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Ein Hospital Building, 177 Fort Washington Avenue, Suite 8-300 Center, Rosiglitazone New York, NY 10032, USACorresponding author: Stephan A Mayer, sam14@columbia.eduPublished: 15 July 2009 This article is online at http://ccforum.com/content/13/4/166 ?2009 BioMed Central Ltd See related research by Derwall et al., http://ccforum.com/content/13/2/RCritical Care 2009, 13:166 (doi:10.1186/cc7929)AbstractDespite significant advances in neurocritical care, it remains difficult to precisely measure the extent of neurological injury in patients affected by stroke, trauma, or cardiac arrest. In the intensive care unit the extent of primary and secondary injury often eludes clinicians, making prognostication imprecise and difficult. Derwall and colleagues present their findings on the dynamics of serum S-100B protein levels in out-of-hospital cardiac arrest survivors. Their study suggests that elevation of S-100B reflects the severity of the primary hypoxic-ischemic insult.cerebrospinal fluid. These proved to be of little use given their lack of specificity for nervous tissue injury. The ideal biomarker would be highly sensitive and specific for neurological injury, rapidly available from the serum or other easily obtained body fluid other than cerebrospinal fluid, and released in proportion to the severity of the injury, with little variability across different diagnostic and demographic groups. Although the ideal biomarker remains elusive, several different molecules have shown promise. Of these, neuron specific enolase, myelin basic protein, glial fibrillary acidic protein, and the S-100B protein have received the most attention. In a recent issue of Critical Care, Derwall and colleagues [1] present their findings on the dynamics of serum S-100B protein levels in a prospectively studied cohort of out-ofhospital cardiac arrest (OHCA) survivors. S-100B is a constitutive protein of glial cells. Due to specificity of its cellular expression, it is considered a potentially useful marker of acute injury to the brain parenchyma and blood-brain barrier. Sixty-eight OHCA patients were enrolled over the course of two years in five different hospitals in the city of Aachen, Germany. Sampling of serum S-100B was performed 6, 12, 24, 72 and 120 hours after the return of spontaneous circulation. About half of these patients were treated with therapeutic hypothermia and half with standard supportive care, according to the preferences of the family and treating physician. Cooling was induced to maintain core temperature at 33 for 24 hours using refrigerated saline and body surface cooling with ice water bags. The results of this study reflect the difficulties that typically hamper the interpretation of small non-randomized studies. No differences were detected in S-100B levels between theThe first decade of the 21st century has witnessed explosive growth in therapies for the critically ill neurological patient. Some of these treatments, such as the use of recombinant tissue plasminogen activator for the treatment of acute cerebral infarction, target very specific pathogenic pathways. Others, such as hypothermia for the treatment of brain injury after cardiac arrest, have multiple additive and synergistic mechanisms of action that culminate in the protection of nervous tissue. To guide these treatments, technological advances in imaging and neuromonitoring can now provide a window PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/7500280 into the metabolic and physiologic status of the injured brain, allowing us to evaluate the.