Tissue hyperosmolality and brain edema in cerebral contusion

Abstract

<jats:p>Severe cerebral contusion is often associated with nonhemorrhagic mass effect that progresses rapidly within 12 to 48 hours posttrauma. The mechanisms underlying such a rapid progression of mass effect cannot be fully explained by classic concepts of vasogenic and cytotoxic brain edema. Data from previous clinical trials, including diffusion-weighted magnetic resonance imaging studies, have indicated that cells in the central (core) area of the contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is located predominately in the peripheral (rim) area during this period. The authors hypothesized that high osmolality within the contused brain tissue generates an osmotic potential across the central and peripheral areas or causes blood to accumulate a large amount of water. To elucidate the role of tissue osmolality in contusion edema, they investigated changes in tissue osmolality, specific gravity, and ion concentration in contused brain in both experimental and clinical settings. Their results demonstrated that cerebral contusion induced a rapid increase in tissue osmolality from a baseline level of 311.4 ± 11.3 to 402.8 ± 15.1 mOsm at 12 hours posttrauma (p &lt; 0.0001). Specific gravity in tissue significantly decreased from 1.0425 ± 0.0026 to 1.0308 ± 0.0028 (p &lt; 0.01), reflecting water accumulation in contused tissue. The total ionic concentration [Na<jats:sup>+</jats:sup>] + [K<jats:sup>+</jats:sup>] + [Cl<jats:sup>−</jats:sup>] did not change significantly at any time point. Inorganic ions do not primarily contribute to this elevation in osmolality, suggesting that the increase in colloid osmotic pressure through the metabolic production of osmoles or the release of idiogenic osmoles can be a main cause of contusion edema.</jats:p>

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

“…Following severe TBI, regions containing necrotic tissue swell and compress the cerebral vasculature such that blood cannot flow to many parts of the brain . Diffuse damage or a stroke may also result in diffuse swelling of the brain, but in all cases, swollen regions are associated with dead, dying or damaged cells (Kawamata et al 2007). Imaging studies have identified cytotoxic swelling as the most probable cause of this oedema (Vorisek et al 2002;Maeda et al 2003;van Pul et al 2005;Marmarou et al 2006b;Kuroiwa et al 2007).…”

“…Brain oedema following TBI has traditionally been subdivided into three major categories: vasogenic (Papadopoulos et al 2005), cytotoxic (Liang et al 2007) and interstitial oedema (Kawamata et al 2007) (for reviews and a historical perspective, see Klatzo 1967;Fishman 1975;Unterberg et al 2004). Indirect measures based on diffusion-weighted imaging have suggested that following TBI without blood-brain barrier (BBB) disruption or with transient BBB disruption, cytotoxic oedema is the dominant cause of persistent brain oedema (Barzo et al 1997;Marmarou et al 2006a).…”

Development of hydrocephalus and classical hypothesis of cerebrospinal fluid hydrodynamics: Facts and illusions

“…It was shown (Katayama et al, 2003) that samples of necrotic brain tissue taken from the central area of the contusion demonstrated a very high osmolarity. The cerebral contusion induced a rapid increase in tissue osmolality of 90 mOsm/kg, 12 hours posttrauma, and a significant decrease in the specific gravity of the contused tissue reflected water accumulation (Kawamata et al, 2007).…”

Effect of osmolarity on CSF volume during ventriculo-aqueductal and ventriculo-cisternal perfusions in cats

“…It was shown (11) that necrotic brain tissue sampled from the central area of contusion demonstrated a very high osmolality. The cerebral contusion induced an increase in tissue osmolality and a significant decrease of specific gravity in contused tissue has reflected water accumulation (13).…”