterized by medial tipping of corniculate processes, medial flattening of the cuneiform processes of arytenoid cartilage, and narrowing of the rima glottis that appears as a slit between the collapsed arytenoids (). Because laryngeal collapse is usually associated with chronic upper airway obstruction, it is rarely seen in puppies or kittens younger than 6 months of age. Congenital malformation of the larynx may, however, result in laryngeal collapse ().
AIRWAY DISEASE IN THE CHINESE SHAR-PEI
The Chinese shar-pei is a breed afflicted by a number of congenital defects. Although this is not a brachycephalic breed, a brachycephalic-like airway syndrome is seen in the young shar-pei, starting as young as 1 week. The spectrum of clinical manifestations is similar to that seen in brachycephalic dogs (). The Chinese shar-pei is also commonly afflicted with congenital hiatal hernia, and respiratory distress may occur secondary to airway disease and/or aspiration pneumonia ().
Laryngeal paralysis is commonly seen as an idiopathic, naturally occurring condition of middle-aged to older large and giant breed dogs. A congenital form of the disease has been seen in Bouvier des Flandres in The Netherlands; Siberian husky, husky crosses, and Dalmatians in the United States; and bull terriers in Great Britain (). In Bouviers, laryngeal paralysis is inherited as an autosomal dominant trait and results from a loss of motoneuron cells in the nucleus ambiguus (). In bull terriers, laryngeal paralysis is associated with generalized muscular disease. Laryngeal paralysis in Dalmatians is associated with a generalized distal axonopathy and may be transmitted as an autosomal recessive trait (). Siberian husky and husky crosses have an inherited form of laryngeal paralysis clinically similar to that described in Bouviers ().
Clinical signs of congenital laryngeal paralysis are primarily due to dysfunction of laryngeal musculature and subsequent obstruction of glottic airflow during inspiration. The arytenoid cartilages are displaced ventromedially, vocal folds are passively drawn toward the midline, and a lack of normal arytenoid abduction occurs during inspiration (). Onset of signs usually occurs at 4 and 6 months of age and includes a change in phonation, gagging, or coughing, especially during eating or drinking. Severe inspiratory dyspnea may be the first sign of laryngeal paralysis. Affected Dalmatians commonly have megaesophagus. Surgical widening of the glottic opening is the definitive treatment for congenital laryngeal paralysis. If there are concurrent motility problems in the pharynx or esophagus or both, subsequent problems with aspiration pneumonia are likely.
Congenital hypoplasia of the larynx is most common in brachycephalic dogs and Skye terriers (). The laryngeal cartilages fail to adequately develop, resulting in a small, narrow, and unusually flexible larynx. The vocal folds fail to adequately abduct during inspiration, and the laryngeal ventricles evert due to the increased pharyngeal pressure. Signs, if present, vary with the degree of laryngeal narrowing. Attempts at surgical correction may result in further collapse and stenosis of the opening. In Skye terriers, the disorder is inherited as a simple autosomal recessive trait.
Congenital subglottic stenosis has been identified in a 5-month-old dog that had signs of laryngeal stenosis (). The subglottic stenosis was caudal to the glottis and cranial to the caudal margin of the cricoid cartilage. Initial signs in the dog were altered phonation and respiratory distress. Laryngeal stridor was present on both inspiration and expiration. Surgical splitting of the cricoid cartilage with or without using an internal splint will increase the glottic opening and relieve obstruction ().
Nasopharyngeal polyps are inflammatory lesions seen in young cats, probably arising from the tympanic cavity or auditory tube. Owners of affected cats often report signs starting before 6 months of age (). Clinical signs include inspiratory dyspnea, stertorous respiration, chronic nasal discharge, sneezing, and dysphagia. Nasopharyngeal polyp is diagnosed by direct examination of the nasopharynx under general anesthesia (); the polyp can usually be visualized after retraction of the soft palate or in the external ear canal (). Treatment is surgical excision of the polyp in combination with a ventral bulla osteotomy.
INFECTIOUS UPPER RESPIRATORY DISEASE
Infectious upper respiratory disease occurs commonly in the young cat and less commonly in the young dog. Several infectious agents may be the cause of upper respiratory infections, including bacterial, viral, fungal, and parasitic agents (Table Causes of Rhinitis). Viral upper respiratory infections in the cat are primarily caused by feline herpesvirus type 1 and calicivirus. Young kittens, especially those in multiple-cat households or catteries, represent the population most prone to severe, sometimes life-threatening infection. In addition, kittens persistently infected with feline calicivirus frequently develop an associated gingivitis, progressive periodontal disease, or limping kitten syndrome ().
Causes of Rhinitis
- Staphylococcus intermedius, Chlamydia psittaci, and other aerobic and anaerobic bacteria
- Young dogs: Canine distemper virus, canine parainfluenza virus, canine adenovirus-2, and canine herpesvirus
- Young cats: Feline rhinotracheitis (herpesvirus type I) virus, feline calicivirus, and feline reoviruses
- Cryptococcus neoformans, Blastomyces dermatitidis, Aspergillus species, and Pythium insidiosum
- Cuterebra species larvae
- Blunt trauma, penetrating wounds, and embedded foreign object(s)
Primary bacterial upper respiratory infections occur sporadically in cats. Bordetella and Chlamydia may cause upper respiratory signs in young kittens, and mycoplasma should be considered in cases of feline upper respiratory disease that are not improving as expected.
In young dogs, canine distemper virus is the most common viral cause of upper respiratory infection, although canine adenovirus-2 and parainfluenza virus infections may also present as a rhinitis. Fungal rhinitis usually presents as a chronic condition and seldom occurs in puppies and kittens younger than 6 months old. Granulomatous rhinitis due to Cryptococcus neoformans infection is more likely to occur in kittens, whereas nasal infection with Aspergillus species is more likely in puppies (). Nasal infections with other fungal organisms (Penicillium species, Blastomyces dermatidis, His-toplasma capsulatum, Alternaria alternata, Exophiala spinifera, and Rhinosporidium seeberi) as well as the Oomycotic organism Pythium insidiosum are rare.
A clinical diagnosis of upper respiratory disease in cats is based on history and clinical signs. It is seldom necessary to pursue definitive identification of the causative agent. Viral or bacterial isolation and identification and immunofluorescent studies of infected tissue can be performed during the early stage of the disease and may be of value in cattery situations. In early canine distemper infections, immunofluorescence of conjunctival scrapings can be helpful; fluorescence may be detected 5 to 21 days after infection. In cryptococcal infections, the most rapid method of diagnosis is cytologic demonstration of organisms in tissue fluid, nasal swabs, or impression smears from tissue specimens. In addition, serologic detection of capsular antigen of Cryptococcus organisms can be performed (). In nasal Aspergillus infections, organisms may be cultured, but interpretation of culture results is difficult because Aspergillus is a common environmental contaminant. A positive culture should be interpreted with biopsy results before making a diagnosis of nasal Aspergillus infection.
For kittens with mild upper respiratory infection, outpatient treatment with antimicrobial agents (Table Therapeutic Asents Used in Respiratory Disorders) is indicated to decrease the severity of bacterial infection. Anorectic, dehydrated kittens may require hospitalization, fluid replacement therapy, and feeding by a nasoesophageal, esophageal, or gastrostomy tube. Other supportive measures include removal of accumulated secretions from the eyes and nose, humidification of inspired air, or saline nebulization (). Intranasal administration of a pediatric phenylephrine-containing or oxymetazoline-containing decongestant once daily for a few days may help relieve upper airway obstruction. Cryptococcal rhinitis is treated with fluconazole (50 mg twice a day) (). Canine Aspergillus infection can be treated with itraconazole (5 mg/kg) or fluconazole (5 mg/kg) (), although topical therapy with enilconazole or clotrimazole is more effective ().
Therapeutic Asents Used in Respiratory Disorders
|Buprenorphine||0.005 mg/kg IV, IM q4-8h||Analgesia in dogs or cats|
|Butorphanol||0.1-0.4 mg/kg IV, IM, SC q2-5h||Analgesia in dogs or cats|
|Meperidine||3-10 mg/kg (dog) IM q2h2-10 mg/kg (cat) IM q2h||Analgesia in dogs or cats|
|Morphine||0.2-1.0 mg/kg (dog) IM, SC q3-4h0.05-0.1 mg/kg (cat) IM, SC q3-4h; given with a tranquilizer||Analgesia in dogs or cats|
|Oxymorphone||0.05-0.1 mg/kg (dog) IM, SC q3-4h0.03-0.05 mg/kg (cat) IM, SC q3-4h; given with a tranquilizer||Analgesia in dogs or cats|
|Nalbuphine||0.03-0.1 mg/kg IM, SC, IV q2-4h||Analgesia in dogs or cats|
|Pentazocine||1-3 mg/kg IM, SC q2-4h||Analgesia in dogs or cats|
|Amoxicillin||22 mg/kg PO bid||Broad-spectrum antimicrobial|
|Amoxicillin/clavulanic acid||12.5-25 mg/kg PO bid||Broad-spectrum antimicrobial|
|Ampicillin||10-20 mg/kg PO tid-qid5-10 mg/kg IV, IM, SC tid-qid||Broad-spectrum antimicrobial|
|Cefadroxil||22 mg/kg PO bid||Broad-spectrum antimicrobial|
|Cefaclor||4-20 mg/kg PO tid||Broad-spectrum antimicrobial|
|Cefazolin||10-20 mg/kg IV, IM tid||Broad-spectrum antimicrobial|
|Cefoxitin sodium||22 mg/kg IV, IM tid||Broad-spectrum antimicrobial|
|Cephalexin||20-30 mg/kg PO, SC, IV bid||Broad-spectrum antimicrobial|
|Cephradine||10-20 mg/kg PO tid||Broad-spectrum antimicrobial|
|Cefotaxime||25-50 mg/kg IV, IM, SC tid||Broad-spectrum antimicrobial|
|Chloramphenicol||50 mg/kg (dog) PO, IV, IM, SC tid25-50 mg/kg (cat) PO, IV, IM, SC bid||Broad-spectrum antimicrobial|
|Clindamycin||5-10 mg/kg (anaerobic bacterial infection) PO bid12.5 mg/kg (toxoplasmosis) PO bid||Broad-spectrum antimicrobial|
|Gentamicin||2 mg/kg IM, SC tid||Broad-spectrum antimicrobial|
|Metronidazole||7.5 mg/kg PO bid-tid||Antimicrobial; effective against anaerobes|
|Tetracycline||20 mg/kg PO tid||Broad-spectrum antimicrobial|
|Trimethoprim and sulfadiazine||15-30 mg (combined)/kg PO bid||Broad-spectrum antibacterial|
|Butorphanol tartrate||0.55 mg/kg PO bid-qid0.055-0.11 mg/kg SC bid-qid||Synthetic opiate partial agonist with potent antitussive activity|
|Codeine||1-2 mg/kg PO tid-qid||Narcotic centrally acting antitussive|
|Dextromethorphan||1-2 mg/kg PO tid-qid||Nonnarcotic centrally acting antitussive|
|Hydrocodone||0.25 mg/kg; not to exceed0.5-1 mg/kg PO bid-qid||Narcotic centrally acting antitussive|
|Morphine||0.1 mg/kg SC bid-qid||Narcotic centrally acting antitussive|
|Aminophylline||6-11 mg/kg (dog) PO tid-qid4-6.6 mg/kg (cat) PO bid||Bronchodilation in dogs or cats|
|Oxtriphylline||10-15 mg/kg (dog) PO tid-qid5-7 mg/kg (cat) PO tid-qid||Bronchodilation in dogs or cats|
|Terbutaline||1.25-5 mg(dog)PO bid0.625 mg (cat) PO bid||Bronchodilation in dogs or cats|
|Theophylline||9 mg/kg (dog) PO qid4 mg/kg (cat) PO bid||Bronchodilation in dogs or cats|
|Oxymetazoline hydrochloride||0.025% 2-3 drops/nostril tid-qid||Topical decongestant|
|Phenylephrine hydrochloride||0.125% or 0.25% 1 drop/nostril tid-qid||Topical decongestant|
|Ethacrynate sodium||0.2-0.4 mg/kg IV, IM bid-qid||Pulmonary edema|
|Furosemide||2-A mg/kg PO, IV, SC bid-qid||Pulmonary edema|
|Acetylpromazine||0.025-0.2 mg/kg (dog) IV, IM once0.05-0.1 mg/kg (cat) IV, IM once||Sedation in dogs or cats|
|Morphine||0.1 mg/kg (dog) IM, SC bid-qid0.1 mg/kg (cat) IM, SC bid-qid||Sedation in dogs or cats|
|Oxymorphone||0.05-0.1 mg/kg (dog) IM bid-qid0.02-0.03 mg/kg (cat) IM bid-rid||Sedation in dogs or cats|
*PO = Oral administration; SC = subcutaneous administration; IV = intravenous administration; IM = intramuscular administration; sid = once daily; bid = twice daily; tid = three times daily; qid = four times daily.
The common causes of infectious laryngitis in puppies and kittens are the same viral and bacterial agents that cause infectious upper respiratory tract disease. Dogs with acute laryngitis usually demonstrate paroxysmal coughing, changes in phonation, gagging, and noisy breathing. Treatment consists of providing rest and avoiding excitement of the animal. Antitussive medications are indicated when coughing is severe enough to limit the dog’s (or the owner’s) ability to rest. In cats, upper respiratory viruses and Bordetella are the most likely causes of infectious laryngitis. Rather than cause coughing, they result in laryngeal edema and stridor.
NASAL TRAUMA AND FOREIGN BODIES
Trauma may result in facial fractures and epistaxis or blood clot formation within the nasal cavity that produces varying degrees of nasal cavity obstruction. If epistaxis is severe, owners may place ice packs over the nose before seeking veterinary care. In most cases, the bleeding will stop before hemorrhage causes significant problems. Foreign bodies occasionally lodge in the rostral portion of the nasal cavity or in the caudal portion of the nasopharynx. The presence of a foreign object in the nasal cavity may be associated with unilateral nasal discharge, epistaxis, sneezing, and attempts to paw at the nose. Epistaxis and paroxysmal sneezing are the most likely clinical signs. Nasal and pharyngeal radiographs may be helpful. Nasal flush procedures can be used to wash foreign material out of the nasal cavity (). A flexible catheter is placed around the soft palate into the caudal nasal cavity; the head is placed down over the edge of the table, and a normal saline solution is flushed vigorously through the catheter and out the nares. Alternatively, a flush and suck technique can be used with a large catheter that is attached to a large syringe inserted through the nares into the rostral area of the nasal cavity. If nasal flush procedures are employed, the animal should be under general anesthesia, and a cuffed endotracheal tube should be in place.
Laryngeal trauma is usually the result of penetrating wounds, especially bite wounds. Other causes of trauma include gunshot wounds, neck collars, and rough endotracheal intubation for inhalation anesthesia (). Bite wounds and gunshot wounds usually result in laryngeal cartilage damage, whereas neck collar trauma often results in fractures or dislocations of the hyoid apparatus. Swelling and edema resulting from the trauma may rapidly worsen and severely compromise respiration over a period of a few hours. Perforation of the upper airway may result in palpable subcutaneous emphysema around the injured site and the dorsum of the head and neck. Supportive therapy for laryngeal injury may include the use of antimicrobial agents and antiinflammatory doses of corticosteroids (see Table Therapeutic Asents Used in Respiratory Disorders). Surgical intervention for debridement and alignment can be important in preventing laryngeal scarring and stenosis (laryngeal webbing) ().
Nasopharyngeal stenosis is an unusual cause of nasal obstructive disease in young cats in which the normal ovoid opening of the caudal nares is reduced to a pinhole-sized orifice by the presence of a thin, tough membrane (). The signs are similar to those described previously for nasopharyngeal polyps. Diagnosis is made by visually observing the stenosed nasopharynx with a dental mirror or endoscope. Surgical enlargement of the stenotic area is the necessary treatment.
Selections from the book: “Veterinary pediatrics: dogs and cats from birth to six months”. Johnny D. Hoskins. (2001)
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