PRESENTING HISTORY AND CLINICAL SIGNS
Since acute lung injury and ARDS are secondary disease processes, animals may have a variety of historical findings and clinical
signs based on the primary disease. Animals will usually be hospitalized for the primary disease before acute lung injury
or ARDS becomes apparent. It often takes one to four days for acute lung injury or ARDS to develop after the onset of the
initial inflammation, so patients may originally be presented without marked respiratory signs and develop these complications
later. If respiratory disease was a patient's admitting complaint, a failure to improve or a decline in respiratory status
may indicate acute lung injury or ARDS.
Tachypnea, respiratory distress, cyanosis, hypoxemia, and, potentially, coughing are some of the more common clinical signs.6 On physical examination increased respiratory noises may be heard, including loud bronchovesicular sounds or crackles. The
patient may also display abdominal breathing, orthopnea, or foamy pink exudate coming from the respiratory tract.4,6,7 The key clinical sign is respiratory distress.
A typical scenario of acute lung injury or ARDS would be a dog that initially presented for one of the disorders listed in
Table 1. This patient may have no evidence of respiratory disease on initial presentation. After a few (one to four) days, the patient's
respiratory rate would begin to elevate, followed by the patient exhibiting increased respiratory effort and, finally, severe
respiratory distress. If the patient had already been managed at another hospital for a few days before referral, it may have
already had time to develop acute lung injury or ARDS and may present in respiratory distress as a complication of one of
those disorders.
Hospital-acquired respiratory distress occurs in animals that have been hospitalized for an unspecified length of time and
develop signs of respiratory distress while in the hospital. It may arise as an acute onset of respiratory signs in an animal
that previously was determined to have a normal respiratory status, or it may be a worsening of clinical signs in an animal
that already had respiratory compromise. The most common differential diagnoses for hospital-acquired respiratory distress
include acute lung injury and ARDS, aspiration or bacterial pneumonia, congestive heart failure (CHF) secondary to fluid overload,
and pulmonary thromboembolism.
DIAGNOSIS
Table 2: Criteria for Diagnosing Acute Lung Injury or ARDS
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Acute lung injury and ARDS were historically difficult to diagnose with confidence. So in 2007, a panel of veterinary experts
published a set of five criteria to accurately diagnose these conditions (Table 2).2 Four of these criteria are required for diagnosis, and the fifth is optional.
No. 1—Acute onset
The rate of onset of tachypnea and dyspnea at rest should be < 72 hours and is easily determined based on a patient's history.
No. 2—Risk factors
Evaluating for risk factors involves establishing whether the patient has a severe primary disease that might have resulted
in acute lung injury or ARDS. This risk factor assessment is easily accomplished by obtaining a thorough history and performing
basic diagnostic tests (complete blood count, serum chemistry profile, urinalysis, imaging) that evaluate the patient for
an underlying disease listed in Table 1.
No. 3—Evidence of pulmonary capillary leak with normal pulmonary capillary pressure
This criterion requires that the patient have fluid in the lungs that does not appear to have been caused by left-sided CHF.2 Acute lung injury, ARDS, and left-sided CHF all cause pulmonary edema. The principal difference is that CHF produces edema
that has a low protein content because of high pressure within the lung vasculature (increased hydrostatic pressure), while
acute lung injury and ARDS produce edema that has a high protein content because of inflamed and permeable vessels and alveolar
epithelial lining.3 To properly evaluate a patient for this criterion, thoracic radiography and a cardiac function evaluation must be performed
to determine whether left-sided heart failure is present.
Figure 1A. A lateral thoracic radiograph of a dyspneic dog that demonstrates intense alveolar infiltrate in the caudodorsal
lung fields. The heart and the pulmonary vessels appear normal. These findings are consistent with a noncardiogenic pulmonary
edema.
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Imaging. The typical fluid distribution in acute lung injury and ARDS results in a bilateral or diffuse pattern of infiltrate on thoracic
radiographs that involves more than one quadrant or lobe (Figures 1A & 1B).2 These changes can be quite variable, however, and may range from increased interstitial and peribronchial patterns to diffuse,
bilateral alveolar infiltrates.6,8 Computed tomography of the lungs can reveal increased lung densities, especially in areas of dependent lung. Affected areas
may demonstrate a hazy increase in lung attenuation, with preservation of bronchial and vascular margins.8 Evidence of proteinaceous fluid in the conducting airways would also be supportive.
Figure 1B. A ventrodorsal thoracic radiograph of the same dog as in Figure 1A. The alveolar infiltrate is visible in the caudodorsal
lung field on each side but is more intense on the right. The heart and pulmonary vessels appear normal.
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Cardiac function assessment. If pulmonary infiltrates are seen, the next step is determining whether the edema is cardiogenic or noncardiogenic. In experimental
settings or in large-animal species, pulmonary capillary pressure can be directly measured by placing a pulmonary arterial
wedge catheter (or Swan-Ganz catheter). But direct measurement is often limited to referral hospitals, so cardiac function
is most commonly determined by history, clinical findings, and echocardiography. Echocardiography evaluates left atrial size
and systolic function quickly and accurately. A lack of left atrial enlargement or systolic dysfunction supports the finding
of noncardiogenic pulmonary edema associated with acute lung injury and ARDS. Echocardiography is also useful to exclude pulmonary
thromboembolism.
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