Abstracto

Resurgent Decompressive Cranial Surgery Following Severe Traumatic Brain Injury

Faupel Marco

Proteases Secondary brain injury results from a first brain injury caused by a variety of intracellular and extracellular processes. ICP, cerebral ischemia, and brain herniation form a pathogenic triad. Subalpine herniation, uncial herniation, central herniation, tonsillar herniation, external herniation by skull fracture, and other types are discussed, along with their clinical symptoms. Medical therapy usually lowers the ICP, improves cerebral perfusion pressure, and improves the clinical condition. In dedicated centres, ICP is measured using various pressure transducers in extradural, subdural, intra parenchymal, and intra ventricular compartments. Measurements of cerebral blood flow, brain tissue oxygenation, and so on are also possible. Cases that are recalcitrant to medical care of ICP are submitted to Decompressive craniotomy in centres where these facilities are not also accessible, based on a periodic clinical assessment. The ICP is reduced, cerebral perfusion is improved, and the clinical result is improved with this DC. Cushing invented the decompression concept for TBI.1-AT is currently known to be a powerful inhibitor of trypsin as well as other serine proteases, with a preference for neutrophil serine proteases, Neutrophil Elastase (NE), and proteinase-3, and is one of the most abundant serine protease inhibitors (serpins) in circulation.

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