Structural Disorders

Laryngeal Paralysis

Pathophysiology

In normal animals, the dorsal cricoarytenoideus muscles contract to abduct the corniculate processes of the arytenoids during inspiration. This muscle is innervated by the recurrent laryngeal nerve, a branch of the vagus that originates near the thoracic inlet and loops around the subclavian artery on the right or the aorta on the left and returns craniad to the larynx. Laryngeal paralysis is recognized as a congenital disorder or as an acquired form in older, large-breed dogs. In the congenital disease in some breeds and in the acquired idiopathic form, laryngeal paralysis can be accompanied by a more generalized polyneuropathy that results in peripheral limb weakness. Electromyographic studies and nerve conduction velocities in peripheral limb musculature of dogs with acquired laryngeal paralysis are suggestive of axonal disease; however, it is unclear whether the neuromuscular supply to the larynx is affected by a similar disease process (Jeffrey et al. 2006). Laryngeal paralysis can also result from trauma via surgery (thyroidectomy or tracheal ring placement), bite wounds, or crush injuries. A mediastinal mass compressing the recurrent laryngeal nerve can also lead to laryngeal paralysis.

In animals with laryngeal paralysis, active contracture to open the glottis is depressed or lost, and this can be unilateral or bilateral. Inspiration against a narrowed glottis results in a pressure drop across the larynx, and turbulent velocity of airflow results in irritation of the mucosa. This leads to mucosal edema and further obstruction of airflow. The larynx serves as an important protective mechanism against pulmonary inhalation of damaging substances. It appears that some dogs with laryngeal dysfunction experience sensory as well as motor loss and this may result in silent aspiration of oropharyngeal or gastroesophageal contents. It is common for dogs with laryngeal paralysis to accumulate secretions around the glottis, resulting in gagging or retching.

Cats are also affected by congenital or acquired laryngeal paralysis but it is less commonly recognized clinically because they are less physically active and regulate activity to avoid respiratory distress associated with inspiratory obstruction.

History and signalment

Laryngeal paralysis results in inspiratory difficulty, dysphonia, excessive or loud panting, gagging, and retching. Exercise intolerance may be the first abnormality noted, and can be mistaken as a sign of aging in the Retriever breeds. Signs are worsened by heat, stress, excitement, or exercise, and severely affected animals may suffer syncope or cyanosis. Careful questioning of the owner is recommended to uncover concurrent esophageal or gastrointestinal dysfunction because the combination of regurgitation or vomiting with laryngeal disease or laryngeal surgery enhances the risk for aspiration pneumonia.

Congenital laryngeal paralysis has been reported in several breeds of dogs and can be associated with additional neurologic deficits in some breeds (Table 5.1). Purebred animals with congenital disease are young when signs are first recognized, although the disease in Shepherds and Leonbergers has a later onset. The acquired form results in clinical signs late in life (10–14 years of age), and traumatic or iatrogenic injury to the larynx during surgery can result in development of signs at any age.

Physical examination

In some animals, upper airway auscultation is difficult because of continual panting. Inspiratory stridor audible over the larynx is the classic finding on physical examination; however, this may be a subtle finding in some dogs. Gently exercising the patient to increase respiratory effort may elicit stridorous sounds; however, caution is warranted to avoid overheating. Some large-breed dogs, particularly those that are obese, can develop life-threatening hyperthermia caused by excessive work of breathing.

Dogs with generalized neuromuscular disease can also display limb weakness exhibited by decreased conscious proprioception or patellar reflexes, and less commonly, a depressed gag or tongue reflex can be detected (Jeffrey et al. 2006). A full neurologic assessment is important in dogs with idiopathic laryngeal paralysis because these dogs may suffer continued weakness or exercise intolerance after surgical treatment of the larynx.

Diagnostic findings

There are no specific laboratory findings associated with laryngeal paralysis. A complete blood count (CBC) should be screened for neutrophilic leukocytosis suggestive of aspiration pneumonia, and a chemistry panel and urinalysis are performed to exclude systemic disease. Several studies have ruled out an association of thyroid dysfunction with laryngeal paralysis and testing is not advocated unless concurrent signs suggest hypothyroidism. If an arterial blood gas is performed, mild hypoxemia might be detected but the more obvious finding anticipated is hypercapnea associated with alveolar hypoventilation (see Chapter 2). In a dog with normal lung function, the alveolar-to-arterial ratio should be normal.

Table 5.1. Congenital forms of laryngeal paralysis

Figure 5.1. This right lateral cervical radiograph of a 9-year-old MC Labrador Retriever with stridor reveals caudal retraction of the larynx and hyoid apparatus consistent with an upper airway obstruction.

Differential diagnosis for laryngeal paralysis includes laryngeal neoplasia, granuloma, foreign body, or inflammatory laryngitis. Cervical radiographs can be helpful in ruling out a laryngeal mass, and indirect evidence of upper airway obstruction can be seen as caudal retraction of the larynx (Figure 5.1). Experienced examiners can document deficient laryngeal motion during ultrasound examination. Chest radiographs are recommended to assess the esophagus and to document evidence of aspiration pneumonia. If vomiting or regurgitation is in the history, videofluoroscopic assessment of esophageal function should be considered because defective function could impact the decision for anesthesia and surgery.

Diagnosis of laryngeal paralysis requires visualization of laryngeal motion under a light plane of anesthesia. The animal is placed in sternal recumbency, and a barbiturate anesthetic agent or propofol is administered to the dose that allows the mouth to be opened safely while preserving respiratory maneuvers. An assistant identifies inspiratory effort while the examiner watches for abduction of the arytenoids. If appropriate laryngeal function is not visualized initially, doxapram hydrochloride (0.5–2.2 mg/kg) can be administered intravenously as a bolus to stimulate respiration. Additional anesthesia is usually required at this point because doxapram can be stimulatory. It is important to time laryngeal motion with inspiratory effort because paradoxical laryngeal motion, where the larynx is pulled inwards by inspiratory effort and then passively opens on expiration, can be mistaken for normal motion. In addition to lack of motion, signs of laryngeal inflammation are often present in animals with laryngeal paralysis, such as hyperemia and accumulation of secretions around the larynx (Figure 5.2).

Dogs with laryngeal disease are at risk for aspiration pneumonia, which is augmented by respiratory depression associated with anesthesia. Therefore, it is prudent to plan for surgical intervention at the time of diagnostic laryngoscopy, if potential complications have been discussed with the client.

Treatment

Dogs and cats with unilateral laryngeal paralysis can usually tolerate the degree of dysfunction that results from partial airway obstruction and are not candidates for surgery. Weight loss and restricted activity during hot or humid weather should be recommended.

Figure 5.2. This endoscopic image of an 11-year-old MC Labrador Retriever shows dramatic hyperemia of the larynx and accumulation of mucoid secretions lateral to the larynx and ventral to the epiglottis.

For animals with bilateral laryngeal paralysis, the decision to go to surgery is based on the quality of life of the dog, the severity of clinical signs, and the time of the year. It can be prudent to perform surgery when approaching the summer to allow sufficient recovery before hot weather develops because warmer weather causes dogs to breathe harder despite less physical exertion. This leads to worsened inflammation and edema, augmenting airway obstruction. Unilateral arytenoid lateralization is currently the surgery of choice for animals with severe clinical signs related to bilateral laryngeal paralysis.

Prognosis

Aspiration pneumonia is the most common complication following arytenoid lateralization and can be seen in 20–30% of patients. It may occur immediately postoperatively or up to 3 years after surgery. Factors significantly associated with a higher risk of developing aspiration pneumonia include preoperative aspiration pneumonia, esophageal disease, temporary tracheostomy placement, and concurrent neoplastic disease (MacPhail and Monnet 2001). However, most dogs survive postoperative aspiration pneumonia with appropriate therapy, and owners are ultimately pleased with the clinical outcome. Other complications following surgical treatment of laryngeal paralysis include suture failure leading to acute upper airway obstruction and incisional seroma.

Figure 5.3. The airways are exposed to atmospheric pressure in the cervical region and intrapleural pressure in the intrathorac region (a). During inspiration, intrapleural pressure drops to create a pressure gradient that results in flow of air from the mouth to the alveolus. The dog with weakened cartilage rings in the cervical region experiences collapse on inspiration (b). During a forced expiration or cough, intrapleural pressure becomes positive and the pressure gradient across the airways favors collapse in the intrathoracic region when cartilage is weak (c). (Modified from Waltham Focus 11(2): 3–8, 2001, with permission.)

Tracheal/Airway Collapse

Pathophysiology

The etiology of tracheal collapse is unknown, but some dogs have been shown to have a reduction in chondrocytes and lack of glycosaminoglycan and chondroitin sulfate in tracheal cartilage. This leads to weakening of cartilage with flattening of the tracheal rings. Typically, tracheal collapse is in a dorsoventral direction with prolapse of an elongated dorsal tracheal membrane into the lumen of the airway. This dynamic collapse leads to mechanical irritation of the opposing mucosa, which enhances tracheal edema and inflammation. The mucociliary apparatus is disrupted and there is increased risk for small airway disease or mucus trapping. The cervical trachea collapses during inspiration while the intrathoracic portion of the trachea collapses on expiration because of the pressure gradients that develop during the respiratory cycle (Figure 5.3). Many dogs with tracheal collapse have collapse of both the cervical and intrathoracic trachea. In some dogs, the principal bronchi also are collapsed, with the right middle and left cranial lobar bronchi affected most commonly. When bronchial collapse is found in conjunction with tracheal collapse, this is termed tra-cheobronchomalacia. In some dogs, only lobar or lower airway collapse is detected and this is termed bronchomalacia. Chronic bronchitis can be found in conjunction with tracheal collapse or bronchomalacia.

History

Tracheal collapse is seen most commonly in small or toy-breed dogs, such as the Yorkshire terrier, Pomeranian, Poodle, Maltese, and Chihuahua, while bronchomalacia can be seen in small- and medium-sized dogs. Tracheal collapse is diagnosed rarely in large-breed dogs and in cats, although large-breed dogs may be affected by bronchial collapse. The condition is less common in the cat, although tracheobronchial collapse may accompany chronic bronchial disease. At the time of presentation, dogs can range from 1 to 15 years of age, depending on the degree of airway collapse and the presence of contributing clinical conditions. Dogs are commonly overweight, and both sexes are equally affected.

Most dogs with tracheal collapse have a chronic history of waxing and waning respiratory difficulty or cough that has grown progressively worse over time or has become refractory to treatment. Exacerbation of cough after eating and drinking or with excitement is common in dogs with tracheal collapse. The cough may be described as paroxysmal, dry, or as a “honking” cough. Owners may mistake the cough for vomiting or will report gagging or retching in association with the cough as the animal attempts to clear secretions from the airways. Worsened tachypnea, exercise intolerance, and respiratory distress tend to occur during physical exertion, with heat stress, or in humid conditions. This may be the result of airway collapse alone, chronic bronchitis, infectious airway disease, and/or concurrent upper airway obstruction (edema, saccular eversion, or laryngeal paralysis). Cyanosis or syncope occurs in severely affected animals due to complete airway obstruction, vagally mediated syncope, or pulmonary hypertension.

Physical examination

Dogs with airway collapse are usually systemically healthy and they are often overweight. The respiratory pattern can appear normal at rest, while marked expiratory effort can indicate bronchial collapse or concurrent bronchitis. Auscultation over the trachea can reveal musical or wheezing sounds caused by turbulent airflow through the narrowed lumen. Dramatic stridor over the upper airway is suggestive of concurrent laryngeal paresis or paralysis, which has been reported in up to 30% of dogs with tracheal collapse. Inspiratory and expiratory stridor can also be heard in dogs with severe tracheal collapse that results in a narrowed and fixed tracheal diameter. A flattened cervical trachea can be palpated in severe tracheal collapse. Most dogs with tracheal or airway collapse have a readily induced cough. Caution is warranted when palpating the trachea in dogs with reports of severe coughing because it may induce a life-threatening crisis of coughing or cough syncope.

Lung sounds can be difficult to assess in dogs with tracheal or airway collapse due to tachypnea, obesity, or referred upper airway sounds. Crackles associated with mucus plugging and airway closure can sometimes be auscultated when concurrent chronic bronchitis or bronchomalacia is present. Careful cardiac auscultation should be performed because 20% or more of middle-aged, small-breed dogs have mitral valve insufficiency in addition to airway collapse. Hepatomegaly is a common finding in dogs with tracheal collapse and may be related to fatty infiltration or a nonspecific hepatopathy.

Diagnostic findings

Although the diagnosis of tracheal collapse can be strongly presumed based on the signalment, history, and physical examination findings, a complete diagnostic work-up should be performed to define concurrent disorders and provide appropriate therapy. Routine hematologic testing may detect predisposing conditions or concurrent disease in dogs with tracheal collapse. Increased liver enzymes are not uncommon in dogs with airway collapse, and elevations in serum bile acids have also been reported, although the cause for this is unclear (Bauer et al. 2006).

Radiographs are essential both to examine airway diameter and to detect concurrent pulmonary or cardiac disorders. Cautious interpretation of the cardiac silhouette is warranted in obese dogs. Fat around the pericardial space and reduced lung volume can lead to the false impression of cardiomegaly. However, right-sided heart enlargement may be present in dogs with severe tracheal collapse, pulmonary disease, or other factors that predispose to the development of pulmonary hypertension.

It is important to note that airway collapse is a dynamic process and radiographs often give a false impression of the presence or absence of collapse. In the cervical region, overlying structures such as the esophagus and neck muscles can obscure details. Evaluation of left and right lateral views may improve distinction of structures; however, differences in positioning and in the phase of respiration may make it difficult to compare these views directly. Obtaining inspiratory and expiratory phases of respiration can be helpful because the cervical region should collapse on inspiration while the intrathoracic airways should collapse on expiration; however, the difficulty in timing these radiographs precisely limits the actual value. In comparison to fluoroscopy, radiographs underestimate the severity of tracheal collapse and are less able to detect intrathoracic airway collapse, which is often more severe than cervical collapse (Macready et al. 2007) (Figure 5.4). Therefore, while radiographs are useful as a screening tool for collapsing airways, they cannot be relied on for the diagnosis and likely will provide inaccurate information regarding the location and severity of tracheobronchial collapse. Fluoroscopy, where available, is beneficial in providing information on the degree of dynamic airway obstruction, and it also allows correlation of airway collapse with cardiac and respiratory cycles. Additional findings such as cranial lung herniation during cough can be detected (Figure 5.5).

Bronchoscopy can document tracheal collapse when radiographs or fluoroscopy is inconclusive and is useful for grading the degree of collapse (Figure 5.6). In addition, bronchoscopy readily identifies bronchomalacia, which can be static or dynamic (Figure 5.7). Bronchoalveolar lavage or an endotracheal wash sample can be used to document bacterial or Mycoplasma infection and to detect inflammation by cytologic examination, although bacteria are rarely involved in tracheal collapse and bronchomalacia. The risk of anesthesia for bronchoscopy can be significant in dogs with airway collapse, especially in obese animals with severe tracheal sensitivity or in hyperexcitable dogs. A slow recovery from anesthesia is advisable to minimize stress, and an oxygen-enriched environment should be available. One milliliter of 1% lidocaine sprayed into the distal trachea at the end of bronchoscopy can help decrease the cough reflex.

Figure 5.4. Inspiratory (a) and expiratory (b) fluoroscopic images from a 13-year-old MC Terrier mix with intrathoracic airway collapse. Note the dramatic reduction in the diameter of the intrathoracic trachea and carina, and the loss of air column within principal and lobar bronchi in (b).

Figure 5.5. Fluoroscopic image from a 15-year-old FS Pug demonstrates dramatic ventral deviation of the cervical trachea and cranial herniation of the lung through the thoracic inlet during a cough.

Figure 5.6. Grade I: The cartilage ring structure of the trachea remains circular and is almost normal. Slight protrusion of the dorsal tracheal membrane into the lumen reduces the diameter by <25% (a). Grade II: Flattening of the tracheal cartilage leads to lengthening of the dorsal tracheal membrane and further reduces the luminal diameter to approximately 50% (b). Grade III: The tracheal cartilage rings are severely flattened and the trachealis muscle contacts the inner surface of the tracheal cartilage. The lumen is reduced by 75% (c). Grade IV: The trachealis muscle is collapsed onto the inner surface of the cartilage, leading to complete obstruction of the lumen. A double lumen may be seen in some cases (d).

Figure 5.7. Bronchoscopic image demonstrating 70–100% collapse of lobar bronchi to the left lung lobe.

Treatment

Animals that have marked respiratory difficulty and coughing may require inpatient management. Stress should be minimized, and oxygen supplementation can be beneficial. Cough suppression and sedation can be achieved with butorphanol (0.05–0.1 mg/kg SC q4–6 hours), and addition of acepromazine (0.01–0.1 mg/kg SC) can have a synergistic effect in producing sedation. Caution should be employed when using the drugs together to avoid oversedation that might require intubation. To decrease laryngeal or tracheal inflammation, a single dose of dexamethasone-SP (0.10–0.25 mg/kg i.v.) or prednisolone sodium succinate (15–30 mg/kg i.v.) can be administered.

Outpatient management should be designed to treat disorders identified in the diagnostic work-up. If the dog is not stable for collection of an airway sample or if cultures are pending, a trial on doxycycline (3–5 mg/kg PO BID) can be employed to treat potential Mycoplasma infection and to provide mild anti-inflammatory effects. Bronchodilators may help reduce cough in animals with bronchomalacia by decreasing the tendency of intrathoracic airway to collapse. Suggested drugs include sustained release theophylline (5–10 mg/kg PO BID), terbutaline (0.625–5 mg/dog PO BID–TID), and albuterol syrup (50 µg/kg PO TID). Airway infection is treated with appropriate antibiotics as determined by airway sampling. If chronic bronchitis is diagnosed, corticosteroids should be employed (see later in this chapter). If marked tracheal inflammation is noted, a short course (5–7 days) of prednisone can be beneficial, although inhaled corticosteroids are preferred because they have limited side effects such as weight gain and panting that can exacerbate airway collapse. Finally, narcotic cough suppressants are often required to control cough and should be administered often enough to control cough without inducing severe sedation. Suggested drugs include hydrocodone (0.22 mg/kg PO BID–QID) and butorphanol (0.55 mg/kg PO BID–QID). Starting with a frequent dosing interval and gradually extending the time between doses and/or reducing the dose appears to be most effective in controlling signs and avoiding the development of tolerance.

Figure 5.8. Tracheal rings used for external support in dogs with cervical tracheal collapse.

Ancillary measures include avoidance of collars and decreased exposure to heat and humidity. Encouraging weight loss in obese animals is essential. This intervention alone can result in a significant reduction in cough and improvement in overall health. Upper airway surgery, if needed, can also reduce clinical signs. Dogs that fail medical management require additional intervention. In dogs with cervical tracheal collapse, placement of tracheal ring prostheses (Figure 5.8) will result in dramatic reduction in clinical signs (Buback et al. 1996). The primary complication of surgery is development of laryngeal paralysis from damage to the recurrent laryngeal nerve during or after surgery. When intrathoracic tracheal collapse is detected, placement of an intraluminal stenting device (Figure 5.9) can be successful in reducing clinical signs (Moritz et al. 2004, Sura et al. 2008). It is critical that the appropriate type and size of stent are used to attain a successful outcome (Weisse 2009). Complications of stent placement include migration, granuloma formation, or breakage of the stent.

Figure 5.9. Catheter delivery system and close-up of a distal deployment stent manufactured for intraluminal support of intrathoracic or complete tracheal collapse. (Courtesy of Infiniti Medical, www.infinitimedical.com.)

Prognosis

Tracheal collapse with or without airway collapse is a common cause of cough in small-breed dogs. Bronchomalacia is found frequently in large-breed dogs also: however, because it requires bronchoscopy for identification, the condition is underdiagnosed. Most animals can be managed successfully with an individualized treatment plan directed against the abnormalities noted during diagnostic testing; however, the underlying pathology of airway collapse is irreversible. Recurrent clinical signs should be anticipated and for dogs that are refractory to therapy, more aggressive intervention should be investigated.

Bronchiectasis

Pathophysiology

Bronchiectasis is described as irreversible dilatation of the bronchi with accumulation of suppurative airway secretions. The disorder is a poorly characterized condition associated with chronic obstructive, inflammatory, or infectious airway diseases in dogs and cats. In the dog, foreign body pneumonia, ciliary dyskinesia, smoke inhalation, chronic aspiration pneumonia, eosinophilic bronchopneumopathy, or chronic bronchitis can lead to the development of bronchiectasis. In the cat, bronchiectasis has been recognized in association with chronic inflammatory airway disease, and the radiographic appearance can be similar to that seen with cystic bronchogenic carcinoma.

History and signalment

Dogs or cats that have bronchiectasis as part of the syndrome of primary ciliary dyskinesia are typically young on presentation and have a chronic history of serous to mucoid nasal secretions and cough that responds to antibiotics but recurs (see Chapter 6).

Animals with acquired bronchiectasis are middle aged to older and have a chronic cough or recurrent pneumonia. Disease is clinically recognized more often in dogs than cats, and Cocker Spaniels are predisposed to the disorder.

Physical examination

There are no specific physical examination features that characterize bronchiectasis. A rapid shallow breathing pattern and abnormal thoracic auscultation may be present in animals with concurrent pneumonia; however, some affected dogs may display only tracheal sensitivity associated with airway inflammation. A moist cough is often induced.

Diagnostic findings

Definitive diagnosis of bronchiectasis is difficult in veterinary medicine because early radiographic lesions are subtle, and dilated, thickened airways are not readily detectable, particularly if pneumonia is absent. When visible radiographically, disease should be considered advanced and irreversible (Figure 5.10). Computed tomography (CT) is used for recognition of dilated airways in human medicine but has only recently been used to aid in the diagnosis of pulmonary disorders in veterinary medicine (Figure 5.11). Visualization of the airways through bronchoscopy allows documentation of bronchiectasis; however, the operator must have knowledge of normal airway anatomy to recognize the abnormality. With bronchiectasis, the normal rounded bifurcations at bronchial branch points are replaced by dilated and more oval or irregular appearing airway openings (Figure 5.12). Airway space is increased as airways are pulled open by the reduction in supporting parenchyma.

Figure 5.10. Right lateral (a) and dorsoventral (b) radiographs from a 10-year-old FS DLH with radiographically apparent bronchiectasis involving the left cranial lung lobe (cranial and caudal segments). A pneumonic infiltrate in the left cranial lung lobe outlines the bronchi and a diffuse bronchial pattern is present throughout the remainder of the lung fields.

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