Page 669 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

656 SPECIAL THERAPY

protect against pulmonary edema. 153 Certain types of The use of colloids in patients with high-pressure pul-
lung injury, such as pneumonia or chemical injury, further monary edema is controversial because of their greater
increase the permeability of the capillary endothelium to propensity for volume overload and because existing
protein. When one considers the Starling equation, it therapies for heart failure are so effective. Therefore col-
becomes obvious that the capillary hydrostatic pressure loid therapy should be used with extreme caution to pre-
becomes the major determinant of edema formation. vent increases in pulmonary capillary hydrostatic
Smaller increases in capillary hydrostatic pressure result pressure. Colloid support in the patient with left-sided
in much greater fluid extravasation than occurs when heart failure should only be used in a critical care environ-
the endothelium remains intact. This finding clearly ment with invasive monitoring capabilities. Increased left
explains clinical and experimental studies that show that atrial pressure secondary to left-sided heart failure results
colloid therapy significantly worsens pulmonary edema in increased pulmonary capillary pressure and increased
caused by increased microvascular permeability. 78 If the fluid extravasation into the pulmonary interstitium. 73
alveolar epithelium is also damaged, interstitial edema Lymph flow in the lung increases to protect against inter-
can rapidly progress to alveolar flooding because there stitial fluid accumulation, 182 but as extravasation
is, in effect, a direct conduit from the vasculature to the increases, fluid begins to accumulate in the interstitium.
alveolar space. In the alveoli, where gas exchange occurs, the capillary
Absorption of water, solutes, and protein occurs via endothelial cell is closely apposed to the alveolar epithelial
different mechanisms and at vastly different rates. cell, and the perimicrovascular interstitium is relatively
Resorption of sodium-containing alveolar fluid occurs noncompliant. In contrast, the peribronchovascular
mainly via active transport by the alveolar epithelium, interstitial tissue is more compliant, and fluid tends to
most likely via a sodium-potassium pump with glucose accumulate as peribronchovascular edema cuffs, thereby
cotransport, which b-adrenergic agonists stimu- protecting gas exchange. 38,39 Eventually, edema fluid
late. 100,136 Fluid absorption occurs against the colloid distends all parts of the pulmonary interstitium and ulti-
osmotic gradient, which increases as fluid is reabsorbed mately fills the airspaces of the lung. Current theory
and protein remains behind. Protein is cleared from the suggests that because the alveolar membrane is so imper-
alveoli at a very slow rate, 99 which is one of the reasons meable to solutes, alveolar filling does not occur by fluid
for the protracted resolution often seen with edema flow through the epithelium, but rather fluid spills into
caused by increased permeability. the airspaces at the junction of the alveolar and airway
Colloid therapy may worsen pulmonary edema if the epithelia. 152 In the absence of increases in permeability,
increase in endothelial permeability is such that the maintenance of intravascular COP via colloid administra-
majority of colloid molecules can pass through the pul- tion can be protective against cardiogenic pulmonary
monary capillary endothelium. 79 This is particularly true edema. 174 Furosemide also increases COP, and, contrary
if a significant increase in pulmonary capillary pressure to popular belief, it does not appear to reduce plasma vol-
occurs simultaneously, as is more likely with colloid infu- ume. 48,142 Because of the opposing effects of intravascu-
sion. Considering the extremely slow clearance of lar hydrostatic pressure and COP, monitoring the
macromolecules from the alveolar space, this increase in gradient between pulmonary artery occlusion pressure
edema may be life threatening. Conversely, if the increase and COP has been suggested in the management of pul-
in permeability is insufficient to allow loss of colloid into monary edema. 48,119,120
the interstitium, prudent colloid therapy can reduce
extravascular lung water. Therefore it is important to crit- CHRONIC HYPOPROTEINEMIA
ically evaluate the patient’s response to a test infusion of The effective COP acting to retain fluid within the intra-
colloid. An increase in COP should be titrated to prevent vascular space is the net difference between the intravas-
an increase in respiratory rate and effort, or, at worst, a cular COP and interstitial COP. As intravascular COP
decrease in arterial oxygen concentration. In more decreases, fluid with a lower COP passes from the vascu-
advanced critical care settings, pulmonary capillary wedge lature and dilutes the interstitial protein concentration
pressure or even measurement of extravascular lung water such that interstitial COP also decreases. Consequently,
may be used to guide fluid therapy. When using colloids the gradient between intravascular and interstitial COP
in the patient with a systemic vascular leak state, and in the is preserved. In addition, increased lymphatic drainage
absence of hemorrhage, failure to retain colloid in the will also protect against edema formation. Hence, a low
intravascular space for an appropriate time period plasma COP per se does not necessitate colloid therapy
suggests that extravascular leakage of colloid could be in the absence of clinical signs such as hypovolemia or
worsening, not helping, hypovolemia and edema. If arte- edema. Indeed, people with an hereditary form of com-
rial oxygenation worsens after colloid therapy in an ani- plete albumin deficiency have plasma COP that still is half
mal with pulmonary edema caused by altered of normal because of increased globulin concentrations,
permeability, one must consider the possibility that the and affected individuals exhibit minimal peripheral
colloid is contributing to the pulmonary edema. edema. 9,49 There also appear to be no serious clinical