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Diseases of the Trachea | Lynelle R. Johnson
CONGENITAL DISORDERS Hypoplastic Trachea
Definition I. Tracheal hypoplasia is a congenital malformation that results in fixed narrowing of the tracheal lumen. II. It can be segmental or may involve the entire tracheal length. III. The ends of the tracheal rings meet or overlap rather than being C-shaped, and the dorsal tracheal membrane is typically short or absent. IV. In some cases, the tracheal cartilages are V-shaped or triangulated.
Causes I. A congenital or inherited lesion is proposed. II. An increased incidence has been reported in the bulldog, Boston terrier, and boxer (Coyne and Fingland, 1992). III. The disorder has also been reported in the Labrador retriever, German shepherd dog, Weimaraner, basset hound, and a litter of husky-mix dogs (Van Pelt, 1988). IV. Males (2:1) are affected more often than females (Coyne and Fingland, 1992).
Pathophysiology I. Narrowing of the tracheal lumen results in primarily inspiratory respiratory difficulty and a failure to clear respiratory secretions. II. Although retained secretions can potentially predispose to recurrent respiratory infections, this has not been documented in retrospective studies. III. Hypoplastic trachea is associated with an increased incidence of other congenital anomalies, including elongated soft palate, stenotic nares, cardiac defects (pulmonic or aortic stenosis), and megaesophagus.
Clinical Signs I. II. III. IV. V.
Inspiratory difficulty Stridorous sounds on inspiration Coughing or gagging frequently noted Exercise intolerance from hypoventilation Syncope related to hypoxia or cardiac defects
VI. Regurgitation, if megaesophagus also present VII. Worsening of signs with excitement.
Diagnosis I. History, signalment, and the presence of typical, clinical signs in a breed commonly affected by tracheal hypoplasia are suggestive of the diagnosis. II. Physical examination can reveal some or all of the following findings. A. The trachea can feel narrow on palpation. B. High-pitched inspiratory sounds may be ausculted over the trachea related to turbulent airflow through the narrowed lumen. C. The opening of the nares must be compared to breed standards to detect stenosis. D. Thorough cardiac auscultation is necessary to detect concurrent congenital anomalies. III. Radiographs of the chest establish the diagnosis. A. The cardinal finding is decreased tracheal diameter. B. Two methods may be used to evaluate tracheal diameter. 1. The ratio of the tracheal lumen diameter (TD) at the thoracic inlet to the diameter of the thoracic inlet (TI) is calculated (Harvey and Fink, 1982). a. Tracheal hypoplasia is present if TD:TI is less than the normal value. b. The normal value for the bulldog is 0.127, for non-bulldog brachycephalic breeds is 0.160, and for nonbrachycephalic dogs is 0.204. 2. The ratio of the TD halfway between the thoracic inlet and the carina to the width of the third rib (3R) is calculated (Suter, 1984). a. Normal is >3.0. b. Tracheal hypoplasia is present if TT:3R is <3.0. C. Radiographs are closely evaluated for evidence of pulmonic or aortic stenosis (see Chapter 8) and for megaesophagus (see Chapter 30), although echocardiography is needed to rule out the former conditions in a dog with a heart murmur.
Differential Diagnosis I. II. III. IV.
Brachycephalic upper airway syndrome Tracheal obstruction or neoplasia Tracheal collapse Primary ciliary dyskinesia 155
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Treatment I. The severity of clinical signs is related to the presence of other disorders rather than the degree of reduction in tracheal diameter. II. Concurrent respiratory or cardiac abnormalities associated with tracheal hypoplasia must be identified and managed. A. Upper airway abnormalities that can be surgically corrected (e.g., elongated soft palate, everted laryngeal saccules, stenotic nares) are managed early in life to reduce clinical signs. B. Respiratory infections must be controlled early in the course of disease. C. Management of obesity is strongly recommended. D. Judicious use of diuretics and vasodilators is indicated for treatment of congestive heart failure (see Chapter 9).
Monitoring of Animal I. Many dogs with tracheal hypoplasia enjoy a good quality of life and can be maintained relatively free of clinical signs or respiratory distress; however, other animals are severely debilitated by disease. II. No specific therapy is available to widen the tracheal lumen. III. Hot and humid conditions adversely affect dogs with tracheal hypoplasia and should be avoided. IV. Recheck examinations are advised at least yearly for early detection of complicating diseases.
DEGENERATIVE DISORDERS Tracheal Collapse
Definition I. Tracheal collapse is characterized by reduction in the luminal diameter of the cervical and/or intrathoracic trachea. II. Flattening of the tracheal rings typically occurs dorsoventrally and leads to lengthening of the dorsal tracheal membrane. III. Prolapse of the dorsal membrane into the tracheal lumen results in dynamic collapse.
Cause I. The etiology is unknown; however, hypocellular cartilage has been detected histologically in some affected dogs. II. Abnormal chondrocyte function with deficient production of the matrix components may result in altered integrity of the cartilage ring structure and a predisposition to collapse. III. An increased incidence of disease is seen in small-breed dogs, such as the poodle, Yorkshire terrier, Pomeranian, and Chihuahua. A. Clinical signs are often seen at an early age, and it is possible that this disorder is congenital. B. Poor nutrition or metabolic influences may contribute to a failure of chondrogenesis and the development of abnormal cartilage metabolism in these breeds.
Pathophysiology I. In normal animals, the trachea is a rigid but flexible structure and exhibits only minor changes in intraluminal diameter in response to pressure changes that occur during respiration. A. As the chest wall expands during inspiration, intrapleural pressure becomes increasingly negative. B. This pressure is translated across the airways and results in airflow from the glottis toward the alveolar region. C. On passive expiration, intrapleural pressure becomes less negative and air flows down the pressure gradient toward an equal pressure point near the thoracic inlet, where the transmural pressure difference is zero. D. In the normal dog, rigid cartilage within the airway walls prevents airway collapse within the thorax on expiration. II. In some dogs with tracheal collapse, there is a deficiency in chondroitin sulfate and glycosaminoglycan in the cartilage ring structure of the trachea, which results in decreased water binding within the cartilage matrix and weakening of the tracheal cartilage (Dallman et al., 1988). A. Decreased rigidity in the cartilage matrix allows the cervical tracheal rings to flatten when negative pressure develops in the airway during inspiration. B. During forced expiration or coughing, intrathoracic pressures rise and exert positive pressure on airway walls, with collapse of the intrathoracic trachea on expiration. III. Chronic intermittent airway obstruction results in respiratory distress and coughing, which perpetuate laryngeal, tracheal, and bronchial irritation (Done et al., 1976). A. Affected animals may suffer frequent, repeated episodes of respiratory distress or coughing before veterinary attention is sought. B. The presence of concurrent disorders, such as upper airway obstruction, chronic bronchitis, or cardiac failure, may produce serious clinical signs in a previously asymptomatic dog. C. Other trigger events include endotracheal intubation and respiratory infections. D. Obesity results in poor thoracic compliance and decreased diaphragmatic excursion, and the ability of the lung to expand on inspiration is diminished, which result in relative pulmonary atelectasis, abnormal pressure gradients along the airways, and an increased tendency toward airway collapse. IV. Two sites of tracheal collapse have been described. A. Cervical (extrathoracic) tracheal collapse is characterized by signs of coughing or distress on inspiration, and upper airway obstruction from laryngeal paralysis, everted laryngeal saccules, or an elongated soft palate as the pressure drops across the upper airway. B. Intrathoracic tracheal collapse causes clinical signs on expiration when intrapleural pressure exceeds intraluminal airway pressure and results in airway collapse. 1. Signs are generally more severe during forced expiration or coughing, and are enhanced by bronchitis or infection.
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2. Collapse of the mainstem bronchi can occur with or without tracheal collapse. C. Cervical and intrathoracic tracheal collapse can occur alone but are found concurrently in many dogs.
Clinical Signs I. Long history of respiratory abnormalities A. Inspiratory difficulty with cervical collapse B. Worsened clinical signs on expiration with intrathoracic tracheal collapse or collapse of the mainstem bronchi II. Paroxysms of coughing, classically described as a “goose honk” cough III. Signs elicited by excitement, pressure exerted on the trachea, high heat or humidity, and eating or drinking IV. Coughing followed by retching V. Respiratory distress, exercise intolerance, cyanosis, and syncope in severe cases
IV.
Diagnosis I. Signalment and clinical signs are often very suggestive of the diagnosis. II. The following may be noted on physical examination: A. Affected dogs are often obese, and hepatomegaly of undetermined etiology may be present. B. The animal may appear normal at rest; however, excitement often induces a honking cough, airway obstruction, or respiratory distress. C. Marked tracheal sensitivity is typical, and even gentle palpation can precipitate a medical crisis. D. When the cervical trachea is severely flattened, the free edges of the cartilage rings can be palpated along their lateral aspect. E. Tracheal auscultation reveals musical inspiratory noises with cervical collapse. 1. Specific attention must be paid to laryngeal auscultation. 2. Stridor on inspiration is suggestive of concurrent laryngeal paralysis, which has been reported in 14% to 30% of dogs with tracheal collapse (Buback et al., 1996; Tangner and Hobson, 1982). F. Intrathoracic tracheal collapse is characterized by respiratory difficulties on expiration, with an end-expiratory snap sometimes heard over the thoracic cage. G. Wheezes or harsh crackles suggest the presence of concurrent bronchitis. H. Cardiac auscultation often reveals the presence of coexisting mitral valve insufficiency. 1. Congestive heart failure may or may not be present. 2. The presence of a right-sided heart murmur, gallop rhythm, or a split-second heart sound indicates that pulmonary hypertension may have developed as a complicating factor. III. Lateral thoracic radiographs are taken on full inspiration and on expiration to detect the dynamic nature of cervical and intrathoracic tracheal collapse. A. The cervical trachea may be collapsed on inspiration or “balloon” open on expiration.
V.
VI.
VII.
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B. The intrathoracic trachea collapses on expiration and may “balloon” open at the carina on inspiration. C. Normal static films do not rule out the diagnosis of tracheal collapse. D. Fluoroscopy is useful in suspected cases of tracheal collapse that have normal chest radiographs. E. When fluoroscopy is unavailable, obtaining radiographs during a cough can aid in the detection of collapsing airways. F. Cervical tracheal collapse also can be detected with ultrasonography; however, a high level of expertise is required because of the difficulty in delineating structures at the air-tissue interface (Rudorf et al., 1997). Both lateral and ventrodorsal thoracic radiographs are closely evaluated to identify concurrent pulmonary disease or cardiac failure. A. Obesity confuses interpretation of pulmonary infiltrates and can lead to artifactual enlargement of the cardiac silhouette. B. The degree of obesity can be demonstrated by measuring the thickness of the fat pad between the ribs and the skin on the ventrodorsal radiograph. Confirmation of tracheal collapse and identification of underlying infectious or inflammatory airway disease are best achieved through bronchoscopy. A. Bronchoscopy can be used to obtain respiratory samples and to visualize dynamic airway changes. B. The grade, extent, and severity of tracheobronchial collapse can be definitively documented. C. Airway sampling is recommended to identify underlying pulmonary infection or inflammation. D. If a tracheal wash is performed, a transoral approach using a small-diameter endotracheal tube is recommended rather than a transtracheal technique in order to diminish tracheal trauma. Perform cytologic analysis and cultures for bacteria and Mycoplasma spp. A. Oropharyngeal contamination is indicated by the presence of squamous cells or Simonsiella spp. bacteria. B. The trachea is not a sterile environment (McKiernan and Smith, 1982). C. Positive qualitative cultures may be found in most dogs with tracheal collapse and must be interpreted in light of clinical and cytologic findings. D. True bacterial infection is supported by septic, suppurative inflammation on cytology and positive bacterial cultures. E. Quantitative bacterial cultures may be required for definitive diagnosis of lower respiratory tract infection. When either a tracheal wash or bronchoscopy is performed, upper airway structure and function should be evaluated at the beginning of the procedure to rule out laryngeal paresis or paralysis.
Differential Diagnosis I. Infectious tracheobronchitis II. Tracheal obstruction
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III. Chronic bronchitis IV. Congestive heart failure
Treatment I. Treatment of coexisting medical and respiratory problems is essential. II. Dogs that have upper airway abnormalities, such as laryngeal paralysis or everted laryngeal saccules, may become less symptomatic for tracheal collapse when these obstructive disorders are corrected surgically. III. Dogs with bronchitis require treatment of their primary airway disease, generally with corticosteroids (see Chapter 17). IV. Dogs with marked epithelial injury from tracheal irritation may require a short course of corticosteroids (5 to 7 days of a tapering dose) to reduce inflammation. V. Inhaled steroids can be used to reduce tracheal or bronchial inflammation and are associated with fewer side effects. A. Administer fluticasone propionate (110 mg/puff) at a dose of 1 puff BID to QID, ensuring that the dog takes 8 to 10 breaths and does not pant. B. Administer via a spacing chamber and face mask. VI. Bronchodilators can result in some reduction in clinical signs in dogs with intrathoracic airway collapse by dilating small airways and reducing the pressure gradient within intrathoracic airways. A. Extended-release theophylline 10 mg/kg PO BID B. Terbutaline 1.25 to 2.5 mg PO BID to TID C. Albuterol 50 mg/kg PO BID to TID VII. Antibiotics are warranted when infection is documented by cytology and culture results. VIII. Cough suppressants are used to reduce mechanical irritation of the tracheal epithelium when infectious or inflammatory processes have been adequately treated. A. The severity of cough in dogs with tracheal collapse may require the use of narcotic agents. B. Give butorphanol 0.5 to 1.0 mg/kg PO BID to QID or hydrocodone 0.22 mg/kg PO every 4 to 8 hours, as needed. IX. Obese animals are started on a gradual weight loss program of regular exercise combined with a low-fat diet. X. During leash walking, the use of a harness is encouraged to avoid mechanical irritation to the trachea. XI. Dogs with tracheal collapse are susceptible to worsening of clinical signs when exposed to heat and humidity, so avoid these elements. XII. Excessive excitement and stress must also be avoided; judicious use of tranquilizers may be considered. XIII. Use of intratracheal stents has shown promise in the short-term management of dogs with life-threatening tracheal collapse (Moritz et al., 2004). A. Migration of the stent may worsen coughing, and the development of granulomatous lesions can limit their use. B. Dorsoventral collapse of stents has also been reported (Radlinsky et al., 1997). XIV. Surgical placement of external ring prostheses can be used in animals with cervical tracheal collapse that fail to
respond to medical management, although controversy exists on the role of surgery in the management of tracheal collapse (White and Williams, 1994). A. Placement of tracheal ring prostheses is technically demanding. B. In one study, laryngeal paralysis occurred postoperatively in 19% and necessitated a permanent tracheostomy or arytenoid lateralization (Buback et al., 1996; White 1995). C. Although a relatively high rate of both immediate and long-term complications such as continued coughing and respiratory distress occur after surgery, these conditions are usually manageable and acceptable to owners. D. Most animals that have undergone surgical intervention have an improved quality of life and reduction in clinical signs. E. Young dogs that undergo surgery may have a better prognosis than older dogs.
Monitoring of Animal I. Dogs with tracheal collapse have variable clinical signs throughout their entire life, and some coughing will always be present. II. It is likely that collapse of the lower airways can progress in severity. III. For dogs that are managed surgically, inform owners that the duration of benefit from surgery varies. IV. Counsel owners regarding risk factors that exacerbate disease and the need for follow-up examinations. V. Concurrent diseases and/or obesity require rigorous monitoring.
INFLAMMATORY DISORDERS Infectious Tracheobronchitis
Definition and Causes I. Tracheitis is characterized by inflammation of the epithelial lining of the trachea and is typically associated with erosion of the mucosal surface, goblet cell hyperplasia, mucus accumulation, and disruption of the mucociliary clearance apparatus. II. Viral agents (e.g., parainfluenza virus, canine adenovirus, canine distemper virus) infect respiratory epithelial cells. III. Viral damage to the epithelium predisposes the animal to secondary infection with bacteria, primarily Bordetella spp. or Mycoplasma spp. (see also Chapter 114). IV. The highly contagious nature of the disease leads to rapid spread among susceptible animals, with clinical signs seen 2 to 10 days postexposure. V. Neonates and immune-compromised animals are susceptible to Bordetella spp. or Mycoplasma pneumoniae.
Clinical Signs I. Sudden development of a dry, paroxysmal, “seal bark” cough II. Absence of systemic signs of illness III. Coughing easily elicited by tracheal manipulation
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Diagnosis I. Diagnosis is often based on the history of exposure to a potential carrier and on detection of the typical clinical signs in an otherwise healthy animal. II. The primary physical examination finding is marked tracheal sensitivity. A. Lung sounds are normal in uncomplicated cases. B. Fever, anorexia, lethargy, or nasoocular discharge are indicators of systemic disease. III. A complete diagnostic work-up is reserved for animals with systemic illness. IV. A complete blood count may reveal the following: A. Lymphopenia suggests a viral etiology but is only present early in the course of disease. B. Neutrophilia can indicate the presence of concurrent bacterial infection, especially bronchopneumonia. V. Thoracic radiographs are often normal. A. A generalized interstitial pattern is compatible with viral pneumonia. B. The presence of an alveolar infiltrate is suggestive of secondary bacterial pneumonia. VI. In complicated cases, a transoral tracheal wash is performed for cytological analysis, bacterial and Mycoplasma spp. cultures, and antibiotic sensitivity testing.
Differential Diagnosis I. II. III. IV. V. VI.
Tracheal collapse Tracheal obstruction Pneumonia Acute bronchitis Parasitic bronchitis or pneumonia Tracheal irritation
Treatment I. Supportive care measures such as maintaining a warm, draft-free environment, ensuring adequate systemic hydration, and providing good nutritional support are implemented. II. Antibiotics are indicated for treatment of secondary infection. A. Local antimicrobial therapy with an aminoglycosides is most likely to reduce bacterial numbers. B. Nebulization or intratracheal injection of gentamicin (3 to 5 mg/kg SID for 5 days) can reduce the number of bacteria present in the trachea and enhance clearance of the organism from the airway surface (Bemis and Appel, 1977). C. Systemic antibiotics may have limited efficacy against Bordetella spp. infection because this organism resides on the surface of airway epithelial cells and does not penetrate cells. D. Antibiotics with in vitro efficacy against Bordetella spp. and Mycoplasma spp. are possibly indicated for 7 to 10 days to reduce the spread of bacteria. 1. Doxycycline 3 to 5 mg/kg PO BID; may stain teeth of young animals 2. Amoxicillin-clavulanic acid 10 to 15 mg/kg PO BID; no efficacy against Mycoplasma spp.
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3. Enrofloxacin 2.5 to 5.0 mg/kg PO SID; possible cartilage deformation in young animals (Speakman et al., 2000) III. Judicious use of antitussives is indicated after infection is cleared. A. Narcotic antitussives are often required. B. If antitussives are used too early, they can encourage development of pneumonia from trapping of bacteria in the lower airways. IV. Owners are instructed to avoid use of a collar to reduce direct tracheal irritation. V. Isolation of infected animals is recommended, humidity in the environment is reduced, and adequate ventilation is ensured.
Monitoring of Animal I. Infectious tracheobronchitis is generally a self-limiting disease, with signs resolving within 7 to 10 days. II. Contact with other dogs must be discouraged given the highly infectious nature of the disease. III. Bleach can be used to disinfect the area contaminated by an infected dog (see Chapter 114). IV. Use of a parenteral or intranasal vaccine against Bordetella bronchiseptica reduces the severity of infection in susceptible animals, and sequential administration of both types of vaccines may provide the highest level of protection (Ellis et al., 2001). Parasitic Tracheitis
Definition and Causes I. Oslerus osleri is a nematode parasite that resides beneath the epithelium of the carina and major bronchi in dogs. II. The parasite has a worldwide distribution, is responsible for disease in both wild and domestic canids, and more commonly infects younger animals.
Pathophysiology I. Transmission from bitch to offspring is believed to occur primarily through grooming activity or possibly regurgitant feeding. II. Direct, horizontal transmission has been demonstrated experimentally (Lappin and Prestwood, 1988) but is unlikely to occur in the natural setting. III. Infection occurs through ingestion of first-stage (L1) larvae that migrate from the intestine to the right heart and then to the tracheal wall during a 10- to 21-week prepatent period. IV. Adult parasites live in nodules within the larger airways, often at the carina, which irritates the trachea and causes coughing. V. Eggs and infective L1 larval stages are coughed up, swallowed, and shed intermittently in the feces.
Clinical Signs I. Chronic, dry cough unresponsive to antibiotic therapy II. Inspiratory respiratory distress, anorexia, and exercise intolerance
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Diagnosis I. Physical examination findings are often nonspecific, and increased tracheal sensitivity is usually present. II. Fecal examination using the Baermann technique or zinc sulfate flotation is performed to detect first stage larvae; however, samples are often falsely negative owing to intermittent shedding. III. Tracheal nodules associated with O. osleri are occasionally visible on radiographs. IV. Bronchoscopy allows visualization of nodules at the carina, and biopsy can be performed for definitive diagnosis. V. Transtracheal wash or bronchoalveolar lavage cytology or tracheal swabs may reveal larvae or eggs. VI. Eosinophilia is variably present on a complete blood count or on cytology of airway washes.
Differential Diagnosis I. II. III. IV.
Chronic bronchitis Parasitic pneumonia or lungworm infection Infectious or irritant tracheobronchitis Tracheal collapse
Treatment I. No single therapy has proven efficacious for eradication of O. osleri, and combinations of drugs may be required for resolution of disease. A. Ivermectin 200 to 400 mg/kg PO or SC once weekly in breeds not susceptible to ivermectin toxicity (Outerbridge and Taylor, 1998) B. Fenbendazole 50 mg/kg/day PO for 10 to 30 days C. Thiabendazole 32 to 140 mg/kg/day PO for 10 to 23 days II. Horizontal transmission in a kennel situation is unlikely; however, routine cleaning and hygienic maintenance are recommended. III. Removal of infected bitches from a breeding colony reduces the incidence of disease in the offspring.
Monitoring of Animal I. Resolution of clinical signs is the easiest method for following response to therapy, although it does not confirm the efficacy of treatment. II. Fecal examinations are unreliable given the intermittent shedding of larvae. III. Use radiographs to follow resolution of tracheal nodules if they were visualized on initial films. IV. Use bronchoscopy to follow regression of intraluminal nodules with therapy.
II. Direct epithelial injury increases mucus production and stimulates a cough. III. Chronic cough then results in a cycle of epithelial erosion and desquamation, increased mucus production, and trapping of secretions that perpetuate tracheal inflammation.
Clinical Signs I. Chronic, nonproductive cough and increased tracheal sensitivity II. Facial burns associated with smoke inhalation or cervical swelling related to choke chain trauma (see Chapter 133)
Diagnosis I. History of smoke inhalation, recent endotracheal intubation, or recent pulmonary disease increases the suspicion of this disorder. II. Other causes of cough must be dismissed. III. Bronchoscopic evaluation of the airway shows irritations, hypervascularity of mucosa, increased mucus, and hemorrhage in the trachea.
Differential Diagnosis I. Infectious tracheobronchitis II. Tracheal collapse III. Parasitic tracheobronchitis
Treatment I. Eliminate environmental features, such as excessive smoke or noxious fumes. II. Antitussives are used to decrease chronic irritation associated with coughing, but infectious diseases must be ruled out first. III. Prednisone 0.5 mg/kg/day PO for 2 to 5 days can help alleviate tracheitis. IV. Alternately, inhaled steroids can be used (see Tracheal Collapse).
Monitoring of Animal I. Use of a harness may facilitate resolution of clinical signs by decreasing pressure on the trachea. II. Cases with severe inflammation may be monitored with repeated bronchoscopy. III. Severely affected cases are at risk for developing tracheal stenosis. IV. Tracheal necrosis can also occur resulting in air leakage into the subcutaneous space.
TRACHEAL OBSTRUCTION Irritant Tracheitis
Definition and Causes I. Tracheal irritation results from direct trauma to the cervical region, inhalation of noxious fumes, use of an overly large endotracheal tube, overdistension of an endotracheal tube cuff, or as a chronic sequela to bronchial or pulmonary disease.
Definition and Causes I. Tracheal obstruction results from narrowing of the tracheal lumen by internal obstruction, stenosis, or by external compression. II. Foreign bodies that may cause airway obstruction include grass awns, tree needles, teeth, or dental tartar. III. Intratracheal mass lesions can be caused by neoplasia, abscess formation, and parasitic or fungal granulomas.
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IV. Tracheal stenosis can result from a congenital deformation, but more commonly occurs secondary to trauma (e.g., endotracheal intubation, automobile crash, tracheostomy, penetrating injury). V. Extraluminal obstruction of the trachea can result from an esophageal mass or diverticulum, megaesophagus, thyroid cyst, lymphadenopathy, or from a mediastinal mass, abscess, or hemorrhage. VI. Tracheal narrowing results in increased resistance to airflow, mechanical irritation of the trachea, stimulation of cough receptors, and increased susceptibility to airway infection.
Clinical Signs I. II. III. IV. V.
Acute or chronic cough, with or without hemoptysis Acute or progressive respiratory distress, panting Anxiety, pawing at the face Dysphagia, halitosis Exercise intolerance
Diagnosis I. History of vomiting, intubation, or trauma raises the suspicion of a tracheal foreign body or obstruction. II. Physical examination often reveals increased tracheal sensitivity. A. High-pitched, musical sounds can be heard over the trachea when the lumen is narrowed by an obstruction or increased secretions. B. Stridor may be detected in animals with high cervical tracheal obstruction. C. A cervical mass or esophageal enlargement may result in palpable thickening of the neck region. III. Radiographs may reveal a radiodense foreign body or softtissue mass within the tracheal lumen, a focal narrowing of the tracheal air column (stenotic lesion), or an external mass impinging on the tracheal lumen. IV. Use bronchoscopy to confirm the diagnosis of an intraluminal mass or foreign body, stenotic lesion, or extraluminal obstruction.
Differential Diagnosis I. II. III. IV. V.
Tracheal collapse Infectious tracheobronchitis Tracheal hypoplasia Parasitic tracheitis Feline bronchial disease
Treatment I. Tracheal foreign bodies are best removed via bronchoscopy when possible. A. Infection with Nocardia spp. may be associated with foreign bodies (Lotti and Niebauer, 1992). B. Both aerobic and anaerobic bacterial cultures are performed, as Actinomyces spp. or anaerobes can be found. II. Bougienage, balloon dilatation, or laser resection can be attempted for tracheal stenosis. A. The inflammatory response generated by the procedure can lead to rapid reformation of the stricture.
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B. The risk of tracheal laceration leading to pneumomediastinum or subcutaneous emphysema must be considered. III. Tracheal stenosis usually requires surgical resection and anastomosis, with lesions involving <8 to 10 tracheal rings being resected without excessive stress on the incision site. IV. Extraluminal compressive lesions are best evaluated by computed tomography, followed by surgical exploration of the region.
Monitoring of Animal I. Recurrent hemoptysis, pneumonia, and chronic coughing are indications that either a foreign body or infection persists. II. After tracheal resection and anastomosis, cough suppressants are used to reduce irritation of the tracheal mucosa. III. Harness-style restraints can also be used to restrict excessive neck motion and reduce tension at the anastomotic site.
NEOPLASIA Definition and Causes I. Neoplasia results from uncontrolled overgrowth of abnormal epithelial or mesenchymal cells within the airways. II. Adenocarcinoma, lymphosarcoma, squamous cell carcinoma, melanoma, plasmacytoma, and chondrosarcoma occur in the dog and cat (Carlisle et al., 1991). III. Osteochondroma is the most common tracheal tumor and is usually found in young dogs (Carlisle et al., 1991). IV. Mass lesions within the trachea cause upper airway obstruction or respiratory distress from narrowing of the tracheal lumen and increased resistance to air flow.
Clinical Signs I. Inspiratory difficulty or respiratory distress, panting, or abnormal respiratory movements II. Exercise intolerance III. Coughing IV. Increased inspiratory noises V. Cyanosis, syncope VI. Systemic signs often absent
Diagnosis I. Physical examination often reveals abnormal respiratory sounds. A. Musical or wheezing noises can be heard over the trachea. B. Increased tracheal sensitivity may also be present. II. Radiographs may show an intraluminal mass lesion. III. Bronchoscopy often allows visualization and biopsy of the mass; occasionally, resection or debulking can be performed.
Differential Diagnosis I. Tracheal collapse II. Tracheal obstruction: foreign body, granuloma, O. osleri III. Laryngeal paralysis
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IV. Congestive heart failure V. Chronic bronchitis VI. Pulmonary hypertension
Treatment I. Prepare for an emergency tracheotomy in any case in which neoplasia of the cervical trachea is suspected. II. Mass removal via bronchoscopy may be possible when the mass is attached to the mucosa by a pedunculated stalk. III. Tracheal resection and anastomosis can be curative in some cases with only local disease. IV. Involvement of >8 to 10 tracheal rings may prohibit surgical treatment because of the risk of excessive tension on the suture line after anastomosis. V. Aggressive neoplasms often require subsequent chemotherapy or radiation therapy. A. Lymphoma involving the trachea often responds to standard chemotherapy regimens. B. Palliation of clinical signs may be achieved through a permanent tracheostomy distal to the tumor, with radiation therapy and/or chemotherapy.
Monitoring of Animal I. Closely monitor the animal for signs of metastasis and local recurrence through bimonthly radiographs. II. Osteochondromas are associated with an excellent prognosis when the tumor can be fully resected. III. Response to therapy is variable for malignant neoplasms affecting the trachea.
TRAUMA Definition and Causes I. Tracheal trauma usually results from penetrating neck injuries, bite wounds, gun shot wounds, or from an automobile accident. II. Iatrogenic trauma most commonly occurs with overinflation of an endotracheal tube cuff. III. In cats, 1.6 ± 0.7 mL of air sufficiently inflates the cuff of most endotracheal tubes (Hardy et al., 1999). IV. Use of excessive force during endotracheal intubation or application of high intrapulmonary pressures during anesthesia or ventilator therapy can lead to tracheal injury or rupture. V. Breakdown of a tracheotomy or tracheostomy site results in clinical signs similar to those found with penetrating injuries to the trachea.
Pathophysiology I. Damage to the tracheal cartilage or annular ligament allows leakage of air into the fascial planes of the cervical region with each inspiration. II. In cats the most common lesion is a linear tear in the dorsal trachealis muscle near the thoracic inlet or in the thoracic trachea (Hardy et al., 1999). III. Excessive air accumulation within the neck region may compress the trachea.
IV. Decreased flow of oxygen into the lung results in alveolar hypoventilation and respiratory embarrassment.
Clinical Signs I. May be delayed with tracheal necrosis II. Subcutaneous emphysema III. Inspiratory dyspnea, tachypnea, and occasionally cyanosis
Diagnosis I. History of a predisposing event increases the probability of tracheal trauma, even if the onset of signs is delayed. II. In cats, tracheal injury occurs most commonly after dental procedures (Hardy et al., 1999). III. Physical examination may reveal the following: A. Subcutaneous emphysema usually originates in the neck region but may extend across the entire body. B. Bite wounds, lacerations, or other evidence of trauma may be found in the cervical region. IV. Radiographs may show subcutaneous air accumulation in the cervical region, pneumomediastinum, or potentially, pneumothorax. V. Tracheoscopy can locate tracheal lacerations in some cases.
Differential Diagnosis I. Infection with gas producing bacteria II. Other causes of tracheal stenosis and obstruction
Treatment I. Conservative management is usually successful when signs are mild, such as in cases of blunt trauma without tracheal or airway penetration. A. Bandage the wound securely to prevent additional air leakage without restricting respiratory effort or venous return. B. Provide an oxygen-enriched environment to reduce respiratory distress and alleviate hypoxemia. C. Forced cage rest is important. II. If significant respiratory distress develops because of severe subcutaneous emphysema, place 18- to 20-gauge needles under the skin to expel air from the subcutaneous space and relieve external compression of the airway. III. Surgical treatment is required in severely affected cases to prevent further leakage of air into the subcutaneous space and to stabilize respiration. A. Surgical debridement and meticulous closure of tracheal rents are indicated in cases refractory to conservative therapy. B. Tracheal resection and anastomosis may be required in cases with substantial tracheal damage.
Monitoring of Animal I. Subcutaneous air accumulation resolves within 7 to 10 days in uncomplicated cases, although it may persist for up to 6 weeks. II. Closely monitor for complications related to laryngeal damage or paralysis, as well as esophageal injury. III. Tracheal stenosis or stricture can occur weeks to months later.
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