Conditions That Predispose to Hypoxemia and Central Cyanosis

The remainder of this section is confined to a discussion of respiratory conditions and cardiovascular anomalies that pre­dispose to hypoxemia and central cyanosis. Impaired pulmonary function may cause hypoxemia and, in some circumstances, cyanosis.

ALVEOLAR HYPOVENTILATION. Alveolar hypoventilation is defined as a reduced volume of inspired air reaching the alveoli per unit time. Alveolar hypoventilation is always asso­ciated with an increased PaCO₂. Conditions associated with alveolar hypoventilation are drug-induced respiratory depres­sion (morphine, barbiturates), brainstem disease (encephalitis,

■ BOX 5.16

Causes of Central Cyanosis in Horses

Common Causes

Bacterial pneumonia, pleuritis, pulmonary abscessation (Rho- dococcus equi, Streptococcus species, other bacteria)

Recurrent airway obstruction (RAO or chronic obstructive pulmonary disease)

Aspiration pneumonia

Viral pneumonia (equine influenza, adenovirus, other viruses)

Equine herpesvirus types 1 and 4 (EHV-1, EHV-4)

Acute bronchointerstitial pneumonia

Prematurity, dysmaturity, immaturity (foals)

Ventricular septal defect with pulmonary hypertension

Tetralogy of Fallot

Toxic methemoglobinemia

Anaphylaxis

Shock (hypovolemic, cardiac, septic)

Less Common Causes

Stenotic nares or choanal atresia

Neoplasia (nose, paranasal sinuses)

Nasal granuloma

Nasopharyngeal cicatrix

Tracheal stenosis, collapse, stricture

Tracheal rupture or perforation

Diaphragmatic hernia

Pneumothorax

Pulmonary edema

Smoke inhalation pneumonia

Interstitial pneumonia

Pneumoconiosis

Atrial septal defect with pulmonary hypertension

Uncommon Causes

Pulmonary lobar hypertrophy (foals)

Embryonal mediastinal cyst

Pulmonary tuberculosis, nocardiosis

Pneumocystis carinii (renamed PneumocystisJtroveci in humans) pneumonia

Air embolism

Pulmonary neoplasia

Transposition of great vessels

Tricuspid atresia

Aortic, pulmonary artery rupture

Interruption of aortic arch

Common ventricle with separate pulmonary outflow chamber

Multiple cardiac anomalies

Methemoglobin reductase deficiency

Lactation tetany

Clostridial diseases

Malignant hyperthermia

Toxic Causes

Sulfur, hydrogen sulfide

α-Naphthyl thiourea (ANTU)

Chlorinated hydrocarbon

Organophosphate, carbamate

Red maple (Acer rubrum)^a

Redroot pigweed (Amaranthus retroflexus)^a

Sudan grass (Sorghum vulgare var.

Mintweed (Salvia reflexa)^a

Lamb's quarters (Chenopodium album)^a

Variegated thistle (Silybum marianum)^a

Winged thistle (Carduus tenuiflorus)^a

^aNitrate accumulator, which causes methemoglobinemia. trauma, hemorrhage, neoplasia), and transection of the cervical spinal cord. All these conditions prevent proper generation and transmission of signals from the respiratory center to respiratory muscles. Other possible causes of alveolar hypoventilation are abnormal respiratory muscle function (diaphragmatic hernia, botulism), thoracic cage abnormalities (rib fracture), increased airway resistance (e.g., stenotic nares, laryngeal stricture or paresis, foreign body obstruction, bronchitis, bronchiectasis), and pleural space disease (inflammatory or neoplastic effu­sions, pneumothorax, hydrothorax, chylothorax, pyothorax, hemothorax).

IMPAIRED DIFFUSION. Impaired diffusion, a second cause of hypoxemia, results from increased thickness of the blood-gas barrier. Equilibrium between alveolar oxygen and pulmonary blood oxygen is not reached because of increases in distance or resistance of barriers through which oxygen must pass to bind to hemoglobin. Because carbon dioxide diffuses more readily than oxygen, the PaCO₂ is not usually increased in conditions that cause impaired diffusion. In fact, PaCO₂ actually may be reduced because of compensatory hyperventilation stimulated by hypoxemia. Conditions that may result in impaired diffusion are pneumonia, pulmonary edema, atelectasis, pul­monary contusions, and pulmonary neoplasms.

VENTILATION-PERFUSION MISMATCH. Ventilation-perfusion mismatch occurs eventually in all generalized pulmonary diseases and is the predominant mechanism by which hypoxemia develops in respiratory conditions. Overall gas exchange is impaired by uneven ventilation and blood flow. Lung areas that are overperfused in relation to ventilation (low ventilation/ perfusion ratio) contribute disproportionate amounts of blood with a low PaO₂ to the systemic circulation.

SHUNTING. Shunting is defined as any mechanism by which blood that has not passed through ventilated areas of the lung is added to arteries of the systemic circulation. The term venous admixture is used to describe venous blood that passes through the lungs without proper oxygenation. Animals with venous admixture often hyperventilate and present with normocapnia or hypocapnia in association with hypoxemia. The most common cause of shunting is congenital heart disease, which allows unoxygenated blood from the right heart to pass directly into the left heart without passing through the pulmonary circulation. Intrapulmonary anatomic shunts can result from pulmonary artery to pulmonary venous fistulae, or from prior to severe lung consolidation that results in large portions of the lung being well perfused but poorly ventilated. Cyanosis or hypoxemia unresponsive to oxygen administration suggests the presence of such congenital cardiac anomalies or intrapulmonary shunts.⁷⁹ Examples of common cyanotic congenital cardiac defects are tetralogy of Fallot, truncus arteriosus, transposition of the great arteries, tricuspid atresia, and hypoplastic left heart syndrome.^77,79 Aside from congenital defects, reversion to fetal circulation should be considered in any critically ill neonatal animal with hypoxemia that is

79 unresponsive to oxygen insufflation.

■ BOX 5.17

Causes of Central Cyanosis in Ruminants

Common Causes

Bacterial pneumonia, pulmonary abscessation (Mannheimia haemolytica [B], Arcanobacterium pyogenes [B], Pasteurella multocida [B], Corynebacterium pseudotuberculosis [O, C], other bacteria)

Viral pneumonia (respiratory syncytial virus [B], ovine progressive pneumonia [O], caprine arthritis-encephalomyelitis [C], other viruses)

Parasitic pneumonia (Dictyocaulus viviparus [B], Dictyocaulus filaria [O, C])

Aspiration pneumonia

Acute bovine pulmonary edema and emphysema (B)

Pulmonary edema

Ventricular septal defect with pulmonary hypertension Tetralogy of Fallot

Toxic methemoglobinemia

Anaphylaxis

Shock (hypovolemic, cardiac, septic)

Rumen bloat

Less Common Causes

Obstruction of nasal passages or paranasal sinuses (neoplasm, granuloma, abscess, other)

Laryngeal abscess

Tracheal stenosis, collapse, stricture

Tracheal rupture, perforation

Diaphragmatic hernia

Prematurity, dysmaturity, immaturity

Inhalation pneumonia (smoke)

Pneumothorax

Hemothorax

Pulmonary contusion

Ventricular septal defect with pulmonic stenosis

Postparturient hemoglobinuria

Clostridial diseases (e.g., malignant edema, blackleg, tetanus) Bluetongue (O)

Obstructive urolithiasis, ruptured urethra

Uncommon Causes

Pleural mesothelioma (B)

Water inhalation (drowning)

Pulmonary adenomatosis (O) Transposition of great vessels Double-outlet right ventricle

Common ventricle with separate pulmonary outflow chamber Acute anthrax

White liver disease (exotic) (O) Sweating sickness (exotic) (B, O)

Toxic Causes

Strychnine Arsenic

Metaldehyde Hydrogen sulfide

Organochlorine, chlorinated hydrocarbon Organophosphate, carbamate

Acute selenium toxicosis Nitrate, nitrite

Perennial broomweed (Gutierrezia microcephala) Oleander (Nerium oleander)

Whitehead (Sphenosciadium capitellatum) Milkweed (Asclepias species) (O) Rhododendron (Andromeda species) Fireweed (Kochia scoparia)

Canary grass (Phalaris species) Kikuyu poisoning (exotic) (B, O) Albizia poisoning (exotic) (B, O) Euphorbia, Sarcostemma poisoning (exotic) (B, O) Acacia poisoning (exotic) (B, O)

Wild onion (Allium validum)^a (O) Variegated thistle (Silybum marianum)^a Redroot pigweed (Amaranthus retroflexus) Sudan grass (Sorghum vulgare var.

Lamb's quarters (Chenopodium album)^a

Many pasture grasses fed during optimum growth conditions^a Locoweeds (Astragalus species, Oxytropis species)^a

^aNitrate accumulator, which causes methemoglobinemia. B, Bovine; C, caprine; O, ovine.

Approach to Diagnosis of Cyanosis

HISTORY. The history should include questions about the duration of the cyanosis (e.g., cyanosis that has been present since birth or an early age may indicate congenital heart disease with right-to-left shunting); possible exposure to toxic plants or chemicals that may result in production of abnormal types of hemoglobin; evidence of an abnormal respiratory pattern (respiratory distress, inspiratory stridor, cough); and signs of episodic weakness or syncope that may be consistent with congenital cardiac anomalies or severe upper airway obstruction (e.g., tracheal collapse or severe laryngeal edema associated with necrotic laryngitis in calves).

PHYSICAL EXAMINATION. A thorough physical examination should include visual inspection to detect abnormalities in the respiratory pattern (e.g., tachypnea, respiratory distress, stridor) and careful auscultation of the larynx, trachea, and lungs to provide information that helps further define the cause of respiratory dysfunction. Rebreathing bags (12- to 52-L capacity for adult horses and cattle; 6- to 12-L capacity for calves, foals, and small ruminants) cause temporary buildup of CO₂, stimulat­ing the respiratory center, prompting deep breathing imme­diately after the bag is removed and the animal is allowed to inspire room air. Loud breath sounds, pulmonary crackles and wheezes, or pleural friction rubs may suggest cyanosis in association with pathologic respiratory conditions. Loud cardiac murmurs accompanied by precordial thrills point to congenital heart disease as the cause of cyanosis.

Palpation and percussion of the thorax are important examina­tion procedures in animals with cyanosis. Chest palpation may reveal pleural friction rubs or the pain and crepitus associated with rib fractures. Increased resonance on percussion may indicate pneumothorax, whereas decreased resonance suggests pulmonary congestion or consolidation, pleural effusion, or a space-occupying lesion in the thorax.

ENDOSCOPIC EXAMINATION. An endoscopic examination should be performed if upper airway obstruction or malforma­tion is suspected (see the Cough, Nasal Discharge, and Respiratory Distress [Dyspnea] sections earlier).

RADIOGRAPHIC EXAMINATION. Radiographs of the upper respiratory tract and thorax can be used to further characterize pathologic respiratory conditions. Abnormalities detected using these modalities include space-occupying lesions in the oro­pharynx, nasopharynx, or larynx; tracheal compression or collapse; enlargement or distortion of the cardiac silhouette; pulmonary consolidation; pneumothorax; pleural effusion; and pulmonary abscessation.

ULTRASOUND EXAMINATION. Ultrasound examination of the chest and heart is indicated to characterize cardiac anomalies and to detect the presence and determine the extent of pleural effusion, pulmonary consolidation, and pulmonary abscessation.

ARTERIAL BLOOD GAS ANALYSIS. Arterial blood gas analysis is indicated to determine O₂ and CO₂ tension (see the Respira­tory Distress [Dyspnea] section earlier).

COMPLETE BLOOD COUNT. A complete blood count should be performed to determine if polycythemia or inflammatory altera­tions in the leukogram are present. Polycythemia may develop secondary to chronic hypoxemia associated with long-standing pulmonary disease or right-to-left shunting. An inflammatory leukogram is consistent with a diagnosis of bacterial or aspiration pneumonia or other inflammatory respiratory condition.

HEPARINIZED BLOOD. A sample of heparinized blood should be shaken gently in the air for 15 minutes. Reduced hemoglobin (cardiovascular or respiratory disease) turns red on exposure to air, whereas methemoglobin remains chocolate brown after shaking.

SPECTROSCOPIC EXAMINATION. Spectroscopic examination is necessary to determine if methemoglobin is present. Met­hemoglobin is stable in refrigerated heparinized blood for only a few hours. To preserve methemoglobin, 1 part of blood can be mixed with 20 parts of phosphate-buffered saline (pH 6.6) or diluted 1:20 in distilled water. These diluted samples can be refrigerated or frozen until they are analyzed.

Abnormal Respiratory Noise (Stridor) thoracic inlet.⁷⁰ Nasal resistance, most of which is caused by resistance just within the external nares, comprises more than 50% of the total upper airway resistance in the horse.^69,82 In most species, including ruminants, this resistance can be bypassed by mouth breathing to accommodate the high airflow rates that accompany strenuous exercise. The horse, in contrast, is limited to nasal breathing even during exercise’’’ because the larynx is firmly maintained in the nasopharynx by the tight seal formed around it by the muscular palatopharyngeal

83 84 ring (intrapharyngeal osteum), except during swallowing., Therefore mechanisms other than mouth breathing are neces­sary to reduce the energy cost of breathing in the horse.^68,81,83 These mechanisms include dilation of the distensible external nares by actively pulling the alar folds laterally, vasoconstriction in the erectile nasal vascular tissues to reduce congestion in the nasal mucosa, straightening of the respiratory tract, and dilation of the larynx by abduction of the vocal folds.⁶⁸,⁷⁰,^80-83,,

The horse is capable of generating high respiratory rates during fast exercise. This is accomplished at the canter and gallop, but not at the trot, by locking respiration to locomotion so that the horse takes one breath for each stride.^84,87-89 Exhala­tion occurs each time the lead forelimb strikes the ground.^83,84,87 The horse can swallow during fast galloping exercise; the entire process is completed in exactly a two-stride sequence.^84,90

At all levels of the respiratory tract, respiratory sounds are thought to result from vibrations in tissue and sudden changes in the pressure of gas moving in the airway lumen.^70,84 Airflow in the normal respiratory tract at rest occurs in a laminar fashion (i.e., the air closest to the wall of the airway is almost stationary, whereas succeeding layers toward the center of the lumen move progressively more rapidly). Respiration in normal horses and in ruminants at rest does not generate easily audible sounds.

High rates of gas flow and airway narrowing increase both the tendency for dynamic collapse and the degree of turbulence and genesis of sounds. High peak flow rates of 125 mL/s/kg have been reported in galloping horses. During exercise significant sound frequencies are generated and can be detected using sound spectrographs or radio stethoscopes, although most of these sounds are of frequencies and amplitudes not detectable by the human ear.^91,92 Deformities in the wall and masses in the lumen of the airway cause airway narrowing and further disturbances in laminar flow, resulting in more severe turbulence and sudden changes in the pressure of moving gas, which may generate audible sounds.⁸⁴ High airflow rates are necessary to induce audible stridor; therefore examination of the horse at exercise is an essential part of the physical examination.^83,84

Stridor is best heard during inspiration in most cases because the usual source of origin, the upper airway, is subject to dynamic narrowing during the inspiratory phase of the respiratory cycle.^68,69,81 In particular, nonfixed obstructions such as the paretic vocal folds of horses with idiopathic laryngeal hemiplegia (ILH) cause obstruction to airflow and turbulence only when dynamically drawn into the airway by the high inspiratory airflow rates that accompany fast exercise. Other obstructions such as arytenoid chondritis are fixed and obstruct airflow during both inspiration and expiration, which frequently result in audible stridor during both phases of respiration.

The pharynx is the site of greatest airway angulation because of flexion of the atlanto-occipital joint. At rest the horse’s head is usually held at about 50 degrees to the horizontal plane.⁸⁴ At gallop the horse extends its head and neck and thus straight­ens the pharyngeal airway.⁸⁴ This maneuver also stretches and straightens the trachea, making it less compliant and less subject to dynamic narrowing during inspiration. When ridden at a collected canter, the horse is forced to flex its poll so that its face is nearly vertical, thereby increasing the angulation of the pharyngeal airway and the obstruction to gas flow at this point.⁸⁴ Therefore abnormal respiratory sounds originating in the pharyngeal region are often more easily heard when the horse is ridden at a collected canter than when it is exercised at a full, extended gallop.⁸³-⁸⁴

Because food animals are not normally expected to perform fast exercise, signs of stridor are usually present at rest when the animals are presented to veterinarians for examination. Stridor in resting animals usually indicates moderate to severe upper airway obstruction of a fixed nature. In ruminants the epiglottis is relatively short and blunt, and the palatopharyngeal ring allows the laryngopalatal dislocation necessary for mouth breathing. In conditions that give rise to respiratory distress and mouth breathing, the turbulence produced is often sufficient to induce abnormal (grunting) expiratory sounds, which may be classified as expiratory stridor. The external nares of cattle are much less compliant than those of sheep, goats, and horses, which prevents dynamic collapse during inspiration; thus conditions such as paresis of the nares that cause stridor in sheep, goats, and horses do not cause stridor in cattle (Boxes 5.18 and 5.19).

Approach to Diagnosis of Stridor

HISTORY. The procedure for taking a history should follow that used in the evaluation of cough and nasal discharge (see the Cough and Nasal Discharge sections earlier). The history should also include the duration of ownership; time of onset of the clinical signs of stridor; progression of clinical signs; presence or absence of the noise at rest; relation of noise to fitness; relation of noise to speed, duration, and direction of work; relation of noise to head position during work; association of noise with poor performance or exercise intolerance; and other signs of respiratory tract, oropharyngeal, or neurologic disease (e.g., nasal discharge, cough, dysphagia, retropharyngeal swelling).

PHYSICAL EXAMINATION. A physical examination of the entire respiratory tract at rest should be performed as described for cough and respiratory distress. In addition, the presence or absence of stridor at rest should be ascertained by listening

■ BOX 5.18

Causes of Stridor in Horses

Common Causes

Idiopathic laryngeal hemiplegia (ILH, roaring)

Dorsal displacement of the soft palate (laryngopalatal dislocation) Epiglottic entrapment

Retropharyngeal abscess

Strangles (Streptococcus equi infection)

Guttural pouch empyema

Chronic pharyngeal lymphoid hyperplasia Arytenoid chondritis

Guttural pouch mycosis

Laxity of the alar cartilage

Less Common Causes

Arytenoid chondroma, chondropathy

Pharyngeal paresis

Botulism, shaker foal

Dynamic collapse of the pharynx Subepiglottal, pharyngeal cyst

Subepiglottal abscess

Epiglottal retroversion

Guttural pouch tympany

Guttural pouch neoplasia

Rostral displacement of the palatopharyngeal arch

Nasal fungal infection (e.g., aspergillosis, rhinophycomycosis) Nasal polyp

Nasal foreign body

Nasal trauma

Nasal tumor

Nasopharyngeal cicatrix

Progressive ethmoidal hematoma

Sinusitis (sinus empyema)

Sinus cyst

Sinus tumor

Atheroma

Laryngeal trauma

Tracheal collapse (scabbard trachea)

Tracheal stricture, stenosis

Tracheal chondroma

Tracheal rupture, perforation

Stenotic nares

Laryngeal edema Purpura hemorrhagica

Anaphylaxis or acute drug reaction

Chronic lead poisoning

Choanal (posterior nares) atresia, hypoplasia (foals) Fracture of laryngeal cartilages

Laryngeal granuloma, scar tissue

Equine influenza Exercise-induced pulmonary hemorrhage (EIPH)

Jugular thrombosis

Hyperkalemic periodic paralysis (HYPP)

Uncommon Causes

Amyloidosis (cutaneous, nasal) Lymphosarcoma, lymphoma Bee or wasp sting

Snakebite

Thyroid adenoma, adenocarcinoma

Vesicular stomatitis

Retrobulbar neoplasia

Dystrophic myodegeneration (white muscle disease)

Neoplasia (oral, mandibular, maxillary, laryngeal, pharyngeal, tracheal)

Coccidioidomycosis

Inhalation pneumonia, smoke inhalation Burns (thermal, chemical)

Congestive cardiac failure

Cutaneous habronemiasis

Unilateral ventral displacement of the roof of the nasopharynx Epiglottiditis

Hyoid bone injuries

Fungal granuloma, maduromycosis, rhinosporidiosis, mycetoma, cryptococcal rhinitis, equine nasal granuloma

Goiter

Hypertrophic ossification of the laryngeal cartilages Abnormalities of the nasal septum

Intramural esophageal cyst

Foreign body (nasal, pharyngeal, laryngeal, tracheal, bronchial) Hyperparathyroidism

Phycomycosis, pythiosis

Anaerobic abscesses (e.g., Clostridium perfringens) Besnoitiosis, globidiosis (exotic)

Glanders (exotic)

Toxic Causes

Organophosphate-induced laryngeal paralysis Lead-induced laryngeal paresis

Reserpine

■ BOX 5.19

Causes of Stridor in Ruminants

Common Causes

Necrotic laryngitis (calf diphtheria) (B, O)

Abscess (pharyngeal, laryngeal, retropharyngeal, oral)

Nose bots (Oestrus ovis) (C, O)

Caseous lymphadenitis (Corynebacterium pseudotuberculosis) (C, O)

Actinobacillosis (wooden tongue, nasal actinobacillosis) Nasal adenocarcinoma, adenoma, adenopapilloma, polyp (C, O) Trauma (oral, nasal, pharyngeal, laryngeal, tracheal) Anaphylaxis or drug reaction

Sinusitis

Foreign body (nasal, oral, pharyngeal, laryngeal, tracheal, bronchial)

Less Common Causes

Actinomycosis (lumpy jaw)

Tracheal stenosis, collapse, stricture

Bovine leukosis (enzootic adult lymphosarcoma) (B)

Sporadic bovine leukosis (adult multicentric lymphosarcoma) (B) Thymic lymphosarcoma (juvenile) (B)

Mannheimia haemolytica or Pasteurella multocida pneumonia (includes shipping fever and enzootic calf pneumonia) (B)

Infectious bovine rhinotracheitis (IBR; BHV-1) (B)

Atypical interstitial pneumonia (B)

Malignant catarrhal fever (B)

Vesicular stomatitis

Clostridial infection of the head (O)

Pulmonary embolism from posterior vena cava thrombosis (B) Snakebite

Bee or wasp sting

Bovine nasal granuloma, atopic rhinitis (summer snuffles) (B) Honker syndrome in feedlot cattle (B)

Neoplasia (nasal, paranasal sinus, oral, pharyngeal, laryngeal, tracheal, maxillary, mandibular, retrobulbar)

Congenital abnormalities

Inhalation pneumonia, smoke inhalation

Uncommon Causes

Tuberculosis (B)

Congenital cystic nasal conchae (B)

Choanal atresia (O)

Salivary cyst, mucocele, ranula, trauma (C)

Photosensitization in Southdown and Corriedale sheep (O)

Fungal granuloma, maduromycosis, rhinosporidiosis, mycetoma (B, C)

Phycomycosis, pythiosis (B)

Goiter, iodine deficiency

Hyperparathyroidism (B, C)

Enzootic ataxia, swayback (C, O)

Besnoitiosis, globidiosis (exotic)

Endemic ethmoid hematoma (exotic) (B)

African bovine malignant catarrhal fever (exotic) (B)

Lumpy skin disease (exotic) (B)

Nasal schistosomiasis (exotic)

Virulent sheep and goat pox (exotic) (C, O)

Peste des petits ruminants (exotic) (C, O) Gedoelstia hasleri nasal bots (exotic) (C, O)

B, Bovine; C, caprine; O, ovine.

at the nostrils, and digital pressure should be applied to the retropharyngeal region and to the larynx during palpation of these areas to evaluate whether stridor or pain (or both) can be induced easily or exacerbated. The dorsal surface of the larynx should be palpated with the fingertips with the horse relaxed and its head and neck in an extended position. This permits comparison of the prominence of the muscular process of the arytenoid cartilages and the thickness of the cricoary- tenoideus dorsalis (CAD) muscle, both of which are affected in horses with atrophy of the CAD muscle in association with ILH. Air turbulence, flattening, swelling, and pain should be assessed during palpation of the extrathoracic airway. The larynx, trachea, and lungs should be carefully auscultated, and the chest should be percussed. A thorough oral examination should be completed, particularly in ruminants; in cattle this should include palpation of the base of the tongue, the oro­pharynx, and, if possible, the larynx through the oral cavity.

FIELD EXERCISE TESTING.⁸⁴ In performance horses most examinations are carried out because the horse makes a noise only when worked, because of exercise intolerance or poor performance, or as part of a prepurchase examination. Unless a high-speed treadmill is available, the exercise testing should be completed under saddle with a competent rider, preferably with an intensity of work that matches the horse's normal activity., It is less satisfactory but often necessary to work the horse on a lunge line, in which case it should be lunged in both directions.⁸³

The horse should be worked in a circle about 30 yards in diameter so that it passes close to the observer on each circuit.⁸⁴ The observer should first identify the expiratory sound by its association with locomotion and then try to fit abnormal sounds into this base rhythm. At fast speeds, respiration is rapid; thus the observer should not stand too far away from the horse because the slow speed at which sound is transmitted confuses interpretation of whether the sound is inspiratory or expira­tory.^84,90 In cold weather the visibility of exhaled breath aids interpretation. It is important to ride the horse in both directions because an abnormal sound is frequently heard more clearly when the horse is exercising in one direction than in the other.⁸³ If the presence or character of a respiratory noise remains in doubt after the horse has been exercised in a circle at a collected canter, the horse should be galloped until it is blowing hard and then ridden past the observer at a fast gallop.⁸³

A satisfactory exercise test should include at least 5 minutes of work at the canter, after which the horse should immediately be brought over to the observer so that the character and sequence of abnormal sounds that persist can be determined. All horses that have been worked adequately make a loud expiratory blowing sound at this time. Turbulence of airflow in the larynx may be audible with a stethoscope.⁸⁴ Inducing adduction of the vocal fold, particularly on the right side, by applying gentle pressure in a rostromedial direction to the muscular process of the arytenoid cartilage often accentuates an inspiratory noise in horses with laryngeal hemiplegia. Noises originating from unilateral lesions in the nasal passages are easily localized because the sound can be eliminated by alternately blocking off airflow through each nostril with the hand. Temporary occlusion of both nostrils simultaneously may provoke laryngopalatal dislocation and a loud gurgling sound in a susceptible horse.^83,84 The presence of nasal discharge or blood at the nostrils should be noted, and the time required for the heart and respiratory rates to return to preexercise values should be interpreted in light of the severity of the exercise test.⁸³

INTERPRETATION OF ABNORMAL SOUNDS. A normal horse makes no audible respiratory sound at rest and when exercised at a canter or slow gallop makes only a blowing expiratory 708384

sound.^,83^, In unfit horses, particularly overweight ones, an inspiratory sound is also frequently audible. This sound can be quite loud, and it may be difficult to differentiate from sounds caused by abnormalities of the respiratory tract.^82,83 Thus evaluation of the horse's “wind” is best carried out when the horse is in fit condition for its intended use. It takes at least 1 month for an older horse that has been turned out to pasture to regain a satisfactory level of fitness to perform a meaningful wind examination. Many normal horses produce a harsh expiratory “high blowing sound” of variable pitch, which results from resonance in the cavity of the false nostril during expiration.^83,84,90 If the source of the stridor remains in doubt, temporary suturing of the alar fold dorsal to the nostril can help localize noises suspected of being caused by vibration of the alar fold.

Horses with ILH make a rather characteristic biphasic sound, the inspiratory sound occurring between successive expiratory sounds. The pitch of the sound can vary from a whistle to a deep roar, the lower-pitched note giving rise to the so-called sawing wood sounds.⁸⁴ Sonographic and spectrographic analysis of the sounds produced by “roarers” indicates that the range of sound frequencies generated by these horses is the same as that produced by normal horses.^91,92 However, horses that make an audible whistle generate an intense band of frequencies centered on 1.9 kHz that are thought to result from amplifica­tion by the still-patent lateral ventricle of the frequency gener­ated by vibration of the incompletely abducted left vocal fold.⁹² In a normal horse the left vocal fold is fully abducted, and the cavity of the lateral ventricle is thus obliterated during strenuous exercise.⁸⁶

The sounds generated by horses with laryngeal chondritis, severe proliferative pharyngeal lymphoid hyperplasia, epiglottic entrapment, and tracheal stenosis can be similar to those caused by ILH.^83,84 Laryngopalatal dislocation (dorsal displacement of the soft palate) gives rise to a transient, vibrant, gurgling 698384

sound. ’ ’ In many instances a severe exercise test is required to induce this condition; thus this sound may be heard only during a race. ’ ’ It is thought that the condition may occur when pharyngeal stimulation causes swallowing during fast exercise.⁸⁴ Instead of the horse completing the process and regaining the laryngopalatal seal consistent with the respiratory position of the larynx in the nasopharynx, the tip of the epiglottis disengages from the rostroventral aspect of the palatopharyngeal ring (the caudal free border of the soft palate), resulting in the entire epiglottis slipping ventral to the soft palate. At the subsequent inspiration the palatopharyngeal arch tends to be drawn into the rima glottis, and at expiration it is driven toward the roof of the pharynx by the airstream. The palatopharyngeal arch acts as an airway obstruction, and the tissue vibration and resulting turbulence generate a sound of varying pitch and intensity, often described as gurgling followed by swallowing.⁸⁴ The horse often slows suddenly or stops when this event occurs, and the jockey often reports that the horse stopped after “choking” or “swallowing its tongue.” If repeated swallowing is successful in relocating the normal laryngopalatal respiratory arrangement, the horse often continues to race after slowing or stopping.⁷⁰

Gross obstruction of the airway by pressure from pus-filled guttural pouches, retropharyngeal abscesses, large subepiglottal cysts or abscesses, or large proliferative lesions (e.g., laryngeal tumors) produces loud, stertorous breathing (snoring) often heard at rest and readily so with exercise; both inspiratory and expiratory sounds are clearly audible.⁸⁴

In a normal horse the pattern of respiratory sounds is regular and synchronized with the pace of the exercise. Laryngeal irritation caused by exudate from the upper or lower airway, pharyngeal lymphoid hyperplasia, or other inflammatory or space-occupying conditions causes the horse to swallow more frequently during exercise, which generates an irregular pattern of respiratory sounds characterized at the canter and gallop by a respiratory cycle of double the normal length.^84,90

Interpretation of stridor in yearlings presented for sale is difficult because these animals are rarely fit and it is usually possible to exercise them only at a canter on a lunge line. It has been shown that resentment of restraint under such cir­cumstances can significantly alter the linking of locomotion and respiration, which complicates recognition of the respiratory phasing of noise production.⁸⁶ In addition, there is not always a close correlation between noise production, endoscopically visible abnormalities, and signs of exercise intolerance even in fit adult horses.^{70, 83}

ENDOSCOPIC EXAMINATION. Endoscopic examination of the upper airway is the most useful diagnostic procedure for investigating stridor. The examination should be performed at rest and, if possible, repeated during exercise in the field or on a high-speed treadmill. Endoscopic examination immediately after cessation of exercise is less satisfactory than endoscopy during exercise because dynamic collapse of the rima glottis terminates rapidly on cessation of exercise. The availability of self-contained portable videoendoscopy equipment allows visualization of the pharynx and larynx during over-the-ground exercise and permits digital video-image capture and analysis. Over-the-ground videoendoscopy has the distinct advantage of allowing the horse to be examined under the exact conditions under which the stridor occurs.

Because sedatives and tranquilizers may alter the tone and function of the muscles supporting laryngeal and pharyngeal anatomy, endoscopic examination should be performed without chemical restraint whenever possible.⁷⁰ The nasal passages, conchae (turbinates) (including the ethmoidal concha), nasal septum, pharynx, guttural pouches, larynx, and trachea should be examined through both nostrils so that the presence, nature, and source of exudates and the presence of anatomic or functional abnormalities or mass lesions can be determined. Because the nasal passages are not positioned on the midline, the larynx is viewed slightly obliquely when examined from the left or the right ventral meatus and may appear slightly asymmetric. Thus visually apparent asymmetry of the larynx should be confirmed by examining these structures through both nostrils.^70,83

Interpretation of the findings of the endoscopic examination of the pharynx and larynx is by no means straightforward. The results can be influenced by the day the examination was done, the use of sedation, the side through which the endoscope was passed, and the observer’s interpretation. The appearance of laryngeal symmetry or asymmetry in resting horses varies considerably and therefore is of limited clinical usefulness unless complete hemiparalysis is present. Many horses have asyn­chronous or asymmetric laryngeal movement at rest but not during exercise, whereas other horses have a normal-appearing larynx at rest but suffer dynamic collapse during exercise. Interpretation of findings is improved by use of an objective grading system, which includes assessment of the ratio of the areas of the left and right half of the rima glottis, and by correlating findings at rest with those observed on video­endoscopy performed during maximal exercise.⁹³ For evaluation of the larynx at rest, full abduction of the vocal folds should be induced by exercise or by temporary occlusion of the nostrils.⁸³ Contralateral adductory laryngeal movement should be stimulated by slapping the horse just behind the withers (slap test).⁹⁴ To induce the horse to swallow, the tip of the epiglottis should be touched with the endoscope, or water should be flushed through the endoscope. These maneuvers help to establish whether movement of the arytenoid cartilages is synchronous and symmetric and increase the predictive value of endoscopic observations, allowing laryngeal function to be graded as follows.⁹³

• Grade 1: Synchronous, full adduction and abduction of the left and right arytenoid cartilages (considered normal).

• Grade 2: Asynchronous movement such as hesitation, flut­tering, or adductor weakness of the left arytenoid cartilage during inspiration, expiration, or both, but full abduction of the left arytenoid cartilage, inducible by nasal occlusion or swallowing. Grade 2 findings are considered a normal variation and are not usually associated with dynamic airway collapse during exercise.

• Grade 3: Asynchronous movement of the left arytenoid cartilage during inspiration, expiration, or both, but full abduction is not inducible by nasal occlusion or induction of swallowing. The true functional significance of grade 3 findings can be determined only by performing endoscopic examination during maximal exercise, a procedure that has led to subclassification of grade 3 findings.⁹⁵ Some grade 3 horses (grade 3A) are able to achieve full abduction during exercise, whereas others maintain a partly abducted position similar to the resting position (grade 3B) or experience dynamic collapse (grade 3C).⁹⁵

• Grade 4: Marked asymmetry of the larynx at rest and no substantial movement of the left arytenoid cartilage during any phase of respiration. These horses have complete left laryngeal hemiplegia, are true “roarers,” and consistently experience dynamic collapse on inspiration during strenuous exercise.⁹³

Performing an endoscopic examination during exercise over ground or on a high-speed treadmill makes it possible for a stationary observer to gain a good dynamic appreciation of the significance of upper airway abnormalities (i.e., dynamic endoscopy)^95-99 (see the Exercise Intolerance and Poor Perfor­mance in Horses section later). Dynamic changes in airway lumen diameter occur quickly during treadmill endoscopy and may be difficult to visualize; therefore the endoscopic examina­tion should be videotaped for later playback in slow motion and freeze frame.⁹⁹ Racehorses should be exercised maximally and to exhaustion because some abnormalities are apparent only at maximal exercise toward the end of a race when pharyngeal or laryngeal muscles become fatigued and are no longer able to resist the transmural pressure gradient, which tends to induce dynamic collapse of the upper airway during inspiration.^95-99 Endoscopic identification of an upper respiratory tract abnormality in a resting horse does not necessarily mean that it is inducing a problem during exercise, and, conversely, the absence of an upper respiratory tract abnormality at rest does not rule out the possibility of intermittent airway obstruc­tion during strenuous exercise. For example, dorsal displacement of the soft palate, epiglottic entrapment, dorsal displacement of the epiglottis, dynamic collapse of the left arytenoid cartilage or vocal fold (or both), and unilateral or bilateral ventral displacement of the roof of the pharynx (dynamic pharyngeal collapse) have been observed during treadmill exercise in horses 9599 with an endoscopically normal upper airway at rest.

RADIOGRAPHIC EXAMINATION. Radiographic examination of the nasal passages, paranasal sinuses, pharynx, retropharyngeal area (including guttural pouches), larynx, and proximal trachea is indicated to confirm anatomic or functional problems or space-occupying lesions not definitively diagnosed by clinical examination and endoscopy (see the Nasal Discharge and Respiratory Distress [Dyspnea] sections earlier). Radiography is particularly useful for visualizing subepiglottic masses such as cysts or abscesses and for evaluating the epiglottis of the horse when it is obscured from endoscopic view by dorsal displacement of the soft palate or other space-occupying lesions. An accurate assessment of epiglottic length can also be made from standardized true lateral radiographs of the larynx by measuring the distance from the body of the thyroid cartilage to the tip of the epiglottis (thyroepiglottic length).¹⁰⁰ The mean ± SD (standard deviation) thyroepiglottic length in normal Thoroughbreds is reported to be 8.76 ± 0.44 cm.¹⁰⁰ Significantly shortened thyroepiglottic lengths have been recorded in Thoroughbreds with dorsal displacement of the soft palate (laryngopalatal dislocation) and in those with entrapment of the epiglottis in the aryepiglottic folds.¹⁰⁰ Tracheal diseases such as chondroma or dynamic collapse may be visualized on radiographs of the trachea, particularly those made during the inspiratory phase.

ULTRASOUND EXAMINATION. Ultrasound examination of externally visible lesions, such as possible retropharyngeal abscesses that may be impinging on the airway, helps to characterize lesions and assist in the collection of samples by aspiration or biopsy. Transcutaneous ultrasound examination of the larynx may also provide useful information.

BIOPSY. Biopsy and histologic evaluation of samples are indicated to diagnose certain mass lesions such as neoplasms, cysts, polyps, fungal granulomas, or foreign body granulomas in or surrounding the airway. Masses in the airway can be biopsied through the biopsy channel of an endoscope, but these samples inevitably are small. Larger samples can be collected from lesions in the nares, nasal diverticulum, and nasal passages using uterine biopsy forceps, laparoscopy forceps, or curettes. Hemorrhage usually accompanies such procedures and should be anticipated before the procedure. Biopsies can also be collected at the time of exploratory or corrective surgery from lesions in the nasal passages, pharynx, larynx, and guttural pouches. Lesions such as habronemiasis involving the external nares and lesions in other accessible areas such as the parotid salivary gland can be biopsied percutaneously using Tru-Cut or similar instruments.

ASPIRATION. Aspiration, performed either blindly or with the assistance of ultrasound, followed by cytologic examination and culture of aspirated material is useful in the evaluation of masses such as retropharyngeal abscesses that are causing stridor by impinging on the upper airway.

SWABBING OR SCRAPING. Nasal or nasopharyngeal swabbing or scraping followed by direct cytologic examination and culture is indicated for confirmation of nasal fungal infection and bacterial infections of the upper airway (e.g., strangles).

COMPLETE BLOOD COUNT. A complete blood count includ­ing fibrinogen concentration can be useful in evaluating patients suspected of having a primary or secondary inflammatory condition or conditions such as ethmoidal hematoma and guttural pouch mycosis in which blood-loss anemia is likely to be a complicating problem.