Fisiopatología del síndrome de hipertensión intracraneal

Abstract

El síndrome de hipertensión intracraneal (HIC) se caracteriza por el aumento de la presión intracraneal (PIC) por encima de límites normales, la cual conlleva a varios signos y síntomas que sufre el paciente, la cual, si no se aborda a tiempo, puede llevar a un desenlace fatal con coma y muerte. La PIC la determina la presión de líquido cefalorraquídeo (LCR), el flujo sanguíneo y el parénquima cerebral. Su etiología es variada, pudiendo ser aguda o crónica lo que determina las diversas manifestaciones clínicas. Las manifestaciones clínicas se dan en varias etapas, produciendo comúnmente cefalea, vómitos, papiledema y signos focales neurológicos. El objetivo es dar a conocer la neuroanatomía involucrada, para así poder realizar un diagnóstico temprano y prevenir patologías irreversibles, así mismo es de suma importancia para comprender el motivo de las manifestaciones clínicas al conocer las estructuras afectadas y poder así realizar un adecuado abordaje.

Decompressive Craniectomy Versus Cisternostomy in Traumatic Intracranial Hypertension. Systematic Review

“…A reduction in CPP below 50 mmHg can lead to ischemic injury and cerebral edema. 2,3,4 The pathological increase in ICP may be due to: injury of extrinsic origin, increased blood volume, increased CSF volume, increased cellular tissue volume. 2 When ICP varies due to any of the given causes, what is known as compensation initially occurs, where blood and CSF move around the spinal axis and normal ICP values are maintained.…”

“…2,3,4 The pathological increase in ICP may be due to: injury of extrinsic origin, increased blood volume, increased CSF volume, increased cellular tissue volume. 2 When ICP varies due to any of the given causes, what is known as compensation initially occurs, where blood and CSF move around the spinal axis and normal ICP values are maintained. 2,5 When the limits of the compensatory mechanisms are exceeded, an increase in ICP occurs.…”

“…2 When ICP varies due to any of the given causes, what is known as compensation initially occurs, where blood and CSF move around the spinal axis and normal ICP values are maintained. 2,5 When the limits of the compensatory mechanisms are exceeded, an increase in ICP occurs. 1 This increase is nothing more than a decompensation resulting from the pressure exerted by the CSF in the cerebral ventricles and the blood volume itself that flows through the central nervous system.…”

“…1 This increase is nothing more than a decompensation resulting from the pressure exerted by the CSF in the cerebral ventricles and the blood volume itself that flows through the central nervous system. 2 Finally, when all the reserve spaces are used, the brain begins to move due to pressure difference, through the folds of dura mater (falx cerebri and tentorium), and through the foramen magnum, in what is called cerebral herniations.…”