The correlation between Tau protein and brain damage in patients with sepsis and septic shock

Sepsis related encephalopathy (SRE) is defined as a diffuse cerebral dysfunction causing systemic response to infection stemming from other regions of the body with no clinical or laboratory evidence of infections directly affecting the central nervous system. SRE is the most widespread metabolic encephalopathy in the intensive care unit and is still generally evaluated using the Glasgow coma scale (GCS). Although the GCS is widely used in the analysis of cerebral dysfunction, it is often not reliable since the majority of septic patients are sedated and taken to a mechanical ventilator before neurological worsening. In addition, scores in non-sedated patients can worsen with acidosis, fever or hypercapnia and poor scores may not always be correlated with fatal outcomes. Brain dysfunction can be evaluated through such imaging techniques as electroencephalography (EEG), computerized tomography (BT) and magnetic resonance imaging (MRI), but daily repetitions in sedated patients are difficult. In addition, they cannot usually be performed on patients whose neurological findings remain unchanged, and such procedures can even be harmful. The frequent injection of contrast products can damage renal functions. In addition, reliable transportation to the radiology department may not always be possible.The easily accessible, effective and practical biochemical markers in SRE analysis may be very useful. The current literature shows that biochemical parameters such as serum Tau protein, neuron specific enolase (NSE) and S100B can be used in the identification of neuronal damage.In addition, Tau protein, a current biochemical marker, is a structural protein linked to the microtubule localized to the axon and its clinical role in sepsis/SRE patients is as yet unknown. This study was intended to determine whether serum Tau protein levels reflect the development of brain damage and encephalopathy in the evaluation of SRE patients, whether they can be used as an additional test to GCS in the diagnosis of SRE and the correlation with mortality and morbidity in SRE patients and with SOFA score.Patients diagnosed with sepsis and septic shock at the Karadeniz Technical University Medical Faculty Emergency Department and Infectious Diseases Department between 01.02.2009 and 30.07.2009 were recorded in this prospective study. The correlation between Tau levels, measured in the first 24 h after application and over the subsequent 3 days, and the development of sepsis-related encephalopathy, clinical course and mortality and morbidity was evaluated.Ninety-eight patients were registered in the study. Twenty-eight patients meeting the exclusion criteria were excluded. Fifty percent of the 70 patients included for analysis in the study were regarded as SRE in the light of GCS determined on the first day; SRE on the basis of GCS developed subsequently in 2.9% of patients.Although serum Tau levels were higher in patients developing SRE compared to those without SRE, the difference was not statistically significant (p>0.05 for all measurements compared). No significant correlation was determined between SRE development and Tau protein levels (p>0.05 for all comparisons). Mean SOFA score in our SRE patients was 7.5 ± 2.3 compared to 3.8 ± 2.8 in non-SRE patients, and this difference was statistically significant (p<0.0001). Thirty-six (51.4%) of the patients enrolled died, 33 (91.7%) of whom were SRE patients and 3 (8.3%) not. This difference was again statistically significant (p<0.0001). No significant correlation was determined between serum Tau levels and mortality and SOFA score (p>0.05).This study established that serum Tau level does not reflect the development of brain damage and encephalopathy, that is cannot be used as an additional test to GCS in the diagnosis of SRE, and that there is no correlation with mortality and morbidity in SRE patients and no correlation with SOFA score.Key words: Sepsis, SRE, Tau, brain damage