Joe Palamara, DVM, DACVS-SA
Description: Dyspnea is defined as difficulty/labored breathing or shortness of breath, and can be a sign of serious disease of the airway, lungs or heart. This lecture will review the process of diagnosing, stabilizing and further localizing dyspnea in dogs. We will discuss recommendations for surgical correction of components of Brachycephalic Airway Syndrome, as well as salvage procedure for Laryngeal paralysis. With appropriate management, the prognosis for these conditions is generally favorable depending on the degree of severity.
Learning Objectives
- Recognize the clinical signs, associated physiology, and diagnosis related to each condition
- Initial stabilization for patients presenting in airway crisis
- Understand the medical and surgical options for each condition
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Part 1. Review dyspnea of the upper airway
Part 2. Examination of the upper airway
Part 3. Brachycephalic obstructive airway syndrome
Part 4. Laryngeal paralysis
OBJECTIVES
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Definition
Difficulty or labored breathing
Clinical Signs
Tachypnea (increased rate of respiration)
Hyperpnea (increased depth of respiration +/- accompanied by increase in rate)
Hyperventilation
Panting
DYSPNEA
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Respiration
Controlled under normal conditions
by arterial CO2 (PaCO2)
PaCO2 is kept under tight control (+ 3mmHg)
Triggers of respiratory distress
Hypoxemia (PaO2 <50-60 mmHg)
Hypercapnia/hypercarbia (PaCO2 >50 mmHg)
DYSPNEA
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*Similarities
Both involve turbulence of airflow in the respiratory tract
Stertor
Respiratory sound characterized by snoring or gasping upon inspiration
Site--Nasopharyngeal, Palatal
Stridor
Respiratory sound, usually high pitched, generated by the larynx during inspiration
Site--Laryngeal
STERTOR VERSUS STRIDOR
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ANATOMY OF THE RESPIRATORY SYSTEM
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1. Posterior nares
2. Pharynx
3. Larynx
4. Trachea
5. Right lung
6. Heart
7. Diaphragm
8. Esophagus
9. Termination of the trachea
Upper Airway
Lower Airway
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Respiration versus deglutition
Protection of the airway
by the epiglottis
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“CROSSROADS”
LUNGS NOSE
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Identify respiratory distress
Stabilize the patient
Determine anatomical origin
of respiratory distress
PATIENT ASSESSMENT
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PATIENT ASSESSMENT
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Objectives of retrospective study
Determine the most frequent underlying diseases in dogs
presenting with dyspnea
Determine if signalment, nature, and duration of clinical signs
might help in assessment of the possible underlying condition and
prognosis
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Groups 1-5
Group 1 Upper airway disease
BOAS, laryngeal paralysis, tracheal collapse, neoplasia
Group 2 Lower respiratory tract
Pulmonary parenchymal disease (inflammatory, infectious, neoplasia), noncardiogenic pulmonary edema, bronchial disease, PTE,
DIC, ARDS, coagulopathies
Group 3 Pleural space disease
Pleural effusion (idiopathic, secondary to systemic disease or lung lobe torsion, and neoplasia), pneumothorax, pyothorax,
neoplasia (thymoma, thymic, ectopic thyroid carcinoma), and PPDH
Group 4 Cardiac disease
Acquired and congenital cardiac diseases casing pulmonary edema, pleural effusion, or both and pericardial effusion Iidiopathic
and neoplasia) associated with pleural effusion
Group 5 Obesity or Stress
NO underlying disease detected
BCS > 7/9
PATIENT ASSESSMENT
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Incidence
# of patients = 1.7% (229/13293) of patients presented to ER 2o to dyspnea
Localization
Most frequent underlying diseases in dogs presenting with dyspnea
• Lower airway (33%) Pleural space disease (19%)
• Upper airway (32%) Cardiac disease (12%)
Obesity and stress (4%)
INCIDENCE AND ANATOMIC SITES
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65% occurred at lower or upper airway
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Most frequent underlying diseases in dogs presenting w dyspnea
DISTRIBUTION / ETIOLOGY
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Breeds of Upper airway disease patients
BOAS
72% of patients were Bulldogs, Pugs, CKCS
Laryngeal paralysis
55% of patients were Mixed breeds, Labs, English Bulldogs
Tracheal collapse
70% of patients were Yorkies, Toy Poodles
BREED PREDISPOSITION
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Distribution of ages and breeds in study
All dyspneic dogs in the study (median age, 6 yrs)
Bulldogs were significantly younger
(median age, < 2 years)
Mixed-breed dogs, Golden Retrievers were significantly older
(median age, > 8 years)
SIGNALMENT
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Medical versus surgical management
Duration of signs in dogs requiring surgical management
(median, 42 days)
Duration of signs in dogs requiring medical management
(median, 7 days)
DURATION OF SIGNS / TREATMENT
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BOAS – 31% (12/39) were emergent
79.5% (31/39) had surgery 84.6% (33/39) survived
Laryngeal paralysis – 64% (14/22) were emergent
82% (18/22) had surgery 77% (17/22) survived
SURGICAL MANAGEMENT /
UPPER AIRWAY PATIENTS
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A greater proportion of dogs 82% (62/76) that underwent
surgical management were discharged than those receiving
medical treatment 48% (74/153)
Survival of all patients in the study with dyspnea 60% (135/229)
PROGNOSIS FOR SURGICAL PATIENTS
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Breed conformational causes of dyspnea
Easily identifiable
Brachycephalic breed
Younger age
Less emergent cases / most stable
Longer duration of clinical signs
Better outcome versus other causes of dyspnea
Surgery significantly improved outcome
SUMMARY OF UPPER AIRWAY PATIENTS
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Lung parenchyma
Cardiac
Systemic causes
Breed conformational changes
Airway obstruction
Pleural space diseases
-------- Surgical --------
-------- Medical --------
DYSPNEA
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Please be alert to:
Acute decompensation (i.e. in a stressful
situation) and emergency examination of a
previously stable patient is possible and should
not be underestimated
SUMMARY OF UPPER AIRWAY PATIENTS
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Pre-oxygenation x 5-10 minutes
IV catheterization (cephalic)
All materials prepared and setup
Laryngoscope, various ET tube sizes,
muzzle gauze, tongue depressor
Medications…?
PROTOCOL
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Premed?
Sedative/Induction?
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Evaluation of the arytenoid movement
The ideal anesthetic protocol = maintain intact laryngeal
reflexes while achieving an anesthetic depth sufficient to allow
for jaw relaxation
Challenge = even light anesthesia may result in apnea or shallow
inspirations, confounding an accurate diagnosis
GOAL OF LARYNGEAL EXAM
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Options
Propofol to effect (~6-7ml/kg)
Alfaxalone to effect (~2mg/kg)
+/- Butorphanol + Acepromazine premedications
What’s best?
SEDATION PROTOCOLS
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SEDATION PROTOCOLS
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Doxapram (Dopram)
Central nervous stimulant that transiently increases respiratory rate and tidal volume
by increasing electrical activity in the inspiratory and expiratory centers of the
medulla
May also stimulate respiration by reflex activation of carotid and aortic
chemoreceptors (Plumb 2002).
Administration normal dogs results
Increased respiratory effort and depth, and intrinsic laryngeal motion
Administration to dog with laryngeal paralysis
Vigorous, paradoxical motion of the arytenoids due to inward motion of the weakened arytenoids
Be prepared to intubate
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Arytenoid motion can be
reliably detected before
doxapram in approximately
50% of dogs, and that the
other 50% will show
definitive arytenoid motion
after doxapram
administration.
Neither propofol nor
alfaxalone alone result in
reliable arytenoid motion
either before or after
doxapram
SEDATION PROTOCOLS
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• Acepromazine
• 0.03 mg/kg
• Butorphanol
• 0.2 mg/kg
PreMed
• Alfaxalone
• 2 mg/kg
• Propofol
• 6 ml/kg
Sedation /
Induction
• Doxapram
• 0.25 mg/kg
Respiratory
Stimulant
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Pre-oxygenate
+/- Premedication
Acepromazine 0.01 mg/kg +/- Butorphanol 0.2 mg/kg IV
Sedation/Induction
Propofol 6-7 ml/kg IV OR Alfaxalone 2 mg/kg IV
Respiratory Stimulant
Doxapram 0.25-1 mg/kg IV = 15-30 seconds of increased respiratory drive
MY CURRENT PLAN
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Assess pharyngeal structures
Palate
Soft palate
Normal length should NOT interfere
with the movement of the epiglottis
Pharynx
Tonsils
Epiglottis
PHARYNGEAL EXAM
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BRACHYCEPHALIC OBSTRUCTIVE AIRWAY SYNDROME
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“Calvin” Palamara
3.5 yr MN French Bulldog
Fall 2018 =
Cyanosis, exercise intolerance
Rhinoplasty, Staphylectomy, Sacculectomy
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2015 AKC
7 of top 25 breeds are brachycephalic
#4 Bulldogs
#6 French bulldogs
#10 Boxers
#18 Cavalier King Charles Spaniel
#19 Shih Tzu
#21 Pomeranian
#22 Boston Terrier
WHY IS BRACHYCEPHALIC DISEASE IMPORTANT?
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UK Kennel Club registrations
Between 2002 and 2013
Pug – 730% increase
French Bulldog – 2,708% increase
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(1) Nares and Nasal Cavity
Stenotic nares
Nasopharyngeal turbinates, incl mucosal contact points
(2) Palate and Larynx
Soft palate elongation and hyperplasia
Everted laryngeal saccules
Laryngeal collapse
COMPONENTS TO BE DISCUSSED
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Normal physiology of the nares
Nose and nasal cavity = contributes ~75% of the total airway resistance during normal
inspiration
Larynx = ~5% Bronchi and bronchiole = ~20%
Primary abnormal anatomy – stenotic nares, abnormal nasal turbinates
Nasal stenosis leads to stertorous breathing (need for increased negative pressure =
increased labored breathing distal to the resistance)
Build up of negative pressure draws soft tissues into the airway lumen, making them
hyperplastic
Elongated soft palate projects into the larynx causing stridor
Excessive, repetitive extreme negative pressure can lead to secondary airway collapse
Inspiratory and expiratory muscle work generates substantial heat precipitating
hyperthermia and heat stroke
BOAS PATHOPHYSIOLOGY
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Other disorders:
Sleep apnea
Cyanosis and syncope
Clinical sign onset
Often severe by 12 months of age
BOAS PATHOPHYSIOLOGY
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Fasanella et al JAVMA 2010. Components of brachycephalic
airway obstructive syndrome (BAOS).
Retrospective study
Goal: report the prevalence of BAOS in dogs (without narrow
case selection), incl everted tonsils*
PREVALENCE OF
ANATOMIC COMPONENTS OF BOAS
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PREVALENCE OF BREEDS WITH COMPONENTS OF BOAS
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English
Bulldogs, 62%
Pugs, 21%
Boston Terriers,
9%
Breeds
English Bulldogs Pugs Boston Terriers French Bulldogs Other
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PREVALENCE OF ANATOMIC COMPONENTS OF BOAS
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Elongated Soft Palate, 94%
Stenotic Nares, 77%
Everted Laryngeal Saccules, 66%
Everted Tonsils, 56%
Elongated Soft Palate
Stenotic Nares
Everted Laryngeal Saccules
Everted Tonsils
0% 20% 40% 60% 80% 100%
Components of BAOS
Percentage of Patients
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Other findings:
Most patients had 3 or 4 components of BAOS
Most common combination = stenotic nares, elongated soft palate,
everted laryngeal saccules, everted tonsils
Comorbidities:
72% of patients had stenotic nares and everted laryngeal saccules
66% of patients had everted saccules and everted tonsils
Corrective surgery post-operative complications = 12% (10/83)
PREVALENCE OF ANATOMIC COMPONENTS OF BOAS
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Skull Conformation
Shorter and wider skull = compressed nasal passages and altered pharyngeal anatomy
(1) NARES AND NASAL CAVITY
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Anatomy
Normal: Free end of the dorsal
lateral cartilage (thick and
vascular) merges with the rostral
extremity of the ventral nasal
conchae
Alar folds: bulbous portion of
the ventral nasal conchae
Brachycephalics: short and thick
alar folds, collapse inward leading
to subsequent stenosis secondary
to cartilaginous or muscular
weakness
NARES
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Physical exam findings:
Varying degrees of obstruction of the nasal vestibule
Surgery is recommended due to development of airway secondary effects
STENOTIC NARES
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4 Severe stenosis 3 Moderate stenosis 2 Mild stenosis 1 Normal
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Stenotic Nares
First reported by
Harvey et al JAAHA 1982.
Rhinoplasty – various techniques
SURGERY: STENOTIC NARES
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Before After
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Stenotic Nares:
Rhinoplasty – various techniques
Trader’s technique
(amputation of the dorsal nasal cartilage)
SURGERY: STENOTIC NARES
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Stenotic Nares
Rhinoplasty – various techniques
Trader’s technique (amputation of the
dorsolateral nasal cartilage)
Vertical, horizontal or lateral alar fold
wedge resection
Alapexy (abduction of the ala)
SURGERY: STENOTIC NARES
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Anatomy
Nasal concha: dorsal, ventral
Ethmoidal labyrinth
Nasal turbinates: ectoturbinates,
endoturbinates
Nasal meatuses
Dorsal, middle, ventral, common
Function
Humidify and warm inspired air
NASAL TURBINATES
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Ginn et al JAAHA 2008. Evidence of nasopharyngeal turbinates.
Retrospective study of brachycephalics undergoing upper airway endoscopy
Goal: report nasopharyngeal turbinates and its incidence in brachycephalics with signs of
upper respiratory disease
NP turbinates identified in 21% of brachycephalic animals – 21% of dogs and 20% cats in study
Pugs accounted for 32% of all dogs in study population; 82% had NP turbinates
NASOPHARYNGEAL TURBINATES
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Oechtering et al Vet Surg 2016.
Intranasal anatomy / aberrant turbinates.
Prospective study of brachycephalics undergoing CT and rhinoscopy
Goal: document intranasal obstruction in brachycephalics with signs of upper respiratory
disease
All dogs (132 of 132) had abnormal conchal growth causing intranasal obstruction
ABERRANT NASAL TURBINATES
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RAT (rostral aberrant turbinates) – 91% of Pugs,
56% French Bulldogs, 36% English Bulldogs
CAT (caudal aberrant turbinates) – 67% of all breeds
Nasal septum deviation - consistent finding in Pugs (99%), less common in Bulldogs
Interconchal and intraconchal mucosal contact points in 91.7% of dogs
Using impulse oscillometry, intranasal obstruction effect was measured and shown to
cause elevated nasal airway resistance
ABERRANT NASAL TURBINATES
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NASAL CAVITY - CT SCAN
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• Normocephalic (German Shepherd) • Brachycephalic (Pug)
• Nasal cavity comparison
– Extreme reduced size
in Pug
– Endoturbinate malformation
resulting in caudal aberrant
turbinate
• Frontal sinus missing in Pug
• Compare nasopharynx in GSD
and Pug
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p1:
Nasal septum
deviation in Pug
p2:
Nasal conchae
extend caudally
and obstruct the
nasopharynx in Pug
NASAL CAVITY
- CT SCAN
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Endoscopy – nasal
vestibule
RAT = rostral
aberrant turbinate
RAT causing severe
nasal meatus
obstruction due to
multiple mucosal
contact points
(1) NARES AND NASAL CAVITY
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• Normocephalic
(German Shepherd)
• Brachycephalic
(French Bulldog)
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Endoscopy – nasal vestibule
Mucosal contact points
Extensive !
NASAL CAVITY - ENDOSCOPY
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• Brachycephalic
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Endoscopy – retroflex,
nasopharynx
CAT = caudal aberrant
turbinate
CAT causing severe
nasopharyngeal/choanae
obstruction
NASAL CAVITY - ENDOSCOPY
• Normocephalic (German Shepherd) • Brachycephalic (Pug)
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Laser-assisted turbinectomy (LATE)
*Complete removal of the following:
Turbinectomy of the nasal vestibule
Turbinectomy of the RAT
Turbinectomy of the CAT
Outcome
Complications
32.3% hemorrhage
6 month followup
Regrowth of turbinates
15.8% received a second resection
ABERRANT TURBINATES
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Most frequently affected breeds: English and French Bulldogs
Anatomy
Divides the nasopharynx
and oropharynx
SOFT PALATE
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SOFT PALATE NORMAL VERSUS ABNORMAL
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• Normocephalic (Shepherd) • Brachycephalic (Boxer)
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Cause
Result of chronic upper airway obstruction
Clinical signs develop when the palate contacts the epiglottis or
extends past the caudal margin of the tonsils
Clinical signs
Stridor
Gagging +/- vomiting
ELONGATED SOFT PALATE
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Pathologic thickening of the soft palate,
observed concurrently with other components of BOAS
Quantitation
CT: allows for precise pharyngeal measurements using transverse slices at multiple
intervals
Grand et al JSAP 2006
Positive correlation between the thickness of the soft palate and the severity of
clinical signs
SOFT PALATE ELONGATION AND HYPERPLASIA
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Davidson et al JAVMA 2001. Laser staphylectomy.
Retrospective study of brachycephalics undergoing staphylectomy
Goal: compare outcomes of laser versus incisional staphylectomy
Findings
Laser staphylectomy was significantly faster
Ease of procedure using laser was advantageous
14-day outcomes were similar
SURGERY: LASER STAPHYLECTOMY
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Cause
Eversion or enlargement of the palatine tonsils
Result of chronic upper airway obstruction
Clinical signs
Debated as to the degree of
contribution to BOAS
*Removal recommended if feel
contributing to upper airway obstruction
ENLARGED/EVERTED TONSILS
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First described in 1957
Cause:
Result of chronic upper airway
obstruction
EVERTED LARYNGEAL SACCULES
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Cantatore et al, ECVS 2010.
*Outcome of laryngeal saccule resection in brachycephalic dogs
Prospective study, 9 dogs
Objective: Investigate whether reduction in airflow turbulence might allow
for spontaneous resolution of saccules (ie resection is not always necessary)
Procedure: rhinoplasty, staphylectomy, and unilateral laryngeal
sacculectomy (persistent everted saccule on one-side acting as control)
Results: Spontaneous resolution was uncommon
One patient with a poor outcome having aberrant proliferation of tissue at the
sacculectomy site
SURGERY: LARYNGEAL SACCULECTOMY
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Surgery
Laryngeal sacculectomy (also
called ventriculectomy)
Procedure: long metzenbaum
scissors to resect reductant
laryngeal saccules
SURGERY: SACCULECTOMY
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Before After
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LARYNX
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NORMAL
a = Corniculate process of the arytenoid cartilage
b = Cuneiform process of the arytenoid cartilage
e = Laryngeal ventricles
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Development of Laryngeal Collapse:
Increased airway resistance, increased negative intraglottic luminal
pressure, and increased air velocity associated with the BAOS (Harvey
1989, Lorinson and others 1997).
Forces displace the rostral laryngeal structures medially with
permanent cartilage deformation (Wykes 1983).
The net result is the gradual collapse of the rostral laryngeal opening.
LARYNGEAL COLLAPSE
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Cause:
Secondary result of chronic upper airway obstruction
Considered an end-stage disease
Patients can do well with medical treatment for mild to
moderate forms
More severe forms require surgery
LARYNGEAL COLLAPSE
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LARYNGEAL COLLAPSE
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http://www.vetfolio.com/respiratory/canine-brachycephalic-airway-syndrome-surgical-management
d = Vocal fold
e = Laryngeal
ventricles
Grade I Laryngeal Collapse
Eversion of laryngeal saccules
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Grade II Laryngeal Collapse
Medial displacement (collapse) or paradoxical motion
of the cuneiform processes of the arytenoid cartilages
LARYNGEAL COLLAPSE
https://www.dovepress.com/strategies-for-the-management-and-prevention-of-conformation-related-r-peer-reviewed-article-VMRR
b = Cuneiform
process of
the arytenoid
cartilage
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LARYNGEAL COLLAPSE
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NORMAL
a = Corniculate process
of the arytenoid cartilage
b = Cuneiform process
of the arytenoid cartilage
e = Laryngeal ventricles
Grade III Laryngeal Collapse
Medial displacement (collapse) or paradoxical motion
of the corniculate processes of the arytenoid cartilages
with loss of the dorsal arch of the rima glottis
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Stage I Laryngeal Collapse
Marked improvement and favorable prognosis
Saccule resection (sacculectomy), soft palate resection (staphylectomy), nares resection
(rhinoplasty)
Stages II and III Laryngeal Collapse
Historic guarded prognosis
Aryepiglottic fold resection, permanent tracheostomy, euthanasia
Recent publications
Left cricoarytenoid lateralization
LARYNGEAL COLLAPSE
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White, JSAP 2011. Surgery of laryngeal collapse with BAOS.
Retrospective study, 12 dogs [stage II (2/12 dogs) or stage III (10/12)
laryngeal collapse]
Goal: Report of 12 BAOS dogs with life-threatening laryngeal collapse
managed with left-sided cricoarytenoid lateralization with
thyroarytenoid caudo-lateralization
LARYNGEAL COLLAPSE
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Results
All patients experienced a progressive deterioration over 6-12
month prior to presentation
Surgery: all cases received – “cut and sew” staphylectomy, wedge
resection rhinoplasty, left and right laryngeal
sacculectomy…combined with bilateral tonsillectomy (9/12 dogs)
and resection of the glosso-epiglottic fold (4/12 dogs)
Each cases had continued, severe upper respiratory obstruction
7/12 dogs: received temporary tracheostomy
Surgery: left cricoarytenoid lateralization (normal cricoarytenoideus
dorsalis muscle/no atrophy)
Surgery: arytenoid cartilage was freed and caudally directed
10/12 had improvement in long-term respiratory function
2/12 dogs were euthanized due to lack of improvement
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Followup (average, 1.5 years)
All 10 dogs were alive and none had required
additional surgical intervention for BAOS
All owners considered that their dogs showed
marked improvement after surgery
(some had rare to occasional mild respiratory
clinical signs )
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Riecks et al JAVMA 2007.
Surgical correction brachycephalic syndrome (BAOS).
Study: Retrospective study, 62 dogs
Goal: assess results of surgical correction of brachycephalic
syndrome (including stenotic nares, elongated soft palate, and
everted laryngeal saccules)
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Findings:
Most common breed for all abnormalities = English Bulldog
Staphylectomy patients had similar outcomes with laser or scissor
resection techniques
Treatment success rate: 94.2%
Overall mortality rate: 3.2%
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Larynx
Opening of the trachea
Suspended ventrally by the
hyoid apparatus (e)
Components of the larynx
Epiglottis, thyroid, cricoid,
sesamoid, interarytenoid, and
paired arytenoid cartilages
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Cricoarytenoideus dorsalis muscle
Abductor of the arytenoid cartilage,
opening the glottis
Origin: cricoid cartilage
Insertion: the muscular process
Recurrent laryngeal nerve
Innervates the Cricoarytenoideus
dorsalis muscle
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Medulla -> Vagus nerve -> Recurrent laryngeal nerves ->
Caudal laryngeal nerves -> Laryngeal muscle innervation
Disruption of this pathway results in Laryngeal Paralysis
LARYNGEAL PARALYSIS
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Clinical signs
Chronic progressive stridor, voice (phonation) changes,
gagging/coughing, exercise intolerance, respiratory distress
Diagnosis
Upper airway examination – unilateral or bilateral paralysis,
paradoxical movement (inward movement on inspiration)
Electromyography [EMG] – dogs as young as 12 weeks
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(1) Congenital Laryngeal Paralysis
Bouvier des Flandres, Bull Terriers, Dalmatians, Rottweilers Pyrenean
Mountain Dogs, Huskies, Malamute, etc
Autosomal recessive, progressive, guarded to poor prognosis
Siberian Huskies, Husky crosses, Bouviers
Progressive degeneration of neurons (nucleus ambiguus) with subsequent
Wallerian degeneration of the laryngeal nerves
Onset: < 1 year of age
LARYNGEAL PARALYSIS
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Von Pfeil et al JAVMA 2018.
Breed: Alaskan Huskies
Phenotype: Blue eyes, white markings, and
oral mucosal tags or tissue bands
Mean age, onset clinical signs: ~ 6 months
Mononeuropathy of the recurrent laryngeal nerve
only
Treatment: cricoarytenoid lateralization
Prognosis: good to excellent
CONGENITAL LARYNGEAL PARALYSIS
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(2) Acquired Laryngeal Paralysis
Labradors and Golden Retrievers,
Saint Bernards, and Irish Setters
Median age – 9 years
LARYNGEAL PARALYSIS
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(2) Acquired Laryngeal Paralysis
Conditions: chronic endocrine (hypothyroidism), infectious, or immune-
mediated polyneuropathy, trauma/cervical, idiopathic polyneuropathy
Generalized idiopathic polyneuropathy
GOLPP – geriatric onset laryngeal paralysis polyneuropathy
Generalized neuromuscular weakness
Esophageal dysfunction – 11% of cases; may require esophagram to diagnosis
Megaesophagus
LARYNGEAL PARALYSIS
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Jeffrey et al. 2006.
Goal: Determined the prevalence of clinical and electrodiagnostic evidence
of a more generalized neurological dysfunction in dogs presented with
idiopathic acquired laryngeal paralysis
Features: Many dogs continuing to exhibit weakness and exercise tolerance
past tieback surgery.
Findings: Clinical neurological deficits and/or electrodiagnostic
abnormalities were found in each case. There was limited evidence that
specific neurological deficits were associated with a poor prognosis for full
recovery of exercise tolerance
GERIATRIC ONSET LARYNGEAL PARALYSIS
POLYNEUROPATHY
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Stanley et al. 2010.
Objectives: To compare esophageal function in dogs with idiopathic
laryngeal paralysis (ILP) to age and breed matched controls; to determine if
dysfunction is associated with aspiration pneumonia over 1 year; and to
compare clinical neurologic examination of dogs with ILP at enrollment and
at 1 year.
Study: Prospective, 32 dogs; tieback surgery, followed out over 1 year
Conclusions: Dogs with ILP also have esophageal dysfunction. Postoperative
aspiration pneumonia is more likely in dogs with higher esophagram scores.
Dogs with ILP will most likely develop generalized neuropathy over the
course of 1 year
GERIATRIC ONSET LARYNGEAL PARALYSIS
POLYNEUROPATHY
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Summary:
Subset of dogs with generalized progressive polyneuropathy
Esophageal dysfunction – greater risk for aspiration
pneumonia
Poor prognosis for return to normal activity
*Educate owners or consider neurology referral if concerns
GERIATRIC ONSET LARYNGEAL PARALYSIS
POLYNEUROPATHY
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Specialty consult – Surgery +/- Neurology
Bloodwork, thyroid
Thoracic radiographs
Upper airway exam
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Gold standard = (“tieback”)
Unilateral cricoarytenoid lateralization
Consistent outcomes
Goal = create a permanent increase in
diameter (one-sided) of the rima glottis
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Complications
Aspiration pneumonia – reported as high as
20% lifelong
Laryngeal distortion – increased risks
Seroma
Persistent cough or gagging
Failure – suture breakage, cartilage
fragmentation
Progression of neurologic signs
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Improvement expected in 90% of cases
70% are still alive 5 years after surgery
Dogs with generalized polyneuropathy at presentation
ALL developed progressive neurologic signs more than 1 year post-surgery
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CONCLUSION:
Our inductive and battery-powered prototypes performed effectively during
in vivo testing, and the 2 units that were implanted for long-term evaluation
held up well. As a proof of concept, we demonstrated that elicited neck strap
muscle or laryngeal EMG potentials could be used as a control signal for
closed-loop stimulation of laryngeal adduction and vocal pitch modulation,
depending on electrode positioning, and that VFs were stimulable in the
presence of synkinetic reinnervation or chronic denervation.
FUTURE OF LARYNGEAL PARALYSIS
TREATMENT
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Brachycephalic obstructive airway syndrome & Laryngeal Paralysis
Anatomic and physiologic abnormal airway function
Clinical signs of upper airway obstruction
Clinical signs typically chronic (median, 49 days) with acute exacerbation
Additional comorbidities – Esophageal / gastrointestinal abnormalities
*Laryngeal paralysis - polyneuropathy
SUMMARY – UPPER AIRWAY DISEASE
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Brachycephalic obstructive airway syndrome & Laryngeal Paralysis
Animals presenting with acute cyanosis or collapse
Medical stabilization
Determine anatomic origin of respiratory distress
Determine any comorbidities
Surgical treatment
SUMMARY – UPPER AIRWAY DISEASE
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Brachycephalic obstructive airway syndrome & Laryngeal Paralysis
Surgery offers improvement in quality of life and improves or resolves
respiratory signs
Considered salvage procedures as abnormalities are not completely
resolved
Prognosis – Good
SUMMARY – UPPER AIRWAY DISEASE
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Brachycephalic obstructive airway syndrome & Laryngeal Paralysis
Recommendations
1) BE MINDFUL of high ambient temperatures and humidity
Walk early morning OR late day
Avoid exercise with increased heat index OR humidity
2) Air conditioning
3) BE MINDFUL that excitement, anxiety, tachypnea, and hyperthermia
can lead to progressive and severe dyspnea, cyanosis and collapse
SUMMARY – UPPER AIRWAY DISEASE
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Joseph Palamara, DVM, DACVS-SA
Jpalamara@uvsonline.com
Tuesday - Friday
Maxwell Bush, VMD, DACVS-SA
Mbush@uvsonline.com
Monday – Thursday
Michele Litterio – Surgery Liaison
UVS SURGERY
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Minimally-invasive surgery
Orthopedic surgery
Soft tissue surgery
Surgical oncology
Questions? – call or email
SURGERY DEPARTMENT
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