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The Predictive Value of Clinical and Immunological Factors in the Development of Pneumonia After Traumatic Brain Injury

This study has been completed.
Sponsor:
Information provided by (Responsible Party):
Demetrios J. Kutsogiannis, Royal Alexandra Hospital
ClinicalTrials.gov Identifier:
NCT00929448
First received: June 26, 2009
Last updated: December 3, 2012
Last verified: December 2012
History of Changes
  Purpose

The development of pneumonia and other infections is one of the most common complications of a traumatic brain injury (TBI). Prior studies have also found that patients suffering from TBI also develop immune dysfunction consistent with an immunosuppressed state shortly after the traumatic event. Specifically, it has been shown that patients with a TBI have impaired delayed type hypersensitivity (DTH), cellular immunity and humoral immunity. The humoral arm of the immune system is particularly involved in defending the host against extracellular bacteria and is primarily composed of B-cells, immunoglobulins and complement. Surgery and trauma impair the clonal expansion of antibody producing B lymphocytes causing hypogammaglobulinemia, through a mechanism involving T lymphocytes. In addition, during the systemic inflammatory process, pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1beta) and interleukin 6 (IL-6) are released. Nuclear factor kappa beta (NF-kB) is a transcriptional regulatory protein that is involved in the expression of proinflammatory cytokines and appears to act at a critical step in the transcription of many proinflammatory genes.

The hypothesis of this study is that the hypogammaglobulinemia from the immune dysfunction and the induction of NF-kB from the inflammatory process are, in part, responsible for the development of pneumonia and other infectious complications identified after TBI. This study has two specific aims: The primary specific aim of this study is to determine the association between serum immunoglobulin or NF-kB levels and the development of pneumonia in patients suffering from traumatic brain injury (TBI). The secondary specific aim of this study is to determine the relative contribution of clinical variables such as APACHE II-III Score and Injury Severity Score as compared to immunological variables (serum immunoglobulins and NF-kB) to the development of pneumonia in patients suffering from TBI.


Condition
Traumatic Brain Injury

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: The Predictive Value of Clinical and Immunological Factors in the Development of Pneumonia After Traumatic Brain Injury

Resource links provided by NLM:

U.S. FDA Resources

Further study details as provided by Royal Alexandra Hospital:

Primary Outcome Measures:
  • The primary outcome of this study will be the development of the composite of either early onset pneumonia (EOP) or ventilator associated pneumonia (VAP [ Time Frame: baseline, d4, d7, d10, d14 ] [ Designated as safety issue: No ]

Secondary Outcome Measures:
  • Secondary outcomes will include ICU and hospital mortality and LOS, duration of mechanical ventilation, Glasgow Outcome Score (GOS) at hospital discharge and at 6-months, and 1-year. [ Time Frame: hospital discharge ] [ Designated as safety issue: No ]

Enrollment: 110
Study Start Date: July 2008
Study Completion Date: February 2010
Primary Completion Date: February 2010 (Final data collection date for primary outcome measure)
Groups/Cohorts
Immunoglobulin

  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population

Intensive Care

Criteria

Inclusion Criteria:

  • > 18 yrs
  • Admitted to ICU in Capital Health region with a TBI and > 1 of the following:
  • An initial resuscitated (Sys BP>90 mmHg and O2 Sat >90%) GSC of ≤ 8
  • A post resuscitation (Sys BP>90 mmHg and O2 Sat >90%) GCS at presentation to the hospital of ≤ 8 in the absence of sedation
  • A post resuscitation (Sys BP>90 mmHg and O2 Sat >90%) GCS within 72 hrs of hospital admission of ≤ 8 in the absence of sedation
  • Intracranial pressure monitoring
  • Decompressive craniectomy
  • Presence of subfalcine, uncal, or supratentorial herniation either clinically or radiologically

Exclusion Criteria:

  • Longer than 5 days since ictus of TBI
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00929448

Locations
Canada, Alberta
Royal Alexandra Hospital
Edmonton, Alberta, Canada, T5H3V9
Sponsors and Collaborators
Royal Alexandra Hospital
Investigators
Principal Investigator: Demetrios Kutsogiannis, MD Royal Alexandra Hospital
  More Information

No publications provided

Responsible Party: Demetrios J. Kutsogiannis, MD, MHS, FRCPC, Royal Alexandra Hospital
ClinicalTrials.gov Identifier: NCT00929448     History of Changes
Other Study ID Numbers: iTBI2009
Study First Received: June 26, 2009
Last Updated: December 3, 2012
Health Authority: Canada: Ethics Review Committee

Keywords provided by Royal Alexandra Hospital:
Traumatic brain injury

Additional relevant MeSH terms:
Pneumonia
Brain Injuries
Lung Diseases
Respiratory Tract Diseases
Respiratory Tract Infections
Brain Diseases
Central Nervous System Diseases
 Nervous System Diseases
Craniocerebral Trauma
Trauma, Nervous System
Wounds and Injuries
Immunologic Factors
Physiological Effects of Drugs
Pharmacologic Actions

ClinicalTrials.gov processed this record on May 23, 2013