Astroglia and Acute Hepatic Encephalopathy: The Mechanisms of Cytotoxic Brain Edema

Astroglia and Acute Hepatic Encephalopathy: The Mechanisms of Cytotoxic Brain Edema

Omar El Hiba, Bilal El-Mansoury, Michael Norenberg, Arumugam Radhakrishnan Jayakumar
Copyright: © 2024 |Pages: 18
DOI: 10.4018/978-1-6684-9675-6.ch013
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Abstract

Acute hepatic encephalopathy (AHE) is a fatal neuro-psychological complication associated with acute liver failure (ALF). While different etiologies were established, over dosage of acetaminophen consumption is still the most frequent. The neuropathological basis of AHE induced death is still not fully understood; however, a body line of evidence sustains the role of rapid onset and progress of brain edema leading to intracranial hypertension, and finally brain herniation and death. The role of astrocytes in the pathogenesis of HE, in general, is well sustained through their role as a detoxifying component of the central nervous system, especially from peripheral generated ammonia, leading to astrocyte swelling, generally associated to brain edema onset. The current chapter will describe the pathomechanisms underlying astrocyte swelling in AHE, with the eventual evolution into macroscopic brain edema and the deathly herniation in humans as well as animal models of AHE.
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Brain Edema: Clinical Features

By definition, cerebral edema refers to increased amount of water within the brain tissue. Knowing that the brain bone is not extensible, water accumulation leads to progressive rise in the intracranial pressure (ICP), and therefore, the onset of intracranial hypertension (ICH). Such abnormality is generally associated to severe neurological complications due to decreased cerebral blood flow, tissue perfusion and ischemia (Larsen 1996).

ICH has been associated to acute forms of hepatic failures since the first description by Ware et al., in 1971(Ware, D’Agostino, and Combes 1971). Such neurological complication was found in up to 80% patients with ALF at the coma stage (fig. 1, fig.2), while studies on animal models of ALF appeared to well mimic such clinical feature.

Figure 1.

(A) Rapid brain edema onset in a patient with acute liver failure; (B) The same patient with normal TC scanner at the admission eight hours earlier

978-1-6684-9675-6.ch013.f01
(Vaquero, Chung, and Blei 2003)
Figure 2.

Association between brain volume and intracranial pressure (ICP). Increased brain volume due to edema leads to increased ICP. Even at the same range of volume increase (A and B), the lower brain compliance results in higher increases of pressure in B. In the acute case, the curve is steeper due to a lesser capacity of compensation.

978-1-6684-9675-6.ch013.f02
(Vaquero et al. 2003)

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