Emergency Imaging. Alexander B. Baxter. Читать онлайн. Newlib. NEWLIB.NET

Автор: Alexander B. Baxter
Издательство: Ingram
Серия:
Жанр произведения: Медицина
Год издания: 0
isbn: 9781604067439
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Hydrocephalus

      • Normal pressure hydrocephalus

      • Meningitis

      • Prior subarachnoid hemorrhage

      • Venous sinus thrombosis

      Obstructive Hydrocephalus

      • Aqueductal stenosis

      • Colloid cyst of third ventricle

      • Tectal glioma

      • Intraventricular tumor

      Parenchymal Hemorrhage

      • Hypertensive hemorrhage

      • Amyloid angiopathy

      • Hemorrhagic metastasis

      • Herpes encephalitis

      • Acute leukemia

      • Arteriovenous malformation

      • Aneurysm

      • Contusion (in trauma)

      Subarachnoid Hemorrhage

      • Ruptured aneurysm

      • Benign perimesencephalic hemorrhage

      • Traumatic subarachnoid hemorrhage

      Global Cerebral Volume Loss

      • Chronic alcohol use

      • Anticonvulsants (particularly cerebellar)

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      pressure leads to transependymal migra-tion of CSF into the periventricular white matter, where it is resorbed via parenchy-mal capillaries.

      On CT, cerebral edema is lower in density than surrounding normal parenchyma. On MRI, signal intensity of edema is lower than that of brain parenchyma on T1-weighted images and higher on T2-weighted im-ages. Diusion-weighted image (DWI) and apparent diusion coecient (ADC) map-ping sequences can distinguish between cytotoxic edema (restricted diusion) and vasogenic or interstitial edema (normal or increased diusion). Fluid attenuation inversion recovery (FLAIR) sequences sup-press intraventricular CSF signal and are sensitive for detecting adjacent areas of in-terstitial edema (Fig. 2.3).

       ◆Cerebral Edema Patterns

      Localized cerebral edema may be classified as cytotoxic, vasogenic, or interstitial, al-though overlap is often present. Cytotoxic edema consists of intracellular swelling caused by depletion of adenosine triphos-phate (ATP) and consequent sodium/potas-sium membrane pump failure. Most typical of cerebral infarct and anoxic injury, cyto-toxic edema aects both white and gray matter similarly on most imaging studies.

      Vasogenic edema, in contrast, prefer-entially involves white matter and results from conditions that increase intracerebral capillary permeability. Vasogenic edema is often due to brain contusion, severe hy-pertensive disease, primary and metastatic neoplasms, or inflammatory conditions.

      Acute hydrocephalus can cause inter-stitial edema, as elevated intraventricular

      Fig. 2.3a–f a,b Cytotoxic edema in cerebral infarction. Extensive right frontal and temporal low-density change with loss of dierentiation between gray and white matter, sulcal eacement, and ipsilateral ventricular eace-ment. The middle cerebral artery is dense, indicating thrombosis.

      c,d Vasogenic edema due to hemorrhagic brain metastasis from lung carcinoma. Left frontal white mat-ter hemorrhage with surrounding low attenuation edema that spares the cortical gray matter. FLAIR MRI shows a hemorrhagic nodule with extensive surrounding high-signal edema limited to the white matter. e,f Interstitial edema in hydrocephalus due to fourth-ventricle obstruction by meningioma. Acute hydro-cephalus with low-density transependymal CSF resorption, most conspicuous at the frontal, occipital, and temporal horns of the lateral ventricles.

      

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       ◆ Anatomic Variants and Incidental Findings

      Common incidental findings on head CT include arachnoid cysts, prominent arach-noid granulations, choroid plexus and choroidal fissure cysts, remote lacunar in-farcts, focal encephalomalacia from prior infarct or trauma, and prominent perivas-cular spaces. The ventricles may be slightly asymmetric, and the septum pellucidum may contain a central CSF-filled cavity (cavum septum pellucidum). Unless symp-tomatic, these conditions usually do not require specific follow-up (Fig. 2.4).

      Fig. 2.4a–f a,b Arachnoid granulation. Whenvisible, arachnoid granulations, which resorb CSF into the venous sys-tem, appear as lling defects in the opacied venous sinuses. They may also cause smooth erosion of the bone adjacent to the sinus. (a) Round lling defect in opacied left transverse sinus. Round osseous ero-sions near the internal occipital protruberance/torcular Hirophili.

      c Choroidal ssure cyst. These small CSF attenuation cysts arise in the choroidal ssure and appear lat-eral to the midbrain or cerebral peduncle on axial images.

      d Enlarged perivascular space. 8-mm CSF attenuation space located in the right posterior putamen. e Cavum septum pellucidum. A developmental variant due to failed embryonic fusion of the leaves of the septum pellucidum, it is present in ~15% of individuals. This CT image also shows cortical contusions, traumatic subarachnoid hemorrhage, and subacute bifrontal frontal subdural hygromas.

      f Arachnoid cyst. CSF attenuation, extra-axial collection due to duplication in the arachnoid membrane, which compresses the adjacent brain and may smoothly expand the overlying calvarium. These are usu-ally asymptomatic; however, larger cysts may predispose to hemorrhage in minor trauma or can cause symptoms by compression of the brain. Epidermoids can have a similar appearance on CT, but they have characteristically high signal on FLAIR MRI.

      

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