Injury to the hepatic microvasculature, the hepatic sinusoids, manifests in several ways. The sinusoidal endothelial cells (SECs) may lose porosity and scavenger function (capillarization); SECs may loosen from their tetherings to the space of Disse or even detach completely (ischemia-reperfusion injury, early sinusoidal obstruction syndrome, peliosis hepatis, early acetaminophen toxicity); the space of Disse may be completely denuded of sinusoidal lining cells that then embolize and obstruct the sinusoid (early sinusoidal obstruction syndrome); or the sinusoid may be obstructed by fibrosis (hepatic sinusoidal fibrosis, late sinusoidal obstruction syndrome). In many of these microvascular injuries, the change to the sinusoid is a primary event that may lead to hepatocyte hypoxia with liver dysfunction and disruption of the portal circulation. With the exception of hepatic fibrosis, which will be reviewed elsewhere in this issue, each of these types of microvascular injuries will be described in this article.