This article is part of the supplement: 28th International Symposium on Intensive Care and Emergency Medicine

Poster presentation

Fatty acid binding protein and tau levels are related to brain damage and outcome after subarachnoid hemorrhage

T Zoerle1, M Fiorini2, L Longhi1, ER Zanier1, A Bersano1, L Cracco2, S Monaco2 and N Stocchetti1

Author Affiliations

1 University of Milano, Fondazione IRCCS Ospedale Maggiore Policlinico, Milan, Italy.

2 Ospedale Borgo Roma, Verona, Italy.

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Critical Care 2008, 12(Suppl 2):P110 doi:10.1186/cc6331


The electronic version of this article is the complete one and can be found online at: http://ccforum.com/content/12/S2/P110


Published:13 March 2008

© 2008 BioMed Central Ltd

Introduction

We measured the fatty acid binding protein (H-FABP) and tau levels in the cerebrospinal fluid (CSF) of patients after subarachnoid hemorrhage (SAH): to evaluate the relationship between SAH severity and H-FABP/tau values; to test the hypothesis that H-FABP/tau might help in the diagnosis of vasospasm; and to evaluate their association with outcome.

Methods

We studied 38 SAH patients, whose severity was assessed by the Glasgow Coma Scale (GCS). Serial CSF samples were obtained in every patient starting on the day of SAH and up 2 weeks post-SAH. H-FABP/tau levels were measured by ELISA. Vasospasm was defined as neuro-worsening (loss of at least one point of the motor component of GCS and/or appearance of a new focal deficit) + angiographic confirmation. The 6-month outcome was assessed by the dichotomized Glasgow Outcome Score (GOS): good (GOS 4–5) and bad (GOS 1–3). Multiple logistic regression analyses were performed to assess the association between H-FABP/tau values and GOS.

Results

H-FABP and tau increased after SAH. We observed a significant association between the peak H-FABP/tau values and admission mGCS (Spearman r = -0.581, P = 0.0001 and r = -0.582, P = 0.0001, respectively). Eight patients underwent brain death. Within the survivors we observed vasospasm in 11 patients. Both proteins were significantly higher in this group compared with those without ischemia (H-FABP = 15,958 ± 21,736 pg/ml vs 2,527 ± 2,427 pg/ml, P < 0.05; tau = 5,821 ± 3,774 pg/ml vs 1,118 ± 1,547 pg/ml, P < 0.05). The H-FABP rise preceded clinical recognition of vasospasm in seven patients and was simultaneous in four patients. Tau increased before clinical recognition of vasospasm in five patients. Patients with bad outcome showed higher peak levels of both proteins than patients with good outcome: respectively, H-FABP = 23,977 ± 25,593 pg/ml and 3,374 ± 2,549 pg/ml, P < 0.001; tau = 6,756 ± 4,544 pg/ml and 1,591 ± 1,639 pg/ml, P < 0.001. Logistic regression showed that, after correction for age, sex and SAH severity, the peak value of tau protein was an independent predictor of outcome.

Conclusion

The H-FABP and tau increase following SAH and might add complementary information for the diagnosis of vasospasm. There is an association between their CSF values and outcome following SAH.