When a serious injury, infection, or shock to a patient’s body occurs, the lungs often receive a damaging blow as a secondary effect. The event that damages lungs is often called Acute Lung Injury (ALI) and its advanced form is called Acute Respiratory Distress Syndrome (ARDS). ALI and ARDS are fatal in 30 to 50% of patients. According to a recent estimate of incidence in the U.S., there are an estimated 150,000 cases of ARDS annually which are associated with 74,500 deaths and 3.6 million hospital days. Many more deaths are attributed to ARDS-related diseases such as sepsis, pneumonia, or pulmonary disease making the probable number of cases much higher.
ALI and ARDS are syndromes commonly found in intensive care units of modern hospitals where patients often receive respiratory support from mechanical ventilators. The inability of patients to adequately oxygenate their blood remains the hallmark of ARDS and ALI.
Reversing ALI and ARDS in the current era would involve a more thorough description of the disease on a molecular basis than is known today. Such a description would map out the molecular pathways involved in ARDS and enable drug strategies to fight the disease, slow it down, or even reverse its harmful effects based on knowledge of how the disease starts, continues through the body, affects the lungs, and eventually causes its damage. The pulmonary arteries of patients with ALI and ARDS are seriously affected in the disease, and the endothelial layer of the arteries is probably the initial site of disease progression in the lungs. We know that molecular changes associated with ARDS and severe sepsis have been found post mortem in the pulmonary arteries of patients who died of the disease. But, the exact molecular steps that lead to ALI and then ARDS are currently not known. Knowledge of the molecular pathways involved in ARDS will allow for the condition to be more effectively diagnosed and treated.
Traumatic injury can also lead to the development of ARDS. The pathophysiology of ARDS secondary to battlefield trauma is poorly understood, and similar to civilian causes of ARDS, therapeutic options are limited. The survival of injured soldiers could be improved if we could accurately predict and diagnose ARDS while there is still time for effective counter-measures. The endoarterial biopsy catheter could advance the development of therapeutic as well as diagnostic solutions for ARDS.
By obtaining pulmonary endoarterial biopsies, we will improve ARDS patient outcomes through better monitoring of the disease cycle, faster response to endothelial decline, and more timely interventions. The lack of minimally invasive tools to obtain samples of the pulmonary vasculature has hindered the in vivo study and treatment of ARDS. The endoarterial biopsy catheter will address this deficiency in the care of ARDS patients by providing pulmonary endothelial and smooth muscle biopsy samples for analysis in a minimally invasive manner. Endoarterial biopsy samples from ARDS patients will indicate the degree of endothelial activation, and state of the patient’s endothelial health. The state of endothelial health can be used to guide therapy and medical management decisions, and establish the connections between therapeutic efficiency and endothelial health in ARDS patients.
WARNING: Investigational Device. Limited by Federal law to investigational use. This device should be used only by physicians with a thorough understanding of percutaneous interventional procedures and training in the use of the endoarterial biopsy catheter.
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