Sepsis-associated encephalopathy is a multifactorially determined process of the brain parenchyma. Among other factors, vasogenic causes have been shown to play a role in its development. The aim of the present work was to assess whether cerebral tissue oxygen saturation is influenced by administration of acetazolamide in septic patients compared to controls.
Patients and methods: 15 patients with severe sepsis and 10 healthy controls were studied. Cerebral oxygen saturation was assessed by INVOS 51 OOC Cerebral Oxymeter (NIRS) before and after administration of 15 mg/kg BW acetazolamide in both groups.
Results: The maximal rise that has been found in the partial pressure of CO(2) in the arterial blood of septic patients after administration of acetazolamide was from 35 ± 5 mmHg to 41.1 ± 6.3 mmHg. For the partial pressure of O(2) the observed increase was from 123.7 ± 47.1 mmHg to 139.9 ± 49 mmHg. Vasodilatory stimulus resulted in a similar maximal increase in cerebral oxygen saturation in septic patients and in controls (8.9 ± 6.5% for septic patients and 9.2 ± 4.6% for healthy persons, respectively).
Conclusions: Cerebral vasoreactivity to acetazolamide is preserved in patients with severe sepsis.
Keywords: acetazolamide; cerebral vasoreactivity; near-infrared spectroscopy; sepsis; sepsis-associated encephalopathy.