Understanding of the etiology of decubitus ulcer formation is fragmentary and the existing literature contains much experimental data that are inconsistent with the idea that pressure sore formation is due extensively to depriving a tissue region of blood. In fact, there is substantial data that illustrate that tissue can remain viable for very extended lengths of time, up to 13 hours, when subjected to externally applied pressures that collapse the blood microvasculature in a region. Based on these observations and on studies done in this laboratory on lymph propulsion and pressure sore prevention, an hypothesis has been formulated that is consistent with the published data and with clinical observations. The hypothesis states that a major contributing factor to pressure sores is the tissue necrosis that is caused by the accumulation of anaerobic metabolic waste products due to occlusion of the lymph vessels.