Patterns of Increased Intracranial Pressure After Severe Traumatic Brain Injury

Abstract

Late rises in ICP were not rare in this cohort. This is clinically relevant as it may impact decisions about ICP monitor removal. Differences between groups in age, CT patterns of injury, fluid therapy, osmotic use, and fever were not statistically significant.

The Course of Intracranial Pressure in Traumatic Brain Injury: Relation with Outcome and CT-characteristics

“…The relation between the time course of ICP and outcome is less clear. Recently, different time patterns of raised ICP have been described [12,15]. However, few data are available on the relation of these different ICP profiles and outcome as mortality is described as main outcome measure.…”

Features of Development of the Brain Oedema in the Acute Period of the Severe Brain Injury

“…После ишемии головного мозга активируется интерферон-стимули-рованный ген 15 (ISG15) [2]. Ряд авторов указывает, что формирование отека головного мозга после тя-желой ЧМТ может развиваться в течение различно-го периода времени: от первых часов до 7 дней [3]. Клинические исследования указывают, что разви-тие отека головного мозга связано преимуществен-но с возрастом пациентов, где наиболее часто этому осложнению подвержены дети [4].…”

Fever and Infection in the Neurosurgical Intensive Care Unit

“…After the initial injury, secondary brain insults are speculated to be caused by several processes including mitochondrial dysfunction, inflammatory response, free radical generation, and excitatory neurotransmitter release. 9 These episodes of secondary brain injury appear to be caused by or temporally associated with hypotension, intermittent hypoxia and ischemia, fever and hyperthermia, cerebral hypertension and elevated intracranial pressure. 9 In terms of trauma to the CNS, it is commonly accepted that elevated temperature exacerbates secondary brain injury.…”

“…9 These episodes of secondary brain injury appear to be caused by or temporally associated with hypotension, intermittent hypoxia and ischemia, fever and hyperthermia, cerebral hypertension and elevated intracranial pressure. 9 In terms of trauma to the CNS, it is commonly accepted that elevated temperature exacerbates secondary brain injury. Fever has been demonstrated to increase glutamate release, provoke diffuse oxygen free radical production, increase cytoskeletal protein degradation, and markedly augment the permeability of the bloodbrain barrier.…”