Urotensinergic system genes in experimental subarachnoid hemorrhage.

OBJECTIVE: Cerebral vasospasm, one of the main complications of subarachnoid hemorrhage (SAH), is characterized by arterial constriction and mainly occurs from day 4 until the second week after the event. Urotensin-II (U-II) has been described as the most potent vasoconstrictor peptide in mammals. An analysis is made of the serum U-II concentrations and mRNA expression levels of U-II, urotensin related peptide (URP) and urotensin receptor (UT) genes in an experimental murine model of SAH. DESIGN: An experimental study was carried out. SETTING: Experimental operating room of the Biomedicine Institute of Seville (IBiS), Virgen del Rocío University Hospital (Seville, Spain). PARTICIPANTS: 96 Wistar rats: 74 SAH and 22 sham intervention animals. INTERVENTIONS: Day 1: blood sampling, followed by the percutaneous injection of 100µl saline (sham) or blood (SAH) into the subarachnoid space. Day 5: blood sampling, followed by sacrifice of the animals. MAIN VARIABLES OF INTEREST: Weight, early mortality, serum U-II levels, mRNA values for U-II, URP and UT. RESULTS: Serum U-II levels increased in the SAH group from day 1 (0.62pg/mL [IQR 0.36-1.08]) to day 5 (0.74pg/mL [IQR 0.39-1.43]) (p<0.05), though not in the sham group (0.56pg/mL [IQR 0.06-0.83] day 1; 0.37pg/mL [IQR 0.23-0.62] day 5; p=0.959). Between-group differences were found on day 5 (p<0.05). The ROC analysis showed that the day 5 serum U-II levels (AUC=0.691), URP mRNA (AUC=0.706) and UT mRNA (AUC=0.713) could discriminate between sham and SAH rats. The normal serum U-II concentration range in rats was 0.56pg/mL (IQR 0.06-0.83). CONCLUSION: The urotensinergic system is upregulated on day 5 in an experimental model of SAH.

[Usefulness of biomarkers in the prognosis of severe head injuries]. / Utilidad de los biomarcadores en el pronóstico del traumatismo craneoencefálico grave.

Severe head injuries have a great socioeconomic and public health impact. Despite progress in diagnosis and treatment, no sufficiently reliable predictive models have been established for developing clinical trials and promoting effective therapeutic strategies capable of improving the prognosis. In the last decades, several brain damage biomarkers have been studied as potential diagnostic and prognostic tools in traumatic brain injury. However, all of them have limitations that preclude their universalized application. The properties of the known biomarkers -both those traditionally shown to correlate with severity and prognosis, and those recently announced as promising options- should be analyzed. New studies are needed to define their properties, both isolatedly and in combined use.

[An experimental model of mass-type brain damage in the rat: expression of brain damage based on neurospecific enolase and protein S100B]. / Modelo experimental de lesión cerebral tipo masa en rata: expresión del daño cerebral mediante enolasa neuroespecífica y proteína S100B.

OBJECTIVE: To determine whether a model of transient mass-type brain damage (MTBD) in the rat produces early release of neurospecific enolase (NSE) and protein S100B in peripheral blood, as an expression of the induced brain injury. DESIGN: An experimental study with a control group. SETTING: Experimental operating room of the Institute of Biomedicine (IBiS) of Virgen del Rocío University Hospital (Seville, Spain). PARTICIPANTS: Fourteen adult Wistar rats. INTERVENTIONS: Blood was sampled at baseline, followed by: MTBD group, a trephine perforation was used to insert and inflate the balloon of a catheter at a rate of 500 µl/20 sec, followed by 4 blood extractions every 20 min. Control group, the same procedure as before was carried out, though without trephine perforation. PRIMARY STUDY VARIABLES: Weight, early mortality, serum NSE and S100B concentration. RESULTS: Differences in NSE and S100B concentration were observed over time within the MTBD group (P<.001), though not so in the control group. With the exception of the baseline determination, differences were observed between the two groups in terms of the mean NSE and S100B values. Following MTBD, NSE and S100B progressively increased at all measurement timepoints, with r=0.765; P=.001 and r=0.628; P=.001, respectively. In contrast, the control group showed no such correlation for either biomarker. CONCLUSIONS: Serum NSE and S100B concentrations offer an early indication of brain injury affecting the gray and white matter in an experimental model of mass-type MTBD in the rat.

Serologic behavior of S100B protein in patients who are brain dead: preliminary results.

OBJECTIVE: The objective of this study is to assess the S100B protein serum concentrations from brain dead (BD) donors to understand whether its level could provide clinical information during BD diagnosis as a potential confirmatory test. METHODS: During 12 months, 26 patients declared BD were prospectively included in this study. Once the diagnosis of BD was achieved, serum S100B protein levels were measured using an electrochemiluminescence assay. For analytical purposes, we selected the maximum S100B serum value reached during the first 5 days of evolution from a historical cohort of 124 survived patients after a severe brain injury (SBI), as well as from 18 healthy donors (HD) and a subgroup of patients who had severe traumatic brain injuries (TBIs) without extracranial injuries. RESULTS: Mean age was 53.48 years (SD, 18.91 years). The BD group had significantly higher S100B serum levels (1.44 µg/L; interquartile ratio [IR], 0.63-3.68) than the SBI (0.34 µg/L; IR, 0.21-0.60) and HD groups (0.06 µg/L; IR, 0.03-0.07; P < .001). Analysis of S100B levels depending on the main cause responsible for BD development showed significant differences between subgroups (P = .012). S100B serum levels were higher in the isolated TBI BD group (P = .004). The S100B value showed an odds ratio for BD diagnosis of 8.38 (95% confidence interval [CI], 1.16-60.45; P = .035). Reciever operating characteristic analysis revealed an area under the curve of 0.92 (95% CI, 0.79-1.00; P = .007). We set a cut-off value of 2 µg/L in S100B serum concentrations. At this level, the diagnostic properties of S100B would reach 100% of specificity and positive predictive value (PPV), and sensitivity and negative predictive value (NPV) of 60% and 86.7%, respectively. CONCLUSION: This preliminary analysis shows for the very first time that BD is associated with higher S100B serum levels, compared with other neurocritical care patients. We also found that the cause of BD development must be considered. Specifically, S100B serum levels in severe isolated TBI patients-with clinical exploration compatible with BD-could be used in a future as confirmatory test.

Clinical variables and neuromonitoring information (intracranial pressure and brain tissue oxygenation) as predictors of brain-death development after severe traumatic brain injury.

BACKGROUND AND PURPOSE: The aim of this study was to ascertain the role of clinical variables and neuromonitoring data as predictors of brain death (BD) after severe traumatic brain injury (TBI). PATIENTS AND METHODS: This prospective observational study involved severe TBI patients admitted to the intensive care unit between October 2009 and May 2011. The following variables were recorded: gender, age, reference Glasgow Coma Scale after resuscitation, pupillary reactivity, prehospital hypotension and desaturation, injury severity score, computed tomography (CT) findings, intracranial hypertension, and low brain tissue oxygenation (Pti02) levels (<16 mm Hg), as well as the final result of BD. RESULTS: Among 61 patients (86.9% males) who met the inclusion criteria, the average age was 37.69 ± 16.44 years. Traffic accidents were the main cause of TBI (62.3%). The patients at risk of progressing to BD (14.8% of the entire cohort) were those with a mass lesion on CT (odds ratio [OR] 33.6; 95% confidence interval [CI]: 3.75-300.30; P = .002), altered pupillary reaction at admission (OR 25.5; 95% CI: 2.27-285.65; P = .009), as well low Pti02 levels on admission (OR 20.41; 95% CI: 3.52-118.33; P < .001) and during the first 24 hours of neuromonitoring (OR 20; 95% CI: 2.90-137.83; P < .001). Multivariate logistic regression showed that a low Pti02 level on admission was the best independent predictor for BD (OR 20.41; 95% CI: 3.53-118.33; P = .001). CONCLUSIONS: Clinical variables and neuromonitoring information may identify TBI patients at risk of deterioration to BD.

Left subclavian artery pseudoaneurysm after a traffic accident: a case report.

The left subclavian artery pseudoaneurysm is a rare entity with few cases reported in the literature. Most injuries were related to iatrogenic manipulation with catheters for canalization of central lines. In rare cases, this injury has been described secondary to a blunt trauma. We present an unusual case of pseudoaneurysm that includes the origin of left subclavian artery in the context of severe multiple injuries after a traffic accident. There were not clavicular or rib fractures, or another type of chest trauma to justify such a vascular injury. Once the injuries that were life threatening for the patient were stabilized, it proceeded to the treatment of the pseudoaneurysm by placing an endovascular prosthesis successfully with a favorable clinical evolution.