Hyperemia and Congestion

Increased blood volume locally in a particular tissue

active process

increased tissue inflow of blood due to arteriolar dilation

affected tissue is redder due to engorgement with oxygenated blood

Usually short-lasting

E.g.

Physiological- Exercise

Pathological - Inflammation

a passive process

results from impaired Outflow from a tissue

affected tissue is of bluish-red color (cyanosis) due to de-oxygenated blood accumulation

May show chronicity

E.g.

Systemic - cardiac failure

local - isolated venous obstruction

DVT(deep venous thrombosis)

TOO Syndrome

Chronic Passive Hyperemia/ Congestion

A long-standing congestion where the stasis of poorly oxygenated blood causes chronic local hypoxia resulting in parenchymal cell degeneration or death

Break down of RBCs and the debris onbeing phagocytosed give rise to hemosiderin laden macrophages

A small foci of hemorrhage may arise at the site of chr. Congestion due to capillary rupture

Micrscopic appearences

Acute pulmonary congestion

alveolar capillaries engorged with blood

associated alveolar septal edema may be present with or without focal minute intra-alveolar hemorrhage

Pasive pulmonary congestion

Alveolar septa – thickened and fibrotic

Numerous hemosiderin laden macrophages referred to as heart failure cells in alveoli

Ac. Pul. Congestion

Chr. Pul. Congestion with heart failure cells

Hemosiderin laden heart failure cells

Acute hepatic congestion

central vein and sinusoids distended with blood

Centrilobular degeneration as the hepatocytes at the periphery receive better oxygenated blood because of their proximity to hepatic arterioles

Chronic passive congestion of the liver

Grossly ‘nut-meg’ liver on cut section

Microscopically –

centrilobular necrosis, hepatocyte drop-out and hemorrhage with hemosiderin laden macrophages

Cardiac Cirrhosis – Hepatic fibrosis in chronic severe passive congestion of liver due to rt. Sided heart failure

Nutmeg liver

Centrilobular necrosis