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. Presenting signs Hyperpnea/tachypnea/dyspnea. Cyanosis. Depends on underlying cause. May present as acute emergency or insidious onset associated with history of left-sided congestive cardiac failure Heart: congestive heart failure. Acute presentation Frothy edematous fluid from the nostrils or from the mouth. Sudden death. Acute dyspnea. Blood-tinged fluid from nostrils and mouth. Cost considerations Treatment relatively inexpensive but further investigations required if any underlying neurological, cardiac or systemic disease present. Special risks Restraint, ie radiography requires very careful handling. Can be sedated if no evidence of shock Shock. Otherwise, only with special care. Anesthesia. Pathogenesis Etiology Cardiogenic pulmonary edema Non-cardiogenic pulmonary edema 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 Presenting problems Dyspnea. Tachypnea. Cyanosis. Cough. Client history Clinical signs Hypernea/tachypnea/dyspnea. Cyanosis. Increased adventitious lung sounds, later crackles and wheezing sounds predominate. Blood-stained froth may be produced by coughing or from nostrils. Diagnostic investigation Radiography See thoracic radiography Radiography: thorax. Diffuse interstitial pattern or patchy mixed interstitial and alveolar pattern . Signs of congestive heart failure, eg pulmonary infiltrates. Lateral view most useful; pulmonary infiltrate if CHF . May also be pleural effusion if related to congestive heart failure. Pleural effusion is a feature of heart failure in cats. Biventricular failure is common in cats, much more so than left-sided CHF. Biochemistry Other Arterial blood gas . Hypoxia and hypocapnia typical of ventilation/perfusion mismatch and lower airway disease. Arterial blood samples are very difficult to obtain in cats with respiratory distress. Confirmation of diagnosis Discriminatory diagnostic features Clinical signs. Radiography. History. Echocardiography will distinguish cardiogenic from non-cardiogenic edema. Definitive diagnostic features Response to treatment. Post-mortem. Gross autopsy findings Some froth in trachea and bronchi is common agonal change, so do not overdiagnose pulmonary edema. Requires thorough, complete PME to establish diagnosis and rule out other conditions. Heavy, congested lungs which pit on pressure and sink in water. Presence of frothy blood-tinged fluid on parenchymal incision. Evaluate cardiac size and structure. Histopathology findings Fix samples of all major organs in addition to respiratory tissues. Consider toxicology sampling (fresh unfixed tissues including liver, kidney, fat, stomach contents, plus urine - consult laboratory). Edema may be lost in tissue processing, but protein residue remains, as does lymphatic dilation. Differential diagnosis Treatment Initial symptomatic treatment Oxygen supplementation Nasal oxygen administration, sedation, eg buprenorphine Buprenorphine or midazolam Midazolam and cage rest may be sufficient, particularly in non-cardiogenic pulmonary edema. Avoid acepromazine for sedation may result in hypotension. Standard treatment Monitoring Clinical signs. Radiography. Arterial blood gases if possible. Pulse oxymetry. Subsequent management Monitoring Radiography. Echocardiography. Electrocardiography ECG: overview. Arterial blood gas. Further investigations and treatment determined by any underlying pathology. Prevention Outcomes Prognosis Good if complete resolution of clinical signs. Guarded if underlying disease process or congestive heart failure poorly responsive to treatment. Some cases respond and have a reasonable medium-term survival. Reasons for treatment failure Severe acute, intractable edema resulting in death from hypoxia. Progressive disease or unresponsive to treatment. Untreatable underlying cause. Owner unable to dose cat. Further Reading Publications Refereed papers Recent references from PubMed and VetMedResource. Drobatz K J, Saunders H M, Pugh C R et al (1995) Noncardiogenic pulmonary edema in dogs and cats - 26 cases (1987-1993). JAVMA 206 (11), 1732-1736 PubMed. Murtaugh R J (1994) Acute respiratory distress. Vet Clin N Am 24 (6), 1041-1055 PubMed.