The term pulmonary edema refers to an abnormal accumulation of fluid within the interstitial space and alveoli, which affects gas exchange and is a common cause of dyspnea. Radiographic diagnosis of pulmonary airspace opacification and lung patterns are important in distinguishing between the two most common causes of pulmonary edema in small animals, high-pressure edema and increased permeability edema, which is valuable since the prognosis and response to treatment differ.

There are two main pathophysiological processes by which pulmonary edema can occur, the first is a high-pressure edema or cardiogenic edema and the second occurs due to an increased permeability or non-cardiogenic edema. The pulmonary barrier between capillaries and alveolar gas exchange has three anatomical layers that are important to consider in the physiopathology of edema. The first layer is composed of the capillary endothelial cells which form loose junctions of cytoplasmic projections; second is the interstitium represented by connective tissue, fibroblasts, macrophages, small arteries, veins and lymphatic channels that control the fluid dynamics within the interstitial space. Lastly there is the alveolar wall, composed of squamous cells with thin cytoplasmic projections forming tight junctions.¹

The governing force of fluid movement across a semipermeable membrane is described in Ernest Starling´s equation² where:

Rate of filtration of fluid = Kf ([Pcap – Pis] – r [IIcap – IIis])
[Where Kf is the coefficient that includes hydraulic conductivity and filtration surface area, P represents hydrostatic pressure and II oncotic pressures. Finally, r defines the endothelial permeability to protein.]

Cardiogenic Pulmonary Edema

Cardiogenic pulmonary edema is present in various left side heart pathologies, which in veterinary medicine are largely represented by mitral valve disease, dilated cardiomyopathy and hypertrophic cardiomyopathy.^2,4 An increase in left atrial pulmonary venous pressure above 25 mm Hg causes edema fluid to accumulate. Initially, the fluid will fill the peribronchovascular interstitial spaces, which can be seen radiographically as "cuffs," and pulmonary venous distention. If the interstitial fluid is saturated, then fluid will move to the alveolar space greatly impacting oxygen perfusion. In general, most cases will have a prior history of heart disease that can assist the clinician in determining the cause of dyspnea and hypoxia.

Non-Cardiogenic Pulmonary Edema

Non-cardiogenic pulmonary edema occurs due to increased vascular permeability secondary to direct or indirect lung damage.^1,3 In general, non-cardiogenic pulmonary edema is an acute presentation as a consequence of some coexisting clinical condition, either systemic or pulmonary.² The accumulated liquid in non-cardiogenic pulmonary edema is high in protein content, which, with decreased lung compliance and damage to epithelium, greatly impacts the lungs ability to remove alveolar fluid, and makes this presentation of pulmonary edema more refractory to treatment. There are several causes of non-cardiogenic pulmonary edema that can be summarized in the following table.^1,3

ALI: acute lung injury; ARDS: acute respiratory distress syndrome; PLE: protein loosing enteropathy; PLN: protein loosing nephropathy.

Diagnosis

Diagnosis of pulmonary edema is often based on clinical history and physical findings. It is valuable to discern between non-cardiogenic pulmonary edema and cardiogenic pulmonary edema since treatment and prognosis differ. The gold standard in distinguishing the two is the measurement of capillary wedge pressure; since this, however, is not a routine test performed in veterinary medicine, radiographic findings play an important role in diagnosis. The following chart helps distinguish the radiographic characteristics of cardiogenic versus non-cardiogenic pulmonary edema.^5,6

When interpreting thoracic radiographs, care must be taken when diagnosing perihilar lung disease in dogs and cats since superimposition on the hilar region by the cardiac silhouette on the VD/DV views or by pulmonary vasculature and left atrium on the lateral views occurs.⁵ It is also important to consider that lungs always look worse on lateral views and if the patient is anesthetized, there will be an increase in general lung opacity secondary to atelectasis.⁷

Conclusions

Pulmonary edema is a common cause of respiratory distress in small animals. The ability to discern between non-cardiogenic pulmonary edema from cardiogenic pulmonary edema is important for adequate treatment options as well as a prognostic indicator. Radiology is one of the most important first line diagnostic tests that can be performed in house and has good sensitivity to orient the differential diagnosis.

References

1.  Kakouros NS, Kakouros SN. Non-cardiogenic pulmonary edema. Hellenic J Cardiol. 2003;44:385–391.

2.  Murray JF. Pulmonary edema: pathophysiology and diagnosis. Int J Tuberc Lung Dis. 2011;15(2):155–160.

3.  Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine. 7th ed. St Louis, MO: Saunders Elsevier; 2010.

4.  Rozanki E. Pulmonary edema (proceedings). http://veterinarycalendar.dvm360.com/pulmonary-edema-proceedings-0. November 1, 2009.

5.  Thrall DE. Textbook of Veterinary Diagnostic Radiology. 6th ed. St Louis, MO: Elsevier; 2014.

6.  Pachtinger G. Noncardiogenic pulmonary edema. http://cliniciansbrief.com. June 2013.

7.  Thrall DE. Lung patterns: Are they overemphasized? http://www.massey.ac.nz/massey/fms/Colleges/College%20of%20Sciences/IVABS/vetschool/NZ%20Lung%20Don%20Thrall.pdf.

8.  Côté E, MacDonald KA, Meurs KM, Sleeper MM. Feline Cardiology. Ames, IA: Wiley-Blackwell; 2011.