Figure 2.

Pathologically elevated serum H₂O₂ levels can account for the general physiological, histological and clinical abnormalities observed in septic shock. Red blood cell glutathione accounts for a major portion of serum redox buffering capacity and is depleted in septic shock non-survivors vs. survivors. Brain neuron function is highly vulnerable to H₂O₂ oxidative stress and is manifested by electroencephalographic changes, which can appear before clinical encephalopathy is evident. Studies show that septic shock survivors upregulate serum antioxidant capacity (which decreases H₂O₂), while non-survivors are unable to do so. This suggests that elevated H₂O₂ is a necessary concomitant to the development of septic shock and recovery is preceded by decreasing H₂O₂. The individual clinical course, bookended by these extremes of H₂O₂, is influenced by parameters such as individual antioxidant capacity, susceptibility to oxidative stress, co-morbidities, age, general health and organ system involved.