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Funded Injury Control Research Centers (ICRCs)

San Francisco Injury Center for Research and Prevention (SFIC)

M. Margaret Knudson, MD
Phone: 415-206-4623
Fax: 415-206-5484
E-mail: pknudson@sfghsurg.ucsf.edu
San Francisco General Hospital
Department of Surgery, 3A
1001 Potrero Ave.
San Francisco, CA 94110

Overview

The San Francisco Injury Center for Research and Prevention (SFIC) is distinguished by having acute care research as its major focus, while maintaining prominent activities in injury surveillance and injury prevention. The San Francisco General Hospital (SFIC) is located at the SFGH campus of the University of California, San Francisco (UCSF), adjacent to the SFGH Trauma Center, one of the first Level I trauma centers in the country. The daily interaction with a large number of severely injured patients admitted to the Trauma Center serves as the impetus for the SFIC investigators to continually re-evaluate methods of treating injuries, and to remain committed to injury prevention. In 1996, with a new administration for the SFIC within the UCSF Department of Surgery and the initiation of a new Surgical Research Center at SFGH, the SFIC expanded its acute care research objectives, while continuing its activities in injury prevention through a subcontract with the Trauma Foundation, a 15-year-old private, non-profit prevention agency also located on the SFGH campus.

The two major objectives for the SFIC are to

  • conduct research in the five phases of acute care management: prehospital, initial resuscitation, definitive surgical care, critical care, and acute rehabilitation
  • continue activities and collaborations in injury prevention.

The specific aims for research, which are designed to parallel the five phases of acute injury management, are

  • examine the effect of prehospital hypoxia and hypotension on outcome following brain injury
  • investigate surgeons' use of ultrasound in the initial evaluation of injured patients
  • study the use of tissue oxygen measurements and cardiopulmonary bypass during resuscitation from hemorrhagic shock
  • describe inflammatory markers and clinical indicators in acute lung injury
  • determine the effectiveness of psychological interventions in reducing stress symptoms following pediatric trauma.

Prevention activities include 

  • continued development of the Trauma Foundation's Injury Prevention Library and the Injury Prevention Network Review
  • improvement of injury surveillance through standardization and analysis of injury data codes for external cause
  • committee and consultative activities in the injury field
  • promotion of educational activities in injury control
  • linkage of acute care research with local and national violence prevention efforts.

Projects*

Project Title: Translating Research to Intervention
Grant Number: CE001178
Project Period: 08/01/2007 - 07/31/2012
Description:
See funded ICRCs page for more information.

Project Title: Traumatic Brain Injury: Development and Refinement of a Swine Model to Study Traumatic Brain Injury
Project Period: 08/01/01-07/31/06
Description:
Brain injury is a leading cause of death and disability following trauma. While the primary injury to the brain produces immediate and irreversible mechanical damage, it appears increasingly that secondary injuries occurring from the moment of the initial traumatic insult may also have a profound effect on outcome. Prevention of these secondary insults will require improvement in methods of monitoring and a redefinition of resuscitation end points. Using a large animal model to simulate the human situation, the investigators will explore three hypothesis and attempt to accomplish three related specific aims.

Hypothesis 1: Direct monitoring of oxygenation and of aerobic and anaerobic metabolites in brain tissue is more sensitive and specific in detecting regional ischemia than are traditional systemic measurements following traumatic brain injury (TBI).
Aim: To characterize focal, regional, and systemic oxygen tension and metabolism in brain tissue during the onset and progression of experimental TBI.

Hypothesis 2: Hyper-oxygenation following TBI produces improved tissue oxygenation, cerebral metabolism, and cellular outcome. Also, hyperventilation results in a decrease in tissue oxygenation, impairs cerebral metabolism, and worsens cellular outcome.
Aim: To determine the effects of alteration in ventilation on cerebral metabolism and cellular outcome following TBI.

Hypothesis 3: Resuscitation and maintenance with a hypertonic hemoglobin-based oxygen-carrying (HBOC) solution results in better tissue oxygenation, metabolism, and cellular outcome as compared with the currently recommended resuscitation protocol using normal saline solution.
Aim: To evaluate the effects that cerebral resuscitation with normal saline solution and a hypertonic HBOC solution have on cerebral metabolism and cellular outcome in a model of TBI.

To address these aims, the investigators will use the model of head injury (controlled cortical impact) that has been successful in small animals and apply it to swine. To measure cerebral metabolism, they will employ calibrated polarographic micro-catheters to measure oxygen tension in the brain tissue and a micro-dialysis technique to evaluate metabolic end products from the interstitial tissue of the brain. These will be added to the traditional systemic and organ-based measurements of homodynamic and oxygen differences. To evaluate extent of injury, the investigators will use gravimetric calibration of cerebral edema and histopathologic analysis. Standard microscopic cross-sections will be used to identify the area of contusion; cellular injury will be measured using histochemical techniques including a fluorochrome (fluorjade) and the TUNEL technique to identify dying or apoptotic cells. Several other immunohistochemical approaches are also mentioned.

Project Title: Metabolic Monitoring: Tissue Oxygen Monitoring of the Brain and Muscle as End-points of Resuscitation during Early Phases of Trauma Care
Project Period: 08/01/01-07/31/06
Description:
Trauma deaths occur early from hemorrhage and later from either head injury or infectious complications. This study uses tissue oxygen monitoring of the brain and the muscle as end-points of resuscitation during the early phases of trauma care. Tissue oxygen values will be compared with micro-dialysis data collected in the same tissue bed to see if measured ischemia correlates with anaerobic metabolism. These two monitored variables will also be compared with the values obtained with more standard measurements, such as cerebral perfusion pressure (CPP) and base deficit. Changes in oxygen and metabolic variables will be observed during alterations in inspired oxygen content and finally during a randomized trial using crystalloid solution versus an oxygen carrying solution in patients with persistent tissue ischemia. Prevention of tissue ischemia and anaerobic metabolism may translate to improved functional outcome from head injury and to a decrease in the mortality and infectious complications resulting from major thoracoabdominal trauma.

The study has several specific aims:

Aim 1: Establishes critically abnormal levels of tissue oxygen in the brain (PbrO2) and muscle (PmO2) of injured patients.
Aim 2: Compare PbrO2 and PmO2 values with levels of aerobic/anaerobic metabolites collected from these same tissue beds.
Aim 3: Correlate PbrO2 and levels of ischemic metabolites with other currently available diagnostic measures used in head-injured patients, including intracranial pressure (ICP), mean arterial blood pressure (MAP), CPP, jugular venous oxygen saturation (SjO2), computerized tomography (CT) findings, neurological examinations, and clinical outcomes from TBI.
Aim 4: Correlate PmO2 and levels of ischemic metabolites with base deficit measurements, standard physiologic variables, infectious complications, and outcomes in critically injured patients.
Aim 5: Describe the changes in PbrO2 and PmO2 that occur with changes in inspired oxygen in critically injured patients and to determine whether improving PbrO2 and PmO2 improves outcome.
Aim 6: Compare the effects of two resuscitation solutions—standard crystalloid and hemoglobin-based oxygen carrying solution (HBOC)—on PbrO2 and PmO2 levels and tissue metabolic measurements.

Project Title: Pediatric Post-traumatic Stress Disorder (PTSD): Identification and Treatment of PTSD Symptoms Resulting from Traumatic Injuries
Project Period: 08/01/01-07/31/06
Description:
This project will clarify the relationship between childhood PTSD and future impairment in social, academic, and psychological functioning. The research evaluates a novel treatment intervention for childhood PTSD that combines the Chapman Art Therapy Treatment Intervention (ART) with Eye Movement Desensitization and Reprocessing (EMDR). Researchers hypothesize that this combination could be an effective tool for reducing PTSD symptoms for hospitalized children and for large numbers of children requiring immediate treatment following natural disasters, school shootings, and other catastrophic events.

Researchers have several aims for the project:

Aim 1: Determine the rate and incidence of PTSD in pediatric patients following an acute traumatic injury.
Aim 2: Determine the effectiveness of a brief psychological intervention, administered at 1 month after a child's injury, in reducing the number and severity of PTSD symptoms.
Aim 3: Examine the influence of child-specific factors on the development, duration and severity of PTSD symptoms following an index trauma event.
Aim 4: Examine the influence of parental and familial factors on the development, duration, and severity of PTSD symptoms in pediatric trauma patients.
Aim 5: Examine the effect of PTSD on a child's overall social, academic, and familial functioning.

This is a prospective, randomized cohort study of children ages 7 to 17 who are hospitalized for physical trauma. Participants will be enrolled during the index trauma admission. One month after injury, they will be tested for PTSD symptoms using the UCLA PTSD Reaction Index (PTSD-RI). Parents will assess their child's level of stress and answer interview questions about their own stress and about the family environment. Children with moderate to severe PTSD symptoms will be randomized to receive either a new intervention that combines ART with EMDR techniques or no intervention. Those randomized to receive the intervention will be treated in two successive weekly sessions. The discrepancy between parental assessment of child stress and the child's assessment will be calculated. Children and parents will be followed at 3 months, 6 months and 12 months post-injury to measure longitudinal development or resolution of symptoms.

There are several primary outcome measures: rate of significant PTSD symptoms at 1 month; the effect of treatment on rates of resolution of significant PTSD; change in PTSD-RI scores from 1 month (pre-intervention) to each follow up; and parent-child discrepancies. The Department of Psychiatry at Children’s Hospital, Oakland (CHO) will be the site for initial and follow-up interviews and the intervention.

Project Title: Biomechanics of Vertebral Fractures for Repetitive Loads: Study of Fatigue Life of Elderly Vertebral Trabecular Bone
Project Period: 08/01/01-07/31/06
Description:
The overall goal of this project is to establish the concept that, after moderate or minor isolated overloads, fatigue failure of human vertebral bone can occur at repetitive cyclic load levels that would otherwise not cause failure. Three hypotheses will be tested: (1) that the fatigue life of elderly trabecular bone cores is reduced by the intensity level of an isolated overload; (2) that the fatigue life is reduced more for older and/or less dense bone than for younger, denser bone; and (3) that fatigue life of a whole vertebral body is reduced after a single overload.

The aims for the project include the following:

1. Determine the fatigue life of elderly vertebral trabecular bone to a single overload of varying intensity.
2. Show that the fatigue life of elderly or less-dense bone to a single overload is less than that of young, denser bone.
3. Show that fatigue life of a whole vertebral body is reduced following a single overload and that the effect is greater for older, less-dense bone.


*Please note: Not all projects may be listed.

 
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