The Pelvic Compartment as Modulator of Intracranial Pressure: The Moscote–Janjua–Agrawal Hypothesis

Introduction

High intracranial pressure (ICP) is the leading cause of death in the patients with traumatic brain injury and contributes to the secondary brain injury if not managed correctly.[1] The Monroe–Kelly doctrine proposes that the rigid skull contains three components: blood, brain tissue, and cerebrospinal fluid (CSF). Any additional component, such as hematomas, cerebral edema, or hydrocephalus, will increase ICP once compensatory shifts in the primary components have been exceeded.[2] The ability to store up to 150 cc of new intracranial volume without a significant increase in ICP occurs through displacement of venous blood into the general circulation, and CSF displacement is time- and age-dependent.[3] Clinical studies have demonstrated that the patients with traumatic brain injury with ICP greater than 20 mm Hg, particularly when refractory to treatment, have a worse clinical prognosis and are more likely to develop cerebral herniation syndromes. Clinical studies have demonstrated that the patients with traumatic brain injury with ICP greater than 20 mm Hg, particularly when refractory to treatment, have a worse clinical prognosis and are more likely to develop cerebral herniation syndromes. There is also recent evidence that cerebral perfusion pressure below 60 to 70 mm Hg is associated with decreased brain parenchymal oxygenation, altered metabolism, and poor prognosis.[4] The goal of neuromonitoring and treatment is to maintain adequate cerebral perfusion, oxygenation, and metabolism while limiting the progression of elevated ICPs, desaturation phenomena, and edema.

Publication History

Article published online:
05 November 2024

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