This is an altered level of consciousness attributed to the effects of an extracranial infection.
An excellent article on the subject earns significant brownie points by quoting Tolstoy in the opening paragraph.

"The doctors said that it was puerperal fever and that it was ninety-nine chances in a hundred it would end in death. The whole day long there was fever, delirium, and unconsciousness. At midnight the patient lay without consciousness, and almost without pulse.
The end was expected every minute."

Septic encephalopathy is present in up to 80% of septic patients. When graded using the Glasgow Coma Scale, it is associated with an increased mortality, ranging from 20% for a GCS of 14-13 to 63% for GCS of 8 and below.

Pathogenesis of septic encephalopathy

In short, nobody knows why this happens. Certainly the bacteria themselves are not to blame - infusing E.coli lipopolysaccharide into healthy volunteers only increased their level of alertness. Several factors are thought to be to blame for the syndrome. A recent review article lists several potential aetiological contributors:

One can represent this complex interaction with a big confusing flowchart.

mechanism of pathogenesis of septic encephalopathy

Diagnosis of septic encephalopathy

This is a diagnosis of exclusion. Certainly, arriving at a diagnosis of septic encephalopathy does not steer one any closer to a specific management strategy, because there is none. One manages this sort of delirium in a similar manner to all other sorts of delirium in the ICU. However, it should be mentioned that in contrast to other forms of delirium, this one should resolve as the septic episode concludes, and thus the management of sepsis should be one's priority (as if it weren't already).

Certainly, it seems imaging and EEG findings in septic encephalopathy are non-specific.

In general, supportive management is geared towards the control of organ system dysfunction and prevention of all the other factors in the "multifactorial aetiology" of delirium. If you can prevent the kidneys and liver from shutting down, if you can control your use of sedating drugs, and if the patient remains normoxic normoglycaemic and normotensive, one can say that one has done everything possible to address the non-septic components, and all that remains is to wait for the antibiotics to have their effect.

References

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Eidelman, Leonid A., et al. "The spectrum of septic encephalopathy: definitions, etiologies, and mortalities." Jama 275.6 (1996): 470-473.

Flierl, Michael A., et al. "Pathophysiology of septic encephalopathy—an unsolved puzzle." Crit Care 14.3 (2010): 165.

van den Boogaard, Mark, et al. "Research Endotoxemia-induced inflammation and the effect on the human brain." (2010).Critical Care 2010, 14:R81

D'Avila, J., et al. "Bioenergetic imbalance and oxidative stress in the pathophysiology of septic encephalopathy." Critical Care 17.Suppl 2 (2013): P22.

Ziaja, Marek. "Septic Encephalopathy." Current neurology and neuroscience reports 13.10 (2013): 1-7.

Green, Rebecca, et al. "Sepsis associated encephalopathy (SAE): a review."Front Biosci 9.5 (2004): 1637-1641.

Berg, Ronan MG, Kirsten Møller, and Damian M. Bailey. "Neuro-oxidative-nitrosative stress in sepsis." Journal of Cerebral Blood Flow & Metabolism 31.7 (2011): 1532-1544.

Jacob, Alexander, James R. Brorson, and Jessy J. Alexander. "Septic encephalopathy: inflammation in man and mouse." Neurochemistry international58.4 (2011): 472-476.

Nico, Beatrice, and Domenico Ribatti. "Morphofunctional aspects of the blood-brain barrier." Current drug metabolism 13.1 (2012): 50-60.

Silvio Taccone, Fabio, et al. "Brain perfusion in sepsis." Current vascular pharmacology 11.2 (2013): 170-186.

Basler, Thomas, et al. "Amino acid imbalance early in septic encephalopathy."Intensive care medicine 28.3 (2002): 293-298.

Kondo, Satoru, Shinichi Kohsaka, and Shigeo Okabe. "Long-term changes of spine dynamics and microglia after transient peripheral immune response triggered by LPS in vivo." Mol Brain 4 (2011): 27.

Zampieri, Fernando Godinho, et al. "Sepsis-associated encephalopathy: not just delirium." Clinics 66.10 (2011): 1825-1831.

Iacobone, Emanuele, et al. "Sepsis-associated encephalopathy and its differential diagnosis." Critical care medicine 37.10 (2009): S331-S336.