Laryngeal Paralysis

Laryngeal paralysis is a clinical syndrome characterized by the failure of the arytenoid cartilages and vocal folds to abduct during inspiration due to dysfunction of the recurrent laryngeal nerves or the cricoarytenoideus dorsalis muscles. This results in partial or complete airway obstruction, leading to inspiratory stridor, exercise intolerance, and respiratory distress. The condition is most commonly acquired and degenerative in older large-breed dogs, but can also be congenital or iatrogenic. Surgical management aims to restore a functional airway lumen, typically via unilateral arytenoid lateralization (tie-back), while preserving airway protection during swallowing. The disease is classified based on etiology (congenital vs. acquired) and severity (graded by laryngeal function during anesthesia).

Laryngeal paralysis can be congenital or acquired. Congenital forms are rare and typically seen in young dogs, with a hereditary basis in certain breeds such as the Bouvier des Flandres, Siberian Husky, and Dalmatian. Acquired laryngeal paralysis is most commonly idiopathic and degenerative, affecting older large-breed dogs, particularly Labrador Retrievers, Golden Retrievers, and Saint Bernards. Other causes include trauma to the neck or recurrent laryngeal nerves (e.g., bite wounds, neck surgery, cervical trauma), neoplasia (e.g., thyroid carcinoma, lymphoma, chemodectoma) compressing or infiltrating the recurrent laryngeal nerves, and iatrogenic injury during cervical or thoracic surgery (e.g., thyroidectomy, cervical ventral slot, thoracic duct ligation). Less common causes include polyneuropathies (e.g., generalized neuromuscular disease, myasthenia gravis, hypothyroidism, hyperadrenocorticism), infectious or inflammatory conditions (e.g., neuritis, polymyositis), and toxic neuropathies (e.g., lead poisoning). The recurrent laryngeal nerve is particularly vulnerable due to its long course through the thoracic inlet and its close association with the carotid sheath and thyroid gland.

Laryngeal paralysis is predominantly a disease of dogs, with a higher incidence in large and giant breeds. The acquired idiopathic form is most common in middle-aged to older dogs (median age 9-12 years). Breed predispositions include Labrador Retrievers, Golden Retrievers, Saint Bernards, Newfoundlands, and Siberian Huskies. Congenital laryngeal paralysis is rare and typically presents in young dogs (<1 year) of specific breeds. There is no strong sex predilection, though some studies suggest a slight male predominance. The condition is uncommon in cats, but can occur secondary to trauma or neoplasia. Working and sporting dogs may be overrepresented due to increased respiratory demands, which exacerbate clinical signs. The incidence of laryngeal paralysis is increasing, possibly due to improved recognition and the popularity of predisposed breeds.

The primary pathophysiological mechanism is denervation of the intrinsic laryngeal muscles, particularly the cricoarytenoideus dorsalis muscle, which is the sole abductor of the arytenoid cartilages. This denervation results from dysfunction of the recurrent laryngeal nerve, which provides motor innervation to all intrinsic laryngeal muscles except the cricothyroid muscle (innervated by the external branch of the superior laryngeal nerve). In acquired idiopathic laryngeal paralysis, the cause is thought to be a progressive, degenerative axonopathy of the recurrent laryngeal nerve, possibly due to chronic microtrauma or an immune-mediated process. The left recurrent laryngeal nerve is more commonly affected than the right, likely due to its longer course and greater susceptibility to injury. As the disease progresses, the arytenoid cartilages and vocal folds fail to abduct during inspiration, leading to dynamic airway collapse. This results in increased inspiratory resistance, turbulent airflow, and stridor. Over time, the increased negative pressure within the airway can cause edema, inflammation, and further compromise. In severe cases, complete airway obstruction can occur, leading to respiratory distress, hypoxia, and hypercapnia. Additionally, the loss of laryngeal abduction impairs the protective function of the larynx during swallowing, increasing the risk of aspiration pneumonia.

Intrinsic predisposing factors include breed-specific anatomical variations, such as a relatively narrow rima glottidis in large-breed dogs, which may exacerbate the clinical impact of laryngeal paralysis. Genetic factors play a role in congenital forms, with an autosomal dominant mode of inheritance suspected in some breeds. Age-related degenerative changes in the recurrent laryngeal nerve are a major risk factor for the acquired idiopathic form. Obesity and underlying endocrine disorders (e.g., hypothyroidism, hyperadrenocorticism) may contribute to the development or progression of the disease. Extrinsic factors include trauma to the neck or thoracic inlet, iatrogenic injury during surgery, and exposure to neurotoxins. Excessive exercise or environmental heat can precipitate acute respiratory distress in affected animals. Concurrent upper airway abnormalities, such as everted laryngeal saccules or stenotic nares, can worsen the clinical signs.

Clinical signs of laryngeal paralysis typically develop insidiously and progress over months to years. The most common presenting complaint is inspiratory stridor, which is often exacerbated by exercise, excitement, heat, or stress. Other signs include exercise intolerance, voice change (dysphonia), coughing, gagging, and respiratory distress. In severe cases, cyanosis and syncope may occur. Physical examination may reveal increased respiratory effort, stertor, and a palpable laryngeal tremor or lack of abduction during inspiration. In advanced cases, signs of aspiration pneumonia, such as fever, productive cough, and lethargy, may be present. The severity of clinical signs can be graded based on the degree of airway obstruction: Grade I (mild) – stridor only during exercise; Grade II (moderate) – stridor at rest, exercise intolerance; Grade III (severe) – respiratory distress at rest, cyanosis; Grade IV (critical) – severe respiratory distress, collapse, and impending respiratory arrest.

Differential diagnoses for laryngeal paralysis include: 1) Brachycephalic airway syndrome – characterized by stenotic nares, elongated soft palate, everted laryngeal saccules, and laryngeal collapse; typically seen in brachycephalic breeds and can be differentiated by breed and concurrent abnormalities. 2) Laryngeal neoplasia – primary tumors (e.g., rhabdomyosarcoma, squamous cell carcinoma) or metastatic disease; may cause similar signs but can be differentiated by laryngoscopic examination and biopsy. 3) Laryngeal trauma – fracture or dislocation of the laryngeal cartilages; history of trauma and imaging findings. 4) Foreign body in the larynx or trachea – acute onset of signs, imaging or endoscopy can identify the foreign body. 5) Tracheal collapse – primarily expiratory dyspnea, cough, and tracheal sensitivity; radiography or fluoroscopy can differentiate. 6) Laryngeal edema – acute onset, often due to allergic reactions or excessive barking; responds to anti-inflammatory therapy. 7) Myasthenia gravis – generalized weakness, megaesophagus, and positive acetylcholine receptor antibody titer. 8) Hypothyroidism – may cause laryngeal paralysis as part of a polyneuropathy; thyroid hormone levels are low. 9) Generalized polyneuropathy – may present with other neurological deficits, such as weakness and proprioceptive deficits. 10) Cricoarytenoid luxation – traumatic injury to the cricoarytenoid joint, diagnosed by imaging or laryngoscopy.

The diagnostic algorithm for laryngeal paralysis begins with a thorough history and physical examination, with particular attention to respiratory effort and laryngeal palpation. If the patient is stable, a laryngeal examination under light anesthesia is the gold standard for diagnosis. The patient is preoxygenated, and a short-acting anesthetic agent (e.g., propofol) is administered to achieve a light plane of anesthesia. Direct laryngoscopy is performed to assess arytenoid cartilage movement during spontaneous respiration. Normal abduction is characterized by symmetrical, synchronous movement of the arytenoid cartilages during inspiration. In laryngeal paralysis, the affected arytenoid(s) fail to abduct, and the vocal fold may be flaccid. The severity is graded based on the degree of abduction: Grade I – normal; Grade II – reduced abduction; Grade III – no abduction; Grade IV – paradoxical movement (collapse during inspiration). If the diagnosis is confirmed, further diagnostic testing is recommended to identify underlying causes. This includes thoracic radiographs to evaluate for megaesophagus, pulmonary metastases, or other thoracic pathology. Cervical radiographs or ultrasound may be useful to assess for masses or trauma. Blood work, including a complete blood count, serum biochemistry, thyroid hormone levels (T4, free T4, TSH), and acetylcholine receptor antibody titer, is recommended to rule out endocrinopathies and myasthenia gravis. Electromyography and nerve conduction studies may be performed if a generalized polyneuropathy is suspected. In cases of suspected neoplasia, advanced imaging (CT or MRI) and biopsy are indicated.

Laboratory findings in laryngeal paralysis are often nonspecific but may reflect underlying systemic disease. A complete blood count may reveal leukocytosis and neutrophilia if aspiration pneumonia is present. Serum biochemistry may show elevated liver enzymes or hypercholesterolemia in cases of hypothyroidism or hyperadrenocorticism. Thyroid hormone levels (total T4, free T4 by equilibrium dialysis, and TSH) are essential to diagnose hypothyroidism. An acetylcholine receptor antibody titer is recommended to rule out myasthenia gravis. In cases of suspected inflammatory or infectious causes, inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated. Arterial blood gas analysis may demonstrate hypoxemia and hypercapnia in severe respiratory distress. Coagulation panel (PT, aPTT, platelet count) is recommended prior to surgery to assess bleeding risk. Synovial fluid analysis is not typically performed unless there is concurrent joint disease.

Imaging plays a supportive role in the diagnosis of laryngeal paralysis. Thoracic radiographs are essential to evaluate for megaesophagus, aspiration pneumonia, pulmonary metastases, or other thoracic pathology. Cervical radiographs may reveal soft tissue masses, laryngeal fractures, or foreign bodies. Ultrasonography of the larynx can assess arytenoid cartilage movement and detect masses, but is operator-dependent and less reliable than laryngoscopy. Computed tomography (CT) provides detailed anatomical information and is particularly useful for evaluating laryngeal neoplasia, trauma, or extraluminal compression. CT can also assess the integrity of the recurrent laryngeal nerves indirectly by identifying masses along their course. Magnetic resonance imaging (MRI) is superior for evaluating soft tissue structures, including the laryngeal muscles and nerves, and may be helpful in cases of suspected polyneuropathy. Fluoroscopy can dynamically assess laryngeal function during respiration and swallowing, but is rarely used in clinical practice. In cases of suspected vascular ring anomaly (congenital), angiography or CT angiography may be indicated.

Cytology and histopathology are primarily used to diagnose underlying causes of laryngeal paralysis, such as neoplasia or inflammatory conditions. Fine-needle aspiration of cervical masses or enlarged lymph nodes can be performed for cytological evaluation. Histopathological examination of biopsied laryngeal tissue may reveal denervation atrophy of the cricoarytenoideus dorsalis muscle, characterized by angular atrophic fibers, fiber type grouping, and increased connective tissue. In cases of neoplasia, histopathology is essential for tumor typing and grading. Immunohistochemistry may be used to differentiate tumor types (e.g., S100 for neuroendocrine tumors, cytokeratin for carcinomas). In congenital laryngeal paralysis, histopathology may show hypoplasia or absence of the recurrent laryngeal nerve or cricoarytenoideus dorsalis muscle.

The definitive treatment for laryngeal paralysis is surgical. The most commonly performed procedure is unilateral arytenoid lateralization (tie-back), which involves suturing the arytenoid cartilage to the cricoid cartilage to permanently abduct the arytenoid and vocal fold. The procedure is typically performed on the left side to minimize the risk of aspiration, as the left side is more commonly affected. Surgical approaches include the lateral approach, which is most commonly used, and the ventral approach. The lateral approach involves an incision over the larynx, dissection through the sternothyroideus and thyrohyoideus muscles, and identification of the cricoarytenoideus dorsalis muscle. The muscle is transected or retracted to expose the arytenoid cartilage. A non-absorbable suture (e.g., polypropylene or nylon) is placed through the muscular process of the arytenoid cartilage and the caudodorsal border of the cricoid cartilage, and tied to achieve abduction. The suture is typically size 0 or 2-0. Postoperative care includes oxygen supplementation, anti-inflammatory doses of corticosteroids, and analgesics. Alternative surgical techniques include partial arytenoidectomy, vocal fold resection, and castellated laryngofissure, but these are less commonly performed due to higher complication rates. Medical management is reserved for patients that are not surgical candidates or as a temporary measure. It includes weight loss, exercise restriction, and avoidance of heat and stress. Corticosteroids (e.g., dexamethasone 0.1-0.2 mg/kg IV) may be used to reduce laryngeal edema in acute crises. Antibiotics are indicated if aspiration pneumonia is present. In cases of underlying endocrinopathy, appropriate medical therapy (e.g., levothyroxine for hypothyroidism) may improve laryngeal function.

The prognosis for laryngeal paralysis after surgical treatment is generally good, with improvement in clinical signs in 80-90% of cases. The most common postoperative complication is aspiration pneumonia, which occurs in 10-20% of cases and can be life-threatening. Other complications include seroma formation, wound infection, suture failure, and persistent stridor. The long-term prognosis is influenced by the underlying cause. In cases of acquired idiopathic laryngeal paralysis, the disease may progress to involve other cranial nerves, leading to megaesophagus and aspiration pneumonia. The median survival time after tie-back surgery is approximately 2-3 years, with many dogs living longer. Negative prognostic indicators include the presence of megaesophagus, aspiration pneumonia at the time of surgery, and concurrent neurological deficits. In cases of congenital laryngeal paralysis, the prognosis is guarded, as the condition is often progressive and may be associated with other congenital abnormalities.

Postoperative follow-up is crucial to monitor for complications and assess surgical outcome. Patients are typically hospitalized for 24-48 hours after surgery for observation and oxygen therapy if needed. The incision should be monitored for swelling, discharge, or infection. Sutures are removed 10-14 days postoperatively. A recheck examination is recommended at 2 weeks, 4 weeks, and 3 months after surgery. At each recheck, the owner should be questioned about respiratory effort, coughing, and exercise tolerance. Thoracic radiographs are recommended at 4-6 weeks postoperatively to evaluate for aspiration pneumonia. Long-term follow-up every 6-12 months is recommended to monitor for progression of underlying disease. Owners should be educated about the signs of aspiration pneumonia and advised to seek immediate veterinary care if they occur. Weight management and avoidance of triggers (e.g., heat, stress) are important for long-term management.

Clinical pearls: 1) Always perform a laryngeal examination under light anesthesia, as deep anesthesia can abolish laryngeal reflexes and mimic paralysis. 2) Preoxygenate the patient before induction to prevent hypoxia during laryngoscopy. 3) Use a short-acting anesthetic agent (e.g., propofol) to allow rapid recovery. 4) When performing tie-back, ensure the suture is placed through the muscular process of the arytenoid cartilage, not the cricoid cartilage, to avoid cartilage fracture. 5) Use a non-absorbable suture material to maintain abduction. 6) Consider performing a left-sided tie-back to reduce the risk of aspiration, as the right side is more important for airway protection. 7) Postoperative corticosteroids can help reduce laryngeal edema. Pitfalls: 1) Failure to identify concurrent upper airway abnormalities (e.g., everted laryngeal saccules) can lead to persistent clinical signs. 2) Over-tightening the suture can cause excessive abduction, leading to aspiration pneumonia. 3) Under-tightening can result in inadequate abduction and persistent stridor. 4) Inadvertent damage to the recurrent laryngeal nerve during surgery can worsen the condition. 5) Failure to address underlying endocrinopathies can lead to poor surgical outcomes. 6) Postoperative aspiration pneumonia is a common complication and should be aggressively treated.

Perioperative drug protocols for laryngeal paralysis surgery are based on Plumb's Veterinary Drug Handbook. Preoperative: Administer a broad-spectrum antibiotic such as cefazolin (22 mg/kg IV) 30 minutes before incision, and repeat every 90 minutes during surgery. For patients with aspiration pneumonia, continue antibiotics (e.g., amoxicillin-clavulanate 13.75 mg/kg PO q12h) for 7-14 days. Analgesia: Administer an opioid such as hydromorphone (0.05-0.1 mg/kg IV) or methadone (0.1-0.2 mg/kg IV) preoperatively, and continue postoperatively as needed. 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 used postoperatively for 3-5 days, but should be avoided in patients with renal disease or dehydration. Local anesthesia: A laryngeal block with lidocaine (1-2 mg/kg) or bupivacaine (1-2 mg/kg) can be performed to reduce laryngeal spasm. Corticosteroids: Dexamethasone (0.1-0.2 mg/kg IV) is often administered intraoperatively to reduce laryngeal edema. Postoperative sedation: Acepromazine (0.01-0.02 mg/kg IV) or butorphanol (0.2-0.4 mg/kg IV) may be used to reduce anxiety and respiratory effort. For patients with hypothyroidism, levothyroxine (0.02 mg/kg PO q12h) is indicated. For myasthenia gravis, pyridostigmine (0.5-3 mg/kg PO q8-12h) may be used. Antiemetics such as maropitant (1 mg/kg SC q24h) may be used to prevent vomiting and aspiration.

Landmark studies on laryngeal paralysis include: 1) A retrospective study by MacPhail and Monnet (2001) evaluating the outcome of unilateral arytenoid lateralization in 50 dogs, reporting a 90% improvement in clinical signs and a 15% incidence of aspiration pneumonia. 2) A study by Hammel et al. (2006) comparing tie-back to partial arytenoidectomy, finding tie-back to have a lower complication rate and better long-term outcome. 3) A study by White (1989) describing the surgical technique of arytenoid lateralization and its modifications. 4) A consensus statement by the American College of Veterinary Surgeons (ACVS) on the management of laryngeal paralysis, recommending tie-back as the treatment of choice. 5) A study by Tobias and Johnston (2012) in Veterinary Surgery: Small Animal, providing a comprehensive review of the pathophysiology and surgical management. 6) A study by Stanley et al. (2010) evaluating the risk factors for aspiration pneumonia after tie-back, identifying megaesophagus and concurrent gastrointestinal disease as significant risk factors. 7) A study by Schofield et al. (2007) on the use of computed tomography in the diagnosis of laryngeal paralysis, showing that CT can accurately assess arytenoid cartilage position. 8) A study by Burbidge (1995) on the congenital form of laryngeal paralysis in Bouvier des Flandres, demonstrating a hereditary basis. These studies collectively support the efficacy of surgical intervention and highlight the importance of careful patient selection and postoperative management.