Laryngeal paralysis in dogs: An update on recent knowledge

Abstract

Laryngeal paralysis is the effect of an inability to abduct the arytenoid cartilages duringinspiration, resulting in respiratory signs consistent with partial airway obstruction. Theaetiology of the disease can be congenital (hereditary laryngeal paralysis or congenitalpolyneuropathy), or acquired (trauma, neoplasia, polyneuropathy, endocrinopathy). Themost common form of acquired laryngeal paralysis (LP) is typically seen in old, large breeddogs and is a clinical manifestation of a generalised peripheral polyneuropathy recentlyreferred to as geriatric onset laryngeal paralysis polyneuropathy. Diagnosing LP based onclinical signs, breed and history has a very high sensitivity (90%) and can be confirmed bylaryngeal inspection. Prognosis after surgical correction depends on the aetiology: traumaticcases have a good prognosis, whereas tumour-induced or polyneuropathy-induced LP has aguarded prognosis. Acquired idiopathic LP is a slow progressive disease, with dogs reachingmedian survival times of 3-5 years after surgical correction.

Full text

Review Arcle
doi:10.4102/jsava.v84i1.909hp://www.jsava.co.za
Laryngeal paralysis in dogs: An update on recent
knowledge
Authors:
Adriaan M. Kitsho1
Bart Van Goethem1
Ludo Stegen1
Peter Vandekerckhove2
Hilde de Rooster1
Aliaons:
1Department of Small
Animal Medicine and Clinical
Biology, University of Ghent,
Belgium
2Veterinary Centre
Malpertuus, Heusden,
Ghent, Belgium
Correspondence to:
Adriaan Kitsho
Email:
adriaan.kitsho@ugent.be
Postal address:
133 Salisbury Avenue,
Merelbeke, Ghent 9820,
Belgium
Dates:
Received: 24 July 2012
Accepted: 18 Dec. 2012
Published: 05 Apr. 2013
How to cite this arcle:
Kitsho, A.M., Van
Goethem, B., Stegen, L.,
Vandekerckhove, P. & De
Rooster, H., 2013, ‘Laryngeal
paralysis in dogs: An update
on recent knowledge’,
Journal of the South African
Veterinary Associaon 84(1),
Art. #909, 9 pages.
hp://dx.doi.org/10.4102/
jsava.v84i1.909
Copyright:
© 2013. The Authors.
Licensee: AOSIS
OpenJournals. This work
is licensed under the
Creave Commons
Aribuon License.
Laryngeal paralysis is the effect of an inability to abduct the arytenoid cartilages during
inspiration, resulting in respiratory signs consistent with partial airway obstruction. The
aetiology of the disease can be congenital (hereditary laryngeal paralysis or congenital
polyneuropathy), or acquired (trauma, neoplasia, polyneuropathy, endocrinopathy). The
most common form of acquired laryngeal paralysis (LP) is typically seen in old, large breed
dogs and is a clinical manifestation of a generalised peripheral polyneuropathy recently
referred to as geriatric onset laryngeal paralysis polyneuropathy. Diagnosing LP based on
clinical signs, breed and history has a very high sensitivity (90%) and can be conrmed by
laryngeal inspection. Prognosis after surgical correction depends on the aetiology: traumatic
cases have a good prognosis, whereas tumour-induced or polyneuropathy-induced LP has a
guarded prognosis. Acquired idiopathic LP is a slow progressive disease, with dogs reaching
median survival times of 3–5 years after surgical correction.
Introducon
It is the authors’ opinion that the incidence of laryngeal paralysis (LP) is higher than commonly
perceived. This is mainly a result of incorrect diagnosis because of a failure to recognise the typical
clinical signs. The authors’ experience has shown that many cases that are correctly diagnosed
are given an improper grave prognosis. New ndings regarding idiopathic LP make the disease
progression and response to therapy easier to comprehend (Stanley et al. 2010). Adaptations of
the surgical techniques and the use of the unilateral arytenoid lateralisation drastically decreased
the associated complications (MacPhail & Monnet 2001; White 1989).
The aim of this article is to sensitise the reader to the clinical signs and treatment options for LP.
An update will also be given on the laryngeal anatomy, aetiology and the diagnosis of LP in dogs.
The most commonly encountered complications are also discussed.
Anatomy
The larynx is a semi-rigid organ composed mainly of hyaline cartilage and muscles (Evans
1993). During inspiration, contraction of the cricoarytenoideus dorsalis (CAD) muscle results in
abduction of the arytenoid cartilages and vocal cords, opening up the glottic lumen and allowing
air to pass freely (Evans 1993). Failure of the CAD muscle to contract will result in narrowing of
the glottic lumen and respiratory stridor (Monnet & Tobias 2012).
The cartilages of the larynx include the epiglottic, arytenoid (paired), sesamoid, inter-arytenoid,
thyroid and cricoid cartilages (Figure 1). The arytenoid cartilages have the most complex
structure. Their irregular shape is the result of the corniculate, cuneiform, muscular and vocal
processes (Evans 1993). The muscular process is situated just lateral to the cricoarytenoid
articulation and acts as an insertion site for the CAD muscle (Evans 1993). The corniculate process
is the longer of the two dorsal processes and forms the dorsal margin of the laryngeal inlet. The
other dorsal process, the cuneiform process, is situated more rostroventrally than the corniculate
process (Evans 1993). The ventral part of this process lies in the aryepiglotic fold forming
most of the lateral boundary of the laryngeal inlet (Evans 1993). The ring shape of the cricoid
cartilage creates a rigid structure that supports the more elastic thyroid and arytenoid cartilages
(Monnet & Tobias 2012).
The thyropharyngeus (TP) muscle is situated on the dorsal and lateral aspect of the larynx
(Hermanson & Evans 1993). This muscle originates on the lateral aspect of the thyroid cartilage
and it extends dorsally to the pharynx to insert on the median plane (Hermanson & Evans 1993).
Contraction of this muscle, together with the cricothyroideus muscle, results in constriction of the
middle pharyngeal area that assists in swallowing and prevents air from entering the oesophagus
(Hermanson & Evans 1993). Opening of the glottis is caused by contraction of the CAD muscle
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(Hermanson & Evans 1993). This muscle originates from the
dorsolateral surface of the cricoid cartilage and inserts on
the muscular process of the arytenoid cartilage (Hermanson
& Evans 1993). Contraction of the muscle results results
in caudodorsal displacement of the arytenoid cartilage
(abduction).
All the intrinsic muscles of the larynx, except the
cricothyroideus muscle, are innervated by the caudal
laryngeal nerve (terminal portion of the recurrent laryngeal
nerve) (Hermanson & Evans 1993). The left recurrent
laryngeal nerve (RLN) arches around the aorta and ascends
on the left side of the trachea, whereas the right RLN arches
around the right subclavian artery and ascends on the right
side of the trachea (Evans & Kitchell 1993). As the recurrent
laryngeal nerves ascend, they give rise to the paralaryngeal
recurrent nerves that run parallel to the RLN (Evans &
Kitchell 1993). The paralaryngeal recurrent nerves supply
sensory innervation to the oesophagus and the trachea
(Evans & Kitchell 1993).
Aeologies and classicaon
Laryngeal paralysis can be congenital or acquired and,
depending on the aetiology, it occurs unilaterally or bilaterally
(Monnet & Tobias 2012; Stanley et al. 2010). A hereditary form
of LP has been described in Siberian huskies and bouviers
des Flandres (O’Brien & Hendriks 1986; Venker-van Haagen
1982). A loss of motor neurons in the nucleus ambiguus as
a result of an autosomal dominant trait, with secondary
Wallerian degeneration of the recurrent laryngeal nerves, has
been identied in the bouvier des Flandres (Parnell 2010).
This disease results in either unilateral or bilateral paralysis
and, generally, presents in dogs less than 12 months of age
(Burbidge 1995; O’Brien & Hendriks 1986; Ridyard et al. 2000;
Venker-van Haagen 1982).
Congenital LP polyneuropathy has been reported in
Rottweilers, bouviers des Flandres, bull terriers, Dalmatians,
German shepherd dogs, Afghan hounds, cocker spaniels,
dachshunds, miniature pinchers and Siberian huskies
(Bennnett & Clarke 1997; Braund 1994; Braund et al. 1994;
Braund et al. 1989; Eger et al. 1998; Harvey & O’Brien 1982;
Mahony et al. 1998; O’Brien & Hendriks 1986; Ridyard et al.
2000; Venker-van Haagen 1982). Clinical signs indicating
the presence of a polyneuropathy can also be present. These
clinical signs include hyporeexia (all four limbs), decreased
postural reactions, hypotonia and appendicular muscle
atrophy (Braund 1994; Braund et al. 1994; Davies & Irwin 2003;
Gabriel et al. 2006; Mahony et al. 1998; Ridyard et al. 2000).
In young Dalmatians and Rottweilers, axonal degeneration
together with loss of myelinated nerve bres of the RLN
and paralaryngeal recurrent nerves are observed (Braund et
al. 1994; Braund et al. 1989; Mahony et al. 1998). Phenotypic
characteristics, such as white coat, freckles and blue eyes,
have been linked to LP in Siberian huskies and German
shepherd dogs (O’Brien & Hendriks 1986; Polizopoulou et al.
2003; Ridyard et al. 2000).
Acquired LP can be caused by trauma to the RLN or
vagus nerves in the cervical or thoracic region (e.g. bite
wounds, surgical trauma, mediastinal tumour) (Monnet
& Tobias 2012). Diseases such as neuropathies, caudal
brainstem disease, endocrine diseases (hypothyroidism and
hypoadrenocorticism), myasthenia gravis, paraneoplastoc
syndromes, idiopathic myositis, systemic lupus
erythematosus and organophosphate toxicity can also result
in LP (Burbidge 1995; Dewey et al. 1997; Kvitko-White et al.
2012; MacPhail & Monnet 2001; Michael 2002; Monnet &
Tobias 2012; White 1989). The term geriatric onset laryngeal
paralysis polyneuropathy (GOLPP) has recently been used to
described the commonly encountered syndrome of acquired
idiopathic laryngeal paralysis (AILP) (Monnet & Tobias
2012; Parnell 2010; Stanley et al. 2010). Strong evidence exists
that this form is a prominent clinical sign of a generalised
peripheral polyneuropathy (Jeffery et al. 2006; Stanley et
al. 2010). It commonly occurs in breeds such as Labrador
retrievers, Rottweilers, Afghan hounds, Irish setters, golden
retrievers, Saint Bernards, Irish setters and standard poodles
(Gaber, Amis & Le Couteur 1985; Monnet & Tobias 2012).
Page 2 of 9
Source: Photographs by M. Doom
Evident in these views are the, (1) stylohyoid, (2) epihyoid, (3) ceratohyoid, (4) basihyoid (5) thyrohyoid, (6) epiglos, (7a) corniculate process of the arytenoid carlage, (7b) cuneiform process of
the arytenoid carlage, (8) thyroid carlage, (9) cricoid carlage and (10) trachea.
FIGURE 1: Embalmed cadaver specimen of a canine larynx, depicted as, (a) rostrodorsal view with the muscles removed, (b) lateral view aer removal of the muscles and
(c) rostrodorsal view with the dorsal aspect of the oesophagus removed.
abc

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Page 3 of 9
In contrast to the congenital form, AILP is typically seen
in middle-aged to older large breed dogs (Burbidge 1995;
Parnell 2010). Male dogs are presented about twice as often
as females (Burbidge, Goulden & Jones 1991; MacPhail &
Monnet 2001; White 1989).
Clinical signs
Dogs with unilateral LP (mostly left-sided) will only display
clinical signs during strenuous activities (i.e. working dogs)
(Monnet & Tobias 2012). Failure to abduct the arytenoid
cartilages during inspiration results in increased resistance
to airow and turbulence through the rima glottidis leads to
the typical inspiratory stridor (Stanley et al. 2010; Venker-van
Haagen 1982). Dysphonia is caused by the inability to tense
the vocal cords, which results in the dog’s voice changing to
a weak, hoarse bark (Parnell 2010). Partial obstruction of the
upper airways by the paralysed arytenoids leads to exercise
intolerance (Burbidge 1995; Parnell 2010).
Respiratory distress (which can lead to cyanosis) can easily be
exacerbated by excitement, exercise, elevated environmental
temperatures, pulmonary oedema or the presence of
bronchopneumonia (Millard & Tobias 2009; Monnet &
Tobias 2012; Parnell 2010). The functional airway obstruction
can also be worsened by secondary laryngeal oedema and
inammation (Harvey & O’Brien 1982; Millard & Tobias
2009). Overweight dogs with LP present with more severe
clinical signs than normally conditioned animals (Broome,
Burbidge & Pfeiffer 2000).
Advanced diagnostics can reveal the presence of concurrent
bronchopneumonia, megaoesophagus, hiatal hernia or
gastro-oesophageal reux (Burnie, Simpson & Corcoran
1989; Stanley et al. 2010). These can lead to excessive
coughing, gagging and regurgitation in affected patients.
In one study, oesophageal motility was decreased in all 32
dogs with AILP (Stanley et al. 2010). This was a result of a
peripheral neuropathy and was more pronounced if a liquid
diet was fed (Stanley et al. 2010). A decrease in oesophageal
motility can be clinically silent (Stanley et al. 2010).
Dysphagia can be a symptom of peripheral polyneuropathy
and can sometimes be seen in patients with LP (Monnet &
Tobias 2012). Congenital LP in dogs is usually the result of
a polyneuropathy complex and presents in dogs less than
12 months of age (Monnet & Tobias 2012). This form of the
disease is characterised by signs of LP together with lenticular
cataracts and neurological signs such as tetraparesis (worse
in the pelvic limbs), hyporeexia in all four limbs, decreased
postural reactions, hypotonia and appendicular muscle
atrophy (Braund 1994; Braund et al. 1994; Davies & Irwin
2003; Gabriel et al. 2006; Mahony et al. 1998; Ridyard et al.
2000). Concurrent diseases, such as megaoesophagus and
aspiration pneumonia, can also be present or can develop
during the course of the disease (Braund 1994; Braund et al.
1994; Mahony et al. 1998; Ridyard et al. 2000).
In 15 dogs with AILP that underwent a full physical
neurological examination in one study, all showed
neurological abnormalities in addition to respiratory-related
problems (Jeffery et al. 2006). These abnormalities included
decreased postural reactions, decits in spinal reexes and
decits in cranial nerve function (Jeffery et al. 2006). Clinical
signs related to the generalised polyneuropathy can be
subtle and care should be taken as they can be overlooked
when dealing with a dyspnoeic dog (Jeffery et al. 2006).
Neurological dysfunction (ataxia) of the hindlimbs in these
older dogs is often misinterpreted as weakness or as an
orthopaedic condition (Jeffery et al. 2006). This generalised
polyneuropathy is a slowly progressive degenerative
condition that affects peripheral nerves (Stanley et al. 2010).
Obvious clinical signs of general polyneuropathy and
dysphagia can take months to years to develop (Jeffery et al.
2006; Stanley et al. 2010).
Diagnosis
Laryngeal paralysis should be suspected in every patient
displaying inspiratory stridor, hoarse voice changes and
exercise intolerance. The inspiratory dyspnoea does not
resolve with open mouth breathing and will worsen with
mild lateral compression over the larynx (Monnet & Tobias
2012).
Clinical signs and signalment are integral parts when
diagnosing LP. Bouviers des Flandres and Siberian huskies
less than 12 months of age with only respiratory problems
are suspected to suffer from hereditary LP (O’Brien &
Hendriks 1986; Venker-van Haagen 1982). Middle-aged dogs
with respiratory problems consistent with LP combined
with neurological dysfunction are suspected of having
congenital LP, which is mostly the result of a peripheral
polyneuropathy (Monnet & Tobias 2012). Older dogs with
exercise intolerance, inspiratory stridor and dysphonia are
suspected of AILP. The signalment, together with the history,
has a specicity of 91.6% and a sensitivity of 98.5% in all dogs
with grade 3 and 4 laryngeal paralysis (Broome et al. 2000).
Laryngeal inspection is essential in order to rule out other
causes of laryngeal stridor (e.g. laryngeal tumour) and
conrm the suspected diagnosis of LP (Broome et al. 2000).
Direct visualisation of the larynx can be achieved via
transnasal or peroral laryngoscopy. As the latter has a 95%
interobserver agreement, it is considered the gold standard
of diagnosis (Broome et al. 2000; Radlinsky et al. 2009; Smith
2000). Transnasal laryngoscopy has the advantage that it
can be performed in large breed dogs using only sedation
and local anaesthesia (Radlinsky, Mason & Hodgson
2004).
Prior to laryngeal examination, an intravenous catheter is
placed and the dog is preoxygenated for at least 3–5 min
(Millard & Tobias 2009; Smith 2000). The dog is placed
in sternal recumbency and the head is held in a normal
anatomic position (Gross et al. 2002; Jackson et al. 2004; Smith
2000). To prevent a false positive diagnosis, only a light
plane of anaesthesia is maintained (Gross et al. 2002; Jackson

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et al. 2004; Monnet & Tobias 2012; Smith 2000). The aim is
to achieve relaxation of the jaw muscles without affecting
the laryngeal reexes or depressing respiratory movements
(Burbidge 1995). Anaesthetic protocols such as diazepam–
ketamine combination are avoided because they result in
suboptimal laryngeal exposure during laryngoscopy as a
result of poor muscle relaxation (Gross et al. 2002). When drug
combinations of acepromazine–propofol, acepromazine–
thiopental or diazepam–ketamine were used, half of the
normal dogs in one study failed to show arytenoid abduction
during inspiration (false positive diagnosis) (Jackson et al.
2004). The same study concluded that intravenous thiopental
as a sole drug was best for maintaining laryngeal function
(Jackson et al. 2004). Although respiratory depression results
when using thiopental as induction agent, a very light plane
of anaesthesia results in tachypnea, which is ideal to evaluate
the larynx (Turner & Ilkiw 1990). Patients suspected of
LP should be examined until they almost reach a plane of
consciousness (Burbidge 1995). When laryngeal inspection is
not conclusive, doxapram HCl (1.1 mg/kg), which induces
deep inspiratory movements, can be useful to differentiate
normal dogs from dogs with LP (Tobias, Jackson & Harvey
2004). The increased velocity of airow, however, will result
in an increase in the negative airway pressure, which results
in paradoxical arytenoid movement that can lead to complete
laryngeal obstruction (Tobias et al. 2004).
Laryngeal inspection involves the evaluation of the arytenoid
cartilages for active abduction during inspiration and passive
adduction during expiration (Monnet & Tobias 2012).
Immobile arytenoids and vocal cords in an appropriately
anesthetised dog indicate bilateral LP, whereas asymmetrical
motion of the arytenoids is indicative of unilateral disease
(Monnet & Tobias 2012). To avoid false negative diagnoses of
LP in patients with paradoxical movement of the arytenoids,
it is helpful if an assistant indicates the inspiration phase
to the clinician who is performing the laryngeal inspection.
Paradoxical movement in LP patients occurs when the
increased negative airway pressure during inspiration
results in adduction of the arytenoids and, subsequently, the
positive pressure during expiration results in passive return
of the arytenoids to their resting position (Burbidge 1995).
This is encountered in up to 45% of dogs with LP (Olivieri,
Voghera & Fossum 2009). Excessive negative pressure can
lead to secondary elongation of the soft palate and eversion of
the laryngeal saccules (Millard & Tobias 2009). The constant
rubbing of the arytenoid cartilages against each other can
result in mucosal ulcerations and oedema at the level of the
corniculate processes (Monnet & Tobias 2012).
Other diagnostic methods, such as sound signature
identication, tidal breathing ow-volume loops,
electromyography, blood gas analysis and plethysomography,
can assist in conrming the diagnosis of LP (Amis &
Kurpershoek 1986; Bedenice et al. 2006; Burbidge 1995; Yeon
et al. 2005). Echolaryngography has been studied but proved
less sensitive for diagnosing LP than direct visualisation
(Radlinsky et al. 2009; Rudorf, Barr & Lane 2001).
Thoracic radiographs should be taken in all dogs suspected of
LP in order to assist in the diagnosis of underlying diseases,
such as cervical and cranial mediastinal masses, and to identify
other pathologies such as megaoesophagus, aspiration
pneumonia and noncardiogenic lung oedema (Monnet
& Tobias 2012). In dogs suspected of a megaoesophagus,
positive contrast oesophograms could conrm the diagnosis;
although, this is not performed routinely because of the
increased risk of aspiration (Millard & Tobias 2009). In
patients with conrmed laryngeal paralysis, 7% – 14% are
subsequently diagnosed with hypothyroidism (Asulp et al.
1997; Dixon, Reid & Mooney 1999; Jaggy et al. 1994; White
1989; Zikes & McCarthy 2012). In dogs showing clinical signs
of weakness, megaoesophagus, other peripheral or central
neurological signs, exercise intolerance, dermatological
abnormalities (hyperpigmentation, alopecia, poor coat
quality and pyoderma), lethargy or obesity, free thyroxine
and thyroid-stimulating hormone should be tested (Jaggy et
al. 1994; Jeffery et al. 2006).
Myasthenia gravis is infrequently associated with LP
(Jeffery et al. 2006). In dogs with LP presenting with clinical
signs of regurgitation (megaoesophagus), dysphagia,
multiple cranial nerve abnormalities, generalised or
focal neuromuscular weakness or exercise intolerances,
acetylcholine receptor antibody titres need to be measured
to rule in or out myasthenia gravis (Shelton 2002). Acquired
myasthenia gravis can be associated with hypothyroidism
or hypoadrenocorticism, or present as paraneoplastic
syndrome associated with thymomas, osteogenic sarcoma,
cholangiocellular carcinoma and cutaneous lymphoma
(Shelton 2002). An attempt should be made to rule out these
primary conditions when a diagnosis of myasthenia gravis
has been made.
Medical treatment of respiratory
distress
Patients with LP can present in acute respiratory distress,
resulting in cyanosis and hyperthermia (Burbidge 1995).
Emergency treatment is essential and consists of oxygen
supplementation, administration of a sedative and cooling of
the patient (Burbidge 1995; Millard & Tobias 2009). The route
of oxygen supplementation depends on what is tolerated by
the patient and can include an oxygen cage, ow-by oxygen,
an oxygen hood, a facemask or a nasal cannula (Mazzaferro
2009). If cyanosis, dyspnoea and hypoxia (SPO2 < 95%) persist
despite oxygen supplementation, a temporary tracheostomy
or temporary intubation under light anaesthesia should be
considered until laryngeal swelling decreases or surgical
correction can be performed (Millard & Tobias 2009).
Temporary intubation is selected if the time of intubation is
expected to be just a couple of hours, whereas tracheostomy
tubes are used for longer-term management (Millard &
Tobias 2009). Fluids are administered with caution as
pulmonary oedema can develop in animals with severe
upper respiratory tract obstruction (Monnet & Tobias 2012).
Sedation using acepromazine (0.005 mg/kg – 0.020 mg/kg)

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and butorphanol (0.200 mg/kg – 0.400 mg/kg) has been
recommended (Millard & Tobias 2009). Additionally,
short-acting corticosteroids, such as dexamethasone
(0.100 mg/kg – 0.500 mg/kg) or prednisolone sodium succinate
(0.200 mg/kg – 0.400 mg/kg), can be administered in the case
of laryngeal oedema (Millard & Tobias 2009). Hyperthermia
should be differentiated from true pyrexia that can occur as
a result of aspiration pneumonia. Temperatures lower than
41.0 °C are not life threatening unless prolonged and therapy
to cool patients should only be instituted if temperatures are
elevated above this level (Mazzaferro 2009; Millard & Tobias
2009). Cooling can be achieved by clipping the fur, by wetting
the animal, by applying ice packs over well-vascularised
regions (neck, axilla and inguinal region), by fanning the
wetted patient or by the rectal administration of cool isotonic
uids (Mazzaferro 2009). Continuous monitoring of the
temperature is important and cooling procedures should
be discontinued as soon as the body temperature reaches
39.4 °C to prevent iatrogenic hypothermia (Mazzaferro 2009).
Conservative management of LP can be considered in older
patients with minimal to moderate clinical signs. This involves
anti-inammatory drugs to decrease laryngeal swelling and
a weight loss programme for overweight patients (MacPhail
& Monnet 2008). The owners should also be educated on the
changes in the patient’s routine and environment. A cool
area should be prepared for the patient, especially in the
warmer months of the year. Patients should not be allowed
to perform strenuous exercise. Short walks using a harness
can be permitted during the cooler periods of the day.
Surgical treatment by cricoarytenoid
carlage lateralisaon
Surgical management is advised in all LP patients with
severe clinical signs (MacPhail & Monnet 2008; Monnet
& Tobias 2012). The aim of surgery is to increase the size
of the rima glottidis (LaHue 1989; Millard & Tobias 2009;
Monnet & Tobias 2012). As resistance of airow is inversely
proportional to the radius to the power of four, according
to Poiseuille’s law, even a small increase in size will make a
substantial difference (Monnet & Tobias 2012).
Many surgical techniques have been developed and
successfully applied. They can be classied as intra-
laryngeal or extra-laryngeal procedures (Figures 2 and 3).
Cricoarytenoid cartilage lateralisation is currently considered
the procedure of choice (Monnet & Tobias 2012). The
objective of this procedure is to prevent passive adduction
of the arytenoid cartilage during inspiration by xing it
to a neutral to slightly lateralised position (low tension
technique) (Bureau & Monnet 2002). This modication still
allows adequate epiglottic coverage of the rima glottidis
during swallowing and is believed to reduce aspiration-
related complications (Bureau & Monnet 2002).
Unilateral cricoarytenoid lateralisation (UCAL) is performed
via a lateral approach (LaHue 1989; Monnet & Tobias
2012). Dogs with unilateral LP are corrected depending on
the affected side, whilst dogs with bilateral LP have the
lateralisation procedure on the left side if the surgeon is right-
handed (MacPhail & Monnet 2001; Monnet & Tobias 2012).
Unilateral correction is sufcient to relieve clinical signs in
most bilaterally affected dogs (Monnet & Tobias 2012).
Placing a sandbag under the neck elevates the laryngeal
region and the skin incision is made over the larynx, just
ventral to the jugular vein (Monnet & Tobias 2012). A
combination of blunt and sharp dissection through the
subcutaneous muscles (platysma and supercial sphincter
colli muscles) and subcutaneous tissue exposes the TP
muscle. This is then incised at the dorsocaudal rim of the
lamina of the thyroid cartilage, avoiding penetration of the
laryngeal mucosa. Alternatively, the TP muscle can be split
along the direction of its muscle bres (Nelissen & White
2011). Cricothyroid disarticulation may be performed in
the adult dog when additional exposure is required. As an
alternative, a stay suture can be placed through the lamina of
the thyroid cartilage to achieve atraumatic lateral retraction.
The muscular process of the arytenoid cartilage is usually
prominent and easily palpable because of the neurogenic
atrophy of the CAD muscle (Grifn & Krahwinkel 2005). A
transverse incision is made through the CAD muscle and
dissection is continued carefully until the cricoarytenoid
articulation is visible (Monnet & Tobias 2012). The cranial
FIGURE 3: Schemac diagram indicang the dierent extra-laryngeal surgical
procedures in dogs with laryngeal paralysis.
Extra-laryngeal
Arytenoid
lateralisaon
Cricoarytenoid
lateralisaon
Thyroarytenoid
lateralisaon
Cricothyroarytenoid
lateralisaon
Neuromuscular
pedicle gras
Nerve anastomosis
Reinnnervaon
FIGURE 2: Schemac diagram indicang the dierent intra-laryngeal surgical
procedures in dogs with laryngeal paralysis.
Intra-laryngeal
Paral
laryngectomy
Implant
augmentaon
Castellated
laryngossure
With
ventriculocordectomy
Without
ventriculocordectomy
With
ventriculocordectomy
Without
ventriculocordectomy

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part of the joint capsule is left intact during dissection of
the cricoarytenoid joint (Bureau & Monnet 2002). A non-
absorbable monolament suture (e.g. polypropylene) on a
tapercut needle is recommended for xing the arytenoid.
Depending on the size of the dog, USP 2/0 (< 40 kg) or USP
0 (> 40 kg) is used (Demetriou & Kirby 2003). The suture
is anchored dorsally on the caudal border of the cricoid
cartilage, taking care not to penetrate the laryngeal lumen. It is
recommended that extubation be attempted after performing
this step as inadvertent suturing of the endotracheal tube
can occur (Weinstein & Weisman 2010). The needle is then
passed through the muscular process of the arytenoid in a
medial-to-lateral direction (Monnet & Tobias 2012). Older
dogs can have brittle laryngeal cartilages that can tear during
suture placement (Monnet & Tobias 2012). For this reason,
needle selection is very important to decrease the risk of
tearing or even fracturing of the cartilage once the suture is
tightened. Some authors advise pre-drilling a small hole in
the arytenoid cartilage using an 18-gauge hypodermic needle
before needle placement (Monnet & Tobias 2012).
The suture is carefully tied until resistance from the tensed
remaining part of the joint capsule is felt (Bureau & Monnet
2002). Alternatively, the suture can be tied under direct visual
endoscopic control after temporary extubation (Weinstein &
Weisman 2010). Adequate abduction is dened as any degree
of abduction resulting in an increase in the glottic diameter
without axial displacement of the dependant (non-surgically
treated) side (Weinstein & Weisman 2010) (Figure 4).
Meticulous apposition of the TP muscle, using a continuous
suture pattern with monolament absorbable suture material
is essential to decrease the chance for postoperative dysphagia
(Nelissen & White 2011). The subcutaneous tissues are closed
in two layers and the skin is closed routinely.
Postoperative complications occur in 10% – 58% of dogs
(Gaber et al. 1985; Hammel, Hottinger & Novo 2006; MacPhail
& Monnet 2001; Snelling & Edwards 2003). These include
gagging or coughing, aspiration pneumonia, recurrence of
clinical signs (caused by implant failure or cartilage tearing),
residual stridor, respiratory distress, gastric dilatation
volvulus, seroma or haematoma formation, and death (Millard
& Tobias 2009; Monnet & Tobias 2012). It should be kept in
mind that dogs carry a lifelong risk for the development of
respiratory tract complications postoperatively (MacPhail &
Monnet 2001). Aspiration pneumonia is the most frequently
noted complication, occurring in about 8% – 24% of dogs
postoperatively (Demetriou & Kirby 2003; Hammel et al. 2006;
MacPhail & Monnet 2001; Snelling & Edwards 2003; White
1989). Low-tension techniques are believed to decrease the
incidence of postoperative aspiration pneumonia (Bureau &
Monnet 2002).
About 5% of patients require a contralateral procedure because
of arytenoid fragmentation, avulsion of the lateralisation
suture or inadequate lateralisation (White 1989). Recurrence
of clinical signs postoperatively is seen more commonly in
small breed dogs (Snelling & Edwards 2003). Complications
during the postoperative period can be minimised by sound
knowledge of the anatomy, meticulous tissue handling and
avoidance of laryngeal lumen penetration (Monnet & Tobias
2012). Factors that negatively inuence the surgical outcome
include age, concurrent respiratory tract abnormalities,
oesophageal disease, neurological disease or neoplastic
disease and the placement of a temporary tracheostomy
tube (MacPhail & Monnet 2001). Unilateral cricoarytenoid
lateralisation has a good clinical outcome, with 88% – 90% of
dogs showing an improved quality of life in the postoperative
period (Hammel et al. 2006; Snelling & Edwards 2003).
Variations of this technique exist in which the arytenoid is
also xed to the thyroid (cricothyroarytenoid lateralisation)
or solely to the thyroid (thyroarytenoid lateralisation)
(Monnet & Tobias 2012). The latter technique results in a
less extensive (but satisfactory) opening of the rima glottidis
when compared to cricoarytenoid lateralisation and takes
less time to perform (Grifths, Sullivan & Reid 2001). The
clinical outcomes of UCAL and thyroarytenoid lateralisation
compare well (Grifths et al. 2001).
Other surgical techniques
Permanent tracheostomy creates a bypass of the larynx
(Monnet & Tobias 2012). It is considered in patients that are
Source: Photographs by B. Van Goethem
FIGURE 4: Laryngeal inspecon in a 10-year-old Maltese dog with laryngeal
paralysis, depicng, (a) preoperave appearance and (b) le arytenoid
abducon aer unilateral arytenoid lateralisaon.
a
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at risk for postoperative aspiration pneumonia. This includes
patients with generalised myopathy, megaoesophagus,
hiatal hernia and gastrointestinal disorders (Monnet &
Tobias 2012).
Partial laryngectomy (Figure 5) is an older technique
involving removal of the vocal cords and a substantial
part of the corniculate and vocal processes (unilateral or
bilateral) in order to ensure unobstructed airow without
inuencing the protective effect on the airway (Harvey
1983a, 1983b). This procedure can result in signicant
postoperative swelling that might necessitate placement
of a temporary tracheostomy tube. Complications are seen
in approximately 50% of the dogs and include persistent
upper respiratory stridor, coughing, vomiting, aspiration
pneumonia, laryngeal webbing and exercise intolerance
(Harvey 1983a; Harvey & O’Brien 1982; MacPhail & Monnet
2001; Ross et al. 1991) (Table 1). This abandoned technique
has recently regained popularity since the introduction of
diode laser arytenoidectomy via transoral approach. No
direct postoperative complications were reported in 20 dogs
and only 10% developed aspiration pneumonia in the long
term (Olivieri et al. 2009).
A recent retrospective study on ventriculocordectomy via
ventral laryngotomy has shown some promising results with
limited short-term and long-term complications. The authors
of this article concluded that because of the ease of the
procedure, the limited complications and minimal surgical
trauma, this technique should be considered for routine use
(Zikes & McCarthy 2012).
Castellated laryngossure is another historical procedure
that creates an enlargement of the ventral laryngeal ostium by
offset closure of a castellated incision on the ventral aspect of
the thyroid cartilage (Figure 6). This procedure is technically
difcult, results in severe postoperative laryngeal oedema
and requires the placement of a temporary tracheostomy
tube for 2–3 days postoperatively (Monnet & Tobias 2012).
Variable results have been obtained and the procedure was
abandoned (Burbidge et al. 1991).
Reinnervation techniques and neuromuscular pedicle grafts
have been used in dogs to restore the abductor function in
experimentally denervated patients (Greeneld et al. 1988;
Paniello, West & Lee 2001; Rice 1982). These techniques might
be of use in patients with acquired LP of traumatic origin. It
is likely to be ineffective in patients with polyneuropathy or
polymyopathy as a primary cause (Monnet & Tobias 2012).
Its routine use is also questioned as it takes a minimum of
5 months for restoration of laryngeal function (Greeneld
et al. 1988).
Laryngeal augmentation with implantable devices has been
reported ex vivo (Cabano et al. 2011) and in vivo (Kwon et al.
2007) in canine patients. No extensive clinical data exist for
the current devices and hence their use can currently not be
recommended.
TABLE 1: Surgical treatment methods with their reported percentages of improvement, aspiraon pneumonia, minor complicaons (persistent stridor, coughing, gagging,
panng, seroma formaon, exercise intoler ance or voming), webbing and mortality rate.
Treatment method Improvement
(%)
Aspiraon pneumonia
(%)
Minor complicaons
(%)
Webbing
(%)
Mortality
(%)
Unilateral arytenoid lateralisaon1,2,3,4,5 90 10–28 9–56 - 0–14
Bilateral arytenoid lateralisaon6,4 - 11–89 - - 67
Bilateral arytenoid lateralisaon with ventriculocordectomy788 15 30 - 0
Castellated laryngossure with ventriculocordectomy6100 - 40 40 -
Paral laryngectomy, transoral approach with or without
ventriculocordectomy4,8,9
88–90 6–33 44 8–14 30
Paral laryngectomy, transoral approach – diode laser10 100 10 - 0 -
Ventriculocordectomy, transoral approach11,12 83 15 40–73 13 -
Ventriculocordectomy, ventral approach13 93 3 6 0 -
1, Demetriou and Kirby (2003); 2, Griths et al. (2001); 3, Hammel et al. (2006); 4, MacPhail and Monnet (2001); 5, White (1989); 6, Burbridge et al. (1998); 7, Schoeld et al. (2007); 8, Ross et al.
(1991); 9, Trout et al. (1994); 10, Olivieri et al. (2009); 11, Asulp et al. (1997); 12, Holt and Harvey (1994); 13, Zikes and McCarthy (2012).
For more informaon on these sources, please see the full reference list of the arcle, Kitsho, A.M., Van Goethem, B., Stegen, L., Vandekerckhove, P. & De Rooster, H., 2013, ‘Laryngeal paralysis
in dogs: An update on recent knowledge’, Journal of the South African Veterinary Associaon 84(1), Art. #909, 9 pages. hp://dx.doi.org/10.4102/jsava.v84i1.909
Source: Photograph by M. Doom
FIGURE 5: Schemac presentaon of unilateral paral laryngectomy on an
embalmed cadaver specimen of the canine larynx, indicang the area of the
arytenoid carlage to be removed in blue (1) and the locaon of the vocal fold
in red (2).
1
2

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Postoperave care
After surgical treatment, partial obstruction of the larynx
will be relieved and the respiratory dyspnoea will resolve
immediately. Oxygen therapy should be administered
as necessary and perioperative dexamethasone sodium
phosphate (0.1 mg/kg – 1.0 mg/kg) can be helpful to decrease
laryngeal swelling and oedema (Monnet & Tobias 2012). Food
and water is withheld until 12 h after the operation. Heavy
sedation in the postoperative period is avoided to preserve
the swallowing reexes (Monnet & Tobias 2012). The patient
is rst offered canned food rolled into balls (Monnet & Tobias
2012). If no coughing or gagging is observed, small amounts
of water can be offered (Monnet & Tobias 2012). The decision
to administer postoperative antibiotic is usually case based.
Prognosis and conclusion
A clear distinction needs to be made between the different
forms of the disease. Prognosis for hereditary LP is excellent
as dogs are cured by surgery. Congenital LP neuropathy
has a poor prognosis and most dogs tend to be euthanased
within 10 weeks as a result of worsening clinical signs
(Davies & Irwin 2003). The prognosis for acquired LP will
vary depending on the cause: trauma cases can be cured;
neoplasia-induced LP will depend on the tumour type.
Evidence strongly suggests that the most common form of
LP in dogs is, in fact, an early stage of GOLPP (Stanley et al.
2010). Even though all complications should be considered
when making a prognosis in any dog developing LP as a
component of polyneuropathy, this condition progresses
slowly, making short-term prognosis more favourable.
Acknowledgements
The authors would like to the Department of Morphology
at the Faculty of Veterinary Medicine, Ghent University for
supplying the embalmed canine larynxes for the photographs
shown in Figures 1 and 5.
Compeng interests
The authors declare that they have no nancial or personal
relationships which may have inappropriately inuenced
them in writing this article.
Authors’ contribuons
A.M.K. (University of Ghent) wrote the manuscript.
H.d.R. (University of Ghent), B.v.G. (University of Ghent),
L.S. (University of Ghent) and P.V. (Veterinary Centre
Malpertuus) made conceptual contributions.
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