Laryngeal Collapse

Laryngeal collapse is a progressive, degenerative condition of the laryngeal cartilages, characterized by a loss of rigidity and structural integrity, leading to medial displacement of the arytenoid cartilages and collapse of the laryngeal lumen during inspiration. It is most commonly a sequela of chronic upper airway obstruction, particularly in brachycephalic breeds, and is classified into three grades based on the severity and anatomical involvement. Grade I is characterized by eversion of the laryngeal saccules, which are normally located in the laryngeal ventricle. Grade II involves medial collapse of the aryepiglottic folds, which are the mucosal folds extending from the arytenoid cartilages to the epiglottis. Grade III represents the most severe form, with collapse of the corniculate processes of the arytenoid cartilages, resulting in a marked reduction of the rima glottidis and severe respiratory distress. The condition is often bilateral and progressive, and it is considered a component of the brachycephalic obstructive airway syndrome (BOAS), though it can also occur secondary to other chronic upper respiratory obstructions such as laryngeal paralysis, tracheal collapse, or neoplasia. Surgical intervention is aimed at alleviating the obstruction and may include laryngeal sacculectomy, aryepiglottic fold resection, and arytenoid lateralization (tie-back) or partial arytenoidectomy, depending on the grade and the underlying cause.

Laryngeal collapse is primarily a secondary condition resulting from chronic, severe upper airway obstruction. The most common underlying cause is brachycephalic obstructive airway syndrome (BOAS), which includes stenotic nares, elongated soft palate, everted laryngeal saccules, and hypoplastic trachea. These anatomical abnormalities create increased negative pressure during inspiration, leading to chronic trauma and fatigue of the laryngeal cartilages. Other etiologies include laryngeal paralysis, which can be congenital (e.g., in Bouviers des Flandres, Siberian Huskies, and Dalmatians) or acquired (idiopathic, traumatic, iatrogenic, or secondary to systemic disease such as hypothyroidism or myasthenia gravis). Tracheal collapse, especially in toy and miniature breeds, can also predispose to laryngeal collapse due to increased inspiratory effort. Less common causes include laryngeal neoplasia, granulomatous laryngitis, and severe obesity. The pathophysiology involves repeated episodes of high-velocity airflow and negative pressure, which cause edema, inflammation, and eventual degeneration of the laryngeal cartilages, leading to loss of rigidity and collapse.

Laryngeal collapse is most commonly diagnosed in brachycephalic dog breeds, including English Bulldogs, French Bulldogs, Pugs, Boston Terriers, and Pekingese. These breeds have a high prevalence of BOAS, with studies reporting that up to 50% of brachycephalic dogs may have some degree of laryngeal collapse. The condition is less common in non-brachycephalic breeds, but can occur secondary to laryngeal paralysis, which is more frequent in large and giant breeds such as Labrador Retrievers, Golden Retrievers, and Saint Bernards. Age of onset varies: in brachycephalic breeds, clinical signs may appear as early as 1-2 years of age, while in laryngeal paralysis, it is typically seen in older dogs (mean age 9-10 years). There is no strong sex predilection, but some studies suggest a slight male predominance. Working and sporting dogs may be at higher risk due to increased respiratory demands, which exacerbate the underlying obstruction. Feline laryngeal collapse is rare but can occur in brachycephalic cats, particularly Persians and Himalayans, as part of BOAS.

The pathophysiology of laryngeal collapse is a cascade of events initiated by chronic upper airway obstruction. In brachycephalic breeds, stenotic nares and an elongated soft palate increase inspiratory resistance, leading to more negative intrathoracic pressure during inspiration. This negative pressure is transmitted to the larynx, causing the laryngeal cartilages to be pulled medially. Over time, the repeated stress leads to edema, inflammation, and degeneration of the arytenoid cartilages and aryepiglottic folds. The laryngeal saccules, which are normally everted only transiently, become chronically everted due to the negative pressure, further compromising the airway. As the condition progresses, the aryepiglottic folds lose their rigidity and collapse medially, and eventually the corniculate processes of the arytenoid cartilages also collapse, resulting in a narrowed rima glottidis. This creates a vicious cycle: the collapse worsens the obstruction, which increases the negative pressure, which further damages the cartilages. In laryngeal paralysis, the underlying cause is denervation of the intrinsic laryngeal muscles, leading to flaccid arytenoid cartilages that are drawn into the airway during inspiration. The resultant airway obstruction and increased respiratory effort can then lead to secondary laryngeal collapse, particularly in the aryepiglottic folds and saccules.

Intrinsic predisposing factors include brachycephalic conformation, which is genetically determined and results in a shortened skull, stenotic nares, elongated soft palate, and a hypoplastic trachea. These features are particularly pronounced in English Bulldogs, French Bulldogs, and Pugs. Age is a factor, as the degenerative changes in the laryngeal cartilages progress over time, and older dogs with BOAS are more likely to have advanced laryngeal collapse. Obesity is a significant extrinsic factor, as it increases respiratory effort and exacerbates the negative pressure on the larynx. Environmental factors such as hot and humid weather can increase respiratory rate and effort, worsening the condition. Prior surgical interventions for BOAS, such as soft palate resection or nares correction, may not prevent laryngeal collapse if the underlying conformational abnormalities are not fully addressed. In laryngeal paralysis, predisposing factors include breed (e.g., Bouviers des Flandres, Siberian Huskies), trauma to the neck, iatrogenic injury during cervical surgery, and systemic diseases such as hypothyroidism, myasthenia gravis, or polyneuropathy.

Clinical signs of laryngeal collapse are primarily respiratory and are exacerbated by exercise, excitement, heat, and stress. Common signs include inspiratory stridor (a high-pitched, harsh sound on inspiration), dyspnea, coughing, gagging, exercise intolerance, cyanosis, and syncope. In severe cases, dogs may present with acute respiratory distress and collapse. On physical examination, affected dogs often have stertorous breathing, which is a low-pitched snoring sound, particularly during inspiration. Auscultation of the larynx may reveal referred upper airway sounds. In brachycephalic breeds, concurrent signs of BOAS are often present, such as stenotic nares, elongated soft palate, and everted laryngeal saccules. In cases secondary to laryngeal paralysis, the arytenoid cartilages may be immobile on laryngeal examination. The severity of clinical signs correlates with the grade of laryngeal collapse: Grade I may cause mild signs, while Grade III can cause severe respiratory distress and is a medical emergency. Dogs may also exhibit signs of gastrointestinal disease, such as regurgitation or vomiting, due to increased negative intrathoracic pressure leading to gastroesophageal reflux.

Differential diagnoses for laryngeal collapse include: 1) Laryngeal paralysis: This condition also causes inspiratory stridor and respiratory distress, but on laryngeal examination, the arytenoid cartilages are immobile, whereas in laryngeal collapse, they are mobile but collapsed. Laryngeal paralysis is often idiopathic or secondary to systemic disease, and may be differentiated by ruling out other causes of neuropathy. 2) Tracheal collapse: This presents with a honking cough and expiratory dyspnea, and is diagnosed by radiography or fluoroscopy showing a collapsed trachea. It can coexist with laryngeal collapse, especially in small breeds. 3) Elongated soft palate: This is a common component of BOAS and can cause stertor and respiratory distress, but it is not the primary cause of laryngeal collapse. It is diagnosed by oral examination and is often treated concurrently. 4) Everted laryngeal saccules: This is a grade I laryngeal collapse, but it can be a primary finding in young dogs with BOAS. It is diagnosed on laryngeal examination. 5) Laryngeal neoplasia: Tumors such as squamous cell carcinoma or lymphoma can cause airway obstruction and stridor. They are diagnosed by laryngoscopy and biopsy. 6) Laryngeal granuloma: This can be caused by chronic irritation, such as from an elongated soft palate or foreign body, and presents with similar signs. It is diagnosed by laryngoscopy and biopsy. 7) Foreign body in the larynx or pharynx: This can cause acute onset of respiratory distress and stridor, and is diagnosed by imaging or laryngoscopy. 8) Brachycephalic airway syndrome without laryngeal collapse: Dogs may have stenotic nares and elongated soft palate but no laryngeal collapse; however, they are at risk for developing it. 9) Severe obesity: This can cause respiratory distress and exercise intolerance, but laryngeal examination is normal. 10) Congenital laryngeal abnormalities: Such as laryngeal hypoplasia or laryngeal web, which are rare and diagnosed by laryngoscopy.

The diagnostic algorithm for laryngeal collapse begins with a thorough history and physical examination, with emphasis on respiratory effort and auscultation of the larynx. If the dog is stable, a sedated laryngeal examination is performed to assess laryngeal function and anatomy. This is typically done using a laryngoscope, and the dog is placed in sternal recumbency with the mouth open. The larynx is evaluated for the presence of everted saccules (Grade I), collapse of the aryepiglottic folds (Grade II), and collapse of the corniculate processes (Grade III). The arytenoid cartilages are also assessed for mobility to rule out laryngeal paralysis. If laryngeal paralysis is suspected, a more detailed neurological examination and further diagnostic tests such as thyroid function tests, electromyography, or muscle biopsy may be recommended. Thoracic radiographs are indicated to evaluate for concurrent tracheal collapse, pulmonary disease, or aspiration pneumonia. In cases where neoplasia is suspected, advanced imaging such as CT or MRI may be performed, and biopsy is necessary for definitive diagnosis. In emergency cases with severe respiratory distress, immediate stabilization with oxygen supplementation, sedation, and possibly intubation or tracheostomy is required before diagnostic procedures.

Laboratory findings in laryngeal collapse are generally non-specific but may reflect underlying conditions or complications. A complete blood count (CBC) may show stress leukogram or, if there is aspiration pneumonia, neutrophilia with a left shift. Serum biochemistry may reveal elevated liver enzymes if there is hypoxemia or if the dog has been on corticosteroids. Thyroid function tests (total T4, free T4, TSH) are recommended if laryngeal paralysis is suspected, as hypothyroidism is a common cause. In cases of chronic respiratory distress, arterial blood gas analysis may show hypoxemia and hypercapnia. Coagulation panel (PT/aPTT) is not routinely indicated unless surgery is planned and there is a history of bleeding disorders. Inflammatory biomarkers such as C-reactive protein (CRP) may be elevated in cases of concurrent infection or inflammation. Synovial fluid analysis is not relevant to this condition.

Imaging plays a supportive role in the diagnosis of laryngeal collapse. Thoracic radiographs are essential to evaluate for concurrent lower airway disease, such as tracheal collapse, bronchial disease, or aspiration pneumonia. In brachycephalic breeds, radiographs may also show an elongated soft palate, but this is better assessed on oral examination. Lateral cervical radiographs may demonstrate a narrowed laryngeal lumen, but this is not a reliable diagnostic feature. Fluoroscopy can be used to assess dynamic collapse of the larynx and trachea during respiration, but it is rarely necessary. Advanced imaging such as CT or MRI is indicated if a mass lesion is suspected, as it provides detailed anatomy of the larynx and surrounding structures. CT can also be used to assess the degree of laryngeal collapse and to plan surgical intervention, but it is not routinely performed. Ultrasonography is not useful for evaluating the larynx due to the air interface. In cases of laryngeal paralysis, electromyography (EMG) of the laryngeal muscles may be performed, but this is specialized and not commonly available.

Cytology and histopathology are primarily used to diagnose underlying causes of laryngeal collapse, such as neoplasia or granulomatous disease. If a mass is identified on laryngoscopy, fine-needle aspiration (FNA) can be performed for cytological evaluation. For example, squamous cell carcinoma may show keratinized epithelial cells with atypia, while lymphoma may show a monomorphic population of lymphoblasts. Histopathology is obtained via biopsy during laryngoscopy or surgery. In cases of laryngeal collapse secondary to chronic inflammation, histopathology may show cartilage degeneration, fibrosis, and infiltration of inflammatory cells. In laryngeal paralysis, histopathology of the recurrent laryngeal nerve or cricoarytenoideus dorsalis muscle may show denervation atrophy. Special stains, such as Masson's trichrome for fibrosis or immunohistochemistry for specific tumor markers, may be used as needed.

Treatment of laryngeal collapse depends on the grade and the underlying cause. In all cases, stabilization of the patient is paramount, especially in acute respiratory distress. This may involve oxygen supplementation, sedation with butorphanol or acepromazine, and in severe cases, intubation or temporary tracheostomy. For Grade I laryngeal collapse (everted saccules), surgical resection of the saccules is recommended, often in conjunction with correction of other BOAS components such as stenotic nares and elongated soft palate. For Grade II collapse (aryepiglottic fold collapse), resection of the aryepiglottic folds may be performed. For Grade III collapse (arytenoid cartilage collapse), more aggressive surgical options are considered, including unilateral arytenoid lateralization (tie-back) or partial arytenoidectomy. However, in brachycephalic breeds, tie-back is often not recommended due to the risk of aspiration pneumonia, and a permanent tracheostomy may be considered as a salvage procedure. In cases secondary to laryngeal paralysis, unilateral arytenoid lateralization is the treatment of choice. Medical management may include weight loss, exercise restriction, and avoidance of heat and stress. Anti-inflammatory doses of corticosteroids (e.g., prednisone 0.5-1 mg/kg PO q12h for 3-5 days) may be used to reduce laryngeal edema, but this is not a long-term solution. Postoperative care includes pain management, antibiotics if indicated, and monitoring for respiratory distress and aspiration.

The prognosis for laryngeal collapse varies depending on the grade, underlying cause, and treatment. For Grade I and II collapse, surgical correction of the saccules and aryepiglottic folds, along with BOAS surgery, can result in significant improvement in clinical signs, with good to excellent outcomes in many cases. For Grade III collapse, the prognosis is more guarded. Unilateral arytenoid lateralization can improve airway function, but there is a risk of aspiration pneumonia, especially in brachycephalic breeds. Permanent tracheostomy is associated with a high rate of complications, including infection, obstruction, and tracheal stenosis, but can be life-saving. In general, dogs with laryngeal collapse secondary to BOAS have a fair to good prognosis if surgery is performed early and complications are managed. Dogs with laryngeal paralysis that undergo tie-back have a good prognosis, with improvement in exercise tolerance and quality of life, but they are at risk for aspiration pneumonia. Negative prognostic indicators include severe obesity, concurrent tracheal collapse, and advanced age.

Postoperative follow-up is crucial for monitoring recovery and detecting complications. After surgery, dogs should be hospitalized for at least 24-48 hours for observation of respiratory status and pain management. Suture removal from the skin is typically 10-14 days postoperatively. Restricted activity is recommended for 2-4 weeks to allow healing. Serial recheck examinations are recommended at 2 weeks, 6 weeks, and 3 months postoperatively to assess respiratory function and overall health. Thoracic radiographs may be repeated if aspiration pneumonia is suspected. Long-term follow-up is recommended every 6-12 months to monitor for recurrence of clinical signs or progression of the disease. In cases of permanent tracheostomy, daily care is required, including cleaning the stoma and monitoring for obstruction. Owners should be educated on the signs of respiratory distress and aspiration pneumonia, and advised to avoid triggers such as heat, exercise, and stress.

Clinical pearls: 1) Always perform a thorough laryngeal examination under light sedation in dogs with suspected BOAS, as laryngeal collapse may be present even if not obvious. 2) When performing laryngeal sacculectomy, use a grasping forceps to evert the saccules and excise them with scissors or a CO2 laser, taking care not to damage the vocal folds. 3) In aryepiglottic fold resection, use Metzenbaum scissors to excise the redundant folds, and ensure hemostasis with bipolar electrocautery. 4) For arytenoid lateralization, place a single suture (e.g., 2-0 or 3-0 polypropylene) through the muscular process of the arytenoid and the caudodorsal aspect of the cricoid cartilage, and tie it to achieve a 2-3 mm abduction of the arytenoid. 5) In brachycephalic breeds, consider a temporary tracheostomy during surgery to secure the airway, as they are at high risk for post-obstructive pulmonary edema. Pitfalls: 1) Failure to address concurrent BOAS components (e.g., stenotic nares, elongated soft palate) may lead to recurrence of laryngeal collapse. 2) Over-resection of the aryepiglottic folds can cause scarring and stenosis. 3) In arytenoid lateralization, over-abduction can lead to aspiration pneumonia, while under-abduction may not relieve the obstruction. 4) Postoperative laryngeal edema can cause acute respiratory distress; therefore, administer corticosteroids (e.g., dexamethasone 0.1-0.2 mg/kg IV) and monitor closely. 5) Avoid the use of acepromazine in dyspneic dogs, as it can cause vasodilation and worsen hypoxemia.

Perioperative drug protocols are based on Plumb's Veterinary Drug Handbook. Preoperative: For prophylactic antimicrobials, cefazolin (22 mg/kg IV) is administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperative antibiotics are not routinely needed unless there is contamination or infection. For pain management, opioids are used: hydromorphone (0.05-0.1 mg/kg IV or IM q4-6h) or buprenorphine (0.01-0.02 mg/kg IV or IM q6-8h) for the first 24-48 hours. Non-steroidal anti-inflammatory drugs (NSAIDs) such as carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) can be started postoperatively for 3-5 days, but caution is advised in dogs with renal or hepatic disease. To reduce laryngeal edema, dexamethasone (0.1-0.2 mg/kg IV) is given intraoperatively and may be repeated postoperatively at 0.05-0.1 mg/kg IV q12h for 24-48 hours. For sedation in dyspneic dogs, butorphanol (0.2-0.4 mg/kg IV) is preferred over acepromazine. If a tracheostomy is performed, humidified oxygen and frequent suctioning are required. For long-term management of BOAS, weight loss and exercise restriction are recommended. In cases of laryngeal paralysis due to hypothyroidism, levothyroxine (0.02 mg/kg PO q12h) is indicated.

Evidence-based literature on laryngeal collapse is limited, but several studies have evaluated surgical outcomes. A study by Poncet et al. (2006) on brachycephalic dogs with BOAS found that surgical correction of stenotic nares, elongated soft palate, and everted saccules resulted in good to excellent outcomes in 80% of dogs, with laryngeal collapse being a negative prognostic indicator. Another study by Torrez and Hunt (2006) reported that dogs with grade III laryngeal collapse that underwent permanent tracheostomy had a median survival time of 12 months, with complications in 50% of cases. For laryngeal paralysis, a study by MacPhail and Monnet (2001) compared unilateral arytenoid lateralization and partial arytenoidectomy, finding that tie-back had a lower rate of aspiration pneumonia (12%) compared to arytenoidectomy (33%), but both procedures improved respiratory function. A more recent study by Schoemaker et al. (2018) evaluated the use of CO2 laser for aryepiglottic fold resection in dogs with grade II collapse, reporting significant improvement in clinical signs with minimal complications. Overall, the evidence supports early surgical intervention in BOAS to prevent progression to laryngeal collapse, and the choice of surgical technique should be tailored to the individual patient and the underlying cause.