INTRODUCTION

Pulmonary edema is the accumulation of extravascular fluid within the pulmonary parenchyma or alveoli. The two main pathophysiologic forms are high-pressure edema (due to increased pulmonary capillary hydrostatic pressure) and increased permeability edema (due to damage of the microvascular barrier and alveolar epithelium in more severe cases). Pulmonary edema is a relatively common disease process in veterinary patients that can be rapidly life threatening.

PATHOPHYSIOLOGY

In normal tissues, transvascular fluid fluxes are determined by Starling forces. The amount of flow is dependent on a number of variables: the capillary hydrostatic pressure, interstitial hydrostatic pressure, capillary colloid osmotic pressure (COP), interstitial COP, and the reflection and filtration coefficients for the tissues.¹

The filtration coefficient is a measure of fluid efflux from the vasculature of specific tissues and is dependent on the capillary surface area and hydraulic conductivity. The reflection coefficient indicates the relative permeability of the membrane to protein. Tissue safety factors protect tissues against the deleterious effects of edema. In normal tissues, extravasation of low-protein fluid results in a fall in interstitial COP, which results in preservation of the COP gradient, thereby protecting against further fluid extravasation.² Other safety factors in nondistensible tissues include increased interstitial hydrostatic pressure and increased driving pressure for lymphatic flow (which can increase up to 10 times normal).

The pulmonary capillary endothelium is relatively permeable to protein compared with other tissues, so the effective COP gradient that can be generated between the intravascular space and pulmonary interstitium is lower than in other tissues. Consequently, increased lymphatic flow is largely responsible for protecting against edema in the lung,³ and hypoproteinemia causing a decrease in COP rarely results in pulmonary edema. Pulmonary edema occurs when the rate of interstitial fluid formation overwhelms the protective fluid clearance mechanisms. Due to the lower COP gradient, hydrostatic pressure is the main determinant of fluid extravasation and edema formation in the lungs,⁴ hence the rationale for using hydrostatic pressure modulators in the treatment of all forms of pulmonary edema. The pulmonary ultrastructure is designed to protect gaseous diffusion. Most interstitial fluid flow is on the side of the capillary opposite to that where gas exchange occurs, and the distensibility of the lung tissue increases toward the peribronchovascular region. This results in initial fluid accumulation in areas not used for gas exchange.⁵

High-pressure edema forms as a result of increasing pulmonary capillary pressures, leading to fluid extravasation that eventually overwhelms the lymphatic removal capacity. Fluid flows initially toward the peribronchovascular interstitium, then distends all parts of the pulmonary interstitium, and eventually spills into the airspaces at the junction of the alveolar and airway epithelia.⁴ In many animals with cardiogenic edema, the increase in pressure occurs gradually, and overt edema may develop over a period of months; however, if there are acute increases in hydrostatic pressure (e.g., chordae tendineae rupture), then edema will form rapidly.

Increased permeability edema occurs secondary to injury to the microvascular barrier and alveolar epithelium, resulting in extravasation of fluid with a high protein content.⁴ The protective fall in COP is thereby diminished, so the hydrostatic pressure becomes the main determinant of edema formation. Interstitial fluid accumulation can then occur at even lower hydrostatic pressures, and relatively small rises in pressure can result in greater edema formation. In more severe cases in which the alveolar epithelium is also damaged, a direct conduit may form in the intravascular space, and interstitial edema progresses to alveolar flooding. This occurs rapidly and explains the greater severity and fulminant course of increased-permeability edema compared with hydrostatic edema.

Although the lymphatic system plays a major role in limiting interstitial fluid accumulation, it has only a minor role in the clearance of pulmonary edema. Most fluid is mobilized to the bronchial circulation, probably because most fluid tends to accumulate in the peribronchovascular areas.⁶ The rate of resolution depends on the fluid type, with pure water being reabsorbed much more rapidly than fluid containing macromolecules and cells.

CLINICAL PRESENTATION

Pulmonary edema results in reduced oxygenation, usually as a result of ventilation-perfusion mismatching; therefore most animals have symptoms of respiratory distress. Some of these patients are extremely fragile, so a risk-benefit assessment should be considered before even performing a physical examination. Oxygen should be given to all patients with respiratory distress, and the benefits of giving a patient time to recover in a quiet, oxygen-enriched environment cannot be overstressed (see Chapter 19, Oxygen Therapy). Initial diagnostic evaluation should be directed toward identifying the severity of the respiratory disease and the underlying cause. Historical information can be useful in some cases, such as smoke inhalation, choking, or a previous diagnosis of congestive heart failure. Neurogenic pulmonary edema may be suspected in animals that have dyspnea after head trauma, upper respiratory tract obstruction, or electric shock.

As with many conditions, the severity is often inversely proportional to the duration of clinical signs. Although typically associated with pulmonary edema, crackles are not heard in all cases; however, most patients will have either loud lung sounds or crackles. Crackles are particularly difficult to hear in patients with rapid respiratory rates and low tidal volumes. Careful auscultation may allow the abnormal lung sounds to be localized to one region and this may aid in the diagnosis, such as a cranioventral distribution with aspiration pneumonia and occasionally a perihilar distribution with cardiogenic pulmonary edema (primarily in the dog).

High-Pressure Edema

Cardiogenic Edema

Cardiogenic pulmonary edema is the most common form of high-pressure edema.⁷ It occurs as a result of left-sided congestive heart failure. Cardiac disease is often chronic, and in dogs there is usually a history of clinical signs consistent with heart disease: cough, exercise intolerance, and usually a heart murmur. Acute onset of signs may be seen, particularly if there has been a precipitating event such as stress. Cats often have no premonitory clinical signs. Due to the chronic progression of heart disease, compensatory mechanisms result in fluid retention to maintain cardiac output and, although beneficial in the short term, this eventually leads to signs of congestion which in its most life-threatening form is pulmonary edema.

As a result of chronic increases in blood volume, the capillary pressure at which edema forms is higher than in the normal dog or cat. In severe cases blood vessel rupture may occur, leading to a serosanguineous appearance of secretions, as evidenced by pink frothy sputum. Fortunately only a few common diseases cause cardiogenic pulmonary edema, and signalment can be extremely useful in forming a differential diagnosis list. Middle-aged, large breed dogs tend to have dilated cardiomyopathy, whereas the smaller breeds tend to have mitral valve disease. Cats are more prone to the myocardial diseases, with hypertrophic, thyrotoxic, and restrictive cardiomyopathies seen most commonly.⁷

Fluid Therapy

Fluid therapy is an uncommon cause of pulmonary edema without preexisting heart or lung disease, due to the effective safety mechanisms within the lung. However, fluid therapy may cause rapid increases in hydrostatic pressure in animals with preexisting (although asymptomatic) heart disease, leading to pulmonary edema. Experimental studies have demonstrated that dogs are able to cope with large volumes: dosages of 360 ml/kg of crystalloid over 1 hour were given before severe fluid overload was seen.⁸ Cats are less able to cope with large volumes, especially those with renal failure, cardiac insufficiency, or lung disease. Synthetic or natural colloid products and hemoglobin-based oxygen-carrying solutions cause much more volume expansion than crystalloids. Approximately 5 times the amount of colloid is retained within the intravascular space, so appropriate reductions in fluid administration rates and dosages should be made, especially in cats. When there are other risk factors such as systemic inflammation, pulmonary parenchymal disease, or hypoalbuminemia, fluid therapy may readily lead to pulmonary edema.

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