Traumatic Brain Injury in Iowa Inpatient Hospital Data, 2003-2005

According to the Centers for Disease Control and Prevention, unintentional injury is the fifth leading cause of death for all age groups and the first leading cause of death for people from 1 to 44 years of age in the United States, while homicide remains the 2nd leading cause of death for 15 to 24 years old (CDC, 2006). In 2004, there were approximately 144,000 deaths due to unintentional injuries in the US; 53% of which represent people over 45 years of age (CDC, 2004). With 20,322 suicidal deaths and 13,170 homicidal deaths, intentional injury deaths affect mostly people under 45 years old. On average, there are 1,150 unintentional deaths per year in Iowa. In 2004, 37% of unintentional deaths were due to motor vehicle accidents (MTVCC) occurring across all age ranges and 30% were due to falls involving persons over 65 years of age 82% of the time (IDPH Health Stat Div., 2004). The most debilitating outcome of injury is traumatic brain injury, which is characterized by the irreversibility of its damages, long-term effects on quality of life, and healthcare costs. The latest data available from the CDC estimated that, nationally, 50,000 traumatic brain injured (TBI) people die each year; three times as many are hospitalized and more than twenty times as many are released from emergency room (ER) departments (CDC, 2006). Besides the TBI registry, brain injury data is also captured through three other data sources: 1) death certificates; 2) hospital inpatient data; and, 3) hospital outpatient data. The inpatient and outpatient hospital data are managed by the Iowa Hospital Association, which provides to Iowa Department of Public Health the hospital data without personal identifiers. (The hospitals send reports to the Agency of Health Care Research and Quality, which developed the Health Care Utilization Project and its product, the National Inpatient Sample).

Traumatic Brain Injury in Iowa: Iowa Brain Injury Resource Network Outcome Evaluation 2007-2009, August 2011

Termed the “silent epidemic,” traumatic brain injury (TBI) is the most debilitating outcome of injury, and is characterized by the irreversibility of its damages, long-term effects on quality of life and healthcare costs. The latest data available from the CDC estimate that nationally, 52,000 people die each year from TBI2. In Iowa, TBI is a major public health problem. The numbers and rates of hospitalizations and emergency department (ED) visits due to TBIs are steadily increasing. From 2006 to 2008, there were on average 545 injury deaths per year. Among the injured Iowans, TBI constituted nearly 30 percent (545) of all injury deaths, ten percent (1,591) of people hospitalized and seven percent (17,696) of ED visitors. 3 The state of Iowa has been supporting secondary prevention services to TBI survivors for several years. An Iowa organization that has made a significant effort in assisting TBI survivors is the Brain Injury Association of Iowa (BIAIA). The BIAIA administers the IBIRN program in cooperation with the Iowa Department of Public Health (IDPH) through HRSA TBI Implementation grant funding and state appropriations.

Brain injury program to ensure greater access to community-based services, July 11, 2006

More than 2,200 Iowans each year experience a traumatic brain injury that requires hospitalization. Of those, more than 750 will experience long-term disability as a result. According to a 2000 CDC report, there are an estimated 50,000 such individuals living in Iowa – a number similar to the population of Ames. As part of an enterprise-wide effort to ensure that all Iowans, including those with brain injuries, have access to quality healthcare, Governor Tom Vilsack signed the Brain Injury Services program bill on May 23. The bill will allow the Iowa Department of Public Health (IDPH) to implement a one-of-a-kind program to help those with brain injuries and their families in navigating and maximizing the Iowa community-based service system.

Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: a microdialysis study.

OBJECTIVES: To analyze the effect of tight glycemic control with the use of intensive insulin therapy on cerebral glucose metabolism in patients with severe brain injury. DESIGN: Retrospective analysis of a prospective observational cohort. SETTING: University hospital neurologic intensive care unit. PATIENTS: Twenty patients (median age 59 yrs) monitored with cerebral microdialysis as part of their clinical care. INTERVENTIONS: Intensive insulin therapy (systemic glucose target: 4.4-6.7 mmol/L [80-120 mg/dL]). MEASUREMENTS AND MAIN RESULTS: Brain tissue markers of glucose metabolism (cerebral microdialysis glucose and lactate/pyruvate ratio) and systemic glucose were collected hourly. Systemic glucose levels were categorized as within the target "tight" (4.4-6.7 mmol/L [80-120 mg/dL]) vs. "intermediate" (6.8-10.0 mmol/L [121-180 mg/dL]) range. Brain energy crisis was defined as a cerebral microdialysis glucose <0.7 mmol/L with a lactate/pyruvate ratio >40. We analyzed 2131 cerebral microdialysis samples: tight systemic glucose levels were associated with a greater prevalence of low cerebral microdialysis glucose (65% vs. 36%, p < 0.01) and brain energy crisis (25% vs.17%, p < 0.01) than intermediate levels. Using multivariable analysis, and adjusting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentration (adjusted odds ratio 1.23, 95% confidence interval [CI] 1.10-1.37, for each 1 mmol/L decrease, p < 0.001) and insulin dose (adjusted odds ratio 1.10, 95% CI 1.04-1.17, for each 1 U/hr increase, p = 0.02) independently predicted brain energy crisis. Cerebral microdialysis glucose was lower in nonsurvivors than in survivors (0.46 +/- 0.23 vs. 1.04 +/- 0.56 mmol/L, p < 0.05). Brain energy crisis was associated with increased mortality at hospital discharge (adjusted odds ratio 7.36, 95% CI 1.37-39.51, p = 0.02). CONCLUSIONS: In patients with severe brain injury, tight systemic glucose control is associated with reduced cerebral extracellular glucose availability and increased prevalence of brain energy crisis, which in turn correlates with increased mortality. Intensive insulin therapy may impair cerebral glucose metabolism after severe brain injury.

Brain Injury Quick Guide: Information and Resources for Teachers and School Staff, July 2013

The Brain Injury Quick Guide was developed as a resource tool for educators and school staff. Functional challenges (including social, physical, communication, and cognitive) are common following brain injury. This booklet serves as a resource outlining common challenges students may face in the classroom as well as strategies for addressing these challenges. Case studies outlining common challenges with possible strategies are provided with suggestions for IEP/504 plan accommodations. Basic brain anatomy and brain injury statistics are also reviewed.

Changes in cerebral compartmental compliances during mild hypocapnia in patients with traumatic brain injury.

The benefit of induced hyperventilation for intracranial pressure (ICP) control after severe traumatic brain injury (TBI) is controversial. In this study, we investigated the impact of early and sustained hyperventilation on compliances of the cerebral arteries and of the cerebrospinal (CSF) compartment during mild hyperventilation in severe TBI patients. We included 27 severe TBI patients (mean 39.5 ± 3.4 years, 6 women) in whom an increase in ventilation (20% increase in respiratory minute volume) was performed during 50 min as part of a standard clinical CO(2) reactivity test. Using a new mathematical model, cerebral arterial compliance (Ca) and CSF compartment compliance (Ci) were calculated based on the analysis of ICP, arterial blood pressure, and cerebral blood flow velocity waveforms. Hyperventilation initially induced a reduction in ICP (17.5 ± 6.6 vs. 13.9 ± 6.2 mmHg; p < 0.001), which correlated with an increase in Ci (r(2) = 0.213; p = 0.015). Concomitantly, the reduction in cerebral blood flow velocities (CBFV, 74.6 ± 27.0 vs. 62.9 ± 22.9 cm/sec; p < 0.001) marginally correlated with the reduction in Ca (r(2) = 0.209; p = 0.017). During sustained hyperventilation, ICP increased (13.9 ± 6.2 vs. 15.3 ± 6.4 mmHg; p < 0.001), which correlated with a reduction in Ci (r(2) = 0.297; p = 0.003), but no significant changes in Ca were found during that period. The early reduction in Ca persisted irrespective of the duration of hyperventilation, which may contribute to the lack of clinical benefit of hyperventilation after TBI. Further studies are needed to determine whether monitoring of arterial and CSF compartment compliances may detect and prevent an adverse ischemic event during hyperventilation.

Iowa State Plan for Brain Injury 2013-2018

Traumatic Brain Injury (TBI) impacts the lives of thousands of Iowans each year. The effects of brain injury (often called the "silent epidemic" because resulting injury is often not visible to others) are cognitive, emotional, and social but may also result in physical disability. This state plan, created by the Governor's Advisory Council on Brain Injuries, is intended to provide guidance for brain injury services and prevention activities in Iowa. This is the fourth Iowa State Plan for Brain Injury. In addition to a statewide needs assessment, development of this plan included recommendations made by the Mental Health and Disability Services Redesign Brain Injury Work-group. For the first time in the history of TBI surveillance in Iowa, the numbers and rates of TBI deaths are decreasing, however hospitalizations and emergency department visits resulting from TBI are steadily increasing. This trend is likely due to the decrease in motor vehicle accidents and improved hospitalization protocols. Looking to the future, the Advisory Council on Brain Injuries identified goals in each of four focus areas. These focus areas are: #1 Individual and family access; dedicated to the enhancement of the lives of individuals with brain injuries and their families. #2 Service and support availability; #3 Service system enhancements; continued funding growth and public awareness campaigns that draw attention to the impact of brain injury. #4 Brain injury prevention; working to prevent and reduce three of the most common causes of brain injury are falls, no helmet use, and motor vehicle crashes.

Molecular Mechanisms of Acute Brain Injury and Ensuing Neurodegeneration

Injury to the central nervous system (CNS), including stroke, traumatic brain injury andspinal cord injury, cause devastating and irreversible damage and loss of function. Forexample, stroke affects very large patient populations, results in major suffering for the patients and their relatives, and involves a significant cost to society. CNS damage implies disruption of the intricate internal circuits involved in cognition, the sensory-motor functions, and other important functions. There are currently no treatments available to properly restore such lost functions. New therapeutic proposals will emerge from an understanding of the interdependence of molecular and cellular responses to CNS injury, in particular the inhibitory mechanisms that block regeneration and those that enhanceneuronal plasticity...

Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury.

OBJECTIVES: We have sought to develop an automated methodology for the continuous updating of optimal cerebral perfusion pressure (CPPopt) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascular pressure reactivity. We then validated the CPPopt algorithm by determining the association between outcome and the deviation of actual CPP from CPPopt. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Neurosciences critical care unit of a university hospital. PATIENTS: A total of 327 traumatic head-injury patients admitted between 2003 and 2009 with continuous monitoring of arterial blood pressure and intracranial pressure. MEASUREMENTS AND MAIN RESULTS: Arterial blood pressure, intracranial pressure, and CPP were continuously recorded, and pressure reactivity index was calculated online. Outcome was assessed at 6 months. An automated curve fitting method was applied to determine CPP at the minimum value for pressure reactivity index (CPPopt). A time trend of CPPopt was created using a moving 4-hr window, updated every minute. Identification of CPPopt was, on average, feasible during 55% of the whole recording period. Patient outcome correlated with the continuously updated difference between median CPP and CPPopt (chi-square=45, p<.001; outcome dichotomized into fatal and nonfatal). Mortality was associated with relative "hypoperfusion" (CPP<CPPopt), severe disability with "hyperperfusion" (CPP>CPPopt), and favorable outcome was associated with smaller deviations of CPP from the individualized CPPopt. While deviations from global target CPP values of 60 mm Hg and 70 mm Hg were also related to outcome, these relationships were less robust. CONCLUSIONS: Real-time CPPopt could be identified during the recording time of majority of the patients. Patients with a median CPP close to CPPopt were more likely to have a favorable outcome than those in whom median CPP was widely different from CPPopt. Deviations from individualized CPPopt were more predictive of outcome than deviations from a common target CPP. CPP management to optimize cerebrovascular pressure reactivity should be the subject of future clinical trial in severe traumatic head-injury patients.

Caveolin expression changes in the neurovascular unit after juvenile traumatic brain injury: signs of blood-brain barrier healing?

Traumatic brain injury (TBI) is one of the major causes of death and disability in pediatrics, and results in a complex cascade of events including the disruption of the blood-brain barrier (BBB). A controlled-cortical impact on post-natal 17 day-old rats induced BBB disruption by IgG extravasation from 1 to 3 days after injury and returned to normal at day 7. In parallel, we characterized the expression of three caveolin isoforms, cav-1, cav-2 and cav-3. While cav-1 and cav-2 are expressed on endothelial cells, both cav-1 and cav-3 were found to be present on reactive astrocytes, in vivo and in vitro. Following TBI, cav-1 expression was increased in blood vessels at 1 and 7 days in the perilesional cortex. An increase of vascular cav-2 expression was observed 7 days after TBI. In contrast, astrocytic cav-3 expression decreased 3 and 7 days after TBI. Activation of eNOS (via its phosphorylation) was detected 1 day after TBI and phospho-eNOS was detected both in association with blood vessels and with astrocytes. The molecular changes involving caveolins occurring in endothelial cells following juvenile-TBI might participate, independently of eNOS activation, to a mechanism of BBB repair while, they might subserve other undefined roles in astrocytes.

Effect of n-3 fatty acids on markers of brain injury and incidence of sepsis-associated delirium in septic patients.

BACKGROUND: Data regarding immunomodulatory effects of parenteral n-3 fatty acids in sepsis are conflicting. In this study, the effect of administration of parenteral n-3 fatty acids on markers of brain injury, incidence of sepsis-associated delirium, and inflammatory mediators in septic patients was investigated. METHODS: Fifty patients with sepsis were randomized to receive either 2 ml/kg/day of a lipid emulsion containing highly refined fish oil (equivalent to n-3 fatty acids 0.12 mg/kg/day) during 7 days after admission to the intensive care unit or standard treatment. Markers of brain injury and inflammatory mediators were measured on days 1, 2, 3 and 7. Assessment for sepsis-associated delirium was performed daily. The primary outcome was the difference in S-100β from baseline to peak level between both the intervention and the control group, compared by t-test. Changes of all markers over time were explored in both groups, fitting a generalized estimating equations model. RESULTS: Mean difference in change of S-100β from baseline to peak level was 0.34 (95% CI: -0.18-0.85) between the intervention and control group, respectively (P = 0.19). We found no difference in plasma levels of S-100β, neuron-specific enolase, interleukin (IL)-6, IL-8, IL-10, and C-reactive protein between groups over time. Incidence of sepsis-associated delirium was 75% in the intervention and 71% in the control groups (risk difference 4%, 95% CI -24-31%, P = 0.796). CONCLUSION: Administration of n-3 fatty acids did not affect markers of brain injury, incidence of sepsis-associated delirium, and inflammatory mediators in septic patients.