Definition

• Acute respiratory distress syndrome (ARDS) is a syndrome of acute onset of respiratory failure typified by diffuse bilateral pulmonary infiltrates on a dorsoventral thoracic radiograph with no clinical evidence of left atrial hypertension or volume overload. ARDS results from an overwhelming inflammatory reaction in the alveolocapillary membrane in response to a systemic or pulmonary inflammatory insult. The end result is increased vascular permeability leading to edema.
• The 2012 Berlin Definition of ARDS defines three categories of severity based on PaO₂/FiO₂ ratio and level of PEEP employed during ventilation, with mild ARDS defined by a PF ratio of 200–300 mmHg with PEEP 5 mmHg, moderate ARDS as a PF ratio of 100–200 mmHg with PEEP 5 mmHg, and severe ARDS as a PF ratio <100 mmHg with PEEP 5 mmHg.

Pathophysiology

• ARDS is due to a diffuse inflammatory insult that causes widespread damage to alveolar endothelial and epithelial cells resulting in thickening of the membrane and impaired gas exchange. This inflammatory insult can be triggered by primary pulmonary disease or it can be of non-pulmonary origin, and leads to exudative, proliferative, and fibrotic changes within the lung:
• First, excessive accumulation and activation of neutrophils, monocytes, and platelets in the pulmonary microvasculature leads to increased alveolar endothelial permeability. This causes protein-rich edema fluid and inflammatory cells to leak into the interstitial and alveolar spaces.
• Alveolar epithelial injury results from release of cytokines and other inflammatory mediators from leukocytes and platelets.
• Epithelial injury involves both type I and type II alveolar epithelial cells, and results in alveolar flooding and surfactant dysfunction. This causes collapse and consolidation of alveoli with development of severe hypoxemia, and hyaline membrane formation in the alveolar spaces.
• Microthrombi in the pulmonary vasculature, hypoxic pulmonary vasoconstriction, and release of endogenous vasoconstrictors lead to pulmonary arterial hypertension, which can lead to right-sided heart failure.
• Proliferation of type 2 alveolar epithelial cells and pulmonary fibrosis occurs in the late stages of ARDS.

Systems Affected

• Respiratory.
• Cardiovascular-right-sided heart failure secondary to pulmonary hypertension; hemodynamic compromise may be associated with aggressive mechanical ventilator settings.

Genetics

Certain humans are more prone to developing ARDS than others due to specific gene polymorphisms. This has not been investigated in the veterinary population.

Incidence/Prevalence

Unknown

Signalment

Signs

Causes

Risk Factors

• SIRS
• Sepsis
• Severity of illness
• Multiple transfusions

Differential Diagnosis

• Left-sided congestive heart failure
• Fluid overload
• Diffuse pneumonia
• Pulmonary hemorrhage

CBC/Biochemistry/Urinalysis

• Leukocytosis or leukopenia
• Other changes dependent on the underlying disease process

Other Laboratory Tests

• Arterial blood gases-low PaO₂/FiO₂ ratio (where PaO₂ is measured in mmHg and FiO₂ is 0.21–1.0). Normal PaO₂/FiO₂ ratio = 500; comparison of this ratio allows evaluation of severity of lung disease and allows direct comparison of blood gases taken at different FiO₂. PaCO₂ is often low; hypercapnia tends to be a late (preterminal) development.
• Total protein of airway edema fluid compared with serum total protein-ratio of edema fluid to serum total protein <0.5 is supportive of low-protein hydrostatic pressure pulmonary edema (e.g., heart failure, fluid overload); edema fluid/serum total protein ratio >0.7 suggests a high-protein, increased permeability pulmonary edema such as ARDS and pneumonia.
• Coagulation panel may reveal hypocoagulable state supportive of DIC or cause of pulmonary hemorrhage.

Imaging

Diagnostic Procedures

Pulmonary artery catheter to measure pulmonary artery occlusion pressure can be used to rule out cardiogenic cause for edema; by definition, ARDS is associated with PAOP 18 mmHg.

Pathologic Findings

Appropriate Health Care

• There is no specific therapy. General aims are to maintain tissue oxygenation and to minimize iatrogenic lung injury while treating the underlying disease.
• Oxygen therapy-no more than is required to maintain PaO₂ >60–80 mmHg to minimize oxygen toxicity.
• Positive-pressure ventilation is essential in the management of ARDS patients. It is indicated in patients that are hypoxemic despite oxygen therapy, patients requiring high levels of inspired oxygen for prolonged periods, or patients working so hard to breathe that they are at risk of exhaustion.
• ARDS is thought to be exacerbated by ventilator-induced lung injury associated with alveolar overdistension compounded by cyclic opening and collapse of atelectatic alveoli. Therefore, lung-protective strategies of positive-pressure ventilation with moderate to high PEEP, low tidal volumes, and permissive hypercapnia are recommended to minimize ventilator-induced lung injury. Tidal volumes of 6 mL/kg have been found to increase survival significantly in human ARDS patients compared to tidal volumes of 12 mL/kg.
• Recruitment maneuvers and high levels of PEEP can both cause significant hemodynamic compromise and patients should have constant direct arterial blood pressure monitoring.
• Intensive supportive care of the cardiovascular system and other organ systems is vital, as these patients are at high risk for development of multiple organ dysfunction.

Nursing Care

• Monitor temperature closely, especially if using an oxygen cage, as animals with excessive work of breathing can easily become hyperthermic.
• Ventilator patients require frequent position changes and physical therapy; regular oral care with a dilute chlorhexidine solution is important to reduce oral colonization with bacteria as a source of sepsis, and frequent endotracheal tube suctioning is needed to prevent occlusion. Inflate cuff carefully and change endotracheal cuff position regularly to prevent tracheal damage.
• Blood pressure monitoring, as septic patients are prone to hypotension.
• Fluid therapy is important to support the cardiovascular system and to maintain normovolemia while avoiding fluid overload, as this will negatively affect lung function.

Activity

If not anesthetized for ventilation, strict cage confinement.

Diet

Nutritional support is important but challenging. Enteral feeding is desired over parenteral nutrition, but must consider high risk of regurgitation and aspiration in a recumbent patient.

Client Education

Clients need to be aware of the guarded prognosis and high costs of therapy.

Surgical Considerations

The underlying disease may require surgery.

Drug(s) Of Choice

• No specific drug therapy.
• Antibiotics for the underlying disease where indicated.
• Vasoactive drugs to maintain blood pressure.
• Anesthetic drugs to allow positive-pressure ventilation.
• Analgesia as appropriate.
• Low-dose corticosteroid-use remains controversial with conflicting reports of efficacy for low-dose steroids in early or late ARDS.

Alternative Drug(s)

Furosemide may produce pulmonary venous dilation and improve lung function, as an intermittent bolus of 1 mg/kg IV q6–12h or as a CRI of 0.2 mg/kg/h IV. Beware dehydration and effects on organ function.

Patient Monitoring

Arterial blood gases, pulse oximetry, end-tidal carbon dioxide, thoracic radiographs, arterial blood pressure, ECG, temperature, urine output, CBC, coagulation profiles, serum chemistry, blood cultures, monitoring for other organ dysfunction.

Prevention/Avoidance

• Aggressive therapy of primary disease processes to reduce the inflammatory insult to the lung.
• Intensive cardiovascular monitoring and support of critically ill animals to ensure adequate tissue perfusion.
• Careful management of recumbent animals to reduce the chance of aspiration, especially if patient has neurologic disease or upper airway disorders that reduce the ability to protect the airway.
• Judicious use of blood products in patients with inflammatory or severe systemic disease.

Possible Complications

• Multiorgan dysfunction syndrome-acute kidney injury, DIC, and gastrointestinal disease are the more common forms of organ dysfunction seen.
• Barotrauma-can result in pneumothorax. Incidence is thought to be less with lower tidal volume ventilation strategies.
• Ventilator-associated pneumonia-patients on PPV have increased risk of pneumonia that may be difficult to differentiate from worsening of the initial lung injury. Airway cultures should be considered in deteriorating patients.
• Oxygen toxicity may be unavoidable due to severity of hypoxemia in spite of PPV. Oxygen toxicity is indistinguishable from ARDS on histopathology making the incidence of this problem impossible to determine.

Expected Course and Prognosis

• Mortality in human patients remains at 40–60%.
• Mortality in veterinary patients likely approaches 100%.

Associated Conditions

Systemic inflammatory response syndrome, multiple organ dysfunction syndrome, sepsis.

Synonyms

• Acute hypoxemic respiratory failure
• Acute interstitial pneumonia
• Adult respiratory distress syndrome
• High-protein pulmonary edema
• Shock lung

See Also

• Dyspnea and Respiratory Distress
• Panting and Tachypnea
• Pulmonary Edema, Noncardiogenic
• Sepsis and Bacteremia

Abbreviations

• ARDS = acute respiratory distress syndrome
• CRI = constant rate infusion
• DIC = disseminated intravascular coagulation
• PAOP = pulmonary artery occlusion pressure (formerly pulmonary capillary wedge pressure [PCWP])
• PEEP = positive end-expiratory pressure
• PF ratio = PaO₂/FiO₂ ratio
• PPV = positive-pressure ventilation
• SIRS = systemic inflammatory response syndrome

Internet Resources

http://www.ardsnet.org