3-s2.0-b9780702047718000260-main

549

26Abnormalities of the upper airwayNorm G. Ducharme Jon Cheethamperformance by decreasing minute ventilation, exacerbating exercise-induced hypoxemia, and decreasing maximal oxygen con-sumption. While some obstructive diseases are static and evident at rest, many obstructive lesions are dynamic and only apparent during exercise. Furthermore, during exercise the coexistence of two or more forms of upper airway obstruction has been reported in 30 to 70% of horses.1,2 This emphasizes the need for dynamic examina-tion to obtain the full identification of all the upper airway abnor-malities in a given horse. A proper assessment including a complete history, signalment, and physical examination, endoscopic exami-nation of the upper airway, both at rest and during treadmill exer-cise, will establish the etiology of the airway obstruction. In addition to sound analysis, imaging modalities such as radiography, ultra-sonography, computed tomography, and nuclear medicine can be valuable in diagnosing performance-limiting lesions of the upper airway.

Redundantalarfolds(alarfoldcollapse) The alar fold is formed by a thick fold of skin and

mucous membrane extending rostrad from the ventral nasal concha.3

Redundant alar folds are a cause of abnormal respiratory noise. In some horses they are also a cause of exercise intolerance and respiratory noise in performance horses.4,5 The prevalence has been reported to reach 9.6% in Standardbred racehorses.

It is seen more commonly in Standardbreds but is also seen in others breeds such as coldblooded trotters and Thoroughbreds.2,4

The diagnosis is made by manually holding the alar folds open during exercise testing, on treadmill exam or securing the alar folds dorsally to document decreased respiratory noise and improved exercise intolerance.2,4

Treatment includes tying the alar folds out of the airway during exercise or alar fold resection.4

Not all horses with alar fold collapse have airway obstruction and therefore improvement in the abnormal noise is not necessarily associated with improvement in performance.

CHAPTER CONTENTS

Introduction 549Redundant alar folds (alar fold collapse) 549Mycotic rhinitis 552Progressive ethmoid hematoma (PEH) 553Sinusitis 554Nasopharyngeal collapse 556Retropharyngeal abscesses 557Dorsal displacement of the soft palate (DDSP) 559Epiglottic entrapment 562Epiglottic retroversion 564Subepiglottic cyst 565Medial deviation of the aryepiglottic folds (previously termed axial deviation) 566Epiglottitis 567Laryngeal hemiplegia 568Arytenoid chondritis 572Rostral displacement of the palatopharyngeal arch (fourth and sixth branchial arch defect, also known as 4-BAD, or cricopharyngeal- laryngeal dysplasia) 575Guttural pouch mycosis 576Avulsion of the longus capitis/rectus capitis ventralis muscles 578Temporohyoid osteoarthropathy 579Tracheal obstructive disease 580References 582

IntroductionUpper airway obstructive diseases result in resistive breathing (an increase in resistance to passage of air through the upper airways) causing either an abnormal upper respiratory noise, exercise intoler-ance, or both. Upper airway resistive breathing limits the athletic

Respiratory system3

550

Fig 26.1 The nose of a horse with rings through the alar folds. The string is used to tie the rings together, pulling the alar fold out of the airway.

Recognition

History and presenting complaintMost horses with redundant alar folds make an expiratory fluttering noise during exercise and a smaller percentage might be exercise intolerant. Horses exhibit no clinical signs at rest.2,4

Physical examinationNo abnormalities are apparent at rest.

Special examinationOther causes of respiratory noise and exercise intolerance should be eliminated by performing an endoscopic examination of the upper airway and evaluating both nasal passages. Confirmation that redundant alar folds are the cause of the airway noise is made by alleviating the abnormal noise by placing a temporary suture through the skin of each nostril, the alar folds, and tying it over the bridge of the nose while the horse exercises (Fig. 26.1).4 The alar folds can also be held out of the nasal passage manually or with clips.2 Because dorsal displacement of the soft palate is seen in association with this abnormality, dynamic endoscopic exam during exercise is also indicated.

Laboratory examinationNone is indicated.

Diagnostic confirmationAbsence of noise and improved exercise tolerance during exercise with the alar folds secured out of the nasal passage confirms the diagnosis.2,4 Differential diagnoses for alar fold collapse include obstructive airway diseases that cause exercise intolerance and abnormal respiratory noise during exercise (Table 26.1). Paralysis or paresis of the levator nasolabialis muscle associated with a tight nose band or caveson can allow collapse of the lateral wall of the nostril and could be confused with alar fold paralysis.

Treatment and prognosis

Therapeutic aimsThe goal of treatment is to remove or secure the alar folds in an open position during exercise. This can be achieved by suturing the alar folds in an open (i.e. abducted) position during exercise, place-ment of a nasal insert, or surgically resecting the alar fold. The first two treatments are not permitted in all racing jurisdictions.

TherapyThe procedure is most commonly done under general anesthesia in dorsal recumbency or with the horse standing after a bilateral infra-orbital nerve block. The alar fold is exposed by retracting or by incising the lateral wall of the nostril. To provide hemostasis in this vascular area, a Glassman intestinal clamp is placed on the dorsal section of the alar fold. Using a blade adjacent to the clamp, the dorsal part of the alar fold is excised, starting immediately caudal to the alar cartilage (Fig. 26.2) and extending caudally along the dorsal limit of the nasal cavity up to the V shape junction of the incisive and nasal bones. At this time a simple continuous pattern uniting the nasal mucosa to the skin at the remnant of the alar fold is done. The Glassman clamp is then placed at the junction of the ventral limit of the alar fold to the ventro-lateral limit of the nasal cavity. A rostral-to-caudal incision completes the alar fold resec-tion.4 Usually, 12 cm of the cartilaginous portion of the ventral nasal concha is excised. The ventral nasal mucosa and the skin of the ventral nasal diverticulum is re-apposed as was done dorsally. If the lateral nasal ala is incised to expose the alar fold, it is closed in two layers.4

PrognosisReportedly, respiratory tract noise improves in 71% of horses fol-lowing alar fold resection and 88% of horses race after surgery.4 Horses with small nares and narrow nasal passages have a poorer prognosis for performance.2,4 As mentioned earlier, alar fold flutters can result in an abnormal noise not necessarily an airway obstruction.

Prevention

There is generally no known prevention.

Fig 26.2 Intraoperative view of the left alar fold. The lateral wall of the nostril has been incised and a Glassman forceps is placed on the dorsal aspect of the alar fold.

26Abnormalities of the upper airway

551

DISEASE

PaO2

PaCO2

TIP

TEP

Ziu

Zeu

IFEF

RF

VT

V E

Normal

132

71.7 (1

.6)

54.7 (1

.9)

42.9 (2.8)

9.2 (3.8)

0.53

(0.02)

0.14

(0.06)

80.4 (4

.2)

66.6 (4

.3)

84 (4

)22

.2 (1

.6)

1858

(109

)

Normal

5175

(2.3)

55 (2

.3)

39 (3.3)

12 (1

.4)

0.42

(0.05)

0.18

(0.02)

90 (5

.2)

91 (4

.1)

109 (11.7)

17.1 (1

.7)

1690

(130

)

Pha

ryng

eal c

ollaps

e131

40.8 (4.4)

22.0 (6

.6)

0.73

(0.02)

0.46

(0.19)

54.2 (4

.0)

55.6 (4

.1)

76 (4

.0)

16.8

1159

.4 (9

4.1)

DDSP

481

8.6 (7.6)

36.2 (1

1.3)

0.41

(0.11)

0.88

(0.38)

44.5 (9

.0)

46.7 (1

0.4)

57 (9

.8)

15 (3

.31)

875.2 (114

.5)

DDSP

5164

(3.6)

66 (4

.9)

29 (3.4)

35 (6

.7)

0.33

(0.05)

0.66

(0.11)

66 (3

.8)

69 (3

.4)

98 (8

.2)

13.6 (2

.5)

1265

(315

)

ILH

6453

58 (8

.3)

59.4

21.3 (0

.47)

1.52

0.49

(9.0)

42.6

42.7 (9

)70

1106

.5 (1

91.5)

Laryng

oplasty +

ventric

uloc

orde

ctom

y64

8339

45.1 (8.4)

0.82

(0.14)

55.5 (5

.0)

77 (2

0)12

11.5 (9

5.4)

Aryteno

idec

tomy +

ventric

ulec

tomy8

84

0.0 (4.4)

0.81

(0.10)

48.0 (2

.0)

1178

.5 (3

8.6)

Epiglottic retroversion6

03

5.7 (3.80)

13.3 (2

.4)

58 (5

)

TIP, trac

heal in

spira

tory pressure (cmH

2O): TE

P, trac

heal exp

iratory pressure (cmH

2O); Ziu, in

spira

tory im

peda

nce (cmH

2O/L/s); Ze

u, exp

iratory im

peda

nce (cmH

2O/L/s); IF, pe

ak in

spira

tory flow

(L); EF, pea

k expiratory flow

(L); RF, respiratory frequ

ency (b

reaths

/min); VT, tidal volum

e (L);

V E, minute ventilatio

n (L/m

in); values in

paren

theses are stand

ard error of the

mea

n.

Tab

le 26.1

Upp

er airw

ay m

echa

nics m

easu

remen

ts and

blood

gas variables in

horses with

obs

truc

tive up

per airw

ay disea

ses

Respiratory system3

552

Laboratory examinationLaboratory tests are generally not warranted, but if the infection is chronic, hyperfibrinogenemia might be present.

Diagnostic confirmationThe diagnosis of fungal rhinitis is confirmed by biopsy and culture of the plaque or mass. Fungi that have been reported to cause mycotic rhinitis in horses include Conidiobolus coronatus, Cryptococ-cus, Rhinosporidium, Aspergillus fumigatus and A. boydii, Coccidioides, and Pseudallescheria.49 The presence of septate hyphae or fungal mycelium on cytological examination is indicative of fungal infection.


Therapeutic aimsThe goal of therapy is to eradicate the fungus from the nasal passage.

TherapySurgical debridement of granulomas and lesions followed by topical antifungal lesions have been reported to be effective in the treat-ment of mycotic rhinitis.5For example, Aspergillus fumigatus is sensi-tive to natamycin solution applied topically.6 Nystatin can be added to the natamycin and used topically or intralesionally.6 Topical and intralesional injection of amphotericin B and intravenous sodium iodide or oral potassium iodide has been used in the past to treat Conidiobolus coronatus infection, but recurrence has been reported.7 Long-term systemic antifungal therapy has also been effective; oral itraconazole, 3 mg/kg, orally, twice daily, for 3.54 months also results in the resolution of Aspergillus sp. infection.8 Alternatively a 1% solution of enilconazole applied topically twice daily for 7 days has been reported to be successful for the treatment of fungal rhinitis.5

PrognosisMycotic rhinitis due to Aspergillus sp. resolves with treatment and recurrence is low.5,6 Conidiobolus coronatus resolves with surgical and medical treatment, but does recur.7,8 Cryptococcus sp. is an inva-sive fungus that can infect the paranasal sinuses and invade the brain and meninges, and the prognosis is generally poor for resolution.7,10

Prevention

No method of prevention is known.

Etiology and pathophysiology

EtiologyFungi isolated from the nasal cavity of affected horses include Conidiobolus spp., Cryptococcus spp., Rhinosporidium, Aspergillus spp., Coccidioides, and Pseudallescheria.

PathophysiologyInhalation of fungal spores and colonization of the nasal mucosa is the most likely route of infection, resulting in mycotic rhinitis.

Epidemiology

Mycotic rhinitis is rare (reported to represent less than 0.1% of all 21 160 admitted patients to a hospital5), but is most commonly seen in hot, humid climates, such as the southeastern USA and tropical areas.


EtiologyThe etiology of redundant alar folds is unknown, but might involve narrow nasal passages and inappropriate function of the transversus nasi muscles.

PathophysiologyA thick fold of skin forms the alar fold and mucous membrane extending rostrad from the ventral nasal concha.3 The space dorsal to the alar fold is the false nostril or diverticulum of the nostril while the true nostril that continues caudally to the nasal passage is ventral to the alar fold. When the nostril is dilated, the alar fold is tensed, obliterating the nasal diverticulum.4 Excessive alar fold tissue or inappropriate nostril dilation can cause the alar fold to collapse across the nostril, causing airway obstruction and exercise intolerance during inhalation, and a fluttering noise during exhalation.

Epidemiology

Standardbred, Scandinavian coldblooded trotters, and American Saddlebreds might be predisposed to this condition.2,4

Mycoticrhinitis Rare fungal infection of the nasal cavity. Often due to Aspergillus spp. Diagnosis by endoscopy and laboratory identification of

fungus. Treatment involves local debridement and topical application

of antifungal agent

Recognition

History and presenting complaintMycotic rhinitis is rare in horses and occurs most frequently in warm, humid climates. The most common clinical signs include nasal discharge that can be foul smelling, sneezing, and intermittent epistaxis.4,5, Horses with nasal granulomas might make an abnor-mal respiratory noise during exercise and show signs of exercise intolerance. If the fungal infection is invasive and involves the paranasal sinuses, extension to the brain and meninges can occur, resulting in cerebral signs such as depression, dementia, ataxia, and recumbency.

Physical examinationHorses with mycotic rhinitis generally have nasal discharge that is malodorous, and if chronic, they can have alopecia along the ventral aspect of the affected naris.4,6 If a nasal granuloma is causing airway obstruction, decreased airflow through the affected nostril is detected by holding the hands over each nostril.

Special examinationEndoscopic examination of the affected nasal passage reveals fungal plaques or granulomas affecting the mucocutaneous junction of the nostril, or mucous membrane of the nasal septum and concha.4,5 Ulceration of the mucosa surrounding the plaque or granuloma can also be seen.6 If the primary site of infection is the paranasal sinus region, exudate at the nasomaxillary opening within the middle meatus can be evident.


553

paranasal sinus region.10,11 If the mass is confined to the maxillary or frontal sinus, sero-sanguineous fluid will be evident at the naso-maxillary opening, yet the mass can be obscured from view.10,11 Differential diagnoses for progressive ethmoid hematoma include fungal granulomas, neoplasia, and nasal polyps which can be con-firmed by biopsy.Lateral, dorsoventral, and oblique radiographic projections of the

paranasal sinus region are taken to define the anatomic limits of the expansile mass (Fig. 26.4).12 A discrete, round density overlying the ethmoid labyrinth or within the maxillary or frontal sinus is suggestive of progressive ethmoid hematoma.13 Fluid lines in the sinuses can be present if secondary sinusitis has occurred. Com-puted tomography is useful to define the extent of the mass prior to surgical excision (Fig. 26.5).12

Laboratory examinationRarely, horses will have evidence of mild, regenerative anemia, though generally blood loss from ethmoid hemotoma is minimal. Depending on the duration, size of the mass, and inflammatory reaction, hyperfibrinogenemia can be present.13

Diagnostic confirmationDifferential diagnoses for PEH include neoplasia, fungal granu-loma, nasal polyp, sinus cyst or abscess. Definitive diagnosis is made based on the histopathology of the mass. Ethmoid hematoma is a non-neoplastic angiomatous mass covered by respiratory epi-thelium and fibrous tissue.11,12 The parenchyma of the mass is com-posed of blood, fibrous tissue, hemosiderin-laden macrophages, neutrophils and necrotic debris, especially in large, chronic masses, with occasional calcareous deposits.


Therapeutic aimsThe goal of treatment is elimination of the mass. This can be achieved by surgical excision, laser photo ablation, or chemical ablation.10,11,13,14 Most commonly, PEH is chemically ablated by intralesional injection of formalin.14,15 In the standing, sedated horse, the mass is injected with 4% formaldehyde or neutral

Progressiveethmoidhematoma(PEH) Clinical signs include unilateral epistaxis and respiratory

stridor. Endoscopy of the nasal passage and inspection of the

ethmoid region demonstrate ethmoid hematoma. The diagnosis is confirmed by histopathology of the mass. Most ethmoid hematoma originate at the ethmoid turbinate,

but can originate from any of the paranasal sinuses. Treatment options include surgical excision, either sharply or

with a laser, or chemical ablation. Recurrence is approximately 43%.

Recognition

History and presenting complaintHorses with progressive ethmoid hematoma (PEH) have unilateral or bilateral epistaxis, which can progress to respiratory stridor and variable facial deformity depending on the duration of the condi-tion, and decreased airflow through the affected nostril.10

Physical examinationUnilateral nasal obstruction can be diagnosed by holding the hands over each nostril and detecting reduced airflow from the affected nostril. Facial deformity can also be observed as asymmetric convex-ity of the facial bones, medial and rostral to the orbit.

Special examinationEndoscopic examination of the upper airway, including both nasal passages, is frequently diagnostic for progressive ethmoid hematoma. Ethmoid hematomas originate from the ethmoid tur-binate region or paranasal sinuses (Fig. 26.3). The masses are smooth, green to purple in color and can be small and discrete or expansile, invading the entire nasal passage, nasopharynx, or

Fig 26.3 Endoscopic image of an ethmoid hematoma.

Ethmoid turbinate

Ethmoid hematoma

Nasal septum

Fig 26.4 Lateral radiograph of the paranasal sinus region of a horse. The large arrow points to the ethmoid hematoma and the small arrow points to the ethmoid turbinates.

Respiratory system3

554

sinuses. Progressive expansion of the mass occurs due to recurrent hemorrhage and local invasion of tissues. Masses can expand rostro-ventrally into the nasal passage or nasopharynx, or within the para-nasal sinuses.

Epidemiology

Progressive ethmoid hematomas have been reported in horses from 6 months to 20 years old, but are most commonly diagnosed in middle-aged and older horses.10,16 Thoroughbred horses are over-represented in case series, though the disease has been reported in many breeds. Bilateral lesions occur 15% of the time.10,16

Sinusitis The paranasal sinuses include the frontal, maxillary,

sphenopalatine, and dorsal and ventral conchal sinuses. Sinusitis can be primary or secondary, and is most commonly

associated with dental disease, masses, and trauma. Clinical signs of sinusitis include nasal discharge and facial

swelling. Surgical debridement of the sinus is frequently recommended

for treatment of primary or secondary sinusitis.

Recognition

History and presenting complaintHorses with sinusitis frequently have unilateral or bilateral nasal discharge. Sinusitis can be primary if no underlying disease is present or secondary if the sinusitis is due to dental disease or fungal infection.15 In the latter case the discharge can be foul smell-ing and is more likely to be bilateral as compared to secondary sinusitis.15,16 Horses with primary sinusitis frequently have a history of recent upper respiratory tract infection. If the sinusitis is second-ary to a cyst or neoplastic mass, facial swelling and deformity of facial bones can be detected as the mass expands within the sinus.15,16

Physical examinationRarely are horses febrile. Facial swelling can be detected and can be painful to palpation.15,16 Deformity of facial bones overlying the sinus can be evident, especially in chronic cases of expansile masses such as sinus cysts and neoplasia.1516Increased respiratory rate and effort is detected if the airway is obstructed. This occurs when the ventral conchal sinus is affected and compresses the ventral meatus16 or secondary to intrasinus lesions such as cyst or neoplasia.15Airflow obstruction is diagnosed by holding the hands over each nostril and detecting reduced airflow from the affected nostril. Submandibular lymphadenopathy has been reported in 7883% of affected horses.16 Epiphora occurs in horses with sinusitis if the nasolacrimal duct is compressed by a mass or swelling in the surrounding tissues.16 Hair loss can be detected on the horses face if the epiphora is chronic.

Special examinationTechniques used to diagnose sinusitis include radiography, com-puted tomography, sinoscopy, endoscopy, and nuclear medicine.16,17 Generally at least four views of the skull are taken if sinusitis is expected, including the left and right oblique, lateral, and dorso-ventral views. The left and right oblique views help to confirm which side of the head is affected. Fluid lines (Fig. 26.6), masses within the sinuses (Fig. 26.7) and periapical tooth root absces-sation and abnormal alveolar bone can frequently be detected

buffered 10% formalin until the mass distends using a trans-endoscopic 23-gauge retractable needle (Mill-Rose Laboratories, Inc., Mentor, OH) or through an injection apparatus constructed from polyethylene tubing and a 22- or 25-gauge needle.13,14 Treat-ments are repeated every 34 weeks until the lesion is obliterated, requiring 118 treatments.15 If the lesion is very large especially if invaded the sinuses surgical excision of progressive ethmoid hematoma is required10,1519 Laser excision is rarely indicated.11 Copious hemorrhage is expected (especially under general anesthe-sia) and controlled using cold saline and pressure applied with sterile gauze packing.Complications from surgical excision include severe hemor-

rhage, chronic sinusitis, surgical site infection, and osteomyelitis of the bone flap.10 Complications following formalin injection include laminitis, dysphagia, and neurologic disease, if the ethmoid hematoma has eroded through the cribiform plate.13,14

PrognosisRecurrence following surgical excision is 43%, necessitating peri-odic re-evaluation should the mass recur. Recurrence is slightly higher in horses with bilateral progressive ethmoid hematomas.1012,15

Prevention

There are no known preventive measures.


EtiologyThe etiology of PEH is unknown.

PathophysiologyProgressive ethmoid hematoma is an expanding angiomatous mass originating from the mucosa of the ethmoid conchae or paranasal

Fig 26.5 Coronal slice of a computed tomographic image of a horse with an ethmoid hematoma. Notice the left sinus region is occupied by the ethmoid hematoma. E = normal ethmoid turbinate; ET = endotracheal tube; M = molars.

Ethmoidhematoma

M M

ET

E


555

gained from the computed tomographic scan aids in surgical plan-ning and the surgical approach. Sinoscopy is performed in the sedated, standing horse by inserting a flexible endoscope or arthro-scope through a trephine in the frontal, rostral maxillary, or caudal maxillary sinus.17 Fluid is aspirated from the sinus and submitted for culture and cytology and the sinus can be irrigated to evacuate exudate. The sinuses can be explored and masses or tooth root abscesses identified and biopsied by use of this technique. Endo-scopic examination of the nasal passages is useful in cases of sinusi-tis to confirm that the exudate is coming from the naso-maxillary opening of the middle meatus. The specific origin of the exudate and inciting cause cannot be determined by endoscopy alone. Despite radiography and computed tomography, identifying the affected tooth can at times be difficult. Nuclear medicine is rarely used in cases of sinusitis, but can be used to confirm infected apical tooth root.

Laboratory examinationThe results of laboratory tests on blood are generally normal. Fluid aspirates are submitted for culture and sensitivity.

Diagnostic confirmationThe diagnosis of primary sinusitis is made based on a history of previous upper respiratory tract infection, nasal discharge originat-ing from the paranasal sinus region, evidence of fluid within the sinuses on radiographs or computed tomography, and the absence of a secondary cause of the sinusitis.1516 Secondary sinusitis is diagnosed based on the presence of an inciting cause of the sinusi-tis, such as apical tooth root abscess, sinus cyst, neoplastic mass, ethmoid hematoma, mycotic granuloma, polyp, or trauma and facial bone fracture into the sinus.1516 Confirmation of the etiology of secondary sinusitis is made by sinoscopy, biopsy, or surgical exploration of the sinuses.


Therapeutic aimsThe goal of therapy is to rid the sinus of infection and remove the inciting cause in cases of secondary sinusitis.

TherapyThe results of culture and sensitivity of fluid aspirated from the sinus dictate the appropriate antimicrobial therapy. Because primary sinusitis frequently is a sequela to upper respiratory tract infection, Streptococcus spp. are frequently isolated. Penicillin or trimethoprim sulfonamides are appropriate antibiotics to use in the treatment of primary sinusitis, prior to receipt of culture results. In addition to systemic antibiotics, repeated lavage of the sinus with balanced polyionic solution decreases the exudate and dilutes the organisms and inflammatory mediators within the sinus.1516 A chronic irriga-tion system can be placed following sinus centesis. Sinus centesis can be performed at the cranial or caudal maxillary sinus or frontal sinus. A point 2.53 cm dorsal to the facial crest and 3 cm rostral to the medial canthus marks the placement for centesis of the caudal maxillary sinus;1516 2.53 cm dorsal to the facial crest and 3 cm caudal to the infraorbital foramen permits access to the cranial maxillary sinus. Centesis of the frontal sinus is performed at a site midway between the medial canthus of the eye and the midline of the head. Following aseptic preparation, a 23 mL bleb of local anesthetic is injected subcutaneously. A stab incision is made through the skin and subcutaneous tissue and a 2 mm Steinmann pin in a Jacobs chuck is used to drill a hole into the sinus. Sterile

radiographically. Computed tomography is performed to localize the lesion more accurately in cases of secondary sinusitis. Sinus cysts, dental disease, neoplasia, ethmoid hematoma, mycotic granu-lomas, polyps, and epidermal inclusion cysts can cause secondary sinusitis and frequently require surgical removal.16 The information

Fig 26.6 Lateral radiograph of the paranasal sinus region of a horse with sinusitis illustrating the fluid line (arrow) within the maxillary sinus.

Fig 26.7 Lateral radiograph of the paranasal sinus region of a horse with a mass (arrow) within the maxillary sinus.

Respiratory system3

556

Horses with hyperkalemic periodic paralysis are at increased risk for developing nasopharyngeal collapse.

Recognition

History and presenting complaintVarious degrees of nasopharyngeal collapse can cause exercise intol-erance and respiratory noise in exercising horses.

Physical examinationThis is normal in the resting horse.

Special examinationIn affected horses, endoscopic examination of the nasopharynx and larynx at rest is generally normal unless a pharyngitis is present. At rest during nasal occlusion the lateral walls, dorsal aspect of the nasopharynx, or rostral portion of the soft palate can collapse into the airway to an abnormal degree in affected horses, especially horses with hyperkalemic periodic paralysis (HYPP).22,23 Be aware that sedation and topical application of local anesthetic can create nasopharyngeal collapse. Some horses show signs of nasopharyn-geal collapse during resting endoscopic examination, and have normal nasopharyngeal function during exercise.Dynamic examination is required to confirm the diagnosis (Fig.

26.8). The interpretation of the endoscopic image at exercise is obvious for lateral wall collapse. The interpretation of billowing of the floor of the nasopharynx (i.e rostral nasopharyngeal collapse) as well as the roof of the nasopharynx (i.e dorsal nasopharyngeal collapse) must be made with caution. Normally, the roof of the nasopharynx minimally projects ventrally at the end of expira-tion due to positive end-expiratory pressure within the guttural pouches resulting in some degree of dorsal pharyngeal collapse at the end of expiration.24 Dorsal nasopharyngeal collapse has recently been proposed to be artificially created in the dressage horse by the excessive thoraco-cervical and atlanto-occipal hyperflexion (i.e. rollkur).25 Dorsal nasopharyngeal collapse is also reported to be secondary to subclinical tympany of the guttural pouch present only during head flexion.26 Billowing of the rostral palate can be due to a ventral position of the endoscope in the most rostral aspect of the nasopharynx or caudal aspect of nasal passage during exercise will visually amplify the normal billowing of the rostral palate and cause an inaccurate identification of this condition.

Laboratory examinationNone is indicated.

Diagnostic confirmationThe diagnosis is best confirmed by dynamic endoscopic exam during exercise.


Therapeutic aimsThe goal of treatment is to resolve the nasopharyngeal collapse.

TherapyHorses with nasopharyngeal collapse may be given local or systemic anti-inflammatory agent if upper airway inflammation is present. Horses that are HYPP positive respond to acetazolamide therapy. Horses with dorsal nasopharyngeal collapse may respond to fenes-tration of the guttural pouches or removal of plica salpingopharyn-geal membrane.26

polyethylene tubing is fed through the centesis site and fluid is aspirated using a needle and syringe attached to the tubing. If elected, a chronic irrigation system can be sutured in place. The chronic irrigation system permits irrigation of the sinus with 13 liters of solution two to four times daily until exudate is no longer produced.The goal of treating secondary sinusitis is to treat the primary

cause. Depending upon the location, sinus cysts, ethmoid hemato-mas, neoplasia, polyps, and infected teeth can be approached sur-gically through a maxillary bone flap or frontal nasal bone flap.15,18 Standing surgery reduces the amount of the bleeding compared to sinusotomy under general anesthesia. Hemorrhage is controlled during surgery by lavaging the site with cold saline and applying pressure to the bleeding area. Occasionally, but rarely, vessels can be located and ligated. After the mass has been removed, continu-ous pressure is applied to the area using gauze (within a stocki-nette) or roll gauze packing placed within the sinus. The end of the packing is exited through a hole in the dorsal or ventral conchal sinus and then out the nose or through a trephine opening in the caudal maxillary sinus. The packing is pulled in 36 to 48 hours.

PrognosisThe prognosis for recovery from primary sinusitis, sinus cysts, trauma, and dental disease is good.15,19,20 Complications can include chronic drainage from the sinus, recurrence of the cyst if a portion of the cystic lining was left within the sinus, oral nasal fistulas from tooth extraction, incisional infection and sequestration of the bone flap overlying the sinus. Prognosis for most neoplastic masses within the sinus resulting in sinusitis is poor due to the expansile, invasive, and metastatic nature of the tumors.

Prevention

There is no known prevention.


EtiologySinusitis can result from a primary infection within the sinus, fre-quently secondary to an upper respiratory tract infection. Sinusitis can also occur secondary to an apical tooth root abscess, sinus cyst, neoplasia, trauma and fracture of facial bones, ethmoid hematoma, and fungal granuloma.15,16

Epidemiology

The prevalence of sinusitis ranges from 0.4 to 1.06%.2021

Nasopharyngealcollapse Horses with nasopharyngeal collapse are usually normal

at rest. The diagnosis of nasopharyngeal collapse is made during

exercise (overground or treadmill) endoscopic examination. Dorsal nasopharyngeal collapse can be a consequence of

excessive thoraco-cervical and atlanto-occipal hyperflexion. Dorsal nasopharyngeal collapse can be a manifestation of

subclinical guttural pouch tympany and treated by addressing the latter surgically.

Clinical signs of nasopharyngeal collapse, in young horses or in horses with pharyngitis, can resolve with time.


557

PrognosisThe prognosis is usually unfavorable, especially in horses with underlying disease such as HYPP. The condition resolves in some horses.

Prevention



EtiologyIn most cases the etiology of pharyngeal collapse is not known. However in some cases the disease is associated with pharyngitis or HYPP and in foal with muscle disease.

PathophysiologyNasopharyngeal collapse can result from some form of exercise-induced guttural pouch tympany or neuromuscular lesion involv-ing the muscles that support the dorsal nasopharynx.23,26 Horses should be evaluated for neuromuscular or primary muscle disor-ders, such as equine protozoal neuropathy, selenium and vitamin E deficiency, hyperkalemic periodic paralysis, or upper respiratory inflammatory disease.22

Epidemiology

The epidemiology of this condition has not been described. However, this disease is most frequently diagnosed in young race-horses, which can be due to the speed and intensity at which they compete. Nasopharyngeal collapse is also frequently recognized in horses with HYPP, and rather than being a distinct entity, represents a muscle group affected by the disorder.

RetropharyngealabscessesRecognition

History and presenting complaintHorses with retropharyngeal abscessation frequently have palpable swelling in the throat region, nasal discharge, abnormal respiratory noise during exercise, dorsal displacement of the soft palate, and exercise intolerance. If the airway obstruction is severe, horses can show signs of respiratory distress at rest.27,28 Additional clinical signs include dysphagia, inappetance, and depression.27

Physical examinationPalpation of the throat in the area of Viborgs triangle can reveal swelling that can be painful and lead to stridorous upper airway noise. If the horse is dysphagic, feed material and saliva can be seen at the nares. If the horse is in respiratory distress, stridorous breath-ing and increased respiratory effort might be apparent.

Special examinationRadiography of the throat area reveals soft tissue density in the retropharyngeal region, dorsal to the pharynx and on the floor of the guttural pouch (Fig. 26.9). Compression of the dorsal nasophar-ynx by the abscessed retropharyngeal lymph node is evident during endoscopic examination of the upper airway (Fig. 26.10). The enlarged lymph node can be best seen within the guttural pouch, on the floor of the medial compartment (Fig. 26.11).

Fig 26.8 Endoscopic images of the nasopharynx of an exercising horse showing progressive nasopharyngeal collapse. Collapse is apparent in the first frame (A) and increases with increasing duration of exercise on the treadmill (B, C).

A

B

C

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the surface protein (SeM) has been used as an epidemiological tool to identify geographically linked outbreak.30


Therapeutic aimsThe goal of therapy is resolution of the abscess.

Therapy

Emergency tracheotomyIf the horse is in respiratory distress, an emergency tracheotomy is performed in the mid cervical area. After infiltration with local anesthetic and aseptic preparation, a 1012 cm linear incision is made through the skin, subcutaneous tissue, and cutaneous trunci with a scalpel along the midline. The fascial plane dividing the right and left sternohyoid muscles is sharply incised with a scalpel, Metzenbaum scissors exposing the tracheal rings. A scalpel is inserted through the tracheal ligament parallel to and in between two tracheal rings. Approximately 40% of the ventral aspect of the tracheal ligament is incised and the tracheostomy tube inserted. The tube must be secured such that when the horse moves its head and neck, the tube lumen is not obstructed and the tube is not dislodged from the trachea.Because most retropharyngeal lymph node abscesses are caused

by streptococcal species, penicillin, 22 00044 000 IU/kg, or sulfamethoxazole-trimethoprim, 15 mg/kg, is administered for 710 days. Judicious use of non-steroidal anti-inflammatory medi-cation is appropriate. If the lymph nodes are large, surgical drainage can be required. Following general anesthesia, the horse is posi-tioned in dorsal recumbency. A modified Whitehouse approach is performed on the affected side, exposing the abscessed lymph node. Confirmation of the abscess is made by inserting a needle into the mass and aspirating material from the lymph node that can be submitted for culture and antibiotic sensitivity. A stab incision is then made in the lymph node and the purulent material evacuated.

Ultrasonographic examination of the throat will show increased soft tissue density containing hyperechoic fluid, or purulent exudates.

Laboratory examinationResults of complete blood count frequently show leukocytosis and neutrophilia with regenerative left shift, and lymphocytosis. Some horses will have hyperfibrinogenemia.

Diagnostic confirmationThe diagnosis is confirmed by aspiration of material from the affected lymph node and real-time PCR or culture of the exudate.29 Retropharyngeal lymph node abscesses are most frequently caused by Streptococcus spp., particularly Streptococcus equi. Sequencing of

Fig 26.9 Lateral radiograph of the pharyngeal region of a horse with an abscessed retropharyngeal lymph node causing collapse of the dorsal nasopharynx.

Mass

Nasopharynx

Fig 26.10 Endoscopic image of the nasopharynx of a horse with abscessed retropharyngeal lymph nodes. Notice how the dorsal nasopharynx is collapsed, such that the larynx cannot be seen. E = epiglottis.

Dorsal nasopharynx

Soft palate

E

Fig 26.11 Endoscopic image of the medial compartment of the guttural pouch. Notice the abscessed retropharyngeal lymph node.

Abscessed retropharyngeallymph node

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is dependent on the activity of the horse. DDSP in show horses generally affects the horses performance because of the noise pro-duction or coughing, although poor performance is also reported.32 Horses that perform with the head and neck flexed, such as upper-level dressage horses and Saddlebreds, suffer exercise intolerance with DDSP due to the more negative inspiratory pressure and airway resistance that occurs with head and neck flexion.33 These horses must be differentiated from horses with collapse of the roof of the nasopharynx, which can also cause a similar abnormal noise and impairment in performance. Dorsal displacement of the soft palate is more common in racehorses, especially 24-year-olds.34,35 The exercise intolerance is often described by trainers and riders or drivers as choking down or hitting a wall because DDSP causes significant expiratory obstruction that limits minute ventilation. Mouth breathing during exhalation is recognized by fluttering of the cheeks as air is diverted underneath the soft palate through the mouth. Occasionally, coughing during exercise is reported in asso-ciation with the disease; this complaint is more common in sport horses.

Physical examinationBecause intermittent DDSP is a dynamic obstructive airway disease that occurs during exercise, most horses are normal at rest. If the soft palate displacement is persistent and associated with dysphagia, feed material can accumulate in the airway, the horse can cough, and have clinical signs of aspiration pneumonia. The primary com-plaint in these horses is dysphagia and aspiration. This is quite different in horses with intermittent DDSP, where exercise intoler-ance and respiratory noise are seen.Some horses with intermittent DDSP have a history of upper

respiratory infection. These horses can have nasal discharge, cough-ing, and enlarged retropharyngeal and submandibular lymph nodes.

Special examination

Intermittent DDSPWatching and listening to the horse exercise at a racetrack and wit-nessing the described abnormal noise, open mouth breathing during exhalation and exercise intolerance can be helpful in diag-nosing DDSP. The noise is somewhat specific in that it occurs during expiration and has a snoring character, quite different from inspira-tory noises associated with laryngeal hemiplegia and other dynamic inspiratory airway abnormalities.Endoscopic examination of the nasopharynx and larynx at rest in

unsedated horses is important to assess nasopharyngeal function and rule in or out other causes of abnormal airway noise and exer-cise intolerance, such as laryngeal hemiplegia/hemiparesis or epi-glottic entrapment. Examination of both guttural pouches can be helpful if dysphagia present. Dorsal displacement of the soft palate is recognized by the dorsal position of the caudal edge of the soft palate obstructing the view of the epiglottis (Fig. 26.12). Occluding the horses nares for 2060 seconds, forcing the horse to breathe against the obstruction, can stimulate increased activity in upper airway muscles and induce DDSP. The observation of induced DDSP during nasal occlusion or resting endoscopy is predictive of DDSP at exercise although it is an insensitive test.36,37 Indeed, the observation of DDSP at rest, coupled with a history of abnormal respiratory noise at exercise, is only correct in approximately half the horses.36 After withdrawing the endoscope, the caudal edge of the soft palate can be examined for evidence of ulcers (Fig. 26.13), or prior staphylectomy. Ideally a laryngeal forceps is used to elevate the epiglottic cartilage to better examine the caudal edge of the soft palate (Fig. 26.14) and the subepiglottic tissue for ulcers, cysts,

The incision is left open, to heal by second intention, and the site is lavaged with saline or dilute iodine solution twice daily.

PrognosisThe prognosis for return to normal function within 45 months following retropharyngeal lymph node abscess is excellent, or approximately 90%.27

Prevention

Decreased exposure to horses infected with Streptococcus equi mini-mizes the occurrence of retropharyngeal lymph node abscess forma-tion. Prophylactic vaccination against S. equi can limit lymph node abscess formation, but vaccination is not without risk.

Etiology

EtiologyMost retropharyngeal lymph node abscesses are caused by strepto-coccal species, principally S. equi.

Epidemiology

Retropharyngeal lymph node abscesses are most commonly seen in horses less than 1 year old, and in horses infected with S. equi.

Dorsaldisplacementofthesoftpalate(DDSP)Recognition

History and presenting complaintHorses with intermittent dorsal displacement of the soft palate (DDSP) are exercise intolerant and often make an abnormal expira-tory noise during exercise. The displaced soft palate billows dorsally during exhalation as air flows beneath the soft palate (Fig. 26.12). The noise associated with DDSP is a gurgling or snoring noise, and is caused by fluttering of the caudal margin of the soft palate. In approximately 2030% of horses with DDSP, noise is not heard.31 The importance of either noise production or exercise intolerance

Fig 26.12 Endoscopic image of a horse with dorsal displacement of the soft palate while exercising on a treadmill. Notice how the soft palate billows dorsally in the airway, obstructing the rima glottidis. Arrow, caudal free margin of the soft palate.

Soft palate

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Persistent DDSPIt is important to evaluate the epiglottis morphology; for instance, subepiglottic masses and epiglottic deformity can result in DDSP. If persistent displacement is present, there are a few techniques that can be used to evaluate the structure and integrity of the epiglottis. Sometimes removing the twitch will relax the horse and allow it to reposition the soft palate appropriately. Sedation can permit replacement of the soft palate.38 Following application of local anes-thetic to the nasopharynx, a laryngeal forceps can be passed in one nostril and used to un-entrap the epiglottis from the soft palate. Evaluation of the epiglottic cartilage and the position of the soft palate can be performed using radiography (Fig. 26.15). Finally, an oral endoscopic examination can be performed on the horse fol-lowing sedation or general anesthesia and application of a mouth speculum. If the horse is anesthetized, manual palpation of the epiglottic cartilage and soft palate can also be performed.

Diagnostic confirmationBecause horses with intermittent DDSP are generally normal at rest (with clinical signs occurring only during exercise) the diagnosis can be very difficult to confirm. DDSP is best diagnosed by a dynamic endoscopic examination.


Therapeutic aimsThe goal of therapy is to prevent DDSP from occurring. Because the etiology of DDSP is varied, treatment should be directed at the cause.

TherapyThe following discussion should be noted with the concerns expressed in a systemic review39 recently performed where no treat-ment could be determined to be superior. This is because most reports in the literature failed to report control or when controls were present, the health status of the control are unknown.39,40

granulomas, or swollen aryepiglottic membrane indicative of inter-mittent aryepiglottic entrapment. During endoscopy, the observa-tions suggestive of DDSP are (1) the ease with which DDSP can be induced by nasal occlusion, (2) more than one swallow is required to correct the DDSP, and (3) ulceration on the caudal edge of the soft palate. Dynamic endoscopic examination of the upper airway is the gold standard to diagnose DDSP.36,37 Diagnosis is made by observation of DDSP during strenuous exercise or by observation of palatal instability with flaccid epiglottis (presumably both are a reflection of caudal retraction of the larynx). Palatal instability (PI) is interpreted as prodromal to DDSP.36,37

Fig 26.13 Endoscopic image of the nasopharynx of a horse with dorsal displacement of the soft palate. Note the ulcer (arrow) at the caudal free margin of the soft palate.

Soft palate

Fig 26.14 Epiglottic cartilage is being lifted with an equine laryngeal forceps, revealing an ulcer on the caudal free edge of the soft palate.

Fig 26.15 Lateral radiograph of the pharyngeal region of a horse with persistent dorsal displacement of the soft palate. Notice the epiglottis (small arrow) positioned ventral to the soft palate (large arrow).

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and muscle is resected bilaterally. The incision is left open to heal or can be sutured if desired. Complications are usually minor and include incisional seromas or abscesses requiring appropriate drainage. However, in experimental horses with normal airway function, resection of the sternothyroid and sternohyoid muscles has been observed to result in a less dynamically stable nasophar-ynx at exercise as measured by an increase in inspiratory tracheal pressure.63

Laryngeal tie-forward is based on an experimental model of inter-mittent DDSP caused by bilateral resection of the thyrohyoideus muscles which was corrected using a suture.59 This was then shown to be effective in 3 subsequent trials in restoring earnings post-operatively in horses with a clinical diagnosis of DDSP.58,59,61 Under general anesthesia in dorsal recumbency, a ventral midline incision is made from the base of the lingual process extending 1 cm caudal to the cricoid cartilage. A non-absorbable suture (No. 5 USP) is passed 34 times in the caudal edge of the thyroid cartilage over a 1 cm span immediately ventral to the ventral limit of the ST tendon. Both sutures are then passed dorsal to the basihyoid bone with the trailer end of the suture emerging adjacent to the base of the lingual process on the contralateral side while the leading end of the suture emerged adjacent to the base of the lingual process on the ipsilateral side. The procedure is repeated on the contralateral side. The ventral sutures are then tied first advancing the rostral edge of the thyroid cartilage dorsal to the basihyoid bone with an overlap of approxi-mately 1.5 cm. The dorsal sutures are then tied together.

PrognosisThe prognosis following treatment ranged from 53 to 80%.39, 4350, 5255,5961 These results must be taken with a grain of salt as all outcomes are using some indices of performance as surrogate of success and not actual resolution of the disease. The reported success rate after bilateral tenectomy/myotomy of the sternothyroid muscle is 60%.45,46 Anecdotally recurrence can occur 36 months after surgery. Following laryngeal tie-forward the success rate is 1020% higher than after bilateral sternothyroid muscle/tendon transection.5961


EtiologyIntermittent DDSP has a multifactorial etiology. Anecdotally physi-cal obstruction (i.e subepiglottic and palatal masses, granulomas, cysts) interferes with the subepiglottic position of the soft palate. Furthermore, epiglottic malformation or chondritis can result in permanent or persistent DDSP.64

Damage of the innervation of the soft palate (i.e palatinus and palatopharyngeus muscles),64 dysfunction of the neuromusculature of the extrinsic laryngeal muscles such as thyrohyoideus muscles,65 and of the hypoglossal nerves66 have all, alone, been sufficient to create dorsal displacement of the soft palate.The innervation of the soft palate is through the pharyngeal

branch of the vagus nerve, which with the glossopharyngeal and hypoglossal nerves which course through the guttural pouch and therefore are susceptible to disease processes that specifically affect the lymph node in the floor of the guttural pouches. The pharyngeal branch of the vagus nerve provides motor innervation to the palati-nus and palatopharyngeus muscles, two muscles that control the position of the caudal portion of the soft palate. Experimentally desensitizing the pharyngeal branch of the vagus nerve bilaterally causes persistent DDSP at rest with dysphagia.65 The thyrohyoideus is a flat rectangular muscle attached to the lateral surface of the thyroid cartilage lamina that inserts on the caudal part of the

Therapy is directed to the likely cause of the DDSP. Pharyngitis has been associated with DDSP due to inflammation of the nerves and perhaps muscles that stabilize the soft palate.64 Upper airway inflam-mation is treated in a plethora of different ways, including systemic administration of corticosteroids (dexamethasone), non-steroidal anti-inflammatory medication, topical anti-inflammatory throat sprays, systemic administration of interferon, and guttural pouch lavage with balanced polyionic solutions with or without dimethyl sulfoxide and corticosteroids. Oral interferon alpha (50200 IU/day for 10 days to two weeks) is sometimes prescribed. An appropriate treatment regimen for moderate-to-severe nasopharyngeal inflam-mation, without bacterial infection, might include treatment first with systemic corticosteroids such as prednisolone or dexametha-sone and a topical anti-inflammatory throat spray for 24 weeks. A common throat spray administered at the rate of 20 cc, orally, every 12 hours consists of: glycerin 250 mL, 250 mL DMSO 90%, nitro-furazone 500 mL, prednisolone 50 mL (25 mg/mL). Horses should be rested (light training without fast speed work) for 1030 days and the upper airway function re-evaluated periodically.If there is a structural abnormality, such as epiglottic deformity,

entrapment, subepiglottic or soft palate cyst or mass, present then these abnormalities should be addressed. Cysts should be removed either through laser surgery or sharp dissection through a laryn-gotomy. Granulomas are treated with local anti-inflammatory agents as described above or rarely through resection. Horses with deformed epiglottic cartilage are more difficult to address. In some cases the epiglottic deformity is worsened by partial entrapment by subepiglottic tissues. Those can be released with laser surgeryWhether secondary to an inflammatory process in the upper

airways, structural abnormalities and when no structural causes are found, tack modifications such as the use of a bit that keeps the tongue under it (i.e., a W bit, Serena song bit), tongue-ties and the figure-eight noseband are traditional approaches (although unproven) that might be of value in reducing the occurrence of DDSP. There is some circumstantial evidence to support the use of a tongue-tie in the prevention of DDSP or improvement of airway mechanics in exercising horses.40,41 Finally the use of an external device which positions the larynx in a more forward and dorsal position has been shown to prevent DDSP during treadmill exercise in an experimental model.42 (Conflict of interest disclosure: one of the authors (N.G.D.) is listed as inventor on a patent owned by both authors employer, i.e Cornell University).Many surgical treatments have been reported, including sta-

phylectomy, various bilateral strap muscle resections (sternohyoid, sternothyroid, and omohyoid alone or in combination), epiglottic cartilage augmentation, and various tension or thermal palatoplasty procedures.4350 These procedures are performed by some surgeons alone or in various combinations.49,50 When comparing the results of these surgical treatments to the results of conservative treatment with or without case-control studies, they appear to be little or no advantage to the above procedures.5155 Two recent studies looked at the biomechanical/histological results following procedure aims to stiffens the soft palate with laser or injection of sclerosing agent.5658 The authors believe that there are two surgical treatments to be considered for treatment of intermittent DDSP: bilateral ster-nothyroid muscle tenectomy/myotomy transection46 and laryngeal tie-forward.5861

The goal of the bilateral resection of the tendon of the sternothy-roideus (ST) muscles is to prevent caudal retraction of the larynx from the caudal edge of the soft palate.46 Through a ventral midline incision centered on the cricoid cartilage, the sternothyroideus tendon/muscle is identified and clamped caudal to the cricoid car-tilage to avoid damaging the cricothyroid muscles which can lead to vocal cord collapse at exercise.62 A 24 cm section of ST tendon

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radiographically. If the soft palate is persistently displaced, due to or associated with the entrapment, a laryngeal forceps can be used to either retract the soft palate, or undisplace the soft palate so that the entrapping membrane can be observed. Alternatively an oral exam during general anesthesia will identify the entrapment.

thyrohyoid bone. It is innervated by the hypoglossal nerve and moves the hyoid bone caudally or the larynx rostrally and dorsally. Experimentally bilateral resection of the thyrohyoideus muscles causes intermittent DDSP during exercise in horses.60 Finally appli-cation of local anesthetic around each hypoglossal nerve at the level of the ceratohyoid bone also resulted in DDSP at exercise in experi-mental horses.66

PathophysiologyDorsal displacement of the soft palate is an expiratory obstructive syndrome that causes increased expiratory impedance, decreased minute ventilation, hypoxia, and hypercarbia (Table 26.1).65,67-69 During inhalation, the soft palate is located ventrally (still dorsal to the epiglottis). During exhalation, the soft palate displaces dor-sally, thus diverting the flow of air through the oropharynx and mouth. This flow pattern is associated with more negative peak tracheal pressure and increased expiratory impedance.65,68,69

PreventionPreventing DDSP is difficult because the etiology of this disease is unknown. However, timely treatment of upper airway inflamma-tion and appropriate vaccination against upper respiratory tract viruses can decrease the chances of horses developing intermittent DDSP.

Epidemiology

Dorsal displacement of the soft palate (DDSP) is a performance-limiting upper airway condition in horses that was reported to be present in 1020% of racehorses.51

Epiglotticentrapment Epiglottic entrapment occurs when redundant aryepiglottic

tissue envelops the epiglottis. Epiglottic entrapment can be an incidental finding during

endoscopic examination of the larynx and not associated with clinical signs.

The entrapping aryepiglottic tissue can be smooth or edematous and ulcerated.

Recognition

History and presenting complaintHorses with epiglottic entrapment can have exercise intolerance and make an abnormal respiratory noise during exercise. It must be realized that the performance of some horses with epiglottic entrap-ment is unaffected70,71 and therefore treatment may not be needed.

Physical examinationExternal physical exam is generally normal. On rare occasion, horses with severely ulcerated, swollen entrapping aryepiglottic membrane can be lead to coughing, dysphagia and have signs of aspiration pneumonia.

Special examinationEndoscopic examination reveals that the epiglottis is in its normal position dorsal to the soft palate but is encased in the aryepiglottic membrane so that the normal serrated edge of the epiglottis and its vascular pattern are not visible. The aryepiglottic tissue can be smooth, fitting tightly around the epiglottis, or swollen and ulcerated (Fig. 26.16A, B). The entrapment can also be observed

Fig 26.16 (A) Endoscopic image of the larynx of a horse with epiglottic entrapment. Note that the epiglottis is encased in the aryepiglottic membrane such that the vascular pattern on the dorsal surface of the epiglottis and the serrated margin of the epiglottis is not visible. (B) Endoscopic image of the larynx of a horse with an epiglottic entrapment. Note the ulcerated area (arrow) of the entrapping aryepiglottic tissue.

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anesthesia through a laryngotomy incision, after everting the epi-glottic cartilage in the larynx.73

Following midline division of the aryepiglottic membrane, topical and systemic anti-inflammatory therapies are recommended to prevent re-entrapment of the epiglottis. A topical anti-inflammatory solution (throat spray) is applied twice daily using a soft rubber tube (i.e. 12 Fr infant feeding tube) placed in alternating nostrils. In addition, dexamethasone (20 mg, IV, SID for 3 days) and an oral phenylbutazone or flunixin meglumine is recommended for 710 days.

Occasionally, the epiglottis is entrapped intermittently, during exer-cise or immediately after swallowing only. In these cases, the diag-nosis can be made by dynamic endoscopic examination during exercise.

Laboratory examinationLaboratory examination is normal, but none is usually indicated.

Diagnostic confirmationDifferential diagnoses for epiglottic entrapment include dynamic upper airway lesions that cause exercise intolerance and abnor-mal respiratory noise during exercise. A definitive diagnosis of epiglottic entrapment is made by static or dynamic endoscopic examination.


Therapeutic aimsThe goal of treatment is to relieve the entrapment. Chronic entrap-ment can result in epiglottic chondritis and/or deformity.

TherapyMidline division of the entrapping aryepiglottic membrane can be performed standing by passing a shielded hook bistoury intra-nasally72 or by use of a hooked bistoury through the mouth with the horse under general anesthesia (Fig. 26.17).73,74 It is ill-advised to use an unshielded hooked bistoury transnasally on standing, even on sedated horses, because it exposes the horse to unnecessary morbidity (possibly career ending) such as palatal, esophageal or guttural pouch laceration if the horse swallows or moves. The entrapping membrane can also be divided with the laser.75 The laser must not come into contact with the epiglottic cartilage, so it is advisable to use a laryngeal forceps or blunt hook to elevate the epiglottic membrane prior to division (Fig. 26.18A,B). The advantage of the laser over the hooked bistoury is that if the aryepi-glottic membrane is ulcerated and swollen, the membrane can be resected. Alternatively this resection can be done under general

Fig 26.17 Endoscopic image through the oropharynx of a horse where an entrapping aryepiglottic membrane is being excised using a hooked bistoury (arrow) with the horse under general anesthesia.

Epiglottic entrapment

Fig 26.18 (A) Endoscopic image of an epiglottic entrapment being elevated by a blunt laryngeal forceps to protect the epiglottic cartilage from inadvertent contact with the laser. The laser first cut is an horizontal incision to allow the blunt hook to come through the membrane. (B) Endoscopic image of the laser-assited midline division of the aryepiglottic membrane.

A B

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retroversion is observed when an exceptionally large subepiglottic cyst is swallowed into the esophagus (see subepiglottic cyst). The horse can then become dyspneic.

Laboratory examinationLaboratory examination is normal, though none is usually indicated.

Diagnostic confirmationDifferential diagnosis of epiglottic retroversion includes those dis-eases that cause abnormal respiratory noise during inhalation at exercise and can result in exercise intolerance (Table 26.1). The diagnosis of epiglottic retroversion is definitively made during endoscopic examination during exercise.


Therapeutic aimsThe goal of treatment is to stabilize the epiglottis and prevent it from obstructing the airway during inspiration.

TherapyLittle is described in the treatment for epiglottic retroversion. Treat-ment of two horses is described, with one horse racing successfully after epiglottic augmentation with polytetrafluoroethylene (Teflon), and another horse showing no improvement.81 The author has performed different fixation (epiglottic tie-down) in five cases (four to basihyoid and one to thyroid cartilage) and only one responded to treatment. Currently better results have been obtained using facilitated ankylosis of the thyroepiglottic articulation.

PrognosisPrognosis is excellent for life, but guarded for athletic endeavors.80,81

PrognosisSeventy-four to 82% of horses have a positive outcome following transoral axial division of the aryepiglottic tissue; 510% of horses have recurrence of the entrapment after surgery, and 1015% of horses develop dorsal displacement of the soft palate following correction of epiglottic entrapment.7275

Prevention

There is no known preventive measure.


EtiologyThe etiology is unknown.

PathophysiologyAryepiglottic tissue is areolar, mucous membrane that attaches along the ventral margin of the epiglottis and continues between the lateral edges of the epiglottis to the corniculate processes of the arytenoid cartilages. The manner by which the entrapment occurs is unknown, but it can be precipitated by airway inflammation and, specifically, inflammation of the aryepiglottic tissue. It has been suggested that horses with epiglottic hypoplasia, diagnosed by use of endoscopy or radiographic measurement of the thyroepiglottic length, are predisposed to epiglottic entrapment.73

Epidemiology

Between 0.74 and 3% of racehorses have epiglottic entrapment.70,71,7679

Epiglotticretroversion Epiglottic retroversion is a rare cause of exercise intolerance

and abnormal respiratory noise in horses. Epiglottic retroversion is diagnosed during dynamic

examination during exercise. When the epiglottis retroverts, it prolapses through the rima

glottides during inhalation, causing airway obstruction. Epiglottic retroversion is probably due to damage to the

hyoepiglotticus muscle or the hypoglossal nerve or some of its branches.

Recognition

History and presenting complaintEpiglottic retroversion is a rare condition that causes abnormal respiratory noise during exercise and exercise intolerance.

Physical examinationThe physical examination is normal.

Special examinationEpiglottic retroversion is diagnosed during dynamic endoscopic examination at exercise.80,81 At rest, the nasopharynx and larynx of affected horses are almost always normal during endoscopic exami-nation. During exercise endoscopy, the epiglottis retroverts such that the ventral surface of the epiglottis faces rostrally (Fig. 26.19). In some horses, the epiglottic retroversion is increased by traction on the lines or reins. Epiglottic retroversion causes dynamic airway obstruction in affected horses (Table 26.1). A rare form of epiglottic

Fig 26.19 Endoscopic image of the larynx of a horse running on a treadmill. Note that the epiglottis (arrow) is retroverted through the rima glottidis, exposing the ventral surface of the epiglottis.


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Therapeutic aimsThe goal of treatment is removal of the cyst.

TherapySubepiglottic cysts are usually excised with the horse using laser in standing sedated horses.82 If the cyst is large it may need to be excised under general anesthesia to allow the procedure to be carried out through the oropharynx. The cyst can also be excised

Prevention

There are no known preventive measures, though care should be taken when performing surgery ventral to the epiglottis (i.e pharyn-gotomy) so as not to damage nerve supply or muscles in this area. In addition, injections lateral to the larynx commonly termed palatal injection can result in injury to the hypoglossal nerve or its branches to the hyoepiglotticus muscle(s).


EtiologyAside from iatrogenic damage to the hyoepiglotticus muscle or its innervation as described above, the cause of epiglottic retroversion is unknown.

PathophysiologyEpiglottic retroversion has been produced experimentally by bilater-ally anesthetizing the hypoglossal nerves, suggesting that trauma or dysfunction of the hyoepiglotticus or geniohyoideus muscle are implicated in the pathogenesis of epiglottic retroversion.82

Epidemiology

Because so few cases have been reported, the epidemiology of this disease is unknown.

SubepiglotticcystRecognition

History and presenting complaintCoughing, abnormal respiratory noise, and exercise intolerance are clinical signs of subepiglottic cysts in mature horses. Dysphagia can occur in foals or horses with a very large cyst.

Physical examinationPhysical examination is usually normal. If the horse is dysphagic, coughing and aspiration pneumonia can be evident.

Special examinationEndoscopic examination of the larynx and nasopharynx is generally diagnostic for a subepiglottic cyst (Fig. 26.20). The cyst is round, pale pink to red, covered with mucosa, and generally seen beneath the epiglottis and average in size, 34 cm.83,84 Occasionally, the cyst is not visible as it rests in the oropharynx and can only be seen briefly in the nasopharynx during swallowing or intermittently during exercise. Most rarely the cyst can be swallowed in the esopha-gus, leading to epiglottic retroversion at rest and obstruction of the rima glottidis and complete airway obstruction (Fig. 26.21).84

Laboratory examinationNone is indicated unless there is a suspicion of aspiration pneumonia.

Diagnostic confirmationEndoscopic examination is diagnostic for a subepiglottic cyst. Fol-lowing resection, the cyst can be submitted for histopathologic analysis if there is any concern that the cyst can instead be a neo-plastic mass.

Fig 26.20 Endoscopic image of the epiglottis of a horse with a subepiglottic cyst.

Epiglottis

Cyst

Fig 26.21 Endoscopic image of a horse that has swallowed its subepiglottic cyst into the esophagus. The glottis is obscured by the ventral aspect of the epiglottic cartilage.

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Recognition

History and presenting complaintHorses with medial deviation of the aryepiglottic folds are exercise intolerant and make an abnormal respiratory noise during exercise.87

Physical examinationPhysical examination is normal.

Special examinationMedial deviation of the aryepiglottic folds is only diagnosed during endoscopic examination of horses during exercise (Fig. 26.22). During intense exercise, the vertical component of the aryepiglottic tissue which connects the corniculate portions of the arytenoid cartilages to the lateral edge of the epiglottis collapses medially across the rima glottidis during inhalation.87 The obstruction is dynamic and worsens as exercise intensity increases. In some horses the medial collapse is seen prior to an imminent occurrence of DDSP.

Laboratory examinationLaboratory examination is normal; none is usually indicated.

Diagnostic confirmationThe definitive diagnosis of medial deviation of the aryepiglottic folds is made during dynamic endoscopic examination.87,88


Therapeutic aimsThe goal of treatment is to alleviate the dynamic airway obstruction by stabilizing the aryepiglottic folds.

TherapyTreatment for medial deviation of the aryepiglottic folds is pre-dominately by surgical resection of the aryepiglottic tissue between the lateral edge of the epiglottis and the corniculate processes of the arytenoid cartilages (Fig. 26.23). This is accomplished using a laser, with the horse sedated and standing. Alternatively,

along with the overlying mucosa by application of a snare device made with obstetrical wire threaded through an infusion pipette.80 Alternatively,the cyst can be excised through a laryngotomy inci-sion, with the horse in dorsal recumbency under general anesthe-sia.80 The cyst is positioned beneath the laryngotomy incision by retroverting the epiglottis. The aryepiglottic mucosa is incised and the cyst is dissected free and removed. In all cases, care must be taken to remove the entire cyst and a minimal amount of aryepiglot-tic tissue.Sclerotherapy is an alternative treatment where the cyst is injected

with ethanol85 or formalin.86 This treatment option should be reserved for cases where economic limitation is present, as the pos-sibility of recurrence and morbidity from excessive fibrosis could lead to dysphagia or displacement of the soft palate.

PrognosisThe prognosis for return to function and resolution of coughing is good to excellent. Occasionally a partial or complete epiglottic entrapment is seen a few weeks postoperatively. Recurrence of the cyst is rare, unless the entire cyst was not removed.

Prevention

There is no known preventive measure.


EtiologySubepiglottic cysts can be either acquired, especially in older horses, or congenital, as in foals. The cysts can develop from remnants of thyroglossal ducts in humans,85 but this has not been proven in horses.

PathophysiologyAirway obstruction and abnormal respiratory noise results from the cyst flipping dorsally across the rima glottidis, causing airway obstruction or leading to DDSP, which results in upper airway obstruction during exhalation.

Epidemiology

Subepiglottic cysts are most frequently diagnosed in young racing horses, both Standardbreds and Thoroughbreds, but have been identified in foals and older horses. There is no known breed predisposition.80

Medialdeviationofthearyepiglotticfolds(previouslytermedaxialdeviation) Medial deviation of the aryepiglottic folds has been

diagnosed in racing Thoroughbreds, Standardbreds, and Arabians.87,88 Diagnosis is made during endoscopic examination of the horse running on a treadmill.

Medial deviation is sometimes seen prior to DDSP at exercise.

Medial deviation is usually bilateral except when seen in a horse with partial or complete arytenoid collapse where contralateral medial collapse is seen.89

Treatment includes rest and anti-inflammatory therapy or surgical removal of the aryepiglottic folds.

Fig 26.22 Endoscopic image of the larynx of a horse with bilateral medial deviation of the aryepiglottic fold collapse during exercise.


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Recognition

History and presenting complaintMost horses have a history of exercise intolerance, abnormal respiratory noise during exercise, and coughing. Occasionally, horses have evidence of airway obstruction at rest, dysphagia, and anorexia.90

Physical examinationGenerally, physical examination is normal, unless the horse is dys-phagic or coughing.90,91 Coughing can be easily elicited by laryngeal palpation. Dysphagic horses can have clinical signs of aspiration pneumonia or rhinitis.90

Special examinationEpiglottitis is diagnosed by endoscopic examination. The epiglottis and subepiglottic tissue are swollen and dark pink to purple and can be ulcerated. Occasionally, the tip of the epiglottic cartilage is visible and is surrounded by granulation tissue. To identify the lesion, exploration with laryngeal forceps under endoscopic control might be needed.92

Laboratory examinationComplete blood count and serum chemistry values are usually normal. When chondritis is present, bacterial culture can help direct antimicrobial therapy.

Diagnostic confirmationDifferential diagnosis of epiglottitis includes epiglottic entrapment, chondritis of the epiglottis, and subepiglottic cyst and granuloma.


Therapeutic aimsThe goal of treatment is to resolve inflammation of the epiglottis.

TherapyHorses should be rested for a minimum of 14 days. Topical admin-istration of throat spray is applied transnasally twice daily for 10 days to 2 weeks.90,91 In addition, systemic anti-inflammatory medi-cation such as phenylbutazone is recommended for 10 to 14 days. If aspiration pneumonia is suspected, broad-spectrum antimicro-bial therapy is recommended.90 Endoscopic examination of the airway should be repeated in 2 weeks.If significant loss/deformity of epiglottic cartilage is present

redundant aryepiglottic membrane may be needed to treat medial deviation of the aryepiglottic fold.92 Additionally a laryngeal tie-forward can be recommended if DDSP is observed.92

PrognosisPrognosis for return to performance is excellent unless epiglottic chondritis is present. Complications resulting from epiglottitis occur in approximately 28% of cases and include epiglottic deform-ity, which can occur if the epiglottic cartilage is exposed and chon-dritis occurs.90 Also, epiglottic entrapment, medial deviation of the aryepiglottic folds and DDSP can occur following epiglottitis due to the subepiglottic inflammation.9093

Prevention


the procedure can be carried out after performing a laryngotomy under general anesthesia and retroverting the epiglottic cartilage to access the left and right aryepiglottic fold. A very small percentage of horses respond to rest and local treatment with topical anti-inflammatory throat spray and systemic anti-inflammatory medication.87

If the disease is seen in association with DDSP, it is not always necessary to treat the condition if treatment of the DDSP is done.

PrognosisSeventy-five percent of horses that have surgery have objective improvement in performance.89

Prevention

There is no known method of prevention.


EtiologyThe cause of this condition is unknown.

PathophysiologyThe aryepiglottic tissue that attaches the lateral aspect of the cor-niculate process of the arytenoid cartilage to the lateral edge of the epiglottis collapses dynamically across the rima glottidis during intense exercise, resulting in inspiratory airway obstruction. Com-puter modeling studies have revealed that the contralateral aryepi-glottic fold in a horse with unilateral laryngeal collapse (or partial abduction) is subjected to more negative inspiratory pressure.89

Epidemiology

Medial deviation of the aryepiglottic folds has been diagnosed in racing Thoroughbreds, Standardbreds, and Arabians.87

Epiglottitis Epiglottis is inflammation of the epiglottic mucosa, and at

times, the tip of the epiglottic cartilage. Treatment includes rest and systemic and topical anti-

inflammatory therapy. The prognosis worsens when epiglottic cartilage chondritis is

present,. Complications of epiglottitis include epiglottic entrapment,

DDSP, and deformity of the epiglottic cartilage.

Fig 26.23 Endoscopic image of the larynx of a horse during resection of left aryepiglottic fold.

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results from perivascular injection of caustic substances or trauma involving the jugular furrow, due to the close proximity of the jugular vein, recurrent laryngeal nerve, and vagosympathetic trunk. Horners syndrome is recognized based upon clinical signs of uni-lateral ptosis, miosis, dropped eyelid, and sweating near the base of the ear, due to loss of sympathetic innervation. An important char-acteristic of Horners syndrome is dilation of the vascular bed of the ipsilateral nasal cavity. Sympathetic nerve damage causes the horse to lose its ability to constrict the nasal vascular bed, leading to reduced airflow that can be detected manually.The larynx is palpated for evidence of atrophy of the cricoaryte-

noid dorsalis (CAD) muscle. This is done by using the index fingers to palpate the dorsal aspect of the cricoid cartilage and muscular processes for symmetry (Fig. 26.24) The laryngeal musculature is best evaluated using external and/or esophageal ultrasound.99

Historically, the absence of arytenoid cartilage adductor move-ment can be identified by the thoracolaryngeal reflex (slap test).100 While standing on the left side of the horse, one could place two fingers of the left hand on the lateral aspect of the larynx, and using the right hand, slap the wither area. A positive slap test will elicit a contraction of the adductor muscles and a twitching can be felt over the contralateral side of the larynx. Horses with RLN tend to make a grunt sound and/or a hoarse whistling noise during inspiration.


EtiologyThe etiology of epiglottitis is unknown, though speculative causes include trauma due to poor-quality hay, the presence of a foreign body, respiratory tract infection, and allergic reaction.

PathophysiologyRespiratory noise and dysphagia are caused by swelling of the epi-glottis with subsequent partial occlusion of the airway and abnor-mal function of the epiglottis.

Epidemiology

Epiglottitis is diagnosed frequently in racehorses but has been seen in older brood mares.90

Laryngealhemiplegia Laryngeal hemiplegia is more commonly a bilateral

mononeuropathy affecting more severely the left recurrent laryngeal nerve: thus it is referred to commonly as recurrent laryngeal neuropathy (RLN).93

Others causes of laryngeal hemiplegia include trauma, arytenoid chondritis, and fourth branchial arch defect.RLN is a distal axonopathy leading to preferential loss of fiber type 2x with clinical implications predominantly on the left side.9395

Laryngeal hemiplegia (grade IV) is frequently diagnosed during endoscopic examination of the larynx at rest, but exercise endoscopy can be required to identify laryngeal collapse on hemiparesis (grade IIII).

The current surgical therapy of choice includes laryngoplasty with ventriculocordectomy for treatment of poor performance and unilateral or bilateral ventriculocordectomy for treatment of abnormal noise.

Recognition

History and presenting complaintHorses with RLN or roarers have a history of making an inspiratory noise during exercise and/or poor performance. The term roaring describes an unnatural sound rattling, snoring, and whistling during inspiration.96,97 The noise is heard only during exercise, immediately after exercise during hyperpnea, or when the horse is startled (grunt test). These horses also have abnormal vocalization. Many sport horses are unaffected until 56 years of age such that a history of normal breathing during exercise followed by progres-sively more noisy breathing is often reported. Exercise intolerance experienced by horses with RLN is associated with decreased venti-lation due to laryngeal collapse.89,98 The degree of impairment reflects a combination of factors such as degree of laryngeal col-lapse, athletic capacity, and the length and intensity of competition. The major complaint of horses performing lower levels of work, such as show hunters and trail horses, is the presence of an abnor-mal inspiratory noise during exercise.

Physical examinationA thorough examination can help to identify the causes of the disease, though the majority of cases of RLN are idiopathic. The throat and cervical areas are inspected for signs of trauma or deform-ity. Horners syndrome can accompany laryngeal hemiplegia that Fig 26.24 Illustration of laryngeal palpation technique.


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access to videoendoscopy. RLN is identified by the presence of sound throughout inhalation and exhalation and the presence of three frequency bands centered on 0.3 kHz, 1.6 kHz, and 3.8 kHz are seen during inhalation (Fig. 26.28A, B).31

Laryngeal ultrasound is becoming one of the most useful diag-nostic modalities in identifying horses with RLN and differentiating them from chondritis. First described in 2006,99 percutaneous

Special examinationEndoscopic exam at rest allows assessment of the laryngeal anatomy as well as some indication of function by categorizing the degree of arytenoid movement and synchrony (see Table 26.2).101,102 The diag-nosis of RLN with complete paralysis (grade IV) is made by endo-scopic examination of the larynx at rest and observation of a midline or paramedian position of the corniculate process without morpho-logical evidence of enlargement or deformation of the cartilage (i.e. arytenoid chondritis). A clinical diagnosis of RLN must not be made solely by observation of motion abnormalities (such as weak, paretic, partially paralyzed, flutter, and/or hesitation) of the aryte-noid cartilage at rest. If one suspects laryngeal collapse (arytenoid cartilage collapse [ACC] (Fig. 26.25) or vocal cord collapse [VCC] (Fig. 26.26)), dynamic videoendoscopy (treadmill or overground) is necessary to confirm the diagnosis and identify concomitant obstruction.1,37,103105 During exercise, the laryngeal grade can also be classified as grade A, B, or C (Fig. 26.27).101 Exercise endoscopy allows the precise diagnosis of collapse as well as co-morbid obstruc-tion such that the optimum treatment can be prescribed. For example, horses with partial arytenoid collapse during exercise often have the same or better degree of arytenoid abduction than that obtained after a laryngoplasty. These horses frequently have vocal cord collapse obstructing the ventral aspect of the rima glottidis, with little collapse of the arytenoid cartilage. Therefore ventriculo-cordectomy might alleviate the obstruction.106 If a dynamic exam at exercise is not possible, there is a reasonable correlation between laryngeal grade as show in Table 26.2 and laryngeal grade at exercise (Fig. 26.27);103 horses with a resting laryngeal grade of I or II have a 7% prevalence of laryngeal collapse, while horses with laryngeal grade of III.1, III.2, and III.3 have a prevalence of laryngeal collapse at 44%, 83%, and 100%, respectively.Another modality less frequently used now that dynamic endos-

copy can be done is sound analysis.31 Frequency analysis of airway sounds during exercise can help quantitate the upper airway sounds of horses such that RLN can be diagnosed during exercise without

Table 26.2 Consensus grading system of laryngeal function performed in the standing unsedated horse104

GRADE DESCRIPTION SUB-GRADE

I All arytenoid cartilage movements are synchronous and symmetrical and full arytenoid cartilage abduction can be achieved and maintained

II Arytenoid cartilage movements are asynchronous and/or asymmetrical but full arytenoid cartilage abduction can be achieved and maintained

1. Transient asynchrony, flutter or delayed movements is seen2. There is asymmetry of the rima glottidis much of the time due to

reduced mobility of the affected arytenoid and vocal fold but there are occasions, typically after swallowing or nasal occlusion, when full symmetrical abduction is achieved and maintained

III Arytenoid cartilage movements are asynchronous and/or asymmetrical but full arytenoid cartilage abduction cannot be achieved and maintained

1. There is asymmetry of the rima glottidis much of the time due to reduced mobility of the arytenoid and vocal fold but there are occasions, typically after swallowing or nasal occlusion, when full symmetrical abduction is achieved but not maintained

2. Obvious arytenoid abductor deficit and arytenoid asymmetry. Full abduction is never achieved

3. Marked but not total arytenoid abductor deficit and asymmetry with little arytenoid movement. Full abduction is never achieved

IV Complete immobility of the arytenoid cartilage and vocal fold

Description generally refers to the left arytenoid cartilage in reference to the right. However, this grading system can apply to the right side (i.e. right grade III.1).)

Fig 26.25 Endoscopic image of the larynx of a horse with grade IV idiopathic laryngeal hemiplegia while the horse is running on the treadmill. Notice how the left arytenoid collapses across the rima glottidis (arrow).

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Fig 26.26 Endoscopic image of the larynx of a horse with grade III idiopathic laryngeal hemiplegia and vocal fold collapse. Notice how the left vocal fold collapses across the rima glottidis (arrow) as well as mild collapse of right aryepiglottic fold.

Fig 26.27 Endoscopic image of a larynx showing the position of the corniculate process of the arytenoids cartilage for each grade of laryngeal position. Zone A represents the position (maximal abduction) for grades I and II; Zone B represents the position for grade III (partial abduction); Zone C represents the position for grade IV laryngeal hemiplegia, or complete paralysis with no abduction.

A

B

C

Fig 26.28 (A) Spectrogram of respiratory sounds from a horse with normal upp

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