Page 366 - Clinical Small Animal Internal Medicine

334 Section 4 Respiratory Disease

Table 34.1 Starling Law applied to pleural membrane and larger particles to be absorbed into the lymphatic
VetBooks.ir Q b = LA[(P c −P pl ) – σ o (π c −π pl )] system through channels called lacunae. The maximal
reabsorption rate through pleural lymphatics is esti-

more than the normal daily rate of fluid accumulation.
Q b Filtration rate across the capillary endothelial barrier in mated to be 0.2–0.3 mL/kg/h, which is considerably
series with the pleural membrane (interstitium) Therefore, the accumulation of pleural fluid occurs when
LA Filtration coefficient = [hydraulic conductivity (L) * the disease process overwhelms fluid reabsorption
surface area (A)] capacity, reduces the ability of lymphatics to reabsorb
σ o Reflection coefficient to protein of the combined fluid, or increases production of fluid while simultane-
endothelial‐interstitial barrier ously decreasing lymphatic clearance.
P c Capillary hydrostatic pressure Pathologic fluid effusions are classified in two broad
P pl Pleural hydrostatic pressure categories: transudates and exudates. Transudative effu-
π c Capillary oncotic pressure sions typically accumulate secondary to an increase in
π pl Pleural oncotic pressure hydrostatic pressure or a reduction in plasma oncotic
pressure while the pleura remains normal, whereas exu-
Source: Adapted from Lai-Fook 2004. dative effusions typically accumulate secondary to vari-
ous pleural pathologic conditions leading to increased
vascular permeability and/or diminished lymphatic fluid
Normal pleural pressure is approximately –3 to reabsorption. Mesothelial cells play a pivotal role in the
–5 cmH 2 O at functional residual capacity, becomes development of exudative effusions by synthesizing
greater (more negative) with deeper breaths, and is more inflammatory cytokines, growth factors, and extracellu-
negative in the dorsal space compared to the ventral lar proteins. A classic example of increased systemic
space, decreasing by 0.5–0.7 cmH 2 O/cm in dogs. This venous hydrostatic pressure leading to a transudative
subatmospheric pleural pressure results from elastic effusion is congestive heart failure. In addition, pulmo-
recoil forces of the lung exerting a force inward with the nary thromboembolism, cardiac tamponade, heartworm
propensity of the chest wall to expand outward and disease, and neoplasia can all lead to increased venous
serves to maintain lung inflation while decreasing the hydrostatic pressure and therefore transudative pleural
work of breathing. Although reported as a single num- effusion. In comparison, a classic example of an exuda-
ber, pleural pressure is a result of the dynamic nature of tive effusion is pyothorax with an influx of inflammatory
the pleural space and represents a summation of the cells, which can increase vascular permeability and
pressure exerted by pleural fluid, regional pleural surface decreased lymphatic drainage (Table 34.2).
deformation, and weight of the lung in dependent areas Regional changes in pleural pressure occur with the
of the thoracic cavity. accumulation of pleural effusion and the mechanism of
pressure change is controversial. Proposed theories to
explain the pressure difference center around the hydro-
Pathophysiology of Pleural Fluid static pressure contribution of a column of fluid in the
Accumulation thorax and the changes in deformation forces as the lung
and thoracic wall become separated by fluid. The hydro-
Pleural fluid volume depends on Starling forces, meso- static theory divides the pleural space into three distinct
thelial cell activity, and lymphatic drainage; however, the pressure zones: the upper (dorsal) zone, middle zone,
exact contribution of each of these mechanisms remains and lower (ventral) zone. In the upper (dorsal) zone, the
somewhat elusive and varies during disease processes. pleural liquid thickness is normal and the pleural liquid
Starling forces which favor the formation of pleural pressure is less than the pleural surface pressure. In the
fluid include increased capillary hydrostatic pressure, middle zone, the pleural liquid thickness increases and
decreased capillary oncotic pressure, and increased cap- pleural liquid pressure equalizes with pleural surface
illary permeability. Mesothelial cells have apical micro- pressure at zero. In the lower (ventral) zone, the pleural
villi that increase the surface area for exchange and fluid thickness increases substantially and the pressure
vesicles that allow for transcytosis of proteins from the becomes positive, displacing the lung from the thoracic
pleural space to the pleural interstitium. In addition, wall. In the other predominant theory, the pleural liquid
indirect evidence suggests mesothelial cells are involved pressure is always equal to pleural surface pressure such
in solute‐coupled liquid transport across the pleural sur- that pressure gradients caused by gravity and regional
face. Lymphatics communicate directly with the pleural differences in pleural surface pressure drive a small
cavity through openings between the mesothelial layer in viscous flow of fluid in the normal pleural space and
the parietal pleura, called stomas, and allow cells, protein, surfaces are never in contact. As pleural effusion