Page 29 - BSAVA Manual of Canine and Feline Head, Neck and Thoracic Surgery, 2nd Edition

BSAVA Manual of Canine and Feline Head, Neck and Thoracic Surgery

bodies, neoplasia, neuromuscular disorders and degener- with mild to moderate congestive heart failure on an emer-
ative diseases. An animal with loud upper airway sounds gency basis. In severely affected dogs, nitroprusside (an
VetBooks.ir proven otherwise. This does not preclude respiratory ning at a constant rate infusion of 1 µg/kg/min and slowly
has to be considered to have upper airway disease until
arterial and venous vasodilator) can also be used, begin-
increasing the rate every 15 minutes whilst monitoring
lesions elsewhere in the tract and these areas should be
investigated as well (e.g. aspiration pneumonia secondary
and may cause severe hypotension). Unfortunately, nitro-
to laryngeal paralysis). blood pressure (nitroprusside is a very potent vasodilator
The two most common abnormalities are laryngeal prusside is not readily avail able any more in the USA. In
paralysis and collapsing trachea. Laryngeal paralysis most dogs, the effective dose is usually 5–10 µg/kg/min.
occurs more commonly in large-breed dogs; collapsing Dogs with dilated cardiomyopathy may also benefit from a
trachea is more common in small-breed dogs. Both con- positive inotrope such as dobutamine (5–10 µg/kg/min). If
ditions represent dynamic airway lesions in which the used judiciously, these drugs are very effective in relieving
collapse varies with the respiratory cycle. Brachycephalic respiratory distress in dogs with severe pulmonary
upper airway syndrome is a common cause for respiratory oedema secondary to heart failure (particularly dilated
stress (see Chapter 6). Loud upper airway sounds inclu- cardiomyopathy). Once stable, the heart disease can be
ding stridor and stertor can be heard depending on the characterized fully and tailored therapy can be instituted.
extent and severity of the condition. Also depending on
the severity of the condition, the respiratory pattern and Pulmonary parenchymal disease
sounds can be consistent with a fixed or dynamic obstruc-
tion (more commonly consistent with extrathoracic Increased lower airway sounds or pulmonary crackles indi-
dynamic obstruction). The harder the animal breathes, the cate small airway or pulmonary parenchymal abnormal-
more severe the obstruction; the more severe the obstruc- ities. These sounds may be due to oedema (cardiogenic
tion, the more hypoxic the animal and the greater the or non-cardiogenic), haemorrhage, infection or infiltrative
respiratory drive; and so the vicious cycle progresses. processes. Some of the more common causes of pulmo-
Heat generated by the respiratory muscles, combined with nary parenchymal disease (in the authors’ experience) are:
the inability to move gas in and out of the pulmonary
system, can result in high body temperature. This also • Pulmonary oedema (cardiogenic or non-cardiogenic)
• Haemorrhage (trauma, anticoagulant rodenticide)
contributes to further demand on the respiratory system.
It is important to break the cycle. Oxygen should be • Pulmonary thromboembolism (PTE)
• Feline asthma
given immediately. This will help slow the respiratory cycle
but is usually inadequate as a standalone therapy. • Pneumonia (aspiration)
• Pulmonary contusion
Sedation with acepromazine maleate (30–50 µg/kg i.v. or
i.m. or butorphanol 0.2–0.4 mg/kg i.v. or i.m.) will help calm • Smoke or toxin inhalation
the animal and slow ventilation. If the animal’s temperature • Acute respiratory distress syndrome (ARDS).
is high (>41°C), spraying water on the hair coat and blow- The absence of audible cardiac abnormalities in the
ing a fan over the body will expedite cooling. This three- face of increased lower airway sounds strongly suggests
pronged approach generally results in stabilization of the pulmonary parenchymal disease or lower airway disease
respiratory system within 30–60 minutes and the animal rather than congestive heart failure. The location of these
can be weaned off oxygen supplementation. Some sounds may help in the diagnosis. For example, a cranio-
patients may benefit from anti-inflammatory doses of ventral distribution or right middle lung lobe distribution
corticosteroids because of laryngeal or tracheal inflam- makes aspiration pneumonia a likely possibility, whilst a
mation and oedema. caudal dorsal distribution suggests neurogenic pulmonary
It is extremely rare that emergency laryngeal surgery is
required in patients with laryngeal paralysis; the above oedema. These findings are not always consistent and,
despite the animal’s instability, thoracic radiographs are
medical therapy is generally quite effective. If a patient is often necessary to characterize the disease so that empir-
in acute distress and there is concern about imminent col- ical therapy can be instituted. A thorough clinical history,
lapse, anaesthesia and intubation will relieve the distress thoracic radiographs, blood tests, tracheal wash, broncho-
immediately if laryngeal paralysis is the cause. It should be scopy or even lung biopsy may be required to diagnose
remembered that waking patients (from anaesthesia) with the problem definitively so that appropriate therapy can be
dynamic upper airway obstruction is extremely difficult.
applied, but often the radiographic distribution of pulmo-
The excitement phase of recovery causes dynamic airway nary infiltrates, appearance of the heart, physical examin-
pressure changes, resulting in collapse of the affected area
ation and clinical history can point towards a diagnosis.
of the pulmonary tree, starting the vicious cycle again.
Non-cardiogenic pulmonary oedema
Heart disease This is oedema not due to cardiac disease, and encom-

If an animal with respiratory distress has increased lower passes nearly all the pulmonary parenchymal types of
airway sounds or breath sounds and an auscultable diseases. Neurogenic pulmonary oedema is a specific
cardiac abnormality, such as a loud heart murmur or a type of non-cardiogenic pulmonary oedema secondary to
persistent arrhythmia, cardiac disease must be consid- a brain insult. The four most common brain insults are
ered as a cause of the respiratory distress. Empirical head trauma, electrocution, seizures and upper airway
therapy for cardiac disease should be administered if obstruction. Neurogenic pulmonary oedema is character-
further diagnostics cannot be pursued. In animals with ized by an acute onset (typically within minutes) of respir-
mild to moderate heart failure, furosemide (2 mg/kg i.v. or atory abnormalities after one of the four listed insults. The
i.m. in dogs; 1 mg/kg i.v. or i.m. in cats) should be admin- degree of pulmonary oedema can vary from mild to
istered. In severely affected animals, these doses can be severe, involving all lung fields. The typical pattern is inter-
doubled. Furosemide therapy combined with oxygen stitial to alveolar, with the distribution initially starting in
supplementation is often successful in stabilizing animals the caudodorsal area. The treatment for this condition is

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