Secondary manifestations induced by the gasblood interface

The embolus acts like a foreign body21. Platelets, leukocytes, fibrinogen and thrombin adhere to the surface of the bubble22. Leukocytes and platelets as well plasma proteins are activated, triggering the activation of complement, coagulation, fibrinolysis and kinine cascades23-27. These phenomena reinforce the forces of adhesion between the bubble and the vascular wall and resist further embolus migration28.

Over time, the embolic obstruction changes to a thrombotic one. Hyperbaric Oxygen is ineffective for the latter which emphasizes the importance of expediency in management.

The vascular wall is also injured29. It becomes increasingly permeable, causing oedema in the tissue, which in turn worsens the ischemia30. In the lungs, this can lead to ARDS due to non-cardiogenic pulmonary oedema31 or severe bronchospasm due to bronchial hyper-reactivity32. In the brain, the oedema effects intra-cranial pressure and impairs brain metabolism33.

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