TBI Poster

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Published on February 23, 2009

Author: akhaku

Source: authorstream.com

Slide 1: Brain Injury Guidelines for Pre-Inpatient Medical Practices (B.I.G. P.I.M.P.)Zarina Ali, Michael Brogan, Matthew Debiec,Aunali Khaku, Seth Pantanelli, Babak Razavi, Solomon Shaftel, Vasisht Srinivasan, John Olschowka University of Rochester School of Medicine and Dentistry, Rochester, NY Background & Significance Methods & Research Plan Relevant Pathophysiology Specific Aims Therapeutic Rationale Timeline Conclusions Traumatic Brain Injury (TBI) is a leading cause of death and disability in the United States. Every year, approximately 1.6 million Americans suffer this injury. Of these, greater than 50,000 will die and as many as 90,000 will have some sort of long-term disability. The cost to society is over $30 billion per year. The Brain Injury Association of America states that TBI occurs every 23 seconds, with the majority of these in children and the elderly. Recent research has greatly contributed to our understanding of the pathophysiology of disease. TBI is related to both the initial primary injury as well as the secondary injury which develops over time. Aggressive control of physiologic parameters in the management of TBI is important in modulating the resulting secondary injury. There is evidence that preventing against hypoglycemia, hypotension, and hypoxia during inpatient management of injuries improves patient outcomes. However, there is no data to recommend a maximum threshold for corrections of these physiologic parameters. Additionally, there is no evidence to suggest that automated management of intracranial hypertension is better than manual control. The purpose of this study is to investigate whether aggressive control against hyperglycemia, hypertension, hyperoxygenation and intracranial hypertension impacts outcomes when compared with standard of care. Outcome measures: All cause mortality ICU Length of Stay Hospital Length of Stay GOS (Glasgow Outcome Scale) Neuropsychological Testing at 6 months post-injury. - Attention: SART (Sustained Attention to Response Task) - Memory: Rey AVLT (Auditory Verbal Learning Test) - Executive Function: Hayling C The sequelae of TBI follow two mechanisms. The primary injury occurs at the time of trauma in several forms, e.g. coup, contra-coup, blast, penetrating, and results from diffuse axonal injury (DAI) and shear forces generated by sudden deceleration. The secondary injury results from the sequelae of the primary injury, namely ischemia, edema, inflammation, and excitatory neurotoxicity. DAI results in axonal damage and cellular swelling from failure of transport, leading to the release of neuroactive compounds (e.g., glutamate) into the brain parenchyma and formation of free radical species. Increased tissue edema causes elevation of intracranial pressure (ICP) leading to decreased tissue perfusion, local ischemia and increased risk of herniation. Excessive glutamate leads to persistent neuronal activation and excitatory neurotoxicity. Vascular injury results in local tissue ischemia, mass effect from hematoma formation, as well as the formation of free radical species. Further, subarachnoid hemorrhage data strongly suggests that the presence of intraparenchymal and subarachnoid blood increases the risk for vasospasm, causing further tissue ischemia and neuronal death. http://www.ninds.nih.gov/disorders/tbi/tbi.htm www.biausa.org/elements/professionals/btf_guidelines_prehospital.pdf http://www.biausa.org/ http://www.guideline.gov/summary/summary.aspx?ss=15&doc_id=10989 Green RE, Colella B, Hebert DA, Bayley M, Kang HS, Till C, Monette G, “Prediction of Return to Productivity After Severe Traumatic Brain Injury: Investigations of Optimal Neuropsychological Tests and Timing of Assessment,” Arch Phys Med Rehabil 89(2); 2008. Draper K, Ponsford J, “Cognitive Functioning Ten Years Following Traumatic Brain Injury and Rehabilitation,” Neuropsychology 22(5); 2008. King JT, Carlier PM, Marion DW, “Early Glasgow Outcome Scale Scores Predict Long-Term Functional Outcome in Patients with Severe Traumatic Brain Injury,” J Neurotrauma 22(9); 2005. Recent data from models of ischemic injury, which shares etiologic mechanisms of cellular injury with TBI, has shown that overzealous correction of physiologic parameters is also important in final outcomes. Application of such principles to inpatient management of TBI may prove to be incredibly important in improving patient outcomes. Hypertension may promote tissue swelling and edema. Hyperglycemia may promote anaerobic glycolysis, leading to the accumulation of lactate, hydrogen ions, causing tissue necrosis and acidosis. Super-oxygenation may promote formation of reactive oxygen species, promoting cell destruction. Low ICP results in increased cerebral perfusion. Heegaard, W.G., Biros, B.H. Marx: Rosen’s Emergency Medicine, Concepts and Clinical Practice. Automated ICP Device. Randomized prospective cohort trial Exclusion Criteria: <18 years old EtOH / Drug Abuse Prior TBI, SAH, ICH, MI Malignancy Other major neurological, psychiatric or cardiopulmonary co-morbidities Extensive non-TBI injuries Chronic use of glucocorticoids, anti-epileptics or other Rx affecting CNS Pregnancy, breast feeding Diabetes Outcomes assessed: 0d, 1d, 1w, 1m, 6m, 1y, 3y & 5y after presentation References We anticipate that this study will elucidate the optimal parameters for control of major physiological variables during inpatient hospital care of TBI. Applying these principles will improve future patient outcomes and guide future basic science research into mechanisms of TBI. More importantly, this study will ensure that patients receive Medicine, of the highest order™.

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