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This chapter reviews available neuroimaging methods and their application in the evaluation and management of the critically ill and injured.
Plain radiography plays a minor role in evaluating the neurologically ill or injured patient. Radiography is not sensitive for the detection of intracranial pathology and is not part of the standard imaging approach for the evaluation of patients with such pathology. Conventional radiography plays a role in the evaluation of suspected spinal pathology, particularly in the setting of traumatic spine injury and assessment of spinal stability and postoperative complications. Plain radiography is also used as a screening tool to assess for metallic foreign bodies, particularly in the orbits and intracranial compartment, in patients requiring magnetic resonance imaging (MRI), as the presence of such foreign bodies may result in injury to adjacent structures secondary to heating and motion from the strong magnetic field.
Computed tomography (CT) uses ionizing radiation to create anatomic images on the basis of differential attenuation of photons between various tissue types. This results in an image composed of grayscale pixels on a spectrum ranging from dark, or hypodense, from tissues with low photon attenuation (air, water, fat) to bright, or hyperdense, from tissues with high photon attenuation (bone, metal). Soft tissues, such as brain parenchyma and muscle, are intermediate attenuators of photons and therefore exhibit grayscale values between low and high attenuators.
CT is widely available, and there are no absolute contraindications to CT imaging in the acute setting. Its use of ionizing radiation does confer minimal risk to the patient related to radiation exposure. However, in the acute setting, the risk–benefit ratio almost always points towards imaging to aid in timely diagnosis. Advances in CT technology, particularly multidetector row CT (MDCT) and volumetric acquisition, allow for rapid imaging with high temporal and spatial resolution. MDCT also allows for thin-slice image acquisition with the ability to manipulate CT data in multiple planes and perform postprocessing, such as volume rendering.
Iodinated contrast may be administered intravenously to increase sensitivity for detection of blood–brain barrier disruption and mass lesions and to evaluate the cerebral vasculature with CT angiography (CTA) techniques. CT perfusion imaging of the brain allows for assessment and quantification of brain perfusion parameters, including cerebral blood flow, cerebral blood volume, mean transit time, and time to peak enhancement. CT perfusion imaging is primarily used in the setting of cerebral ischemia.
MRI uses a strong external magnetic field and a series of radiofrequency pulses (nonionizing radiation) to confer energy to protons in tissues. Images are constructed based on the differential responses of these energized protons in different tissues (protons in water versus protons in fat). Imaging parameters are adjusted to allow for variable tissue weighting, thus highlighting specific tissues and pathologic processes.
MRI is more sensitive than CT for detection of brain and spine pathology in almost all circumstances. However, longer imaging time precludes particularly unstable patients, given the required time away from the intensive care unit. Patients with certain medical devices and known or suspected retained ferromagnetic foreign bodies may not be eligible for MRI.
MRI uses nonionizing radiation. Therefore no radiation risk is conferred to patients. Gadolinium-based contrast media can be administered intravenously to detect blood–brain barrier disruption, masses, and vascular lesions. Contrasted imaging may also be used to assess the cerebral vasculature and brain perfusion parameters, similar to that described with CTA and CT perfusion. Noncontrast MR angiography (MRA) and perfusion techniques are also available for patients who cannot receive gadolinium-based contrast. Gadolinium is now known to be retained in the brain and in other organ systems. There are no known clinical sequelae to date; however, many investigators are studying the potential long-term effects of gadolinium retention.
Several advanced MRI techniques are used in the evaluation of critically ill patients. Diffusion-weighted imaging (DWI) is based on the principle of water molecules being freely mobile and able to diffuse freely in all directions. Some pathologic processes, such as ischemia, cytotoxic edema, and abscess, restrict this free diffusion of water, which can be represented visually with DWI techniques. Diffusion restriction is also seen in pathologic processes associated with high cellularity, such as high-grade neoplasms. Diffusion-tensor imaging (DTI) is based on the same principles as DWI and allows for anatomic mapping of white matter tracts in the brain. This can be used to assess for alterations in brain connectivity in the setting of traumatic brain injury and to assess the anatomic relationship of white matter tracts to focal brain lesions.
Several nuclear medicine studies are encountered in the neurocritical care setting. Planar brain scans using Tc-99m–labeled radiotracers assess brain perfusion and are used in the determination of brain death. Nuclear medicine cisternography is used to confirm and localize the site of a suspected cerebrospinal fluid (CSF) leak. Positron emission tomography (PET) and single-photon emission tomography (SPECT) play a role in the evaluation of epilepsy and seizure focus localization. Nuclear medicine scans using gallium-68 and radiolabeled white blood cells are used to localize occult infection and are useful in monitoring response to therapy, particularly in the skull base and spine.
Cerebral edema is a common response to brain pathology and is classified as either cytotoxic, vasogenic, or interstitial. Cytotoxic edema results from failure of adenosine triphosphate (ATP)–dependent transmembrane ion channels, leading to intracellular accumulation of fluid. The major causes of cytotoxic edema are ischemia and excitotoxicity. Vasogenic edema is the result of blood–brain barrier disruption, resulting in extravascular extravasation of serum proteins and fluid into the extracellular space. Common pathologic processes that cause vasogenic edema include neoplasms, infection, hemorrhage, and acute hypertensive syndromes. Interstitial edema occurs in the setting of increased ventricular pressure, which results in CSF flow through the minor CSF drainage pathways in the periventricular white matter. Interstitial edema is seen in the setting of acute hydrocephalus. Regardless of subtype, edema appears as areas of hypodensity on CT and increased intensity on T2-weighted and fluid-attenuated inversion recovery (FLAIR) MRI sequences.
Cytotoxic edema presents on CT as areas of hypodensity involving the cerebral cortex to a greater extent than the underlying white matter, resulting in loss of normal gray matter–white matter differentiation. Gyri become swollen, and sulci are effaced ( Fig. 52.1 A). MRI will show increased signal, or hyperintensity, on T2-weighted and FLAIR sequences, which are sensitive to water. T1-weighted sequences will show corresponding regions of decreased signal, or hypointensity. DWI sequences will show hyperintensity, implying the presence of restricted diffusivity of water molecules within swollen neurons and glial cells. In contrast to cytotoxic edema, vasogenic edema preferentially involves white matter with relative sparing of gray matter. CT and fluid-sensitive MRI sequences show hypodensity and hyperintensity, respectively, throughout the involved white matter extending up to adjacent cortex and deep gray structures (see Fig. 52.1 B). Interstitial edema presents in the setting of acute hydrocephalus and will show hypoattenuation on CT and increased signal on T2/FLAIR MRI sequences in the periventricular white matter, especially near the frontal and occipital horns of the lateral ventricles ( Fig. 52.2 ).
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