No. 4—Evidence of inefficient gas exchange

Inefficient gas exchange is confirmed by the presence of hypoxemia and, occasionally, hypercapnia. The best way to determine whether a patient has hypoxemia is to obtain an arterial blood gas sample for analysis (see sidebar titled "How to obtain arterial samples for blood gas analysis"). Many bench-top and point-of-care analyzers are reliable sources of blood gas information. The partial pressure of oxygen in arterial blood (PaO₂) provides information about blood oxygenation. A normal PaO₂ should be about 80 to 110 mm Hg if the patient is breathing room air.⁹ If the patient is receiving oxygen supplementation, the PaO₂ should be about five times the percentage of oxygen being supplemented. For example, a patient receiving 40% oxygen in an oxygen cage should be expected to have a PaO₂ around 200 mm Hg (40 x 5), while an anesthetized patient receiving 100% oxygen should have a PaO₂ near 500 mm Hg (100 x 5).

If blood gas analysis is not available in a practice, pulse oximetry measurement can be performed to get a general idea of blood oxygenation. However, blood gas analysis is necessary for true diagnosis of acute lung injury or ARDS; it is also necessary to distinguish between these two conditions.

SpO₂. Pulse oximetry is a widely available noninvasive tool that can also be used to provide a quick assessment of oxygenation by indirectly measuring the oxygen saturation of hemoglobin (SpO₂). This tool may be useful when blood gas analysis is not available, but it has several disadvantages. SpO₂ measurement can be difficult to perform in animals with a thick coat, pigmented skin, or poor perfusion. SpO₂ results may also be inaccurately low in these circumstances. The best ways to ensure accurate readings include minimizing movement of the patient, using the probe on thin skin that is adequately perfused, comparing the measured heart rate to the actual heart rate of the patient, and taking several consistent SpO₂ readings. Finally, SpO₂ cannot differentiate PaO₂ values > 100 mm Hg; the results will all be 99% to 100%. Therefore, animals receiving oxygen supplementation that have significant lung dysfunction may still have a SpO₂ of 99% to 100% as long as their PaO₂ remains above 100 mm Hg.

PaO₂/FiO₂ ratio. Arterial blood gas results can be further analyzed to determine the ratio of PaO₂ to the fraction of inspired oxygen (FiO₂). FiO₂ is equal to 21% (or 0.21) when the patient is breathing room air. Most oxygen cages supplement up to at least 40% oxygen, so the FiO₂ is 40%, or 0.4.¹⁰ Oxygen (100%) delivered through bilateral nasal cannulas can supplement an FiO₂ of 50% if the patient is not panting.¹⁰ An anesthetized patient is receiving 100% oxygen, barring any leak in the system, so the FiO₂ is 100%, or 1. However, in nonventilated dogs it can be difficult to determine FiO₂ because of wide variation in the character of respiration demonstrated by the patient.

The PaO₂/FiO₂ ratio is used to determine the severity of respiratory compromise and is the one factor that distinguishes acute lung injury from ARDS. A ratio of < 300 indicates acute lung injury, and a ratio < 200 is diagnostic of ARDS.² The PaO₂/FiO₂ ratio also allows accurate comparison between different arterial samples taken when different levels of oxygen (FiO₂) were being supplemented to the patient. The ratio is calculated by dividing the PaO₂ by the FiO₂ percentage (expressed as a decimal). A normal animal should have a value > 400. For example, an animal breathing room air with a PaO₂ of 60 mm Hg would have a PaO₂/FiO₂ ratio of 60/0.21, which = 285 and is consistent with acute lung injury when other criteria that indicate acute lung injury are present.

Because ARDS is a more severe form of acute lung injury, distinguishing between these two respiratory disorders might indicate the severity of the disease and provide prognostic information for the owner.

Table 3: Alveolar-Arterial Gradient Calculation*

No. 5—Evidence of pulmonary inflammation

The last criterion for diagnosing acute lung injury or ARDS, and the only criterion that is optional, is evidence of pulmonary inflammation. Transtracheal wash or bronchoalveolar lavage samples taken from animals with acute lung injury or ARDS demonstrate characteristic types of inflammation. Cytologic examination of respiratory fluid reveals a predominance of neutrophils (suppurative inflammation).² When these diagnostic samples are tested for inflammatory cytokines such as tumor necrosis factor alpha and interleukin-beta, these substances are also increased from normal values.^2,6 However, performing these diagnostic tests in a dyspneic animal may be contraindicated because of the risks associated with anesthesia or the procedure itself. So while these diagnostic procedures may provide useful information, they are not currently a requirement in diagnosing acute lung injury or ARDS. These tests might be more practical if a dog is already being ventilated or if samples are necessary for diagnosis and treatment of pneumonia.

TREATMENT

A variety of treatment strategies have been attempted, but strong clinical evidence for the best approach to these patients is lacking. In general, managing acute lung injury and ARDS should focus on early recognition with treatment of the underlying disease and supportive care for the respiratory system. The underlying disorder (risk factor) should be fully evaluated and treated aggressively and specifically, if possible. In patients that require transfusions, use blood products cautiously because, in people, transfusion-related acute lung injury is another cause of noncardiogenic pulmonary edema.

Supportive therapy

Fluid therapy. Supportive care should include maintaining organ perfusion with appropriate fluid therapy. Some clinicians advocate the conservative use of fluids since the lung vasculature is already more permeable than normal and it might be easy to cause fluid overload in these patients. Additionally, the hope is that mild dehydration may help pull some of the interstitial lung fluid back into the vasculature.^3,4,7 But if you use this conservative approach to fluid therapy, monitor blood pressure closely to make sure the patient does not become hypotensive, which is especially likely in septic patients. If the patient has been sufficiently volume-loaded and hypotension is still present, use vasopressors such as dobutamine, dopamine, vasopressin, or norepinephrine to stabilize systemic blood pressure and achieve adequate organ perfusion. Other clinicians advocate aggressive fluid management to maximize oxygen delivery and organ perfusion as a more appropriate approach, but no consensus has been reached at this time.

A recent study in people evaluated these two philosophies of fluid therapy, placing patients in either a conservative or liberal fluid management group. No difference in 60-day mortality was seen between the groups, but patients in the conservative fluid group had significantly more days alive, ventilator-free, and spent outside of the intensive care unit.¹¹ These findings suggest that providing as small a fluid volume as possible while maintaining organ perfusion may be the most appropriate fluid plan for patients with acute lung injury or ARDS. Colloid therapy may help improve systemic blood pressure by increasing the volume of fluid in circulation, but it should generally be avoided in patients with suspected pulmonary capillary leaks. The colloid may leak from the capillary into the pulmonary interstitium, worsening the existing pulmonary edema.¹²

Oxygen therapy. Oxygen therapy is also a vital part of treatment for these patients. Oxygen may be provided by intranasal cannulas or nasal prongs, an enclosed hood, or an oxygen cage (Figure 2). Animals can tolerate up to 60% oxygen without concern for oxygen toxicosis,⁴ but high concentrations may be difficult to obtain unless a tightly sealed oxygen cage is available. Closely monitor the patient for response, and consider obtaining samples for serial blood gas analysis to check for hypoxemia. If a patient persistently has a PaO₂ < 60 mm Hg, a PaCO₂ > 60 mm Hg, or increased respiratory effort despite receiving oxygen therapy, consider ventilator therapy.⁹

Other therapies. Other supportive care measures that have been attempted in people include antibiotic therapy, gastric ulcer prophylaxis, nitric oxide administration, surfactant replacement, specific cytokine therapy, glucocorticoid therapy, and nutritional management.^13,14 While no strong evidence supports or negates some of these treatment options, we do know that early nutritional interventions are important in human critical care and are probably equally important in our veterinary patients.¹⁵ Nutrition can be provided either enterally or parenterally. Most patients with dyspnea will be unwilling to eat on their own, so parenteral therapy may be necessary. If the patient must be anesthetized, consider placing a feeding tube to provide enteral nutrition since early enteral nutrition improves gastrointestinal mucosal barrier function and may decrease the incidence of bacterial translocation.¹⁶