Noncardiogenic pulmonary edema in small animals

Abstract

Objective To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs. Etiology NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be due to changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature, or a combination thereof. Possible causes include inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post‐obstructive pulmonary edema), neurologic disease such as head trauma or seizures (neurogenic pulmonary edema), electrocution, after re‐expansion of a collapsed lung or after drowning. Diagnosis Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left‐sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis. Therapy The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases. Prognosis Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE.

Successful treatment of acute respiratory failure following hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma

“…The dog was extubated after mechanical ventilation for 24 hours. Similar to the present case, rapid onset and recovery of neurogenic pulmonary edema have been reported in dogs ( Drobatz et al , 1995 ; Drobatz, 2019 ; Herrería-Bustillo et al , 2022 ; Nemi et al , 2023 ; Unger and Martin, 2023 ). A high mortality rate was observed in dogs treated with mechanical ventilation for neurogenic pulmonary edema ( Drobatz et al , 1995 ; Nemi et al , 2023 ).…”

“…The cause of noncardiogenic pulmonary edema in cases of pheochromocytomas is similar to that of neurogenic pulmonary edema. The pathogenesis of neurogenic pulmonary edema is also associated with catecholamine storms ( Davison et al , 2012 ; Drobatz, 2019 ; Unger and Martin, 2023 ). In this pathology, high catecholamine concentration can cause a sudden increase in pulmonary capillary pressure due to massive vasoconstriction and alter pulmonary capillary permeability ( Davison et al , 2012 ; Drobatz, 2019 ; Unger and Martin, 2023 ).…”

“…The pathogenesis of neurogenic pulmonary edema is also associated with catecholamine storms ( Davison et al , 2012 ; Drobatz, 2019 ; Unger and Martin, 2023 ). In this pathology, high catecholamine concentration can cause a sudden increase in pulmonary capillary pressure due to massive vasoconstriction and alter pulmonary capillary permeability ( Davison et al , 2012 ; Drobatz, 2019 ; Unger and Martin, 2023 ). Unfortunately, we did not measure plasma catecholamine levels during the hypertensive crisis and, therefore, lack direct proof of a catecholamine storm in the present case.…”

“…A high mortality rate was observed in dogs treated with mechanical ventilation for neurogenic pulmonary edema ( Drobatz et al , 1995 ; Nemi et al , 2023 ). The unfavorable outcomes are attributed to the severity of the underlying disease rather than to the complications of pulmonary edema or mechanical ventilation ( Drobatz et al , 1995 ; Drobatz, 2019 ; Unger and Martin, 2023 ). In the present case, no additional hypertensive crisis was observed during mechanical ventilation.…”

Biophysical properties of alveolar surfactant in drever dogs with hunting associated pulmonary edema

“…Fluid balance is regulated by the Starling forces, an interplay between intravascular and interstitial hydrostatic and oncotic pressures. Pulmonary edema forms, when the pressure difference favors fluid shift from the vasculature to the interstitium or when vascular permeability increases [5]. A classic example is the formation of cardiogenic pulmonary edema, where vascular pressure increases due to left sided cardiac dysfunction.…”