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The terms hyperemia and congestion both indicate a local increased volume of blood in a
particular tissue. Hyperemia is an active process resulting from augmented blood flow
due to arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during
exercise). The affected tissue is redder than normal because of engorgement with
oxygenated blood. Congestion is a passive process resulting from impaired venous return
out of a tissue. It may occur systemically, as in card iac failure, or it may be local,
resulting from an isolated venous obstruction. The tissue has a blue-red color (cyanosis),
especially as worsening congestion leads to accumulation of deoxygenated hemoglobin in
the affected tissues (Fig. 4-3).

Congestion of capillary beds is closely related to the development of edema, so that
congestion and edema commonly occur together. In long-standing congestion, called
chronic passive congestion, the stasis of poorly oxygenated blood causes chronic
hypoxia, which in turn can result in degeneration or death of parenchymal cells and
subsequent tissue fibrosis. Capillary rupture at such sites of chronic congestion can also
cause small foci of hemorrhage; phagocytosis and catabolism of the erythrocyte debris
can result in accumulations of hemosiderin- laden macrophages.


Cut surfaces of hyperemic or congested tissues are hemorrhagic and wet.
Microscopically, acute pulmonary congestion is characterized by alveolar capillaries
engorged with blood; there may also be associated alveolar septal edema and/or focal
minute intra-alveolar hemorrhage. In chronic pulmonary congestion the septa become
thickened and fibrotic, and the alveolar spaces may contain numerous hemosiderin- laden
macrophages ("heart failure cells"). In acute hepatic congestion the central vein and
sinusoids are distended with blood, and there may even be central hepatocyte
degeneration; the periportal hepatocytes, better oxygenated because of their proximity to
hepatic arterioles, undergo less severe hypoxia and may develop only fatty change. In
chronic passive congestion of the liver the central regions of the hepatic lobules are
grossly red-brown and slightly depressed (because of a loss of cells) and are accentuated
against the surrounding zones of uncongested tan, sometimes fatty, liver ("nutmeg liver";
Fig. 4-4A). Microscopically, there is centrilobular necrosis with hepatocyte drop-out,
hemorrhage, and hemosiderin- laden macrophages (Fig. 4-4B). In long-standing, severe
hepatic congestion (most commonly associated with heart failure), hepatic fibrosis
("cardiac cirrhosis") can develop. It is important to note that because the central portion
of the hepatic lobule is the last to receive blood, centrilobular necrosis can also occur
whenever there is reduced hepatic blood flow (including shock from any cause); there
need not be previous hepatic congestion.
Figure 4-3 Hyperemia versus congestion. In both cases there is an increased volume and
pressure of blood in a given tissue with associated capillary dilation and a potential for
fluid extravasation. In hyperemia, increased inflow leads to engorgement with
oxygenated blood, resulting in erythema. In congestion, diminished outflow leads to a
capillary bed swollen with deoxygenated venous blood and resulting in cyanosis.
Figure 4-4 Liver with chronic passive congestion and hemorrhagic necrosis. A, Central
areas are red and slightly depressed compared with the surrounding tan viable
parenchyma, forming a "nutmeg liver" pattern (so called because it resembles the
alternating pattern of light and dark seen when a whole nutmeg is cut). B, Centrilobular
necrosis with degenerating hepatocytes and hemorrhage. (Courtesy of Dr. James
Crawford, Department of Pathology, University of Florida, Gainesville, Florida.)