HYPEREMIA AND CONGESTION

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 cardiac 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.

Morphology

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.)