Renato Hoffmann Nunes Ana Lorena Abello - Critical Findings in Neuroradiology

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Part I
Brain

Springer International Publishing Switzerland 2016

Renato Hoffmann Nunes , Ana Lorena Abello and Mauricio Castillo (eds.) Critical Findings in Neuroradiology 10.1007/978-3-319-27987-9_1

1. Cerebral Edema

Juan Manuel Gonzlez 1

(1)

Department of Radiology, Hahnemann University Hospital, Drexel University College of Medicine, 230 North Broad Street, Philadelphia, PA 19102, USA

(2)

Department of Neuroscience, School of Medicine, Universidad Catlica de Chile, Luz larrain, 3946 Lo Barnechea, Santiago, Chile

(3)

Department of Radiology, University of North Carolina, Chapel Hill, NC, USA

Juan Manuel Gonzlez

Email:

Florencia Alamos

Email:

Ana Lorena Abello (Corresponding author)

Email:

Abstract

Brain edema is a pathologic increase in the amount of brain water as a result of several etiologies, either cellular damage and ionic pump dysfunction, bloodbrain barrier disruption, or increased transependymal flow from the intraventricular compartment to the brain parenchyma. Brain edema can have focal or global distribution.

Diagnostic imaging can help detect the onset or progression of edema in patients with worsening clinical condition. CT is the modality of choice as the initial study to evaluate injuries that may require intervention. MRI is very sensitive to detect edema and has excellent tissue contrast to detect underlying lesions and may be used when the cause of the edema is not readily apparent on CT.

Keywords

Cerebral edema Cytotoxic edema Vasogenic edema Interstitial edema Pseudo-subarachnoid hemorrhage Excitotoxicity Posterior reversible encephalopathy syndrome

Background

Cerebral edema may be defined as a pathologic increase in the amount of total brain water content leading to an increase in brain volume [].

Symptoms of cerebral edema are nonspecific and related to mass effect, vascular compromise, and herniations. Clinical and imaging changes are usually reversible in the early stages as long as the underlying cause is corrected. Rapidly progressive edema overwhelms cerebral autoregulatory mechanisms, resulting in structural compression, cerebral ischemia, and ultimately fatal cerebral herniation [].

Most fundamental pathophysiological processes following brain injury start with brain edema followed by increased intracranial pressure (ICP) leading to the reduction of cerebral blood flow, inadequate oxygen delivery, energy failure, and further edema. One of the treatment goals is to interrupt this vicious cycle by controlling swelling and maintaining an adequate blood and oxygen supply [].

Glucocorticoids are very effective in ameliorating vasogenic edema that accompanies tumors or inflammatory conditions [].

Key Points

Etiology

According to its location, cerebral edema may be classified as:

• Focal : Generates a pressure gradient in adjacent regions and may result in tissue shifts and herniations. Examples of focal edema can be found around tumors, hematomas, and infarctions [].
• Global : Diffusely affects the whole brain and, when critical, may cause intracranial hypertension and compromised perfusion and lead to generalized ischemia. Cardiopulmonary arrest, severe traumatic injury, multisystem organ failure, hypertensive crisis, infection or inflammation, hypoxicischemic injury, and toxic and metabolic conditions are common causes of global cerebral edema [].

Edema in the brain may be also classified according to its pathophysiological mechanisms (Table ]:

Table 1.1

Pathophysiology of edema

Cytotoxic

Arterial infarction

Small vessel disease

Vasogenic

Neoplasm

Hemorrhage

Venous thrombosis

Arteriovenous shunts

Interstitial

Hydrocephalus

Combined

Trauma

Hypoxicischemic encephalopathy

Osmotic

Hydrostatic

Infection or inflammation

• Cytotoxic edema : Cytotoxic edema is defined as a cellular process, where extracellular Na+ and other cations enter neurons and astrocytes and accumulate due to failure of energy-dependent mechanisms. This incapacity to maintain cellular homeostasis is called cytotoxic edema. Ischemia and profound metabolic derangements are the most common causes [].
• Vasogenic edema : It is caused by breakdown of the tight endothelial junctions comprising the bloodbrain barrier, secondary to either physical disruption or release of vasoactive compounds. As a result, intravascular proteins and fluid escape into the extracellular space [].
• Interstitial edema : Results from increased transependymal flow from the intraventricular compartment to the brain parenchyma. It typically occurs in the setting of obstructive hydrocephalus [].

Best Imaging Modality

Non-enhanced computed tomography (CT)

CT is the modality of choice for initial assessment of suspected cerebral edema because it can be promptly performed, is widely available, and is highly accurate in detecting associated injuries (tumors, hemorrhage, fractures) and in evaluating injuries that require intervention [].

Magnetic resonance imaging (MRI)

MRI is highly sensitive to detect edema and provides excellent soft tissue contrast resolution to evaluate for underlying lesions. On MRI, edema produces high signal on T2-weighted image (T2WI) and low signal on T1-weighted image (T1WI). Diffusion-weighted images (DWI) and apparent diffusion coefficient (ADC) maps distinguish between cytotoxic edema (restricted diffusion) and vasogenic or interstitial edema (increased or facilitated diffusion) [].

Major Findings

Global Edema

CT and MRI show generalized loss of graywhite matter differentiation, effacement of sulci, ventricles, and basal cisterns. If the cause is not addressed, these findings can progress to transtentorial and fatal brain herniations [].

The pseudo-subarachnoid hemorrhage appearance in non-enhanced CT makes reference to diffuse brain edema associated with increased attenuation of the basal cisterns and subarachnoid space, the falx, and the tentorium probably as consequence of slow venous blood circulation (Fig. ].

Fig. 1.1

Global edema. Axial NECT shows diffuse global hypodensity of the brain parenchyma with loss of graywhite matter differentiation and relative increase density of the subarachnoid spaces ( black arrow in a ), posterior falx, and tentorium ( white arrow in b ) compatible with a pseudo-subarachnoid hemorrhage appearance

Cytotoxic Edema

Infarction is the most common cause of cytotoxic edema. In acute arterial infarction, the gray matter is the first to be affected because of its high metabolic activity and greater cellular density; later, both the gray and white matter become involved. CT shows edema as decreased density compared to the surrounding normal parenchyma, which can be more readily visualized using a narrow stroke window (width, 30 HU and level, 30 HU) [].

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