Drotrecogin alfa (activated) may attenuate severe sepsis-associated encephalopathy in clinical septic shock.docVIP

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Drotrecogin alfa (activated) may attenuate severe sepsis-associated encephalopathy in clinical septic shock.doc

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Drotrecogin alfa (activated) may attenuate severe sepsis-associated encephalopathy in clinical septic shock

Spapen et al. Critical Care 2010, 14:R54 /content/14/2/R54 RESEARCH Open Access Drotrecogin alfa (activated) may attenuate severe Research sepsis-associated encephalopathy in clinical septic shock Herbert Spapen*1, Duc Nam Nguyen1, Joris Troubleyn1, Luc Huyghens1 and Johan Schiettecatte2 Abstract Introduction: Sepsis-associated encephalopathy (SAE) is a diffuse cerebral dysfunction induced by the immuno- inflammatory response to infection. Elevated levels of the brain-specific S100B protein are present in many septic patients and reflect the severity of SAE. Adjunctive treatment with drotrecogin alfa (activated) (DrotAA), the human recombinant form of activated protein C, has been shown to improve mortality in patients with severe sepsis-induced organ failure. We studied the effect of DrotAA on S100B levels in patients with acute septic shock who presented with increased baseline values of this biomarker. Methods: All patients received standard goal-directed resuscitation treatment. Patients with pre-existing or acute neurological disorders were excluded. Based on the Glasgow coma scale (GCS), patients were classified into two groups: GCS ≥ 13 and GCS 13. DrotAA was given as a continuous infusion of 24 μg/kg/h for 96 h. S100B was measured before sedation and the start of DrotAA (0 h) and at 32 h, 64 h and 96 h and at corresponding time points in patients not treated with DrotAA. The lower limit of normal was 0.5 μg/L. Results: Fifty-four patients completed the study. S100B was increased in 29 (54%) patients. Twenty-four patients (9 with GCS ≥ 13 and 15 with GCS 13) received DrotAA. S100B levels in DrotAA-treated patients with a GCS 13, though higher at baseline than in untreated subjects (1.21 ± 0.22 μg/L vs. 0.95 ± 0.12 μg/L; P = 0.07), progressively and significantly decreased during infusion (0.96 ± 0.22 μg/L at 32 h, P = 0.3; 0.73 ± 0.12 μg/L at 64 h, P 0.05; and 0.70 ± 0.13 μg/L at 96 h, P 0.05 vs. baseline). This patient group had also s