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Edema refers to abnormal, excessive accumulation of fluid in the cells, tissues, or body cavities. Brain edema results from excess accumulation of water in the extracellular and/or intracellular compartments of the brain. The brain is protected by a closed, rigid cranial cavity that contains brain tissue, cerebrospinal fluid (CSF), and intravascular blood. Any increase in either of its components is compensated by reduction or displacement of the other (known as the Monro-Kellie doctrine). If the brain volume increases, the first component to decrease is blood followed by displacement of CSF. The compensation is limited due to the fixed rigid space after the fusion of fontanelles. In adults, due to an unyielding skull, the initial compensatory mechanisms get exhausted early and any further increase in volume of intracranial components leads to a rise in the intracranial pressure (ICP).
Brain swelling, leading to tense brain, may even occur after opening the cranial cavity during a craniotomy. If the tension within the cranial cavity is high, after a craniotomy, the brain may bulge along with the dura mater through the cranial opening. Intraoperatively, brain swelling may occur due to various reasons, causing the brain to become tense. The brain swelling may be classified into four types (see Table 1 ).
Vasogenic | Due to shift of fluid from intravascular compartment to extracellular space |
Cytotoxic | Due to shift of fluid from extracellular to intracellular compartment |
Interstitial | Due to shift of cerebrospinal fluid into the extracellular space |
Hyperemic | Due to increase in intravascular volume |
The brain has three anatomical compartments where the excessive fluid can accumulate: the cellular compartment (neurons and supporting cells), the extracellular compartment (interstitial and CSF spaces), and the vascular compartment (arteries, veins, and capillaries). Volume expansion of any one or more of these compartments causes bulk enlargement of brain.
Excessive uptake of fluid by cellular elements of the brain can lead to brain swelling. Derangement of cellular metabolism results in inadequate functioning of energy-dependent Na + -K + pump of the cell membrane, causing cellular retention of Na + and water. This process causes the cell to swell ( cytotoxic edema ) ( Figure 1(b) ). Such swelling occurs during cerebral ischemia. Cytotoxic edema is typically seen after exposure to various intoxicants such as methionine sulfoximine, hydrogen cyanide, lead, hexachlorophene, isoniazid, and so forth; it is also seen in Reye’s syndrome.
Excessive accumulation of fluid in the interstitial space and/or CSF cavities causes the brain to swell. It may occur as a consequence of disruption of the blood–brain barrier (BBB) with increased permeability of cerebral capillaries ( vasogenic edema (VE)); osmotic gradient between the plasma and brain extracellular fluid with intact BBB ( osmotic edema ); or due to obstruction of interstitial fluid or CSF outflow ( compressive and hydrocephalic edema ).
VE is the most common type of extracellular edema and is seen in response to head injuries, tumors, infections, inflammations, and cerebrovascular accidents. Disruption of BBB causes intravascular proteins and fluid to penetrate into brain parenchymal extracellular space ( Figure 1(c) ). The magnitude of edema depends on various factors like severity of BBB dysfunction, size of the lesion, and duration of barrier opening. It increases proportionally with the increase in mean arterial pressure. VE is seen more in the white matter due to lower resistance compared to gray matter which has greater density.
Osmotic edema results when an unfavorable osmotic gradient is established between the plasma and the extracellular fluid of the brain. If the osmolarity of the plasma decreases (e.g., inappropriate secretion of antidiuretic hormone, water intoxication, excessive hemodialysis of uremic patients, etc.) or the osmolarity of the brain tissue increases, the passage of water down the gradient occurs, creating cerebral edema. For osmotic edema to develop, the BBB must be intact to maintain effective osmotic gradient.
Obstruction to the flow of interstitial fluid due to compression by any mass (e.g., a large tumor) may cause the edema of the surrounding tissue (compressive edema). Similarly, in hydrocephalic edema, obstruction to the drainage of CSF leads to collection of CSF proximal to the block, thus causing distention of cavities and retrograde flooding of the extracellular compartment (periventricular edema).
Cerebral engorgement results from an increase in the cerebral blood volume (CBV). It may be caused by vasodilatation or venous outflow obstruction. In the normal brain, the cerebral autoregulation maintains the cerebral blood flow (CBF) according to the physiologic requirement of the brain by regulating the tone and caliber of cerebral arteries and arterioles. However, various pathological conditions (e.g., febrile infections, seizures, malignant hypertension, global ischemia, etc.) may alter metabolic demand and/or disturb arterial tone and caliber. This causes profound arterial dilatation, which may lead to hyperemia and congestion of brain. Obstruction of the cerebral veins or venous dural sinuses also causes congestion of the brain. Venous outflow obstruction can be caused by bacterial meningitis, parasagittal tumors, subdural abscesses, polycythemia, head injury, compression of neck veins, right heart failure, and so forth.
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