Introduction

• Accumulation of fluid within the interstium and alveoli.
• Cause:
  • Left-sided congestive heart failure.
  • Hypoalbuminemia.
  • Inhalation or ingestion of toxic substances and irritants.
  • Electrocution Electrocution.
  • Anaphylaxis.
  • Multisystemic inflammatory and non-inflammatory, eg uremia, diseases and sepsis.
  • Disseminated intravascular coagulation (DIC).
  • CNS trauma or seizure.
• Signs: respiratory distress, blood-tinged frothy fluid from the nostrils/mouth in severe cases. Crackling and bubbling sounds on auscultation in moderately to severely affected animals.
• Diagnosis: history, clinical signs, radiography.
• Treatment: oxygen, cage rest, diuretics, vasodilators, bronchodilators, corticosteroids, antibiotics.
• Prognosis: guarded, depends on successful treatment and management of any underlying cause.

Pathogenesis

Etiology

Cardiogenic pulmonary edema

• Left-sided congestive heart failure Heart: congestive heart failure; resulting from cardiomyopathy Heart: hypertrophic cardiomyopathy  Heart: dilated cardiomyopathy (DCM)  or congenital defects Congenital heart disease: overview.

Non-cardiogenic pulmonary edema

• Bronchopneumonia Pneumonia.
• Hypoalbuminemia Hypoproteinemia.
• Inhalation of toxic substances and irritants.
• Ingestion of toxins, eg paraquat Paraquat poisoning, organophosphates Organophosphorus poisoning, alpha naphthyl thiourea (ANTU).
• Anaphylactic reaction Anaphylaxis.
• Multisystemic inflammatory and non-inflammatory disease, eg uremia Uremia.
• Septicemia Shock: septic.
• Overzealous administration of intravenous fluids.

Neurogenic pulmonary edema

• Electrocution.
• Cranial trauma or following severe seizures Seizures.

Pathophysiology

• Various mechanisms lead to increased capillary permeability   →   fluid leakage into interstitium and alveoli.
• Reduced plasma colloid osmotic pressure, eg in hypoalbuminemia may be important where capillary permeability is normal but fluid still leaks due to reduced oncotic pressure. Really important when hydrostatic pressure decreases or vascular permeability increases.
• Accumulation of fluid in the interstitium and alveoli results in varying degrees of respiratory distress and cyanosis due to reduced oxygen transport into pulmonary capillaries.

• Left heart failure   →   raised pulmonary venous pressure   →   increased capillary hydrostatic pressure   →   pulmonary edema.
• Damage to pulmonary blood vessels by toxins/irritants   →   fluid leakage into pulmonary interstitium and alveoli.
• Cranial trauma, seizure or electrocution   →   activation of sympathetic nervous system   →   blood volume shift from systemic to pulmonary circulation   →   elevated pulmonary capillary pressure   →   edema.
• Presence of fluid   →   impaired gas exchange   →   hypoxia   →   increased alveolar capillary permeability.

Timecourse

• May present as acute onset respiratory distress.
• Gradual onset associated with congestive heart failure.

Diagnosis

Treatment

Outcomes