The cat presenting with respiratory distress poses unique challenges. Not only do clinical signs often appear to occur suddenly, creating an emotional situation for owners, but the cat is often in an unstable condition where decompensation can occur because of the stress associated with handling and procedures. Intensive care and support are vital, but the number and frequency of procedures must be minimised in order to promote patient stability. The clinician must maintain a logical and calm approach, by formulating a list of differential diagnoses that is revised on an ongoing basis as diagnostic test results are revealed.

Presenting Signs, Initial Stabilisation and Historical Findings

Most cats with respiratory distress present acutely, often at an inconvenient time and with little notice. We recommend that the patient is provided with supportive oxygen therapy as soon as they are known to have respiratory distress. As a result, history taking is often curtailed early on, but this can be resumed once initial stabilisation is under way. Whilst the clinician is working with the cat, a third party (possibly a veterinary nurse) should obtain a signed consent form for stabilisation and initial procedures, including thoracocentesis.

It is imperative that the dyspnoeic cat is handled minimally, in a quiet and calm environment, with adequate oxygen provision. Intravenous access or blood work is often contraindicated early in the timeline of case management. Sedation should be considered if the patient is distressed. Pharmaceuticals that dramatically alter systemic vascular resistance or promote bronchoconstriction should be avoided. The authors typically use butorphanol (0.2–0.4mg/kg IM, SC or IV if access is present), and avoid using medetomidine or ketamine because of their profound effects on systemic vascular resistance.

Observation of respiratory pattern is a very useful way of narrowing the list of possible differential diagnoses in cats with respiratory distress (Table 1). It can be performed whilst the cat is in a carrier, whilst they are receiving oxygen, and without any patient restraint which may contribute to stress. It is worth noting that a paradoxical pattern represents non-specific respiratory fatigue, although it is common in patients with pleural space disease and diaphragmatic rupture. Respiratory fatigue is a concern, because further decompensation may be associated with respiratory failure. When clinical signs of respiratory distress in cats are accompanied by postural adaptations (for example, orthopnoea, represented by a sternal recumbency with an extended neck and abducted elbows to reduce the resistance to airflow) or persistent open mouth breathing, the situation should be considered grave and the patient highly unstable. Owners and other staff handling the patient should be cautioned, and equipment for endotracheal intubation and cardiopulmonary resuscitation should be prepared.

Once the cat is settled in a calm, oxygen rich environment, a full history can be obtained from the owner. Alternatively, this may be carried out by another veterinarian or experienced veterinary nurse whilst the primary clinician is overseeing initial stabilisation. In most cases it is appropriate for owners to be provided with reassurance that their cat is being cared for appropriately whilst they wait. In the event that an owner has left the premises, a telephone call to update them and take a history should suffice, provided that signed consent was previously obtained.

Table 1. The observation of respiratory pattern can be used to help localise the disease and narrow the list of differential diagnoses.
CHF, congestive heart failure

As always, a thorough history and establishing a timeline of events is vital in achieving a diagnosis and formulating an appropriate treatment plan. The duration, intensity and progression of respiratory signs should be interrogated thoroughly, as should any concurrent clinical signs. Historical reports of a persistent or chronic cough should assist in identifying lower airway disease, but may also be attributable to respiratory tract neoplasia. Coughing is rare in cats with congestive heart failure (CHF), which tend to present primarily with tachypnoea. Retching or gagging is highly suggestive of nasopharyngeal or laryngeal disease, but the sounds are easily confused with a cough by owners. For this reason, we would encourage clinicians not to be shy in performing impressions of the different respiratory noises, to aid in owner differentiation and thus assist in appropriately narrowing your list of differential diagnoses. An alternative would be to record a series of videos to demonstrate the different clinical signs to owners. Syncope, collapse, episodic weakness or even evidence of partial seizures (such as facial motor activity or periods of absence) in the history of a cat presenting with respiratory distress hint at cardiac arrhythmias, and may lead the clinician to prioritise the investigation of possible heart disease if other clinical findings support this diagnosis.

Physical Examination

Once a cat has stabilised and calmed somewhat, physical examination is likely to be permitted. Again, this should be performed so that stress is minimised, potentially in the kennel or ward where the patient has acclimatised (preferably a cat only area). A quiet environment is essential for accurate auscultation and temporary cessation of oxygen therapy may be necessary to facilitate this.

The minimum physical examination of a cat presenting with respiratory distress should consist of noting the respiratory rate and pattern exhibited, assessment of mucus membrane colour and capillary refill time, noting heart rate and rhythm, auscultating heart and lung sounds, performing thoracic compression and thoracic percussion, and assessment of bilateral femoral pulses. Abdominal palpation may be useful if a diaphragmatic rupture is suspected (subjective absence of a normal volume of abdominal contents is uncommon but supportive), but should be performed with care in such patients. Also, the presence of a fluid thrill on abdominal ballottement may indicate ascites, which may occur concurrently with a pleural effusion in patients with severe heart disease, neoplasia or feline infectious peritonitis (FIP).

The presence of a heart murmur in a cat is a non-specific finding. Studies performed in a non-selected population of cats in rehoming centres suggest that only 1 in 3 cats with murmurs have any identifiable echocardiographic abnormalities. However, the specificity of murmur to identify heart disease is greater if the murmur is louder (grade III–IV/VI or above) or if the cat is older (Wagner et al. 2010). In the authors’ experience, some cats with very severe heart disease and clinical signs of CHF do not have an audible murmur. Other auscultatory findings, such as a gallop sound or an arrhythmia are far more specific for significant heart disease. As such, the findings of a loud murmur, an arrhythmia or a gallop sound in an older cat with respiratory distress are highly supportive of a cardiogenic cause. Young cats are sadly not exempt from severe heart disease, and some cats seem to develop overt hypertrophic cardiomyopathy even in the first year of life.

Pulmonary auscultation and thoracic percussion are vital tools in identification of pleural space disease. In cats with a pleural effusion, the breath sounds are expected to be reduced and percussion should sound dull in the sternal portion of the thorax. A fluid line may be identifiable by performing auscultation and percussion at different heights. In contrast, pneumothorax may be identified by an absence of breath sounds dorsally and hyper-resonant percussion in the same region.

Abnormal airway noises are useful in identifying lower airway disease. Cats with chronic bronchitis or asthma may have loud, coarse pulmonary crackles accompanied by terminal inspiratory or expiratory wheezes. In CHF, pulmonary oedema is associated with soft, subtle crackles that may be focally distributed or even inaudible. Abnormal respiratory sounds in cats with upper-respiratory tract disease are, in contrast, less subtle. Inspiratory noise (stertor/stridor) may be audible without the use of a stethoscope, and laryngeal auscultation may detect loud or high-pitched inspiratory noise.

Thoracic Ultrasonography

For cats with a restrictive, paradoxical or mixed respiratory pattern (or where the clinician is uncertain as to the localisation of respiratory compromise), thoracic ultrasonography is an invaluable initial diagnostic test. Most practices have access to a basic ultrasound machine, and the identification of air or fluid using ultrasound is a straightforward skill that is easy to learn (for a thorough review, see Lisciandro 2011). Although many clinicians are tempted to perform thoracic radiography, perhaps because of a low level of confidence in their sonographic skills, the use of ultrasound has several advantages to the patient. In contrast to relocating a patient and using manual restraint techniques for radiography, ultrasound can be performed with minimal restraint, patient-side in a kennel or ward, whilst oxygen supplementation in sternal recumbency is ongoing. This constitutes the lowest-risk handling possible, whilst a lateral radiograph would be considered very high risk for a patient with respiratory compromise (Figure 1). In addition, ultrasound may be able to identify significant cardiac enlargement, a large mediastinal mass or a diaphragmatic rupture without the necessity for additional tests.

Figure 1. Contrasting imaging techniques used to identify a pleural effusion: ultrasonography (left) is low-risk and may identify a mass or significant cardiac enlargement, whist radiography (right) is high-risk and further information regarding a mediastinal mass or cardiac remodelling is lost because of fluid effacement of soft tissue structures. (VIN editor: Figures were not provided in the original document.)

In the absence of obvious pleural fluid, identified as an anechoic space between the thoracic wall and intrathoracic structures on ultrasound, lung ultrasound can assist in further narrowing the list of differential diagnoses. Normal lung ultrasound shows a bright pleural line in the near-field, which slides back and forth as the animal breathes (known as the “glide sign”). Deep to this line are parallel “A lines”, which represent the scatter of ultrasound in normal, aerated lung (Figure 2). In patients with pneumothorax, the glide sign is absent but A lines remain present, because the pleura are no longer adjacent to the thoracic wall and so cannot be visualised beyond the scatter caused by air in the pleural space. In contrast, the presence of B-lines excludes a pneumothorax (as does the normal glide). B-lines are vertical, hyperechoic artefact caused by an air-fluid interface within the pulmonary interstitium or alveoli (Figure 2). These are highly suggestive of pulmonary oedema and should raise the concern of CHF in a cat presenting with respiratory distress. Recently, a prospective study determined that in cats with dyspnoea, thoracic ultrasound to look for B-lines had the same accuracy as thoracic radiography for both experienced and novice users (Ward et al. 2017).

Figure 2. Schematic diagrams (inspired by Lisciandro 2011) of lung ultrasound in cats: the normal appearance of A lines (top left) and an abnormal appearance with B lines (top right, and below on ultrasound images) which are highly suggestive of pulmonary oedema and exclude the presence of pneumothorax. B lines move back and forth during respiration and cause a “twinkling” appearance (also see Video 6). A pneumothorax is detected when the normal glide of the pleura, moving back and forth during respiration, is absent. A lines are present in both a pneumothorax and a normal lung, due to ultrasound scatter in air. (VIN editor: Figures and videos were not provided in the original document.)

R, rib causing hypoacoustic shadow artefact

Thoracocentesis

Drainage of pleural fluid or air is indicated in cats with respiratory compromise caused by a pleural effusion or pneumothorax. It should be considered not only a diagnostic procedure but a therapeutic one. Diuretic therapy alone is not sufficient to reduce pleural fluid volume with the rapidity required to provide patient stability, and will certainly not work if the effusion is non-cardiogenic. Thoracocentesis, on the other hand, provides a rapid benefit to the patient and will be effective regardless of the cause of the effusion. It may also be performed blind where a clinical suspicion of pleural space disease exists but ultrasound is unavailable, as a diagnostic procedure.

Thoracocentesis may be carried out in the calm conscious patient, or one lightly sedated with butorphanol (0.2–0.4 mg/kg IM or SC). We recommend pre-oxygenation during equipment set-up and flow-by oxygen administration during drainage. A butterfly needle, three-way tap and 10 ml syringe are the equipment of choice, with a strict aseptic technique if time and patient stability permits. At the very least, hair should be clipped and surgical spirit applied with a short contact time to reduce the likelihood of contamination by skin flora.

To drain pleural effusion, ultrasound guidance may be used to select an accessible pocket of fluid and position the needle. Alternatively, needle placement blind may be achieved by using intercostal spaces 7-9, in the ventral one-third of the thorax. Slowly inserting the needle perpendicular to the skin (tolerated better than a fast movement) whilst applying gentle negative pressure will result in fluid entering the hub of the needle and extension tubing once the pleural space is reached. At this point, the butterfly wings may be used to flatten the needle against the inner aspect of the pleural, to minimise risk of trauma to the lung surface. The procedure for draining a pneumothorax is identical, but the needle should be positioned dorsally where air accumulates. Fluid should be drained as completely as possible, sampling some in EDTA and plain tubes for fluid analysis, cytology and bacteriology. Fluid analysis can help to narrow the possible list of differential diagnoses (Table 2). A fresh, air-dried smear may assist cytologists by minimising fluid preservation artefacts. Also, if possible, a second EDTA sample should be obtained for measurement of pleural fluid NTproBNP (a cardiac biomarker, see below). It is anecdotally reported that 20ml/kg pleural fluid causes clinical signs of tachypnoea and 50 ml/kg is associated with severe dyspnoea. Although these figures are likely to be a crude representation of the individual patient’s pathophysiology, they may be a guide as to how much fluid the clinician should expect to drain in a particular patient. For example, in a 4 kg cat with orthopnoea and a large pleural effusion on ultrasound, drainage of 80 ml is unlikely to resolve clinical signs. In our experience, 200–250 ml could be expected in a cat with severe dyspnoea caused by a pleural effusion.

Table 2. Characteristics of pleural fluid and their association with common differential diagnoses

TNCC, total nucleated cell count; FIP, feline infectious peritonitis (wet form), CHF; congestive heart failure
*Please note: cats with wet FIP typically have high protein effusions, but only moderate cell counts (500–5000 x10e9/L)

Identifying Cardiac Disease

Once haemothorax, pyothorax, diaphragmatic rupture and trauma are excluded, the most likely differential diagnoses for the dyspnoeic cat are cardiac disease, lower airway disease and neoplasia. Detection of a chylothorax may be associated with CHF, neoplasia or idiopathic disease. In cats with an obstructive pattern, lower airway disease is highly likely and empirical treatment should be considered to help stabilisation and facilitate further imaging of the thorax, such as radiography or computed tomography. In patients with either a pleural effusion or a restrictive respiratory pattern, lower airway disease can be all-but excluded.

Where analysis of a pleural effusion detects a modified transudate, or thoracic ultrasound/thoracocentesis have not yielded a diagnosis in cats with a restrictive or paradoxical dyspnoea, CHF and neoplasia should be considered the most likely causes. Significant heart disease is the easiest rule-out in this scenario, and two tests should be considered: focused assessment of left atrial size and measurement of NTproBNP (N-terminal pro B-type natriuretic peptide; a hormone released by the atrial and ventricular myocardium by the stimulus of wall stretch or stress).

Subjective assessments of atrial size in cats with respiratory distress are often preferable to absolute measurements, because standard echocardiographic views in lateral recumbency are rarely safe to obtain in dyspnoeic patients. Standard images of the left atrium are best obtained from the right hemithorax, over the palpable apical impulse. It is reassuring that the dilation of the left atrium associated with CHF is rarely subtle or equivocal (Figure 3). Whilst normal left atrial to aortic root ratio (LA:Ao - usually measured in short axis where the three cusps of the aortic valve are symmetrical and clear, like a Mercedes-Benz logo) is less than 1.5, many cats with CHF have an LA:Ao ratio over 2. Where the findings of echocardiography are unclear, cardiac biomarkers offer a good alternative to identify significant heart disease, but there is an increase observed in the circulating levels associated with respiratory distress in cats, which leads to a “grey-area” in measurements (Fox et al. 2009). For this reason, it should be considered only after thorough assessment of respiratory pattern and cardiac auscultation, and attempts to assess left atrial size using ultrasound.

Figure 3. Normal (top) and abnormal (bottom) left atrial size in the cat. The normal feline left atrium is relatively square in appearance and its size should appear to be approximately half the area of the left ventricle in long-axis and less than 1.5 times the aortic diameter in short-axis. (VIN editor: Figures were not provided in the original document.)

LA, left atrium; LV, left ventricle; PF, pleural fluid

NTproBNP can be measured quantitatively using reference laboratories (the best validated assay is Cardiopet proBNP Feline, run by IDEXX laboratories Ltd, United Kingdom) or qualitatively using a benchtop, patient-side SNAP test (IDEXX). The patient-side test has a positive cut-off value that is useful for detecting subclinical cardiomyopathy (around 120–130 pmol/L, Machen et al. 2014). However, it has not been validated in a population of dyspnoeic cats and this relatively low cut-off may lead to a high rate of false positive results in this population. Using the quantitative assay at a reference laboratory would be more useful in cats with respiratory distress because a significant increase (>265 pmol/L) has been shown to reliably differentiate cardiac from noncardiac causes of respiratory distress (Fox et al. 2009), but the transport time and laboratory turnaround mean that results take several days and are not useful in cats with acute dyspnoea. Despite these limitations, a negative NTproBNP SNAP test is highly likely to exclude CHF as the cause of respiratory distress. A positive test is less discriminatory.

Recent research has shown that the quantitative NTproBNP assay can be reliably run using pleural fluid (stored in an EDTA tube and handled as recommended by the laboratory for blood samples) instead of plasma (Humm et al. 2013). This is hugely advantageous in cats with acute dyspnoea, because samples for laboratory submission can be achieved from therapeutic thoracocentesis instead of taking an additional blood sample from a patient where minimal handling is a priority. Although not validated, the SNAP test should have the same reliability on pleural fluid as the quantitative test (good negative predictive value, but likely to have a high rate of false positive results).

Considerations for Cats with Upper Airway Obstruction

Patients with suspected upper-respiratory tract obstruction usually require direct visual examination of the nasopharyngeal/laryngeal area, possibly with cross-sectional imaging (e.g., computed tomography) if available. Radiography may have limited value, owing to the complex bony anatomy of the area, and ultrasonography of this area requires considerable expertise and high-frequency ultrasound transducers to obtain diagnostic images. A light plane of anaesthesia induction is required to facilitate examination of the larynx, but the clinician should be prepared for endotracheal intubation or even emergency tracheostomy if significant upper airway obstruction is detected. If detected, nasopharyngeal polyps can be removed by gentle traction (described in detail elsewhere). If suspected laryngeal neoplasia is present, fine needle aspiration might prove useful - laryngeal lymphoma should exfoliate sufficiently for a confident cytological diagnosis.

Empirical or Initial Treatment

Thoracocentesis is the definitive emergency treatment for stabilisation of cats with a pleural effusion or pneumothorax. It has a great therapeutic and diagnostic potential so should be performed wherever indicated.

Where a convincing obstructive respiratory pattern is present on observation, lower airway disease is most likely and empirical treatment with a bronchodilator (inhaled salbutamol or systemic terbutaline) and an anti- inflammatory dose of steroids should be considered. It is worth noting that beta-agonists can promote tachycardia and arrhythmias, which may lead to deterioration of a cardiac patient, and corticosteroids can increase circulating volume and promote congestive signs. For these reasons, if the clinician is unsure of the likelihood of cardiac disease, left atrial assessment or NTproBNP measurement should be considered prior to empirical treatment for lower airway disease. Also, steroid use may lead to uncertainty in the interpretation of diagnostic bronchoalveolar lavage samples obtained at a later date, or a worsening of clinical signs if an infectious cause of respiratory signs is present (e.g., Mycoplasma spp).

If a cat with respiratory distress has an audible gallop sound, CHF is highly likely and furosemide should be administered empirically at a dose of 2 mg/kg, with reassessment of respiratory rate and effort in 30 minutes. If a pleural effusion is present, thoracocentesis should be performed. Furosemide not only reduces the severity of pulmonary oedema through its diuretic effect, but has a rapid venodilatory effect if given intravenously (if circumstances and stability permits), which helps to reduce left atrial pressure and pulmonary congestion. In addition, furosemide has mild bronchodilatory effects, so cats with signs of lower airway disease should not be put at risk by a single dose and may in fact show a favourable response even when CHF is not the cause of respiratory distress. This positive response, referred to by some as a “furosemide response test”, may be interpreted as diagnostic for CHF. This test should be interpreted in light of furosemide’s non-cardiovascular effects and the patient’s other clinical findings (e.g., respiratory pattern at presentation).

References

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3.  Hogan D, Fox PR, Jacob K, et al. (2015). Secondary prevention of cardiogenic arterial thromboembolism in the cat: the double-blinded, randomized, positive-controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). Journal of Veterinary Cardiology 17 S.306–S.317.

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