Definition

Accumulation of edema fluid in the pulmonary interstitium and alveoli, in the absence of heart disease.

Pathophysiology

• Associated with increased pulmonary vascular permeability and leakage of fluid into the interstitium and alveoli; if severe, can be accompanied by an inflammatory response and accumulation of neutrophils and macrophages in the interstitium and alveoli.
• Several mechanisms contribute to changes in pulmonary vascular permeability.
• Stimulation of brainstem (medulla) vasomotor centers can lead to a reflex systemic release of catecholamines resulting in systemic vasoconstriction, temporary shunting of blood into the pulmonary circulation, transient pulmonary circulatory overload, and endothelial damage; probably occurs in patients with neurogenic edema, electric cord bites, and upper airway obstruction.
• In patients with upper airway obstruction, negative intrathoracic pressure from inspiratory attempts against an airway obstruction contributes to edema formation.
• Increased vascular permeability can be part of a generalized inflammatory response that develops in patients with SIRS, sepsis, or pancreatitis.
• The inciting insult can trigger a cascade inflammatory response that often worsens over 24 hours following the initial episode.
• Severity of clinical manifestation-varies, ranging from mild to severe; the most seriously affected patients can progress from normal to death in as little as a couple of hours after the incident.

Systems Affected

• Respiratory.
• Cardiovascular-hypotension, tachycardia, and shock.
• Hemic/Lymphatic/Immune-if severe and causing respiratory failure, can be associated with DIC.
• Renal/Urologic-acute renal failure.

Genetics

Unknown

Incidence/Prevalence

Uncommon

Signalment

Signs

Causes

• Upper airway obstruction-laryngeal paralysis; choke-chain injury; mass; abscess.
• Electric cord bite.
• Acute neurologic disease-head trauma; prolonged seizures.
• Smoke inhalation.
• Aspiration pneumonia.
• Systemic inflammatory response syndrome-sepsis; endotoxemia; pancreatitis.
• Anaphylaxis (cats).
• Near drowning.
• Adverse drug reactions including certain anesthetic drugs (ketamine), thiazides, or certain antineoplastics (vincristine, cisplatin in cats).
• Transfusion-related acute lung injury-not reported in veterinary medicine.

Risk Factors

• Hypoproteinemia
• Crystalloid fluid resuscitation

Differential Diagnosis

• Cardiogenic pulmonary edema
• Pulmonary infection-bacterial, viral, or fungal pneumonia
• Pulmonary neoplasia
• Pulmonary hemorrhage (e.g., anticoagulant rodenticide exposure)
• Pulmonary thromboembolism

CBC/Biochemistry/Urinalysis

• Leukocytosis common, leukopenia and thrombocytopenia possible-owing to neutrophil sequestration in the lung and platelet consumption.
• Biochemistries-usually normal; may note hypoalbuminemia owing to pulmonary protein loss; mild stress-related hyperglycemia.
• Urinalysis-usually normal.

Other Laboratory Tests

• Pulse oximetry and arterial blood gas analysis-usually demonstrates mild to severe hypoxemia and hypocapnia; results are not specific but indicate the severity of pulmonary dysfunction.
• Coagulation testing (severely affected patients)-mild to moderate prolongation of PT and PTT in animals with consumption and DIC. Severe coagulopathy could indicate hemorrhage as the cause for respiratory signs rather than noncardiogenic pulmonary edema.

Imaging

• Thoracic radiographs-vital; can reveal prominent interstitial pattern with mild or early disease; alveolar infiltrates with moderate or severe disease; alveolar infiltrates commonly in dorsocaudal lung fields but can be seen in other lung fields, are sometimes asymmetrical and predominantly right-sided. Cardiac silhouette generally normal.
• Echocardiography-rule out cardiogenic pulmonary edema.

Diagnostic Procedures

• Cytology of airway fluid-inflammatory with neutrophils and some alveolar macrophages. Fluid tends to have high protein values >3 g/dL. Culture typically negative unless concurrent bacterial pneumonia.
• Edema fluid to plasma ratio (EF:PL) compares protein in the edema fluid to plasma protein. An increased ratio (>0.65) is indicative of non-cardiogenic pulmonary edema.
• Pulse oximetry-non-invasive, continuous monitoring of arterial hemoglobin saturation with oxygen; provides information about the severity and progression of pulmonary dysfunction.
• Pulmonary artery wedge pressure-normal value confirms noncardiogenic origin; not commonly performed.
• NT Pro-BNP testing in cats and dogs can suggest underlying heart disease and thus support a diagnosis of cardiogenic edema.

Pathologic Findings

• Gross-lungs usually heavy, red, or congested; fail to collapse; often exhibit a wet cut surface; can ooze foam from major airways.
• Histopathology-depends on severity of the insult; early, mild: may note eosinophilic amorphous material filling the alveoli or can be near normal because fluid removed in processing; severe: alveolar hyaline membranes, alveolitis, and interstitial inflammatory infiltrates with neutrophils and macrophages evident and accompanied by atelectasis, vascular congestion, and hemorrhage; lesions can be found within hours of a severe insult.

Appropriate Health Care

• Inpatient versus outpatient-depends on the severity of respiratory dysfunction and the underlying cause of disease (e.g., dogs with upper airway obstruction or severe seizures generally require hospitalization).
• Make every effort to resolve and treat the underlying cause (e.g., relieve airway obstruction or treat seizures).
• Mild to moderate-patients generally improve on their own within 24–48 hours with complete resolution; offer support of pulmonary and cardiovascular function while the lung repairs.
• Severe-difficult to treat; usually requires PPV because of respiratory failure; many patients die despite intensive supportive care.

Nursing Care

• Minimize stress.
• Oxygen therapy-vital in moderate to severe disease; administer via mask or hood, nasal catheter, or oxygen cage; inspired oxygen concentration depends on the severity of disease; most patients do well on 40–50% oxygen, but severe disease can require 80–100% to sustain life.
• Severe-can require PPV and PEEP.
• Fluid therapy with a balanced electrolyte-give as replacement solution with dehydration or shock; use cautious fluid administration.
• Plasma or synthetic colloids-consider with hypoproteinemia or low colloid osmotic pressure measurements; improve oncotic pressure, minimizing movement of fluid into the lungs.

Activity

Dogs with moderate to severe hypoxemia and respiratory distress-rest and minimal stress vital for minimizing oxygen requirements.

Client Education

• Warn client that the condition can worsen before improving.
• Inform client that severe disease that progresses rapidly to fulminant pulmonary edema and respiratory failure is associated with a very poor prognosis.

Surgical Considerations

Relevant only for treating the underlying cause.

Drug(s) Of Choice

• Damaged endothelium in the pulmonary vasculature-no specific treatment available.
• Inflammatory response-generated by a variety of mediators and cascades; cannot be blocked by one specific anti-inflammatory drug to resolve edema.
• Diuretics-usually minimally effective; edema is caused by changes in permeability, not high hydrostatic pressure; can use furosemide cautiously in boluses of 0.5–2 mg/kg IV, IM or at 0.1–1 mg/kg/h IV in a continuous infusion. Additional beneficial effects may include decreases in bronchospasm and bronchodilation.
• Corticosteroids-used to reduce swelling in patients with upper airway obstruction; generally ineffective for pulmonary inflammatory response; may predispose patients to infectious complications (e.g., bacterial pneumonia); if used, recommend an anti-inflammatory dosage (e.g., dexamethasone sodium phosphate at 0.05–0.1 mg/kg IV).
• The use of beta-adrenergic agonists such as terbutaline may increase clearance of alveolar fluid.
• Sedatives can be used cautiously if patient's anxiety is contributing to respiratory distress or upper airway obstruction. The patient should be carefully monitored as sedation can decrease central respiratory drive leading to progression of respiratory failure.
• Additional therapy as indicated by underlying cause, such as anticonvulsants, analgesics for oral ulcerations.

Precautions

• Diuretics (e.g., furosemide)-excessive use can cause dehydration and a marked decrease in intravascular volume with minimal resolution of edema; low intravascular volume can exacerbate cardiovascular collapse or shock.
• Corticosteroids-can predispose patients to infectious complications (e.g., bacterial pneumonia).

Patient Monitoring

• Observe respiratory rate and pattern and auscultate frequently (every 2–4 hours) for the first 24–48 hours, depending on severity of disease.
• Assess pulmonary function by pulse oximetry or arterial blood gas analysis (initially every 2–4 hours).
• Assess PCV and total solids and evaluate mucous membranes, pulse quality, heart rate, blood pressure, and urine output every 2–4 hours to monitor cardiovascular status and possible progression to shock.

Prevention/Avoidance

• Avoid contact with electric wire.
• Correct and avoid airway obstruction.
• Treat seizures and high intracranial pressure.

Possible Complications

Usually none if patient recovers from the acute crisis.

Expected Course and Prognosis

• Mild to moderate-resolution of signs in 24–72 hours; no specific treatment required except for oxygen and careful fluid supplementation.
• Severe-difficult to treat; can require PPV because of respiratory failure.
• Overall survival rates-80–90%.
• Long-term prognosis-excellent for recovered patients.

Associated Conditions

Acute respiratory distress syndrome

Synonyms

• Acute alveolar failure
• Acute lung injury
• Capillary leak syndrome
• Congestive atelectasis
• Hemorrhagic lung syndrome
• Progressive respiratory distress
• Shock lung
• Traumatic wet lung

See Also

Acute Respiratory Distress Syndrome

Abbreviations

• DIC = disseminated intravascular coagulation
• PCV = packed cell volume
• PEEP = positive end-expiratory pressure
• PPV = positive-pressure ventilation
• PT = prothrombin time
• PTT = partial thromboplastin time
• SIRS = systemic inflammatory response syndrome