PET Imaging in Patients at Risk for Acute Lung Injury (PET-ALI)
|ClinicalTrials.gov Identifier: NCT01486342|
Recruitment Status : Completed
First Posted : December 6, 2011
Last Update Posted : January 4, 2013
Despite decades of research, the mortality in acute lung injury remains very high and treatment options are very limited. Given these facts, the best treatment modality may be in prevention of this lethal syndrome.
Historically, imaging has played a crucial role in understanding ALI. The appearance of chest radiography is one of the consensus criteria in defining ALI, and commuted tomography (CT) scans further advanced the understanding of the pathoanatomy of ALI. While valuable, these imaging modalities are nonspecific and do not incorporate functional cellular physiology.
PET imaging measures concentrations of radioisotopes in the body. By embedding in, but not altering molecules, the natural fate of these tracers can be studied with PET imaging. Advances in the understanding of ALI include blood flow distribution, as well as the response to alveolar recruitment maneuvers and prone positioning. Not all patients who are receiving mechanical ventilation develop ALI. Inflammation in the lungs is known to play a key early role in the development and progression of ALI. Secondary to inflammation, the lungs develop edema and do not exchange oxygen as well. This early inflammation is in part driven by a specific type of immune cell called the neutrophil. These cells seem to travel and become sequestered in the lung- they are "recruited" to the lung during this inflammatory stage. When there, these neutrophils release inflammatory substances which are integral in the development of ALI. Neutrophils use primarily glucose as a fuel source. The radio isotope [18F]Fluorodeoxyglucose (FDG)is a glucose analog and therefore taken up/ingested by the neutrophils as a part of their normal metabolism. Because of this fact, positron emission tomography (PET) using the radio isotope [18F]FDG is a highly sensitive marker to look at the recruitment of neutrophils to the lung, therefore quantifying the degree of pulmonary inflammation prior to the development of ALI.
The investigators seek to examine the relationship of pulmonary inflammation in patients at risk for ALI, but without clinical evidence of the syndrome. The investigators seek to enroll ten patients in a pilot trial.
|Condition or disease||Intervention/treatment|
|Acute Lung Injury Early Pulmonary Neutrophilic Inflammation||Radiation: PET-CT scan|
|Study Type :||Observational|
|Actual Enrollment :||5 participants|
|Official Title:||Positron Emission Tomography With [18F]Fluorodeoxyglucose in Patients at Risk for Acute Lung Injury|
|Study Start Date :||October 2011|
|Primary Completion Date :||October 2012|
|Study Completion Date :||October 2012|
Mechanically ventilated patients without acute lung injury and lung injury prediction score < 4
Radiation: PET-CT scan
PET-CT imaging with [18F]FDG will be performed within 24 hours of admission to the ICU. All patients imaged will be those remaining on mechanical ventilation at the time of PET imaging.
A low-dose CT scan (50 effective mAs) will be obtained with placement of the participant such that the lungs are centered within the field of view. After completing the transmission scan, 10 mCi of [18F]FDG will be injected intravenously at the start of a 60-minute dynamic scan acquisition and the intravenous (IV) catheter flushed with 10 ml saline. Imaging will be obtained with the following framing schedule: 24 5-sec, 6 3-minute and 8 5-minute frames.
- The influx constant (Ki) of FDG uptake [ Time Frame: 3 days ]The influx constant describes the rate of FDG uptake and represents pulmonary inflammation
- Correlation of the influx constant (Ki) with lung injury prediction score [ Time Frame: 3 days ]
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01486342
|United States, Missouri|
|Washington University in St. Louis School of Medicine|
|St. Louis, Missouri, United States, 63110|
|Principal Investigator:||Brian Fuller, MD||Washington University School of Medicine|