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Pushing boundries – exploring the importance of jugular venous distention as a sign of tention pneumothorax. a Bio-Engineering solution for clinical research introducing really dangerous conditions
Tristan van Leest, Matthijs Vogels, Igor Paulussen, Bart Spruijt, Gerrit Noordergraaf
Session: Poster Session 1 (Even numbers)
Session starts: Thursday 26 January, 16:00
Presentation starts: 16:00
Tristan van Leest ()
Matthijs Vogels ()
Igor Paulussen ()
Bart Spruijt ()
Gerrit Noordergraaf ()
Abstract:
Introduction: Tension pneumothorax is a potentially lethal injury by leading to respiratory and circulatory arrest. As a simple pneumothorax may progress to tension, clinicians must identify and treat it early. In trauma courses signs of tension pneumothorax are respiratory distress, hypoxia, tracheal deviation and particularly (early) jugular venous distention (JVD). However, disagreement exists in JVD’s timely (early/late) appearance and its relationship to volume status. We aim to identify the limits of unilateral pressure thresholds to better understand the role of jugular venous distention as a symptom in tension pneumothorax. This will show if JVD is a clinically important entity in diagnosing (early) tension pneumothorax allowing recognition of the danger for imminent collapse.
Methods: Elective videoscopic thoracostomy (VATS) patients would be a suitable population as animal models (i.e. swine) are less suitable due to their anatomy. However, introducing enough (air) pressure to induce circulatory collapse is potentially an ethically challenging form of clinical research. While resolution of the circulatory collapse should be uncomplicated, inclusion seems daunting.
Therefore, we explore a bio-engineering approach using an ex-vivo digital model based on the Donders model for CPR. The extended model should simulate the transmural effect of pressure on the central veins, the effect of mediastinal lateralisation on lumen collapse (vascular twisting), in addition to the effect of global increase in intra-thoracic pressure on the vasculature and right heart. These are deemed contributing factors to the circulatory collapse (Pulseless Electrical Activity). Nonetheless, finding behaviour variables for the model is difficult and validation more so.
Results: We hypothesise that increasing the unilateral, intra-thoracic pressure, will non-linearly diminish venous return. This should result in venous distention of the right external jugular vein as Niemann’s valve will not operate, plus increased vessel diameter of the internal jugular veins above a certain pressure threshold.
Discussion & Conclusion: Clinical limits suggest bio-engineering approaches to address relevant clinical dilemma’s. Jugular distention is only useful as a marker if it has a consistant and timely appearance. We believe that this will advance not only current daily clinical practice, but also future education of medical professionals.