Thorax injury in relation with systemic neutrophil activation

Trauma is the major cause of morbidity and mortality in people under the age of
50. Morbidity and mortality are the direct result of the sustained injuries or
indirectly due to post-injury complications like organ failure. Currently the
treatment of organ failure is symptomatic. Prevention of organ failure is
essential for a reduction in morbidity and mortality. Unfortunately, to date
there is no tool for this, partically because the pathofysiologal processes
that lead to organ failure are not completely understood. More insight in these
processes is needed.

For the development of organ failure two factors are required: local
endothelial activation or damage AND systemic inflammation. Severe thorax
trauma is frequently followed by pulmonary failure (ARDS). In thorax trauma
there is always a certain amount of local tissue damage and systemic
inflammation present. The development of ARDS is therefore dependent on the
combination of systemic inflammation and local injury. This organ failure
(ARDS) is mainly mediated by neutrophils. We developed profiles of receptor
expression on neutrophils that reflect the systemic inflammatory status of the
patient. The local (micro) injury can be identified by lung specific proteins
in the circulation.

The projects*goal is to gain insight in the pathofysiological processes after
trauma that lead to organ failure. The hypothesis is that for the clinical
presentation both severe systemic inflammation and severe local injury is
needed. In the patient population of this study both factors are always present
in different amounts. This results in the following questions:

Primary question:

Is there synergy between inflammation and tissue damage in the development of
ARDS?

Secundary question:

Is there a relation between clinical scores for injury severity and the amount
of inflammation and/or local tissue injury?

Is the cause of trauma (penetrating or blunt) of influence on the inflammatory
response?

Patient, admitted to the hospital with an isolated thorax trauma (blunt or
penetrating), are included. Patient informed consent or proxy consent is
obtained as soon as possible. The severity of trauma is scored by various
scoring systems (ISS, NISS, HTTSS). During admission the development of
pulmonary complications and extra-pulmonary organ failure is recorded. These
clinical start (traumascores) and endpoints (complications) are analyzed in the
context of neutrophil expression profiles indicating the systemic inflammatory
status of the patient and local injury by lung specific proteins.

On admission 5 ml Natrium-Heparin blood is set aside when regular laboratory
assessment is done. Three and six hours after the trauma was sustained
additional blood samples (5 ml Natrium-Heparin) is obtained. Twenty-four hours
after the sustained injury 5 ml Natrium-Heparin is set aside when regular
laboraty assessment is done. The samples are analyzed directly for their
receptor expression profiles by flowcytometry.

No risks, burden of 2 additional vena punctures.