Larynx

Introduction

Brachycephalic animals (especially English bulldogs, Boston terriers, Chinese Pugs, Pekinese, Shar Pei dogs, and Himalayan and Persian cats) often exhibit signs of upper airway obstruction due to anatomic and functional abnormalities. Brachycephalia is a local chondrodysplasia that occurs as a result of domestication. Brachycephalic animals are characterized by having a compressed face with poorly developed nares and a distorted nasopharynx. Their head shape is the result of an inherited developmental defect in the bones of the base of the skull. These bones grow to a normal width but reduced length. The soft tissues of the head are not proportionally reduced and often appear redundant. These anatomic exaggerations result in increased airflow resistance and increased inspiratory effort which lead to functional airway abnormalities. Brachycephalic animals with these anatomic exaggerations and clinical signs are diagnosed as having the “Brachycephalic Syndrome”.

The major components of the “Brachycephalic Syndrome” include 1) stenotic nares, 2) elongated soft palate, and 3) eversion of the laryngeal saccules. Most dyspneic brachycephalics have more than one and often all components of the syndrome. Some animals, especially English bulldogs, also have tracheal hypoplasia. These abnormalities may restrict airflow so severely that the condition progresses to include laryngeal and pharyngeal inflammation and edema, tonsil eversion from their crypts, and epiglottic, laryngeal and/or tracheal collapse.

Presentation and Diagnosis

Affected brachycephalics exhibit mild to severe signs of respiratory distress depending on the degree and location(s) of the obstruction. Signs of upper airway obstruction include exercise intolerance, stertorous breathing, mouth breathing, gagging, restless sleep (“sleep-disordered breathing”), cyanosis and collapse. Other signs may include restlessness, tachypnea, dysphagia, fever and an abnormal posture. Excitement, stress, and increased heat and humidity frequently make clinical signs worse. Dogs present for stridorous breathing and exercise intolerance, gagging or episodes of cyanosis and collapse.

Clinical evaluation of patients with severe respiratory distress should be conducted in a manner that does not upset the animal to avoid exacerbating its condition. The animal should be allowed to maintain a position of comfort and be minimally restrained during initial evaluation. Prior to a more thorough evaluation and work-up, patients with severe respiratory distress are provided emergency therapy. Emergency treatment includes controlling the environment to keep the animal cool and minimize stress, providing supplemental oxygen and a patent airway, and administering corticosteroids, sedatives and other drugs as needed to stabilize the patient. Sedatives given to relieve anxiety or facilitate examination sometimes exacerbate signs by relaxing upper airway dilating muscles. Further diagnostics and treatment follow stabilization of the patient.

A tentative diagnosis of the patient’s upper respiratory tract obstruction is usually achieved by obtaining a complete history, thorough physical examination, and clinical pathology results. Clinical pathology results are usually normal but may reveal polycythemia in animals with chronic hypoxia.¹ These diagnostic measures are followed by lateral neck and routine thoracic radiographs or other imaging modalities, endoscopic respiratory tract examination, and sample collection for bacterial culture and biopsy as needed. Additional diagnostic measures might include blood gas analysis and respiratory function testing.

Components of the Syndrome

Stenotic Nares

Stenotic nares are congenital malformations of the nasal cartilages which are commonly seen in brachycephalic breeds. The nasal cartilages of animals with stenotic nares lack normal rigidity and collapse medially causing occlusion of the external nares. Normally during inspiration the levator nasolabialis muscle contracts dilating the nares to facilitate air intake. In animals with stenotic nares there is little or no dilation during inspiration, and in severe cases, collapse of the opening. Airflow into the nares is restricted and greater inspiratory effort is necessary, causing mild to severe dyspnea. Severe inspiratory dyspnea results if airflow obstruction is marked. Marked occlusion of the nares results in open-mouthed breathing and can interfere with olfaction, and air warming, moisturizing, and filtering. Stenotic nares are diagnosed on physical exam by recognizing that the external nares opening in the nasal planum is narrowed, restricted or compressed by this collapsed tissue.

Elongated Soft Palate

Congenital soft palate elongation is the most commonly recognized component of the Brachycephalic syndrome. The normal soft palate just touches or slightly overlies (1 to 3 mm) the tip of the epiglottis. The elongated soft palate extends more than 1 to 3 mm caudal to the tip of the epiglottis, is often thickened and obstructs the dorsal aspect of the glottis (Figure 25-1). The elongated palate is pulled caudally during inspiration and is sometimes pulled between the corniculate processes of the arytenoids. Consequently, increased inspiratory effort is required and airflow is more turbulent. The arytenoids and palate become inflamed and irritated due to the movement of the palate against the arytenoids and airflow turbulence. At times the soft palate may obscure the epiglottis by displacing it dorsally. Diagnosis of soft palate elongation is made during laryngoscopic or endoscopic examination of the nasopharynx and larynx.
 

Laryngeal Saccule Eversion

Laryngeal saccule eversion,or prolapse of the mucosa lining the laryngeal crypts, is the first stage of laryngeal collapse.

In their normal position between the vocal cords and the ventricular bands (false vocal cords), the laryngeal saccules are not visualized. Increased airflow resistance and increased negative pressure generated to move air past obstructed areas due to stenotic nares and soft palate elongation pulls the saccules from their crypts and causes them to swell. Everted and edematous saccules obstruct the ventral aspect of the glottis further restricting airflow (See Figure 25-1). Diagnosis of laryngeal saccule eversion is made during laryngoscopic or endoscopic examination. The everted saccules are recognized as edematous or fleshy soft tissue masses immediately rostral to and often obscuring the vocal folds. Acutely everted saccules are whitish and glistening in appearance. Chronically everted saccules are pink and fleshy. It is difficult to visualize and thoroughly evaluate the laryngeal saccules and larynx prior to soft palate resection as the soft palate obscures the other structures, and the severely affected patient may become cyanotic. For these reasons, laryngeal saccule eversion is diagnosed less often than elongated soft palate or stenotic nares. Saccule eversion may also be suspected during ultrasonographic examination of the larynx when there is a narrowed air shadow within the rima glottis.²

Advanced Laryngeal Collapse Advanced laryngeal collapse is caused by chronic upper airway obstruction which results in increased inspiratory efforts and causes the cartilages to fatigue and lose their rigidity. Stage two and three laryngeal collapse may be recognized during laryngoscopic or endoscopic evaluation of animals with the brachycephalic syndrome. In stage two collapse or collapse of the aryepiglottic fold, the cuneiform process of the arytenoid cartilage and the fold of tissue connecting it to the epiglottis weaken and deviate medially (Figure 25-2). Medial deviation of this aryepiglottic fold causes further obstruction of the ventral aspect of the glottis. In stage three collapse or collapse of the corniculate processes of the arytenoid cartilages, the corniculate processes loose their rigidity and deviate medially obstructing the dorsal aspect of the glottis (See Figure 25-2). The normal glottic diameter at rest is narrowed and widening of the glottis during inspiratory abduction of the corniculate processes is reduced.
 

Associated Abnormalities

During laryngoscopic and endoscopic examination of the airway the pharynx should be assessed for degree of inflammation and edema, evidence of redundant dorsal pharyngeal mucosa, and tonsil eversion. Tonsil eversion, inflammation and edema are secondary to air turbulence and increased breathing effort. Aberrant nasal turbinates and gastrointestinal lesions have also been described. Tracheoscopy is performed to assess the tracheal conformation and degree of inflammation. Many brachycephalics have concurrent tracheal hypoplasia and a few have tracheal collapse. Hypoplasia results in a narrow lumen due to the cartilages meeting or overlapping. These cartilages are often abnormally rigid and the trachealis muscle is often obscured or rolled into the lumen. Tracheal collapse is usually a dorsoventral narrowing of the trachea with cartilages being more flaccid than normal and the trachealis muscle is stretched and droops into the lumen. These abnormalities further restrict airflow.

Treatment

After definitive diagnosis, the syndrome is treated with the goal of achieving long-term relief from respiratory distress and preventing progression of the disease. Partial resection of the nares, soft palate and laryngeal saccules is recommended for all patients with these brachycephalic abnormalities. Patients with advanced laryngeal collapse who do not improve adequately following palate and saccule resection or those who improve and then later relapse with severe signs of respiratory distress often benefit from a permanent tracheostomy which allows airflow to by-pass the upper airway. In addition to surgery, medical management may be beneficial. A weight reduction program is instituted for obese animals. Exercise restriction and elimination of precipitating causes may be beneficial. Provision of a cool environment and exclusion of respiratory irritants from the animal’s environment (smoke, fragrances, sprays, etc) are beneficial. Perioperative administration of metaclopramide and gastroprotectants may decrease signs associated with gastrointestinal lesions.

Before surgical evaluation and treatment, special precautions must be taken because brachycephalic animals with respiratory distress are at extreme risk for hypoxia, especially during anesthetic induction and recovery. Sedatives and anesthetic agents relax the upper airway by dilating muscles and relaxing accessory muscles employed by brachycephalics to facilitate breathing. This allows the upper airway to collapse and reduces respiratory drive. Risk of complete airway obstruction at induction can be minimized by pre-oxygenating the patient, rapid induction of anesthesia with an injectable agent, and then quickly intubating the patient. Risk of complete airway obstruction during recovery are minimized by intensive monitoring and prevention of nasopharyngeal and laryngeal edema. I recommend administering an anti-inflammatory dose of corticosteroids (dexamethasone 0.5 to 2 mg/kg SQ, IM ) immediately prior to or after induction of anesthesia. This reduces swelling and edema of pharyngeal and laryngeal tissues during and after surgery. Corticosteroid administration may be repeated as needed after surgery to reduce airway obstruction caused by swollen pharyngeal and laryngeal tissues. Nasopharyngeal and laryngeal inflammation and edema are also minimized by using atraumatic examination and surgical techniques. Sedation of the patient as anesthetic recovery begins will allow a slow, smooth recovery with the endotracheal tube in place for as long as possible. Administration of oxygen through a nasal catheter facilitates a slow smooth recovery and minimizes anxiety due to hypoxia. Alternatively, a tracheostomy tube is placed at the beginning of surgery and removed when the animal is fully recovered from anesthesia and shows minimal signs of respiratory distress.

Surgical Techniques

Various surgical techniques have been described to resect portions of the nares, soft palate and laryngeal saccules. Resections should be performed early in the animal’s life (often before 1 year of age) to prevent progressive deterioration of airway function. I prefer resection using sharp incisions with a scalpel or scissors rather than using electrosurgical, heat sealing or laser instruments. Prior to surgery, the patient is positioned to allow for optimal visualization and lighting of the oral and pharyngeal cavities (Figure 25-3). The patient is positioned in sternal recumbency with the neck extended and the maxilla suspended from an overhead rod. The mandible is pulled ventrally with tape to maximally open the mouth and the tongue is retracted rostrally. The cheeks may also be retracted laterally to further improve visualization.
 

Soft Palate Excision

Surgery is begun by resecting the elongated soft palate. This will allow subsequent resection of the laryngeal saccules if necessary with a less obstructed view. An Allis tissue forceps is used to grasp the tip of the soft palate and retract it cranially (Figure 25-4A). The line of excision is along an imaginary line at the level of the caudal pole of the tonsil. The epiglottis may also be used for anatomic reference and the finsished resected palate should just touch the tip of the epiglottis. Once the length of palate to be resected is determined, stay sutures using 3-0 or 4-0 poliglicaprone 25 (monocryl, Ethicon, Inc., Somerville, NJ) are placed and tied in the lateral margins of the palate adjacent to the line of incision. Cranial retraction using the tissue forceps and stay sutures provides good visualization.

A scalpel blade or a sharp pair of Metzenbaum scissors is used to incise half the width of the soft palate (Figure 25-4B). The incised edges of the nasal and oral palatal mucosa are apposed using a simple continuous pattern of 3-0 or 4-0 poliglicaprone 25. Care is taken to include the nasal mucosa which tends to retract from the incision line. The remaining palate is incised, and suturing continued to the opposite margin (Figure 25-4C). The stay sutures can be used as part of the suture placed in the palate or remain separate from the incision line. Blood clots or mucus should be aspirated from the pharynx prior to recovery and extubation of the patient.

Laryngeal Saccule Resection

Stay sutures previously placed on the edges of the soft palate are maintained to facilitate retraction of the palate and improve visualization of the everted laryngeal saccules. Blood and mucus are aspirated from the glottis as necessary. The endotracheal tube is elevated dorsally and deviated to one side to allow access to the laryngeal saccule on the opposite side. Alternatively, the endotracheal tube may be temporarily removed to allow less restricted access to the laryngeal saccules, this however increases the intraoperative risks of aspiration and hypoxia. An Allis tissue forceps is used to grasp and gently retract the everted saccule rostrally and medially to allow positioning of a long-handled, curved Metzenbaum scissors across the base of the saccule. (Figure 25-5). The everted tissue is excised using the scissors. Amputation may also be accomplished using laryngeal cup forceps or similar biopsy instruments, laser or electrosurgery. Hemorrhage is usually mild but some surgeons twist the saccule after it is grasped to reduce hemorrhage post-excision. More severe hemorrhage is rare and is controlled with direct pressure. Care is used during excision to not inadvertently resect the vocal fold which lies immediately caudal to the everted saccule. The procedure is repeated to remove the opposite laryngeal saccule and the resection sites are allowed to heal by second intention.
 

Stenotic Nares Wedge Resection (Alaplasty)

The patient is positioned in sternal recumbency and the head taped to the table to avoid rotation. The obstructing portion of the lateral nasal planum is grasped with Brown-Adson thumb forceps to delineate and stabilize the segment of nares to be resected. Maintaining this grip, make a “V” shaped incision around the forceps with a #11 scalpel blade. First make a medial incision angled in a caudolateral direction. Then make a second incision from the lateral aspect of the nares in a caudomedial direction to meet the first incision at the vortex of the wedge (Figure 25-6) Remove the wedge of nasal planum and cartilage. Hemorrhage is controlled by applying pressure and apposing the cut edges. Occasionally, vessels are identified which may be occluded with hemostats or electrocoagulation. Align the ventral margin of the nares and mucocutaneous junction and appose the incised edges with three or four simple interrupted sutures using a monofilament absorbable suture (4-0 polydioxanone). Repeat the procedure by removing a similar wedge of tissue from the opposite naris and apposing the edges. Alternative techniques include removal of wedges of various shapes and orientations from the lateral aspect of the nasal planum or alapexy.

Aryepiglottic fold resection is occasionally performed in patients with aryepiglottic fold collapse. It is performed when other resection techniques have not adequately alleviated the patient’s respiratory distress or concurrently with resection of palate, nares and saccules if respiratory distress is extreme and permanent tracheostomy is not acceptable to the client. Aryepiglottic fold resection is performed unilaterally through an oral approach. The fold is grasped and stabilized with thumb forceps and the fold and cuneiform process excised with Mayo scissors or uterine biopsy forceps. The tissue defect is allowed to heal by second intention.
 

Postoperative Management

The nasopharynx and larynx are aspirated and a nasal catheter placed for oxygen administration during recovery. Advance the catheter to the end of the soft palate if possible. Suture or glue the catheter to the skin and fit the animal with an appropriately sized Elizabethan collar to prevent the patient from removing the catheter. Keep the animal quiet and sedated to allow a slow quiet recovery with the endotracheal tube in place for as long as possible. Remove the tube with the cuff slightly inflated to withdraw any blood clots that may have entered the trachea. Begin supplemental oxygen through the nasal catheter (50 ml/ kg/min) just before or after the endotracheal tube is removed. Continue nasal oxygen administration until the patient is fully recovered from anesthesia and breathing with minimal or no distress, usually 2 to 3 hours. Provide continuous monitoring during recovery and postoperatively for 24 to 72 hours as inflammation and edema may result in airway obstruction. The clinician should be prepared to reanesthetize and re-intubate or perform a tube tracheostomy in patients which experience severe dyspnea. Additional doses of corticosteroids may also be necessary and gastroprotectants are continued. Analgesics are continued for 48 to 72 hours. A weight reduction program should be instituted for obese animals.

Serious surgical complications include death due to glottic obstruction from inflammation and edema, and nasal regurgitation and rhinitis/sinusitis due to excessive soft palate resection. Inadequate resection of tissue results in persistent signs of upper airway obstruction. Excessive glottic manipulation may cause vagal induced bradycardia. Hemorrhage, gagging and coughing and aspiration may also occur in the early postoperative period.

Dehiscence of the nares may occur if the patient frequently licks or rubs its nose. Healing then occurs by second intention and may cause a pink scar. Scarring or stenosis following laryngeal saccule or aryepiglottic resection cause voice change, loss of bark, respiratory noise or progressive signs of upper airway obstruction.

Prognosis depends on the severity of the condition at the time of surgery. Partial resection of the soft palate, laryngeal saccules and nares is expected to relieve moderate to severe signs of respiratory distress in patients who do not have laryngeal collapse. Patients breathe with less effort and noise and are more tolerant of exercise and excitement. Some patients who have initially responded well to resection sometimes deteriorate and again show signs of severe respiratory distress months to years later. Laryngeal collapse has often become severe in these patients. Patients with advanced laryngeal collapse at the time of diagnosis and resection may respond unsatisfactorily to resection and require permanent tracheostomy to relieve their respiratory distress.

Suggested Readings

Bright RM, Wheaton LG: A modified surgical technique for elongated soft palate surgery. J Am Anim Hosp Assoc 19:288-292, 1983.

Clark GN, Sinibaldi KR: Use of a carbon dioxide laser for treatment of elongated soft palate in dogs. J Am Anim Hosp Assoc 204:1779-1785, 1994.

Ellison GW: Alapexy: An alternative technique for repair of stenotic nares in dogs. J Am Anim Hosp Assoc 40: 484-489, 2004.

Harvey CE: Upper airway obstruction surgery 1: Stenotic nares surgery in brachycephalic dogs. J Am Anim Hosp Assoc 18:535-537, 1982.

Harvey CE: Upper airway obstruction surgery 2: Soft palate resection in brachycephalic dogs. J Am Anim Hosp Assoc 18:538-544, 1982.

Harvey CE: Upper airway obstruction surgery 3: Everted laryngeal saccule surgery in brachycephalic dogs. J Am Anim Hosp Assoc 18:545- 547, 1982.

Harvey CE: Upper airway obstruction surgery 4: Partial laryngectomy in brachycephalic dogs. J Am Anim Hosp Assoc 18:548-550, 1982.

Hendricks JC: Brachycephalic airway syndrome. Vet Clinics North Am: Small Anim Pract 22:1145-1153, 1992.

Poncet CM, Dupre GP, Freiche VG, Bouvy BM: Long-term results of upper respiratory syndrome surgery and gastrointestinal tract medical treatment in 51 brachycephalic dogs. J Sm Anim Pract 47: 137-142, 2006.

Rudorf H: ltrasonographic imaging of the tongue and larynx in normal dogs. J Sm Anim Pract 38: 439-444, 1997.

Wykes PM: Brachycephalic airway obstructive syndrome. Problems in Veterinary Medicine: Head & Neck Surgery 3:188-197, 1991.
 

Introduction

Bilateral laryngeal paralysis is a common cause of upper airway obstruction in older dogs. Although the disease has been reported in many breeds of dogs and in cats the large sporting breeds (Labrador and Golden Retrievers) are most commonly affected. The disease is characterized by clinical signs of inspiratory stridor, exercise intolerance, and respiratory distress, which gradually worsen over a period of months. Severely affected dogs will often progress to cyanosis and collapse. Other signs include voice change and coughing or gagging. Clinical signs are usually not evident in dogs unless the disease is bilateral. The long-term prognosis for patients with laryngeal paralysis is usually poor unless the disease is managed surgically.¹

The surgical technique described here is a form of arytenoid lateralization called unilateral cricoarytenoid laryngoplasty. This procedure or other forms of unilateral arytenoid lateralization have been successfully used by many surgeons to obtain consistently good results in the surgical treatment of laryngeal paralysis. Partial laryngectomy has been used successfully in the past but is not recommended for the treatment of laryngeal paralysis because of the high incidence of postoperative complications. Modified castellated laryngofissure has shown acceptable clinical results in dogs with laryngeal paralysis however the procedure is relatively complex, requires tracheostomy and is not widely used.

If proper surgical treatment is performed, the prognosis for affected dogs is good, however aspiration pneumonia remains a potential life-long risk.

Etiology

The most common form of laryngeal paralysis is the acquired, idiopathic form, which occurs primarily in older, large breed, male dogs. Congenital laryngeal paralysis is uncommon. A hereditary form has been reported in Bouviers des Flandres, with clinical signs observed at four to six months of age.² An association between laryngeal paralysis and generalized polyneuropathy has been reported in young Dalmatians.³ A hereditary form of the disease has also been reported in Siberian huskies and husky cross breeds.² Direct injury to the recurrent laryngeal nerves due to trauma or surgery is an uncommon cause of laryngeal paralysis.

The primary cause of laryngeal paralysis is dysfunction of the recurrent laryngeal nerves. The specific etiology of this dysfunction in acquired laryngeal paralysis is unknown, although a demyelinating disease has been suggested.⁴ This would preferentially affect longer nerve fibers such as the recurrent laryngeal nerve.⁴ A possible association with hypothyroidism has been reported.¹ The possibility of laryngeal paralysis being an early or initial clinical sign of a generalized polyneuropathy has been suggested.⁵

Neurogenic atrophy of intrinsic laryngeal muscles, particularly the cricoarytenoideus dorsalis muscle, causes failure of arytenoid cartilages and vocal folds to abduct, resulting in upper airway obstruction. The obstruction can worsen with exercise, excitement, or hot weather as increased oxygen demand causes greater inspiratory effort (greater negative pressure), which draws the arytenoid cartilages and vocal folds medially. This can become a vicious cycle, leading to cyanosis and collapse.

Diagnosis

The importance of an accurate diagnosis cannot be overemphasized. Laryngeal paralysis occurs primarily in older, larger breed dogs. It is rare in toy and small breed dogs. Other causes of respiratory distress such as upper airway obstruction caused by intraluminal or extraluminal (thyroid) neoplasia should be considered and ruled out before laryngeal paralysis is considered the primary cause. The most common clinical signs are respiratory distress, stridor, and exercise intolerance, often with a slow, insidious onset over a period of months to years. Other clinical signs observed less commonly include voice change and coughing or gagging. Although the onset of signs is gradual, it is not uncommon for patients to have acute, severe, life threatening episodes of upper airway obstruction, particularly during hot weather and when the dog is excited or exercising.

Physical examination of patients with suspected laryngeal paralysis should include auscultation of the laryngeal region with and without mild laryngeal compression both before and after exercise.⁶ In dogs with laryngeal paralysis, auscultation usually reveals increased respiratory noise (stridor) over the laryngeal region, especially during inspiration. Dogs with normal laryngeal function should not have an appreciable change in upper airway noise with mild laryngeal compression. Dogs with laryngeal paralysis will exhibit a distinct worsening of the stridor as laryngeal compression is applied because they already have a fairly narrow, relatively fixed laryngeal glottis. This may be noted while listening as the dog is panting or upon auscultation of the laryngeal region. Thoracic auscultation will often only demonstrate referred upper airway sounds, but it is extremely important in order to evaluate the patient for possible concurrent disease. Aspiration pneumonia and/or bronchial disease can occur in patients with laryngeal paralysis because these patients are unable to fully close the glottis during swallowing.

Thoracic and cervical radiographs should be obtained to rule out other causes of respiratory compromise and to document concurrent disease. In addition to a CBC and chemistry profile, thyroid status is evaluated (T4 or TSH stimulation). There is an increased incidence of hypothyroidism in dogs with laryngeal paralysis, although there is not a proven cause and effect relationship. Hypothyroidism, like acquired laryngeal paralysis, tends to be a disease of older dogs. Hypothyroidism has been reported as a cause of generalized polyneuropathies.⁷ Supplementation with thyroxine will not reverse the laryngeal paralysis, but it could help prevent or slow the progression of possible hypothyroid-induced generalized neuromuscular disease that may cause peripheral weakness.

Definitive diagnosis of laryngeal paralysis is made with laryngoscopy under very light anesthesia. In lightly anesthetized dogs with laryngeal paralysis, there is a failure of the arytenoid cartilages to abduct during inspiration. The arytenoid cartilages can also fail to abduct if the level of anesthesia is too deep. In order to make an accurate diagnosis, the patient must be under as light a plane of anesthesia as possible and the evaluation must be of adequate duration to be sure there is no effective arytenoid abduction during inspiration (at least 5 to 10 minutes). In some cases, paradoxical movement of the arytenoid cartilages may occur where the arytenoids are drawn medially due to the negative pressure created at inspiration.⁸ Similarly, the arytenoids may appear to abduct weakly on expiration; this is caused by the arytenoids being moved from their paramedian position by passive expiratory efforts. It is extremely important to correlate any laryngeal movement with the phase of respiration. Various anesthetic protocols have been used effectively to assess arytenoids function. I currently use propofol (2 to 6 mg/ kg, IV). After initial induction and arytenoid evaluation, I administer doxapram (1.0 to 2.2 mg/kg) and continue laryngoscopy. Use of doxapram is very useful in more clearly differentiating normal dogs from those with laryngeal paralysis. It increases respiratory effort and increases any intrinsic laryngeal motion (if present).²¹ In dogs with bilateral laryngeal paralysis, use of doxapram may increase paradoxical arytenoid motion. Close monitoring of the patient’s ventilatory status during laryngeal examination is important and the examiner should be prepared for patient intubation with the appropriate sized endotracheal tube. Laryngoscopy often reveals laryngeal (arytenoid) edema and inflammation, which may worsen the signs of laryngeal paralysis, and may change the character of dyspnea from primarily inspiratory to both inspiratory and expiratory.⁸ If laryngeal paralysis is strongly suspected in patients with moderate to severe clinical signs, based upon history and physical examination, it is advantageous to schedule laryngoscopy so that surgery can be performed immediately following laryngoscopy if the diagnosis is confirmed.

Treatment

The recommended emergency medical treatment for an acute respiratory crisis due to laryngeal paralysis is sedation and endotracheal intubation, followed by gradual wakening of the animal.⁶ These severely affected patients should be observed continuously and may need emergency surgery to relieve the upper airway obstruction. It is best to perform a definitive corrective procedure if possible rather than a temporary tracheostomy.

Alleviation of upper airway obstruction caused by laryngeal paralysis can be best achieved with surgery.² Medical therapy, including the use of tranquilizers, oxygen, and corticosteroids may be helpful in management of severely affected patients prior to surgery. Patients with preexisting aspiration pneumonia should be treated prior to surgery and may be more likely to develop postoperative aspiration pneumonia. Patients with laryngeal paralysis and megaesophagus (or any cause of regurgitation) have a poor prognosis due to the extremely high likelihood of developing severe aspiration pneumonia after surgery.

The goal of surgery is to provide complete relief of upper airway obstruction while minimizing discomfort and postoperative complications. After surgery, patients should be able to breathe comfortably and have a normal activity level for their age.

Unilateral arytenoid lateralization in some form (cricoarytenoid laryngoplasty is described here) has been used successfully to achieve these goals in treating laryngeal paralysis and is the procedure of choice of many surgeons.^1,2,6,8-16 Other reported surgical techniques for treatment of laryngeal paralysis include partial laryngectomy (partial arytenoidectomy with vocal fold resection) using either an oral or ventral laryngotomy approach^17,18 and modified castellated laryngofissure with vocal fold resection.^19,20

Surgical Technique

There are several variations of unilateral arytenoid lateralization. The procedure described here has been called cricoarytenoid laryngoplasty.^6,8 The procedure involves the placement of two sutures in the same location as the cricoarytenoideus dorsalis muscle, from the caudal dorsolateral aspect of the cricoid cartilage to the muscular process of the arytenoid cartilage (through the articular surface). Arytenoid lateralization has been used as a general term or to describe the procedure where sutures are placed from the caudal border of the thyroid cartilage to the muscular process of the arytenoid cartilage.^2,9,10,15,16 Regardless of the technique used, it is advisable to become familiar with the anatomy of the cervical and laryngeal region and the specific surgical procedure. The surgical technique should be observed prior to performing it and practiced on cadavers, or performed with an experienced surgeon present if possible.

Routine endotracheal intubation is performed following laryngoscopy. The unilateral cricoarytenoid laryngoplasty can be performed on either side. I perform the procedure on the left side for consistency only. Right handed surgeons usually prefer to perform left side lateralization because needle advancement through the cricoid is easier and less awkward. The patient is placed in right lateral recumbency with a slight rotation towards dorsal recumbency. It is helpful to place a small rolled towel under the neck at the level of the larynx. A ventrolateral approach to the larynx is made, beginning with a 5 to 8 cm long skin incision over the larynx, just ventral to the external jugular vein (Figure 25-7). It is helpful to palpate the caudal border of the cricoid cartilage and the wing of the thyroid cartilage as anatomic landmarks during the approach. Dissection is continued to the lateral and dorsal aspects of the larynx through the subcutaneous tissue and the superficial muscles of the neck, being careful to avoid the external jugular, linguofacial and maxillary veins.
 

The dorsal margin of the wing of the thyroid cartilage is palpated and retracted laterally by use of a “stay” suture or a hand-held retractor. The thyropharyngeus muscle is incised along the dorsal rim of the thyroid cartilage (Figure 25-8). Lateral retraction of the thyroid cartilage is important in order to avoid the esophagus. A layer of connective tissue is incised just medial and parallel to the rim of the thyroid cartilage and separated bluntly. The cricothyroid articulation at the caudal edge of the thyroid cartilage is separated with scissors and/or a Freer septum elevator (Figure 25-9A). This disarticulation is necessary to provide adequate exposure. The cricoarytenoideus dorsalis muscle and muscular process of the arytenoid cartilage are identified. The cricoarytenoideus dorsalis muscle is undermined and incised close to the muscular process, leaving enough muscle on the muscular process to attach mosquito forceps to facilitate gentle manipulation (Figure 25-9B). The cricoarytenoid articulation is separated using blunt dissection with a Freer elevator, being careful not to damage the muscular process or penetrate the laryngeal mucosa (Figure 25-9C). The rostral aspect of the cricoarytenoid joint capsule is left intact, as this almost always allows adequate mobility of the arytenoid cartilage. The purpose of cricoarytenoid joint disarticulation is to gain mobility of the arytenoid cartilage in relation to the cricoid cartilage so the arytenoid cartilage can be adequately abducted. Laryngoplasty procedures have been described where cricoarytenoid disarticulation is not done.¹³ However, some dogs have fibrosis and ankylosis of this joint. If disarticulation is not performed in these patients, adequate abduction of the arytenoid cartilage will not be achieved.
 

When performing this procedure, I no longer incise and separate the sesamoid band that connects the two arytenoid cartilages because mobilization of the arytenoid cartilage and optimal abduction can be achieved without dissection of the described band.

The left arytenoid cartilage is now movable in relation to the cricoid cartilage. Two sutures of monofilament nylon or polypropylene (0 in large dogs, 2-0 in medium dogs) are passed closely under the caudal edge of the cricoid cartilage and directed cranially to penetrate through the cartilage on the dorsolateral aspect (approximately 5 to 8 mm from the caudal edge), being careful not to penetrate laryngeal mucosa (Figure 25-10A). These sutures are then passed from medial to lateral through the central portion of the articular surface of the muscular processs of the arytenoid cartilage at least 2 to 3 mm from the cartilage edge (Figures 25-10B and 25-10C). The sutures are tied separately (Figure 25-10D). The intact rostral portion of the cricoarytenoid joint capsule helps to prevent over-abduction of the arytenoid cartilage. Either at this point or following closure, the dog is extubated briefly while laryngoscopy is performed to confirm adequate abduction of the left arytenoid cartilage, followed by replacement of the endotracheal tube. Closure of the thyropharyngeus muscle is completed using fine (3-0 or 4-0) monofilament absorbable suture material in a simple continuous pattern. Subcutaneous tissues and skin are closed routinely.
 

Postoperative Management

Postoperative care includes continuous (24 hour) monitoring for dyspnea, intravenous fluid therapy, and withholding of food and water for 12 to 24 hours. Cefazolin (20 mg/kg, IV) is given at the time of anesthetic induction and repeated two hours later. Antibiotic therapy (ampicillin 20 mg/kg, PO, TID) is only continued if the laryngeal mucosa is penetrated. Patients most often do well postoperatively and are discharged from the hospital within 1 to 2 days of surgery. The most common serious complication that can occur postoperatively is aspiration and development of aspiration pneumonia. Depression, fever or coughing postoperatively should prompt the surgeon to take thoracic radiographs to rule out aspiration pneumonia. A soft, canned food consistency diet with no excess gravy or crumbs is recommended to minimize the risk of aspiration pneumonia. I also counsel owners to avoid any food that might result in vomiting, as that increases the risk of aspiration pneumonia. A voice change (similar to a debarked dog) is expected after cricoarytenoid laryngoplasty and other laryngoplasty techniques. Occasional coughing after drinking water occurs commonly in the postoperative period, but usually decreases after a short period of adaptation.⁹

Surgical Results

Surgical techniques other than arytenoid cartilage lateralization techniques utilized in the treatment of laryngeal paralysis include partial laryngectomy and castellated laryngofissure. Partial laryngectomy usually involves partial arytenoidectomy with vocal fold resection using either an oral or ventral laryngotomy approach.

Arytenoid Lateralization/Cricoarytenoid Laryngoplasty

Unilateral cricoarytenoid laryngoplasty or some form of unilateral arytenoid lateralization has been shown to relieve signs of upper airway obstruction such as stridor, dyspnea and exercise intolerance in 82% to 100% of patients.^{1,8,10-12,15,16,23} Lane reported a 97% overall success rate in surgical treatment of 167 cases of laryngeal paralysis using several modifications of arytenoid cartilage lateralization.¹⁰ My success rate with unilateral cricoarytenoid laryngoplasty in over 500 dogs has been consistent with these results. White reported alleviation of exercise intolerance or stridor after arytenoid lateralization (with attachment of arytenoid cartilage to cricoid and/or thyroid cartilage) in 82% of dogs with laryngeal paralysis.¹⁵ Greenfield and Venker-van Haagen reported alleviation of clinical signs of upper airway obstruction in 89% and 95% respectively with unilateral arytenoid lateralization.^2,11 Payne, et al reported results of abductor muscle prosthesis in 11 dogs, where placement of the sutures from cricoid cartilage to muscular process of the arytenoid cartilage is done without cricoarytenoid disarticulation.¹³ Three of seven dogs where the procedure was done bilaterally died of aspiration pneumonia. There were no cases of aspiration pneumonia with unilateral procedures. In another study by Hammel, et al, the incidence of aspiration was reported in 7 dogs (18%).²² Six of those dogs recovered with treatment. Snelling, et al reported 87.7% improvement in quality of life, with a 10.7% overall complication rate in 100 patients.²³

Modified Castellated Laryngofissure

Modified castellated laryngofissure widens the glottic lumen by performing a stepped incision in the thyroid cartilage. The procedure also includes vocal fold resection and placement of mattress sutures through the arytenoid and thyroid cartilages to stabilize the arytenoid cartilages. In a report of four dogs treated with castellated laryngofissure,¹⁹ two (50%) had no clinical signs of upper airway obstruction at 7 and 12 months postoperatively, and two (50%) had no clinical signs of upper airway obstruction at 10 and 12 months postoperatively. Another study evaluated a modified castellated laryngofissure in 12 dogs with laryngeal paralysis.²⁰ Signs of upper airway obstruction had either decreased in severity or disappeared in 11 of these dogs 15 to 452 days after surgery. One dog died immediately after surgery from hyperthermia, and three dogs died 1, 9, and 11 months postoperatively from non-related or unknown causes. Tracheotomy tubes were used during the operation and were maintained for a minimum of three days postoperatively in both studies. Duration of postoperative hospitalization noted in only one case was eight days.

Modified castellated laryngofissure and arytenoid abduction techniques were evaluated using 30 canine postmortem specimens.¹⁴ There was a greater change in cross-sectional area of the rima glottidis with modified castellated laryngofissure than with unilateral arytenoid lateralization techniques. The authors of this study suggested using modified castellated laryngofissure when subglottic luminal compromise, such as traumatic fibrosis, is present. They felt the procedure was technically more demanding, more time consuming, and more traumatic than arytenoid abduction (lateralization) techniques.

Partial Laryngectomy/Bilateral Ventriculocordectomy

Several studies have shown a high incidence of postoperative complications associated with partial laryngectomy for the treatment of laryngeal paralysis. Long term results of partial laryngectomy (oral approach) in 25 dogs with idiopathic laryngeal paralysis were as follows:¹³ (52%) could breathe, eat and drink normally; four (16%) were considerably improved but still were noisy or had a cough, gag, or retch; six (24%) died of airway disease postoperatively; and two (8%) had initial improvement but were lost to follow-up.¹⁷ Aspiration was the cause of death in three dogs. Tracheotomy tubes were placed prior to performing surgery in all cases. Duration of maintenance of the tracheotomy tube and length of postoperative hospitalization were not described. Granulation tissue or web formation across the glottic region causing airway obstruction has been reported after partial laryngectomy, particularly when a ventral laryngotomy approach was used.

Complications and long term results after partial laryngectomy for the treatment of idiopathic laryngeal paralysis were reported in 45 dogs.¹⁸ Good or excellent results were obtained in 29 dogs (65%). Six dogs (13%) had some improvement, but residual respiratory compromise, exercise intolerance and consistent coughing. Ten dogs (22%) either showed no improvement over preoperative condition or developed fatal postoperative complications related to the partial laryngectomy. Death occurred in the immediate postoperative period (3 to 11 days) either because of pneumonia (8 dogs) or complete upper airway obstruction (1 dog). Nine dogs died of respiratory disease. Three dogs developed web stenosis across the glottis. The authors of this study did not recommend partial laryngectomy for the treatment of laryngeal paralysis because of the high incidence of postoperative complications. They felt that unilateral arytenoid lateralization may be a superior technique because unilateral lateralization provides relief from respiratory distress with a low complication rate.

Twenty four dogs with laryngeal paralysis treated with bilateral ventriculocordectomy through an oral approach at the University of Wisconsin-Madison were evaluated.¹² There was an unacceptably high incidence of postoperative complications after the bilateral ventriculocordectomy procedure. Complications occurred in 58% (14 of 24) of the dogs. The reported complications included increased respiratory stridor, exercise intolerance, and difficulty cooling off after exercise. Transverse laryngeal webbing occurred in nine of the 24 dogs (37.5%), requiring further surgery. The authors of this report recommended unilateral cricoarytenoid laryngoplasty for treatment of laryngeal paralysis in dogs.

Summary/Prognosis

It is important to recognize that while bilateral laryngeal paralysis is a significant cause of upper airway obstruction in older dogs, it is surgically treatable, with a good prognosis. Consistently good results have been obtained by many different surgeons with unilateral cricoarytenoid laryngoplasty or other forms of unilateral arytenoid lateralization. Familiarity with the laryngeal anatomy and the procedure is essential to a successful surgery. I recommend the unilateral cricoarytenoid laryngoplasty or other form of arytenoid lateralization because it achieves the goals of surgery in treating laryngeal paralysis, by relieving the respiratory distress, stridor, and exercise intolerance with a minimum of complications.

Editor’s Note: Recent studies seem to confirm that dogs with laryngeal paralysis likely have a polyneuropathy. See references 24 and 25.

References

1. Gaber CE, Amis TC, LeCouteur RA: Laryngeal paralysis in dogs: A review of 23 cases. J Am Vet Med Assoc 186:377-380, 1985.
2. Harvey CE, Venker van Haagen AJ: Surgical management of pharyngeal and laryngeal airway obstruction in the dog. Vet Clin North Am (Small Anim Pract) 5:515-535, 1975.
3. Braund KG, Shores A, Cochrane S, et al: Laryngeal paralysis-polyneuropathy complex in young dalmatians. Am J Vet Res 55:534-542, 1994.
4. Smith MM, Child G, Cardinet GH, et al: Muscle and nerve abnormalities associated with canine laryngeal paralysis. Vet Surg 21:239, 1992 (abstr).
5. Braund KG, Steinberg HS, Shores A, et al: Laryngeal paralysis in immature and mature dogs as one sign of a more diffuse polyneuropathy. J Am Vet Med Assoc 194:1735-1740, 1989.
6. LaHue TR: Laryngeal surgery: Lateralization techniques: 1994 Scientific Proceedings, 22nd Annual Surgical Forum, Washington, D.C., American College of Veterinary Surgeons, 1994, pp 255-257.
7. Harvey HJ, Irby NL, Watrous BJ: Laryngeal paralysis in hypothyroid dogs,in Kirk RW, (ed): Current Veterinary therapy VIII, Small Animal Practice. Philadelphia, PA, Saunders, 1983, pp 694-697.
8. LaHue, TR: Treatment of laryngeal paralysis in dogs by unilateral cricoarytenoid laryngoplasty. JAAHA 25:317-324, 1989.
9. Lane JG: ENT and Oral Surgery of the Dog and Cat. Bristol, England, Wright, 1982, pp 113-118.
10. Lane JG: Diseases and surgery of the larynx, in: 1986 Scientific Proceedings, 53rd Annual Meeting of the American Animal Hospital Association, Denver CO, American Animal Hospital Association, 1986, pp 620-623.
11. Greenfield CL: Canine laryngeal paralysis. Comp Cont Ed 9:1011-1020, 1987.
12. Peterson SW, Rosin E, Bjorling DE: Surgical options for laryngeal paralysis in dogs: a consideration of partial laryngectomy. Comp Cont Ed 13:1531-1540, 1991.
13. Payne JT, Martin RA, Rigg DL: Abductor muscle prosthesis for correction of laryngeal paralysis in 10 dogs and one cat. JAAHA 26:599- 604, 1990 .
14. Lozier S, Pope E: Effects of arytenoid abduction and modified castellated laryngofissure on the rima glottidis in canine cadavers. Vet Surg 21:195-200, 1992.
15. White RAS: Unilateral lateralization: an assessment of technique and long term results in 62 dogs with laryngeal paralysis. J Small Anim Pract 30:543-549, 1989.
16. Venker van Haagen AJ: Laryngeal diseases of dogs and cats, in Kirk RW, (ed): Current Veterinary therapy IX, Small Animal Practice. Philadelphia, PA, Saunders, 1986, pp 265-269.
17. Harvey CE, O’Brien JA: Treatment of laryngeal paralysis in dogs by partial laryngectomy. JAAHA 18:551-556, 1982.
18. Ross JT, Matthiesen DT, Noone KE, et al: Complications and long-term results after partial laryngectomy for the treatment of idiopathic laryngeal paralysis in 45 dogs. Vet Surg 20:169-173, 1991.
19. Gourley IM, Paul H, Gregory C: Castellated laryngofissure and vocal fold resection for the treatment of laryngeal paralysis in the dog. J Am Vet Med Assoc 182:1084-1086, 1983.
20. Smith MM, Gourley IM, Kurperschoek MS, et al: Evaluation of a modified castellated laryngofissure for alleviation of upper airway obstruction in dogs with laryngeal paralysis. J Am Vet Med Assoc 188:1279-1283, 1986.
21. Tobias KM, Jackson AM, Harvey RC: Effects of doxapram HCl on laryngeal function of normal dogs and dogs with naturally occurring laryngeal paralysis. Vet Anaesth Analg 31(4): 258-263, 2004.
22. Hammel SP, Hottinger HA, Novo RE: Postoperative results of unilateral arytenoid lateralization for treatment of idiopathic laryngeal paralysis in dogs: 39 cases (1996-2002). J Am Vet Med Assoc 228(8): 1215-20, 2006.
23. Snelling SR, Edwards GA: A retrospective study of unilateral arytenoid lateralisation in the treatment of laryngeal paralysis in 100 dogs (1992- 2000). Aust Vet J 81(8):464-8, 20.
24. Stanley BJ, Hauptman JG, Fritz MC,et al: Esophageal dysfunction in dogs with idiopathic laryngeal paralysis: a controlled cohort study. Vet Surg 39:139, 2010
25. Thieman KM, Krahwinkel DJ, Sims MH, et al: Histopathological confirmation of polyneuropathy in 11 dogs with laryngeal paralysis J Am Anim Hops Assoc 46:161,2010