Examination of the equine respiratory system (Proceedings)


Sensitivity is poor diseases such as IAD can be clinically silent for many years. Specificity is also poor, as many diseases share similar signs such as cough

What can we learn?

·         Location of pathology

o    For example, upper v. lower airway

·         Pathophysiology

o    For example, obstructive v. restrictive

·         Etiology

o    For example, infectious v. allergic v. parasitic

What limits the physical exam?

Sensitivity is poor – diseases such as IAD can be clinically silent for many years. Specificity is also poor, as many diseases share similar signs such as cough.

What do we need to know?


(Age, Breed, Sex):  In examining the equine respiratory system, the only one of these that really matters is age.

Chief complaints

Important things to notice are:

·         Abnormal breathing pattern

·         Cough

·         Sneeze

·         Nasal rubbing

·         Nasal discharge

·         Epistaxis

·         Abnormal lung sounds

·         Loss or increase in chest resonance (with percussion)

·         Tachypnea (increased rate)

·         Hyperpnea (increased minute volume)

·         Dyspnea (labored breathing)

·         Noisy breathing

·         Voice changes

·         Malodorous breath

·         Anatomical deviations

·         Subcutaneous emphysema

·         Chest pain

·         Exercise intolerance

·         Weight loss



History is exceptionally important. You can often make your preliminary diagnosis before you ever touch or see the horse. You should make sure to note the following:.

·         Involvement of individual or multiple animals

·         Onset (slow progressive to peracute)

·         Duration (hrs, days, weeks, months, years)

·         Seasonality

·         Association with time of feeding

·         Diet

·         Activity (exercise, discipline)

·         Indoor vs. outdoor living periods

·         Outdoor environment –dust, particulates, pollutants, toxins

·         Hygiene of the indoor environment (e.g. tobacco smoke, ventilation, dust exposure, heat, moisture, mold, fresh water)

·         Exposure to healthy animals (on or off premise)

·         Exposure to sick animals (e.g. viral infection)

·         Immunizations

·         Anthelminthics

·         Recent travel / transport

·         Previous medications and response to treatments

Physical examination

Breathing patterns

Stand back from the animal and observe the breathing pattern from both sides and if possible from the top. It is especially useful if the animal is standing during this examination.  In particular, note the contribution of the rib cage and abdomen to ventilation, the animal's head position (e.g., is it extended to promote air intake), and the extent of nasal flaring.  

‘Normal breathing pattern'

There is near equal contribution from the rib cage and abdomen, although the abdominal component may be more evident clinically during quiet breathing.  Nasal flaring is just barely discernible during inspiration.  Head – neck is maintained in a natural (slightly flexed) posture.

‘Accentuated breathing pattern'

·         Increased abdominal effort

o    increased force and length of excursions of the diaphragm

o    recruitment of accessory muscles such as the rectus abdominus during expiration

o    abdominal effort is typically accentuated during expiration

o    typically increased abdominal effort is associated with lower airway obstruction

o    it is also heightened with chest wall / pleural restriction (rib fractures, pleuropneumonia, trauma, and after surgical invasion (thoracotomy) of the chest cavity.

·         Increased rib cage and abdominal effort

o    Synchronous rib and abdominal movement – hyperpnea in response to hypoxemia, hypercapnia, pain, excitement, and hyper-thermia.  Recruitment of accessory inspiratory muscles (scalenus) and expiratory muscles (rectus abdominus).

o    Asynchronous – i.e. “thoracoabdominal asynchrony”

o    Abdominal leads rib (common finding) – increased respiratory drive with airway obstruction results in strong dominance of diaphragmatic contraction causing indrawing of chest wall in particular where chest wall compliance is high (neonates, for example).

o    Rib cage leads abdomen (uncommon finding)– diaphragmatic fatigue or paralysis, such that intercostals muscles drive ventilation, and abdominal compartment moves in the opposite direction (see Paradoxical breathing).

o    Paradoxical breathing – diaphragm is weakened or paralyzed (lesions involving C3-5 or phrenic nerve(s)), so it is displaced cranially rather than caudally during inspiration in opposite phase from rib cage.  The rib cage moves appropriately / in synchrony with inspiratory and expiratory flow. Respiratory failure may ensue if increased load (obstruction, stress, exercise) is imposed on this situation. Externally the abdominal component of breathing moves outward passively with exhalation, and is drawn inward passively upon inspiration. This condition can be seen in horses with heaves due to diaphragmatic fatigue or failure.

o    Diaphragmatic breathing – abdominal motion (coincident with diaphragmatic displacement) in synchrony with inspiration or expiration, whereas the rib cage appears to move passively in the wrong direction.  Intercostal nerve damage may be the cause at the level of the spinal cord (nerves branch off cord at same level of ribs). However, this pattern usually does not result in respiratory failure due to the competency of the diaphragm to maintain ventilation, unless increased demand beyond quiet breathing is imposed on the diaphragm.  

o    Cheynes-Stokes breathing – typically the result of severe hypoxemia or CNS disease involving respiratory centers, there are prolonged periods of apnea interspersed with deep compensatory breaths (in response to hypercapnia).  There appears to be delayed sensation of CO2 reaching the brain, or a delayed response, hence the periods of apnea followed by rapid compensatory ventilation. Prognostically this is a poor sign in general.  One should provide supplemental oxygenation and mechanical ventilation may be necessary.  A thorough neurological workup is warranted.



Cough reflexes are initiated by the particle/chemical/stretch stimulation of receptors (myelinated rapidly adapting pulmonary stretch receptors – RAR's, and/or unmyelinated C-fibers that stimulate RAR's) in the airways. The purpose of cough is to protect the respiratory system from foreign particles, and to expulse mucus.  

There are important receptors in the larynx as well; local anesthesia is applied to block laryngeal receptors during intubation for instance.  The afferent impulses go to the brainstem cough center, and back to the respiratory system.  The neural pathways of cough and bronchoconstriction are distinctly different, but frequently activated in tandem.  A single cough involves transient glottic closure, active buildup of airway pressure distal to the glottis, followed by rapid opening of the glottis to expulse secretions. Series of coughs are produced by glottic interruptions of expiratory flow (cough…cough… cough…gasp) from tidal volume down into the expired reserve volume as low as residual volume.

Clinically, cough can be observed either without intervention, or stimulated by (1) forcing the animal to rebreath into a plastic back (as done for better auscultation in large animals) or (2) gentle compression of the proximal trachea.  Normal animals do not cough with rebreathing, but 1-2 coughs upon tracheal stimulation is normal.


Irritation or inflammation of the nasal mucosa or associated sinuses cause firing of afferent nerve endings (facial or trigeminal nerves), that are responsible for the ‘sneezing reflex.'  Sneezing manifests as short bursts of blowing in large animals rather than the more explosive bursts accompanied by head tossing / twisting in small animals. Nasal secretions (arising locally or distally) may stimulate sneezing without pathology in the nasal passages. Local anesthesia of the superior maxillary nerve at the level of the infraorbital foramen, can reduce sneezing in horses with photic (light induced) or allergic sneezing.  This may be a useful diagnostic procedure

Nasal rubbing

Irritation, inflammation, foreign bodies, infiltrative, and secretions (particularly those that are serous) may elicit a rubbing response from the animal.  Animals rub their nose on themselves, other animals, fomites, and in the case of horses, on fences and waterers. It is important to establish seasonality (e.g. allergic rhinitis) vs. non-seasonality (non-allergic, or contact sensitivity).   The nasal passages should be examined with a pen-light, initially for the presence of pathology, foreign bodies, and infiltrative masses, for example. Endoscopy, radiography, and CT, are excellent tools to define the extent of pathology in the nasal passages. 

Nasal discharges

We usually classify nasal discharges as serous, mucoid, or mucopurulent, and whether unilateral or bilateral.  Furthermore, the color and viscosity are noted.  Nasal discharges arise from any segment of the respiratory tract, so it is imperative that direct examination (penlight, endoscope) or indirect examination (auscultation) are used to define the point source of secretions.   

Epistaxis or Hemoptysis

Bleeding may occur from one or both nares (epistaxis), or may be coughed up from the oral cavity (hemoptysis). Epistaxis may arise from any segment of the respiratory tract.  The goal of physical examination is to locate the source.  Common sources include ethmoids, nasal passages (hematoma, foreign bodies or tumors), guttural pouches (fungal infections in horses), or the lung (exercise induced pulmonary hemorrhage or EIPH in horses, pulmonary thromboembolism in dogs).  

Sources behind the nasal septum bleed into both nasal passages (e.g. guttural pouch, lung), and sources rostral to the caudal border of the nasal septum bleed unilaterally (e.g. ethmoid hematoma, sinus, conchae).  The sound of gurgling (crackles) in the trachea associated with epistaxis indicates pulmonary origin. The color (bright red vs dark red) may indicate arterial vs venous blood and hence the urgency of the problem.  

Abnormal lung sounds

Lung sounds are evaluated during quiet unprovoked breathing and during deep inspiration. The latter can be brought about by forcing the animal to rebreath into a plastic bag, holding off the nostrils temporarily, or by exercise.   Rebreathing is essential for auscultation of all but the most obvious, severe, lung pathology.

Normal lung sounds:

·         Bronchial sounds – generated in the large airways

·         Vesicular sounds – generated in the large airways but heard peripherally after attenuation though aerated parenchyma

Changes in sound transmission

·         Consolidated areas and pleural effusion – more efficient acoustical conduction, so sounds may be amplified (heart sounds more-so than bronchial sounds).

·         Hyper-inflation and pneumothorax – quieter than normal sounds ipsilaterally.

Increased intensity of normal sounds

·         Increased flow rate via hyperpnea/tachypnea, or, narrowing of airways increasing velocity of flow

·         ↑ inspiratory sounds – extrathoracic or large airway obstruction

·         ↑ expiratory sounds – partial collapse of intrathoracic airways promoted by increased alveolar pressure generation -- characteristic of lower airway obstructive diseases (e.g. feline asthma, equine heaves/recurrent airway obstruction).

Abnormal (adventitial) sounds – changes in sound production

·                     Discontinuous (<20 msec):

o    crackles (‘rales').  Explosive equilibration of pressure on either side of unopened airway. The process of opening airways and subtended regions of parenchyma is referred to as recruitment, with the opposite (closure/atelectasis) referred to as derecruitment.  Recruitment – derecruitment cycling is one cause of repetitive crackles.  In obstructive airway disease, opening of bronchoconstricted zones results in crackles. As well, inflammation causes excessive secretions that obstruct airways and these secretions are rapidly mobilized causing crackles.  Rupture of fluid films or bubbles are in part responsible for crackles in small airways. 

o    pleural friction rubs:  sheering movements of pleural surfaces containing irregular inflamed, fibrinous or fibrous adhesions.  Pleural rubs that are synchronous with breathing, should be distinguished with (1) pericardial rubs that are synchronous with heart sounds, and (2) bowel sounds that are random.

·                     Continuous (>250 msec):

o    wheezes (rhonchi). Vibration of constricted airway walls, or walls that contain intraluminal masses.  Secretions may narrow the airway lumen, and induce turbulent flow and vibrant musical sounds. Low pitched musical continuous sounds associated with secretions in the airways may change (improve, worsens) after coughing, deep inspiration (temporary relief of wheezes), or repositioning (e.g. from lateral to sternal, wheezes from the down lung may disappear).

 Loss or increase in chest resonance (with percussion)


Percussion is an age-old but extremely valuable tool to isolate regions within the sinuses, pleural cavity, or lung parenchyma where there is loss of air, due to infiltration, effusion, or space-occupying lesions.  In large animals, percussion is still practiced, whereas in small animals, it is generally not, due to the availability of radiography (Dr. Liz Rozanski, personal communications). One taps over the sinus (maxillary, frontal) or chest (between the ribs, preferably) in a systematic fashion to delineate resonant borders corresponding to normal or abnormal anatomical architecture.

One percusses the chest by tapping on your fingers, or on a flat metal device (“pleximeter”) in order to listen for the hollow sound of air (resonance).  Percussion of the sinus is performed similarly with the fingers. Loss of the normal hollow sound within the expected sinus or lung field indicates pathology.  Sometimes, the loss of resonance is related to accumulation of gravid fluid (pleural effusion, sinus empyema) in which case there is a horizontal fluid line and loss of resonance below.  Sometimes there are focal spots of dullness that signify abscessation.  Consolidated lung, enlarged heart or pericardial sac, and hemorrhage within the lung parenchyma also elicit loss of resonance.  Large masses (lymph nodes, tumors) within the chest cavity can contribute to loss of resonance.  

Alternatively, an increase in the resonance indicates a loss of tissue density, most likely (1) pneumothorax (increased resonance but normal lung field), and less likely (2) hyper-inflation (expanded lung field), or (3) emphysema (expanded lung field) which is rare in animals.  Increased resonance following trauma is most certainly pneumothorax, so use your stethoscope!   Decreased resonance after trauma may indicate hemothorax, pulmonary contusion, or diaphragmatic hernia. This is a very useful clinical tool to screen for pathology of the lung and chest cavity.

Tachypnea (increased rate)

Normal resting respiratory rates

·                     Cattle: 15-35/min     cat: 20-30/min

·                     Horse: 12-20/min    dog: 10-30/min

·                     Sheep:     20-40/min (highly variable depending on excitement, temperature, wool).

Causes of tachypnea include hypoxemia, hypercapnia, metabolic acidosis, and hyper-thermia (e.g. exercise induced).  The latter effect demonstrates the importance of the respiratory system to thermoregulation.  Tachypnea may not increase minute ventilation (MV = VT * freq).  Low tidal volume (VT) tachypnea (‘panting', 120 / min) is seen commonly in dogs with excitement and involves oral and nasal breathing, but can be seen in any facultative oral breathing (not horses) species. Low VT tachypnea may also occur with respiratory restriction.  When an animal breaths at low tidal volume, there is a greater amount of dead space ventilation.  

This limits the effectiveness of nasal insufflation for oxygenation, since much of the oxygen delivered is mixed with dead space.  Oxygenation using a mask, intubation, or tracheostomy may be necessary to increase the fraction of inspired oxygen, and thus contend with hypoxemia during tachypnea.   Tachypnea at higher lung volumes (hyperpnea) is a more common response to the above stimuli, and responds better to oxygenation, as well as improves alveolar ventilation. Pulmonary function tests (spirometry) are necessary to quantify tidal volumes and minute ventilation, as they can not be estimated on the basis of clinical examination.

Hyperpnea (increased minute ventilation, usually increased VT and freq.)

Hyperpnea is the typical response to exercise, in an effort to increase oxygen delivery to the alveoli and therefore maintain alveolar oxygen tensions.  It is commonly seen with tachypnea in response to hypoxemia (with exception of central depression), hypercapnia, metabolic acidosis, hyper-thermia, pain, exercise, and excitement.   To quantify hyperpnea as for tachypnea, pulmonary function tests are required.   Hyperpnea in the case of excitement or pain would result in respiratory alkalosis (syn:  hyperventilation, hypocapnia) since the animal is eucapnic during quiet (non-hyperpneic) breathing.

Dyspnea (labored breathing)

This is a subjective term that requires anthropomorphism to attribute to the animal.  Once can not ask the veterinary patient to describe their difficult with breathing, which is required for dyspnea grading, for instance, in humans.  However, it is an acceptable description of the signs of labored breathing, including a combination of abnormal breathing pattern, nasal flaring, abduction of elbows, extension of the head, and even refusal to lie down.  Dyspnea can worsen in animals that are recumbent presumably from the increased abdominal pressure limiting functional residual capacity (FRC) and inspiratory capacity (IC).

Examples of conditions commonly associated with dyspnea are asthma, heaves, ARDS, pulmonary thromboembolism, pulmonary edema, interstitial- or broncho- pneumonia, and pulmonary fibrosis.  These conditions cause a marked decrement in gas exchange evoking the sensation of dyspnea in the animals. Dyspnea may also be elicited with normal gas exchange in the lung where there is obstruction or restriction of breathing (i.e. mechanical dysfunction rather than gas exchange dysfunction). The sensation of inspiratory or expiration limitation due to obstruction or restriction causes marked dyspnea (e.g. choanal atresia in llamas and alpacas, empyema in the cat).


Noisy breathing

Noise is produced either during inspiration, expiration, or both. If the noise only occurs during inspiration or expiration it is considered to be a dynamic obstruction, vs. a fixed obstruction that causes turbulence and noise during inspiration and expiration.  The noise implies airway obstruction, but cannot be used to grade the obstruction since loud noises sometimes eminate from small obstructions.  They are generally caused by upper airway (nasal, pharyngeal, laryngeal) pathologies. 

Whereas severe obstructions are audible during quiet tidal breathing, mild airway obstructions can be heard only during exercise or high flow rates (ie provocations).   Familiarity with noises can pinpoint abnormalities (e.g. laryngeal paralysis in horses and dogs, tracheal collapse in dogs and calves, dorsal displacement of the soft palate in horses) but in no way are these sounds pathognomic.  

Careful examination of the upper airway structures using laryngoscopy, endoscopy, radiography, CT, or MRI may be necessary to discern the significance of a respiratory noise.   Newer techniques of evaluation couple endoscopy with a provocation to induce higher flow rates that exacerbate dynamic obstructions (e.g. laryngeal paralysis, dorsal displacement of the soft palate, pharyngeal collapse).  Chemical challenge (lobeline, dopram), CO2, and exercise are common provocations.  Lower airway constriction (‘bronchoconstriction') can produce wheezes and accumulations of blood or secretions audible crackles (‘gurgling') that are heard without a stethoscope, but this is only observed in severe cases.

Change in phonation

Phonation is performed by domestic animals by passing flow over the vocal cords whose tension is tightly controlled. In addition, the oral and nasal cavities, and paranasal sinuses, serve as resonant chambers.  Vocalizations can be altered by diseases that affect the vocal cords, including paralysis (cranial nerve X), inflammation, infection or abscessation, as well as physical deviations of the cord due to extrinsic factors (tumors, foreign bodies).   Disease of the resonant chambers can change the nature of phonation as well. For example, inability to open the mouth (e.g. temporomandibular joint arthritis) will alter and reduce the sound pitch and intensity of a horse's “whinny.” 

Owners will report a change in phonation as one of the earliest signs of laryngeal / vocal cord disease, sometimes before noisy breathing ensues.  Correction of phonation does not always coincide with correction of the primary anatomical or functional disturbance (e.g. laryngeal paralysis corrected by tie-back operation does not always correct “roaring”).

Malodorous breath

It is important to distinguish malodor arising from the oral vs nasal cavity.  There is no easy way to do this. One must isolate the odor by attempting to smell during normal respiration with the mouth closed, and to search for the odor with the mouth open.  This does not always work.

Any segment of the respiratory tract may be involved in an infectious (bacterial, fungal) or neoplastic condition, giving rise to malodorous breath.  A classic respiratory malodorous finding is pleuropneumonia associated with abscessation (horses), pulmonary abscessation (cattle), or empyema (cats). In some cases (horses with pleuropneumonia associated with anaerobic bacteria) the odor is detected at some distance from the horse.

Swellings / mal-positioning of respiratory tissues

The external appearance of the respiratory tract is revealing, especially when coupled with simple palpation of external structures, including nares, nasal bones, paranasal sinus bones, laryngeal cartilages, tracheal rings, and ribs.  Common findings include nasal tumors, bacterial sinusitis, laryngeal muscle atrophy, collapsing trachea (extrathoracic type) or ruptured trachea, and rib fractures, respectively.

Subcutaneous emphysema

Disruption of the respiratory tract anywhere distal to the larynx may result in subcutaneous emphysema.  Examples include tracheal rupture with tracking of air subcutaneously and into the mediastinum (pneumomediastinum – causes dyspnea and radiographic evidence of air in mediastinum), and ruptured lung bullae in the lung with air tracking around the chest wall, penetrating foreign bodies of the trachea or chest wall (coupled with pneumothorax). Iatrogenically this can be caused by tracheostomy, pneumonectomy, or lobectomy.  

Chest pain

Chest pain can be detected by applying gentle pressure on the chest wall. This distorts deeper structures, including intercostals muscles, ribs, parietal pleura, and visceral pleura. In the case of pleuritis, inflammation causes marked pain over the parietal pleura, and palpation (pushing gently) of the rib cage over the region of infection results in flinching and avoidance.  Rib fractures are another source of chest pain. Guarded breathing (shallow and/or abdominal) and reluctance to move or lay down, are clinical manifestations of chest pain.

Exercise intolerance

The respiratory tract is the first in a chain of oxygen delivery systems, followed by the cardiovascular system (red blood cells, hemoglobin, capillaries, heart, etc.), that bring oxygen to working muscles during exercise.  Respiratory compromise results in decreased oxygen available for work, and therefore decreased maximal oxygen consumption (decreased VO2) or decreased “aerobic capacity” --- see Dr. Mazan's section on Exercise Pathophysiology.   

Upper airway obstruction causes a marked increase in the work (and metabolic cost) of breathing, and eventually hypoventilation (hypoxemia, hypercapnia).  Lower airway obstruction causes an increase in the expiratory work of breathing and ventilation-perfusion mismatch, resulting similarly in hypoxemia (if severe, hypercapnia as well). 


Restrictive / infiltrative / diffuse parenchymal lung disease (e.g. pulmonary fibrosis) causes an increase in inspiratory work of breathing due to loss of lung compliance (increased elastic recoil), and hypoxemia results from poor diffusion capacity and intrapulmonary shunting during exercise.  The most common respiratory causes of exercise intolerance are found in dogs and horses, and include upper airway obstructions (dogs, horses) and lower airway diseases associated with inflammation and bronchoconstriction in horses.   Reduced speed, endurance, and decline in normal abilities that are specific to athletic discipline are observed in these athletic species.

Weight loss

In chronic lung disease, the metabolic cost of breathing is so high that weight loss ensues. Most animals can not increase caloric intake sufficiently to compensate. Examples where weight loss is an important finding in respiratory disease, include heaves in horses and pulmonary fibrosis and neoplastic (primary of metastatic) processes in small animals. Lung diseases that are sufficient to cause weight loss are usually readily identifiable clinically, exhibiting tachypnea or dysnpea with the animal at rest.

Ancillary diagnostic tests

Tests of gas exchange- arterial blood gases (see Respiratory Physiology Review for background)

Ventilation is best assessed using PaCO2 as a guide.  Decreased alveolar ventilation results in hypercapnia (hypoventilation, respiratory acidosis).  Hyperventilation results in hypocapnia (respiratory alkalosis).  Hypoxemia may be accompanied by hyper-capnia, eucapnia, or hypo-capnia.  Causes of low PaO2 include hypo-ventilation, right to left intrapulmonary shunt, ventilation-perfusion mismatch, and decreased diffusion capacity.

The clinical examination and ancillary procedures discussed are used to sort out the cause.  Furthermore, shunt respond poorly to oxygen supplementation as opposed to the other cause.  Hypoventilation responds readily to mechanical ventilation.  Ventilation perfusion –mismatch exhibits a large gradient between alveolar and arterial oxygen usually with minimal hypercapnia, but responds well to oxygen supplementation. In this way, the clinical utility of the arterial blood gas is widened.

Macroscopic tests


A flexible fiberoptic endoscope can be extremely useful for direct inspection of the airways.  The nasal passages, nasomaxillary meatus opening, pharynx, larynx, trachea, mainstem bronchi, segmental and subsegmental bronchi, are accessible by endoscopy.  The endoscope itself is chosen on the basis of the diameter of the structures to be traversed and evaluated, and range from 15mm down to 2-3 mm outside diameter. Endoscopy requires anesthesia in small animals, but can be easily performed in sedated or unsedated large animals including horses (adults and foals), cattle (adults and calves), and sheep, but not pigs. 

Upper airway pathology may produce static or dynamic dysfunction. Static dysfunction is observed during quiet breathing as a fixed and obvious anatomical derangement (e.g. narrowing of nasal or tracheal diameters). The description of dynamic dysfunction is made possible by inducing the conditions (e.g. hyperpnea) under which the animal is clinically affected (e.g. makes noise, exercise limited).   Dynamic inspection therefore requires provocation to induce hyperpnea.  The latter is brought about by chemical injection of a respiratory stimulant (e.g. lobeline), CO2 challenge, partial nasal occlusion to alter pressure gradients across the upper airways, or exercise. Endoscopy in the horse during exercise is a classic example of dynamic endoscopy.

Tracheo-bronchial masses, edema, constriction, and secretions can be visualized distal to the upper airways.  Biopsies can be taken via the endoscope for histopathologic examination.

Parenchyma cannot observed directly using endoscopy.  However, the pleura can be visualized with a rigid thoracoscope (i.e. laparascope) or flexible endoscope.  The latter procedures are more appropriate for inspection and surgical manipulation of the pleural surfaces, for example for “pleurectomy” (removal of fibrous pleural adhesion).


Indications for radiography include auscultation of adventitious sounds (wheezes, crackles, absence of sounds), abnormal percussion of the sinuses or chest, dyspnea, unexplained tachypnea, other abnormal breathing patterns, presence of lower airway secretions, exercise intolerance, external trauma, cyanosis, and chronic cough.  The size of the lung fields can be determined, and vascular, airway (tracheal, bronchial), and interstitial components can be evaluated.  Common terms for pathology observed in the lung include bronchial (ring shadows, donuts), vascular, alveolar (fluffy, coalescent), interstitial (transparent but cloudy area), and consolidated (white, non-translucent).


Ultrasound performed at the surface of the chest wall is indicated when there is abnormal percussion, auscultation, or abnormal radiography that does not fully characterized the disease. Resolution of ultrasounds vary considerably, but one can discern masses as small as 1 cm diameter with a high resolution probe and good technique. The difficulty is distinguishing a normal from abnormal structure that size.  

The normal lung, full of air, reflects all ultrasonic signals, so only when there is disruption of the usual air content of the chest, do we see beyond the visceral parietal surface.  Hence, ultrasound is an excellent technique to investigate pleural effusion, diaphragmatic herniation, lung consolidation or atelectasis, but not for lower airway obstruction or bronchiectasis for instance.


Pulmonary function testing (PFT)

These tests are aimed at describing the mechanical function or gas exchange capacity of the respiratory system.  They are indicated primarily when clinical diagnosis fails to describe the entity, or its severity or prognosis.   PFT are indicated where this is airway obstruction or restrictive lung disease where more thorough characterization is required.

In particular, upper and lower airway obstructions lend themselves to measurements of airflow limitation (“resistance) and restrictive diseases to quantification of lung or chest wall stiffness (elastance = reciprocal of compliance).  At the current time, PFT are in clinical use to characterize lower airway obstruction in horses, and the dynamic upper airway obstruction in dogs. Lung size (functional residual capacity) and diffusion capacity (DLco) are other PFT that have value in characterizing chronic parenchymal disease. These tests are described in detail in the section by A Hoffman called Pulmonary Function Testing.

Computed tomography (CT)

The advantage of CT is the imaging of the lung in cross-sections. This allows for considerable more detail of intrapulmonary, pleural, and mediastinal structures, and the separation of these by axial (cross), saggital (lateral to medial), coronal (top down) images. Reconstruction of selected parts into 3 dimensional images, enhances analysis of structures such as tumors, abscesses, masses within the airways, bullae, and pleural adhesions.  Images can be analyzed with regard to area, volume, and density.

Gamma scintigraphy (‘nuclear scan')

Radionuclides are administered intravenously or by aerosol and tracked using the gamma camera.  Intravenous radionuclides lodge in the pulmonary capillaries or are engulfed by pulmonary intravascular macrophages, resulting in a whole lung image.  This is called a perfusion image, and maps the region of normal and abnormal perfusion. Aerosols lodge by sedimentation and inertial factors on airway walls (fine particles, 2-10 um) or in the alveoli (0.5-2 microns, ultrafine particles).  The image is called a ventilation image.  Comparison between simultaneous perfusion and ventilation images gives a ‘functional image' relating to ventilation/perfusion matching.

This is most notably abnormal with lower airway obstructions.  Perfusion is abnormal with thromboembolism of pulmonary vessels.  Alternatively, leucocytes can be removed from the individual and labeled, then injected intravenously and traced. Areas with enhanced inflammation will attract and adhere to leucocytes, causing enhanced radioactivity in those zones.  These techniques are available at referral centers but not used for pulmonary diagnosis as frequently as the other methods discussed due to their cost, technical difficulties, and lack of sensitivity.

Microscopic sampling

Respiratory cytology

These techniques are described in detail in the Small and Large Animal Medicine and Surgery courses.   The indications for recovering respiratory secretions for cytologic evaluation are numerous, but inflammation, infection (bacteriology), and neoplasia are the main objectives.  In general when infection of the lower respiratory tract is suspected, a aspirate of tracheal secretions (“tracheal aspirate”, “transtracheal wash” or “TTA”) is indicated.  If disease produces a more diffuse, chronic, peripherally located lesion that is non-infectious (e.g. allergic, inflammatory, neoplastic) a more peripheral sampling method is indicated.  This can be achieved with a bronchoalveolar lavage (BAL).  

Samples are observed grossly for surfactant (foam) content, turbidity, flocculence (i.e. mucus), blood or hemosiderin (yellowish). Odor of respiratory samples is hard to discern. Microscopically the sample is enumerated after appropriate concentration, smearing, and staining for typical cells (macrophages, lymphocytes, neutrophils, metachromatic cells, eosinophils, and columnar epithelium and goblet cells) and the presence of morphologically abnormal (e.g. atypical, giant, neoplastic) cells.  Normal cytology is available for each species (horse, cattle, dog, cat, sheep, goat).

Thoracocentesis for effusions and pneumothorax

The main indication for thoracocentesis is pleural effusion.  Sampling can be undertaken on one side (“representative sample”) or both sides if the effusion is bilateral.  Samples of pleural fluid can be drawn by sterile, percutaneous insertion of a cannula or needle. Sampling location is guided on the basis of areas of reduced resonance or normal anatomical borders, usually as ventral as possible at the 8-10th intercostals space to avoid the heart. 

If sampling AND therapeutic drainage are intended, a large bore cannula (e.g. chest tube) will be required since fibrin, mucupurulent exudates, or clots can obstruct small cannulae and needles.  The samples are evaluated for color, viscosity, specific gravity (high SG indicating modified transudate or exudates), protein, blood, total nucleated cell count, pH, lactate, and cell differential.  Low pH or high lactate content is highly suggestive of sepsis. Generally less than 5,000 cells per microliter are considered normal, but this varies from species to species.

Complications associated with thoracocentesis are rare, but pneumothorax is the one we dread the most – fortunately, it can be reversed quickly. If pneumothorax (spontaneous or iatrogenic) is identified by percussion, auscultation, and/or radiography, a needle can be inserted for suction using a closed system, and the chest drains attached to a one-way (evaluation) valve called a Heimlich valve left in place for a period of time.

Lung biopsy

Lung biopsy provides the only means by which one can directly diagnosis airway or lung pathology.  In many diseases of the respiratory system, pathology is minimal or non-existent at the histologic level.  Hence, lung biopsy is reserved for situations where lung pathology is likely to exist (e.g. lung fibrosis) and other methods have failed to describe this pathology indirectly.  Lung biopsies are obtained percutaneously, via endoscope, or surgically via thoracotomy.

  Table 1

Normal sinus borders (horse)

:   Medial canthus of the eye rostrally parallel to the facial crest, ventrally the facial crest, lines that connect these two borders cranially and caudally       Normal lung fields:     Equine Tubercoxae 17th intercostal space   Tuber ischii 16th space   Pt shoulder 11th space   Olecranon 6th space Bovine Tuber coxae 11th space   Mid-thorax 9th space   Olecranon 5th space Ovine Tuber coxae 11th space   Mid-thorax 8th space   Olecranon 5th space

Diagnostic post-mortem 

In cases where there may be a threat to herd health and the value of the animal is perceived by the owner to be minimal, euthanasia followed by diagnostic post-mortem is preferred, over spending time and money on ante-mortem diagnostics.  This is the best way to get fresh tissue. The lung undergoes rapid autolysis, although less rapid than gastrointestinal and other tissues.  It is important to perform a gross and microscopic examination. Tissues can be cultured for bacteria, fungus, and viruses, and preserved in 10% formalin for standard histopathology.


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