Estimated Specific Gravity with Quantitative CT Scan in Traumatic Brain Injury

Abstract

An uncontrolled increase in intracranial pressure (ICP), often due to cerebral oedema, is the most common cause of death in traumatic brain injury (TBI) patients. Different types of oedema coexist in TBI patients: vasogenic oedema and cytotoxic oedema. Vasogenic oedema occurs with the extravasation of fluid into the extracellular space following blood brain barrier (BBB) disruption. Cytotoxic oedema results from a shift of water from the extracellular compartment into the intracellular compartment due in part to alterations in normal ionic gradients. The description of the localisation, and the knowledge of the chronology, the determinants, and the kinetics of the BBB disruption are necessary to adapt therapeutic strategy. Although nuclear magnetic resonance is not advisable during the acute phase of human TBI, especially in unstable TBI patients, this imaging is one of the most accurate for the study of brain oedema. Diffusion-weighted imaging provides a useful and non-invasive method for visualizing and quantifying diffusion of water in the brain associated with oedema. Apparent diffusion coefficients (ADC) can be calculated and used to assess the magnitude of water diffusion in tissues. For example, a high ADC value indicates more freely diffusible water which is considered as a marker of vasogenic oedema. On the other hand, cytotoxic oedema restricts water movement and results in decreased signal intensities in the ADC map. In a rat model of diffuse TBI, an early increase in ADC values during the first 60 minutes was observed, followed by a decrease in ADC values reaching a minimum at one week [1]. This result suggests a biphasic oedema formation following diffuse TBI without contusion, with a rapid and short disruption of the BBB during the first hour post injury, leading to an early formation of vasogenic edema. Contrary to the non-contused areas, there are numerous arguments in favour of a profound and prolonged alteration of the BBB in traumatic areas of contusion appearing on CT [2-7]. Several methods have been used to study oedema formation and the BBB changes following animal and human TBI, however its underlying mechanisms are still not well understood. For these reasons, it might be interesting to investigate a new and more accessible technique to study the oedema formation at the acute phase of human TBI, particularly to compare the non-contused and the contused areas and to follow the BBB state in these areas with time.