The present study was undertaken to study the pathophysiology of SMOF from the aspect of tissue hypoxia. Seventeen postoperative SMOF patients (9 survivors, 8 non-survivors) and 14 control ICU patients were evaluated their oxygen delivery (DO2I) and oxygen consumption (VO2I) in relation to cellular injury score (CIS) derived from 3 different intracellular metabolic indices, arterial ketone body ratio (AKBR), osmolality gap (OG) and blood lactate. In the early stage, SMOF patients showed hyperdynamic state and increased VO2I, reflecting increased oxygen demand in tissue. However, CIS of SMOF was significantly higher than that of control in spite of increased VO2I, indicating relative tissue hypoxia might exist in vital organs resulting in cellular injury. Further deterioration of CIS was accompanied with decreased VO2I. These data suggest that impaired tissue oxygen metabolism correlates with cellular injury and might be one of mechanisms of organ failure in SMOF patients.