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Laryngeal paralysis in dogs and cats: pathogenesis, clinical signs and diagnosis (Part I)

Last updated September 06, 2013

Laryngeal paralysis (LP) is a well recognised and potentially life threatening condition seen predominantly in older large-breed dogs. However, it is increasingly being recognised also in cats. The condition results either from dysfunction of the caudal laryngeal nerves, which are terminations of the recurrent laryngeal nerves, or from damage to the dorsal cricoarytenoid muscles. The caudal laryngeal nerves control the contraction of the crycoaritenoideus dorsalis muscle and subsequently the abduction of the arytenoid cartilages during inspiration. Dysfunction of these nerves or muscles and secondary muscle atrophy result in failure of arytenoid abduction and medial displacement of the vocal folds during inspiration leading to upper airway obstruction. Clinical signs include voice change, inspiratory stridor, and dyspnoea. LP is diagnosed by observing the absence of arytenoid abduction during laryngeal examination under a light anaesthetic plane. LP can be unilateral or bilateral and congenital or acquired. Most studies report that male dogs are more commonly affected then female dogs.

 

PATHOGENESIS & CLINICAL SIGNS


CONGENITAL LP
A hereditary form of laryngeal paralysis in young dogs has been reported in Bull Terriers1, Bouviers des Flandres2, Siberian Huskies and Siberian Husky cross-breeds,3,4 Dalmatians,5,6 Rottweilers,7 white-coated German shepherd dogs,8 Leonberger9 and Pyrenean mountain dogs10. In Bouviers des Flandres, the condition is secondary to Wallerian degeneration of the recurrent laryngeal nerves.2 In Siberian Huskies, Husky crossbreeds and white-coated German Shepherd dogs, the condition is thought to be associated with the white colour of their coat.3,4,7 A laryngeal paralysis-polyneuropathy complex (LP-PNC) due to neurogenic atrophy of intrinsic laryngeal and appendicular skeletal muscles has been described in young Dalmatians, Rottweilers and Pyrenean mountain dogs.5,6,7,10 In these dogs, LP was found in conjunction with other neurological signs, such as gait abnormalities (ataxia, paresis, head and muscle tremors) and megaoesophagus.5,6 Recently, an X-linked, recessively inherited polyneuropathy and laryngeal paralysis has been reported in young and adult Leonberger dogs.9

In most cases, clinical signs are noticed at young age, usually before 1 year and include increasing loss of exercise tolerance and respiratory dysfunction reflected by progressive upper airways stridor, dysphonia, dyspnoea and collapse.10 Furthermore, regurgitation, vomiting and progressive inhalation pneumonia have been described.7 Survey thoracic radiographic findings in young Rottweilers were consistent with hiatal hernia, reported as a complication of upper airway obstruction secondary to LP.7  Prognosis for dogs with LP-PNC appears to be poor, even with palliative treatment. Surgical correction of LP in these animals should be considered with caution as the polyneuropathy may continue to progress. Congenital LP may occur also in cats.11

ACQUIRED LP
A
cquired LP is most commonly reported in Labrador and Golden Retrievers, Great Danes, Irish Setters, Afghan Hounds and Saint-Bernards.12,13 Potential underlying causes of acquired LP include iatrogenic injury to the recurrent laryngeal nerve during surgeries such as thyroidectomy, trauma, infection and neuromuscular diseases. However, in older dogs the acquired form of LP is most often considered idiopathic. Acquired LP may also occur as part of a paraneoplastic syndrome, or be associated with endocrine or metabolic disorders such as hypothyroidism or diabetes mellitus.14 Hypothyroidism could represent a causative or predisposing factor; however resolution of LP in supplemented hypothyroid dogs has been poorly described.15 LP has been diagnosed in cats after bilateral thyroidectomy and in dogs from stretching or compression of the laryngeal recurrent nerve by a cranial mediastinal or paratracheal mass.

Recent evidence strongly suggests that dogs with idiopathic LP may have an underlying chronic progressive, non-inflammatory, degenerative polyneuropathy or neuromuscular disorder and LP may be only one manifestation of a more complex condition. In support of this theory Thieman and others (2010) reported neurogenic atrophy in laryngeal and pelvic limb muscles, and nerve axonal degeneration in laryngeal and peroneal nerves in dogs affected by acquired LP. In these cases electrophysiological tests also supported peripheral nerve abnormalities. Clinical signs of a neuromuscular disease include generalised or focal muscle weakness, normal to depressed spinal reflexes, and muscle atrophy.14 Stanley and others (2010) demonstrated that dogs with acquired LP also have abnormal cervical and cranial thoracic oesophageal motility compared with unaffected dogs in a similar breed and age distribution. In fact, the cervical and cranial thoracic oesophagus are supplied by the pararecurrent laryngeal nerves (pRLNs), branching off the recurrent laryngeal nerves (RLNs) as they arise from the vagus nerve. Because of the common origin of the RLNs and the pRLNs, it is possible that the pRLNs also degenerate in dogs with acquired idiopathic LP leading to cranial oesophagus dysfunction and increased risk of aspiration pneumonia. Bilateral LP occurs in 81% to 100% of dogs presented for LP surgery.16

Video 1The presenting signs of the acquired form of LP are quite similar to the signs of the hereditary form. Median age of dogs affected by acquired LP is 9 years. Early in the disease, owners may notice voice change, inspiratory stridor and exercise intolerance (Video 1). Dysphagia can also occur, possibly in association with peripheral neuropathy. Regurgitation from concurrent oesophageal disease or gagging and retching from a soft palate that has hypertrophied as result of inspiratory dyspnoea may also be reported. Progression of signs is often slow and it can take few months to years before a dog develops severe respiratory distress. Owners may initially believe that the dog’s reluctance to move is simply a sign of aging. Once the disease progresses and laryngeal muscles are paralysed bilaterally, dogs may develop severe dyspnoea, cyanosis and syncope. Dogs with unilateral LP are usually asymptomatic. Exercise, obesity, excitement and increased environmental temperature generally can rapidly exacerbate the signs.  These dogs may develop an inspiratory dyspnoea that is not alleviated with open-mouth breathing (see Video 1). Because the primary means of heat loss in dogs is evaporation while panting, dogs manifesting acute severe signs of LP are more susceptible to hyperthermia due to a lack of heat dissipation through an obstructed respiratory tract. Rectal temperature should be always obtained at initial assessment and dogs should be also evaluated for systemic signs of heat stroke. These include petechial haemorrhages associated with disseminated intravascular coagulation and hyperaemic mucous membranes. Heatstroke from sustained hyperthermia can progress to multi-organ failure and death. Dogs affected by LP may develop pneumonia secondary to oesophageal dysfunction and regurgitation or pulmonary oedema as result of changes in intra-thoracic pressure.

LP IN CATS
Congenital or acquired LP has been only sporadically reported in cats and no breed or sex predilection has been identified. The median age of presentation of the signs of the acquired form is 11 years and clinical symptoms include tachypnea or dyspnea, inspiratory stridor, weight loss, cough, anorexia, lethargy, cyanosis, and fever. While regurgitation is often reported in dogs with LP, this seems not to be obvious in cats. As in dogs, LP in cats may occur in conjunction with polyneuropathy. Other causes of acquired LP in cats include neoplastic, trauma or surgical complication in the cervical or thoracic region. Reports of LP in cats have shown primarily bilateral paralysis, with few cases of left-sided unilateral paralysis. The left RLN has been hypothesised to be more susceptible to damage because of its longer course and fewer nerve fibres as compared to the right RLN.11

 

DIAGNOSIS


Clinical suspicion is an important tool in diagnosing LP (Fig.1). If an affected animal is stable, it should undergo a through physical examination. The thorax and the cardiovascular system should be assessed for evidence of pneumonia, pulmonary oedema or abnormalities that could contribute to exercise intolerance. Neurological examination should also be performed to evaluate for signs of polyneuropathy. Complete blood count and serum biochemistry profile are usually within normal limits, unless concurrent disease is present. Hypercholesterolemia, hyperlipidaemia and increased liver enzymes may be suggestive of hypothyroidism. Thyroid function should therefore be tested measuring free thyroxin and endogenous thyroid-stimulating hormone (TSH) concentrations to rule out thyroid hypofunction. Thoracic and abdominal radiographs as well as abdominal ultrasonography should also be routinely performed. These are aimed to rule out other causes of dyspnoea and for determining whether concurrent conditions are present such as lung lobe tumours, mediastinal or abdominal masses. Thoracic radiographs also permit to look for concurrent inhalation pneumonia, non-cardiogenic pulmonary oedema or megaoesophagus. Oesophageal dysfunctions may not be visible on plain x-rays, but may be detected on oesophagrams. However, as the risk of aspiration largely outweighs the diagnostic benefits of contrast oesophagraphy, this procedure is not performed routinely in dogs with LP.17

Laryngoscopy and observation of the movements of the arytenoid cartilages under a light plane of anaesthesia is the diagnostic method of choice for LP (Fig. 2).  Patients with LP fail to abduct their arytenoid cartilages and the vocal folds are medially displaced during inspiration (Fig. 3) (Video 2). These patients should have an intravenous catheter placed before the examination and receive pre-procedure oxygen via facemask. It is important to be aware of the patient’s breathing pattern during laryngoscopy since expiration passively moves the vocal folds laterally simulating abduction. This paradoxical vocal folds movement must be recognised, since maximum arytenoid cartilage lateralisation and subsequent vocal folds abduction should be during inspiration, not expiration. When laryngoscopy is performed, the diagnosis of LP is based on either the vocal folds remaining stationary or moving toward midline during inspiration.

Video 2 - Laryngoscopy

A potential problem with diagnosing LP is that anaesthetic agents normally depress laryngeal movements. The animal should be anaesthetised to the point at which the mouth can be easily opened but a laryngeal reflex is still present. The guideline is that if I am afraid I may be bitten during the examination, then the plane of anaesthesia is appropriate. If the anaesthesia is too deep, the patient will not have normal vocal fold movement and even a normal larynx may appear paralysed. In this case the clinician should wait for drug redistribution allowing the patient to approach consciousness and repeat the examination.

Gross and others (2002) compared thiopental, propofol and diazepam-ketamine for evaluation of laryngeal function in dogs premedicated with butorphanol-glycopyrrolate and concluded that normal laryngeal function was observable with the three investigated protocols. However, the exposure of the larynx was more readily accomplished with thiopental or propofol than with diazepam-ketamine.18 In a comparison study of seven anaesthetic protocols, Jackson and others (2004) reported that arytenoid motion is significantly greater during inspiration when thiopental as a single agent or intramuscular acepromazine with intramuscular butorphanol plus isoflurane by mask was used.19 The animal is placed in sternal recumbency with the head elevated. A portable laryngoscope can be used to visualise the rima glottidis. However, retraction of the tongue and pressure on the epiglottis with the blade may affect laryngeal function. Therefore, some clinicians prefer to use a trans-oral video endoscope.

Anaesthetic regimens for diagnosing laryngeal paralysis in dogs include:

  1. Preoxygenation for 3-5 minutes (Fig. 4);
  2. Butorphanol (0.2-0.3 mg/kg IV) 5 minutes before induction;
  3. Propofol (2-3 mg/kg IV slowly over 1 minute to effect) or
  4. Diazepam (0.5 mg/kg) and Ketamine (10 mg/kg) mixed in the same syringe

To complete the neurological assessment of patients affected by acquired LP, electro diagnostic testing should be performed followed by muscle and peripheral nerve biopsies in order to establish whether a concurrent polyneuropathy is present and to determine a long-term prognosis (Fig. 5). Abnormalities in electro diagnostic procedures performed on the thoracic and pelvic limbs may indicate a generalised polyneuropathy. Fibrillation potentials and positive sharp waves are indicative of denervation and occur when lower motor neurons are lost. A decrease in motor neuron conduction velocity is also indicative of lower motor neurons functional impairment. Collection of samples of the crycoarytenoideus dorsalis muscle and muscular branch of the RLN and of the cranial tibial muscle with peroneal nerve can be performed during anaesthesia for laryngeal surgery.

Clinicians should be aware that even though LP could be part of a generalised polyneuropathy, these animals will likely develop the signs of it over the course of 1 year. This should not discourage from performing corrective surgery for the LP. Surgery is therefore warranted, however owners need to be informed of the potential long-term prognosis and the possibility for development of additional, slowly progressive, neuromuscular abnormalities.

 

References


  1. Cook WR. Observation on the upper respiratory tract of the dog and cat. Journal of Small Animal Practice 1964;5:309-329.
  2. Venker-van Haagen AJ, Hartman W & Goedegebuure SA. Spontaneous laryngeal paralysis in young Bouviers.  Journal of the American Animal Hospital Association 1978;14:714-720.
  3. O’Brien JA & Hendrix J. Inherited laryngeal paralysis. Analysis in the husky cross. Veterinary Quarterly 1986;8:301-302.
  4. Polizopoulou ZS, Koutinas AF, Papadopoulos GC & Saridomichelakis MN. Juvenile laryngeal paralysis in three Siberian Husky x Alaskan malamute puppies. Veterinary Record 2003;153:624-627.
  5. Braund KG, Steinberg HS, Shores A, Steiss JE, Metha JR, Toivio-Kinnucan M & Amling KA. Laryngeal paralysis in immature and mature dogs as one sign of a more diffuse polyneuropathy. Journal of the American Veterinary Medical Association 1989;194:1735-1740.
  6. Braund G, Shores A, Cochrane S, Forrester D, Kwiecien JM & Steiss JE. Laryngeal paralysis- polyneuropathy complex in young Dalmatians. American Journal of Veterinary Research 1994;55:534-542.
  7. Mahony OM, Knowles KE, Braund KG, Averill DR & Frimberger AE. Laryngeal paralysis-polyneuropathy complex in young Rottweilers. Journal of Veterinary Internal Medicine 1998;12:330-337.
  8. Ridyard AE, Corcoran BM, Tasker S, Willis R, Welsh, EM, Demetriou JL & Griffith LG. Spontaneous laryngeal paralysis in four white-coated German shepherd dogs. Journal of Small Animal Practice 2000;41:558-651.
  9. Shelton DG, Podell M, Poncelet L, Shatzberg S, Patterson E, Powell HC & Mizisin AP. Inherited polyneuropathy in Leonberger dogs: a mixed or intermediate form of Charcot-Marie-Tooth disease? Muscle & Nerve 2003;27:471-477.
  10. Gabriel A, Poncelet L, Van Ham L, Clercx C, Braund KG, Bhatti S, Detilleux J & Peeters D. Laryngeal paralysis-polyneuropathy complex in young related Pyrenean mountain dogs.  Journal of Small Animal Practice 2006;47:144-149.
  11. Thunberg B & Lantz GC. Evaluation of unilateral arytenoid lateralization for the treatment of laryngeal paralysis in 14 cats. Journal of the American Animal Hospital Association 2010;46:418-424.
  12. Burbidge HM. A review of laryngeal paralysis in dogs. British Veterinary Journal 1995;151:71–82.
  13. MacPhail CM & Monnet E. Outcome of and postoperative complications in dogs undergoing surgical treatment of laryngeal paralysis: 140 cases (1985–1998). Journal of American Veterinary Medical Association 2001;218:1949–1956.
  14. Thieman KM, Krahwinkel DJ, Michael H & Shelton DG. Histopathological confirmation of polyneuropathy in 11 dogs with laryngeal paralysis. Journal of the American Animal hospital Association 2010;46:161-167.
  15. GriffinJG & Krahwinkel DJ. Laryngeal paralysis: pathophysiology, diagnosis and surgical repair. Compendium on Continuing Education for the practicing veterinarians 2005;27:857-868.
  16. StanleyBJ, Hauptman JG, Fritz MC, Rosenstein DS & Kinns J.  Oesophageal dysfunction in dogs with idiopathic laryngeal paralysis: a cohort study. Veterinary Surgery 2010;39:139-149.
  17. Millard RP & Tobias KM. Laryngeal paralysis in dogs. Compendium on Continuing Education for the practicing veterinarians 2009;31:212-219.
  18. Gross ME, Dodam JR, Pope ER & Jones BD. A comparison of thiopental, propofol and diazepam-ketamine anaesthesia for evaluation of laryngeal function in dogs premedicated with butorphanol-glycopyrrolate. Journal of the American Animal Hospital Associaton 2002;38:503-506.
  19. JacksonAM, Tobias KM, Long C, Bartges J & Harvey R. Effects of various anesthetic agents on laryngeal motion during laryngoscopy in normal dogs. Veterinary Surgery 2004;33:102-106.

Vetpedia is translated by a team of expert scientific translators coordinated by Alberto Scalcerle (InterMed - Italian Association Medical Interpreters - coordinator) and Rachel Stenner (MA (Cantab) MB BS (Lon) - lead translator). 
For further information please contact: alberto.scalcerle@alice.it  www.scalcerle.net

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