Cerebral Edema. Hydrocephalus. The effects of traumatic head injuries

Cerebral Edema

Cerebral edema, or brain swelling, is an increase in tissue volume secondary to abnormal fluid accumulation. There are 4 types of brain edema.

Vasogenic Edema. Vasogenic edema results from an increase in the extracellular fluid that surrounds brain cells. It occurs with conditions such as tumors, prolonged ischemia, hemorrhage, brain injury, and infectious processes (e. g. , meningitis) that impair the function of the blood-brain barrier and allow water and plasma proteins to leave the capillary and move into the interstitium.

Cytotoxic Edema. Cytotoxic edema involves the swelling of brain cells. It involves an increase in fluid in the intracellular space, chiefly the gray matter, although the white matter may be involved. Cytotoxic edema can result from hypoosmotic states, such as water intoxication or severe ischemia, that impair the function of the sodium-potassium membrane pump. Changes in cerebral function, such as stupor and coma, occur with cytotoxic edema. The edema associated with ischemia may produce cerebral infarction with necrosis of brain tissue.

Ischemic: Due to cerebral infarction and initially confined to intracellular compartment; after several days, released lysosomes from necrosed cells disrupt blood brain barrier.

Interstitial: Movement of CSF from ventricles to extracellular spaces increases brain volume.

Hydrocephalus

Enlargement of the CSF compartment occurs with hydrocephalus, which is defined as an abnormal increase in CSF volume in any part or all of the ventricular system. There are two types of hydrocephalus: noncommunicating and communicating. Hydrocephalus refers to dilation of the ventricular system and a compensatory increase in CSF volume, secondary to a loss of brain tissue.

Noncommunicating or obstructive hydrocephalus occurs when obstruction in the ventricular system prevents the CSF from reaching the arachnoid villi. CSF flow can be obstructed by congenital malformations, tumors, inflammation, or hemorrhage.

Communicating hydrocephalus results from impaired reabsorption of CSF from the arachnoid villi into the venous system. The cerebral hemispheres become enlarged, and the ventricular system is dilated behind the point of obstruction. Acute-onset hydrocephalus is usually marked by symptoms of increased ICP, including headache vomiting, and by edema of the optic disk (papilla edema). If the

obstruction is not relieved, mental deterioration eventually occurs. Slowly developing hydrocephalus is less likely to produce an increase in ICP, but it may produce deficits such as progressive dementia and gait changes.

The effects of traumatic head injuries

The effects of traumatic head injuries can be divided into two categories: primary or direct injuries, in which damage is caused by impact, and secondary injuries, in which damage results from the subsequent brain swelling, an intracranial hematoma, infection, or cerebral ischemia. Ischemia is the most common cause of secondary brain injury. It can cause the hypoxia and hypotension or the impairment of regulatory mechanisms that maintain cerebral blood flow and oxygen supply. Even if there is no break in the skull, a blow to the head can cause severe and diffuse brain damage. Such closed injuries can be classified as focal or diffuse. Diffuse injuries include concussion and diffuse axonal injury.

  Foca l injuries include contusion, laceration, and hemorrhage. Brain injury is manifested by alterations in sensory and motor function and by changes in the level of consciousness.

Global brain injury, caused by head trauma, stroke, or other pathologies, is manifested by alterations in sensory and motor function, by changes in the level of consciousness and brain death.

Stroke, or “brain attack, ” is an acute focal neurologic deficit caused by a vascular disorder, that injures brain tissue. There are two main types of stroke: ischemic and hemorrhagic. Ischemic stroke, which is the most common type, is caused by cerebrovascular obstruction by a thrombus or emboli. Hemorrhagic stroke, which is associated with greater morbidity and mortality, is caused by the rupture of a blood vessel and bleeding into the brain. The acute manifestations of stroke depend on the location of the blood vessel that is involved and can include motor, sensory, language, speech, and cognitive disorders.

 Most subarachnoid hemorrhages are the result of a ruptured cerebral aneurysm. Presenting symptoms include headache, nuchal rigidity, photophobia, and nausea. Complications include rebleeding, vasospasm, and hydrocephalus. Arteriovenous malformations are congenital abnormal communications between arterial and venous channels that result from failure in the development of the capillary network in the embryonic brain. The vessels in the arteriovenous malformations may enlarge to form a spaceoccupying lesion, become weak and predispose to bleeding, and divert blood away from other parts of the brain; they can cause brain hemorrhage, seizures, headache, and other neurologic deficits.