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Cerebral Edema Cerebral edema, or brain swelling, is an increase in tissue volume secondary to abnormal fluid accumulation. There are two types of brain edema: vasogenic and cytotoxic. Vasogenic edema occurs when integrity of blood-brain barrier is disrupted, allowing fluid to escape into the extracellular fluid that surrounds brain cells. Cytotoxic edema involves the actual swelling of brain cells themselves. Brain edema may or may not increase ICP. The impact of brain edema depends on the brain’s compensatory mechanisms and the extent of the swelling. Vasogenic Edema. Vasogenic edema occurs with conditions that impair the function of the bloodbrain barrier and allow transfer of water and protein from the vascular into the interstitial space. It occurs in conditions, such as tumors, prolonged ischemia, haemorrhage, brain injury, and infectious processes (e,g,. meningitis). Vasogenic edema occurs primarily in the white matter of the brain, possibly because the white matter is more compliant than the gray matter. Vasogenic edema can displace a cerebral hemisphere and can be responsible for various types of herniation. The functional manifestations of vasogenic edema include focal neurologic deficits, disturbances in consciousness, and severe intracranial hypertension. Cytotoxic Edema. Cytotoxic edema involves an increase in intracellular fluid. It can result from hypoosmotic states such as water intoxication and severe ischemia that impair the function of the sodium-potassium membrane pump. Ischemia also results in the inadequate removal of anaerobic metabolic end products such as lactic acid, producing extracellular acidosis. If blood flow is reduced to low levels for extended periods or to extremely low levels for a few minutes, cellular edema can cause the cell membrane to rupture, allowing the escape of intracellular contents into the surrounding extracellular fluid. This leads to damage of neighboring cells. The altered osmotic conditions result in water entry and cell swelling. Major changes in cerebral function, such as stupor and coma, occur with cytotoxic edema. The edema associated with ischemia may be severe enough to produce cerebral infarction with necrosis in brain tissue. Treatment. Although cerebral edema is viewed as a pathologic process, it does not necessarily disrupt brain function unless it increase the ICP. The localized edema surrounding a brain tumor often responds to corticosteroid therapy (e.g., dexamethasone). But use of these drugs for generalized edema is controversial. The mechanism of action of corticosteroid drugs in the treatment of cerebral edema is unknown, but therapeutic doses, they seem to stabilize cell membranes and scavenge free radicals. Osmotic diuretics (e.g., mannitol) may be useful in acute phase of vasogenic and cytotoxic edema when hypoosmolality is present. 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. The two causes of hydrocephalus are decreased absorption of CSF and overproduction of CSF. There are two types of hydrocephalus: noncommunicating and communicating.
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 malformation from tumors encroaching on the ventricular system, and by inflammation or haemorrhage. The ependymal (i.e., lining of ventricles and CSF-filled spaces) is especially sensitive to viral infections, particularly during embryonic development; ependymitis is believed to be the cause of congenital aqueductal stenosis. Communicating hydrocephalus results from impaired reabsorption of CSF from the arachnoid villi into the venous system. Decreased absorption can result from a block in the CSF pathway to the arachnoid villi or a failure of the villi to transfer the CSF to the venous system. It can occur if too few villi are formed, if postinfective (meningitis) scarring occludes them, or if the villi become obstructed with fragments of blood or infectious debris. Adenomas of the choroid plexus can cause an overproduction of CSF. This form of hydrocephalus is much less common than that resulting from decreased absorption of CSF. Similar pathologic patterns occur with noncommunicating types of hydrocephalus. The cerebral hemispheres become enlarged, and the ventricular system is dilated beyond the point of obstruction. The gyri on the surface of the brain becomes less prominent, and the white matter is reduced in volume. The presence and extent of the ICP is determined by fluid accumulation and the type of hydrocephalus, the age of onset, and the rapidity and extent of pressure rise. Acute hydrocephalus usually is manifested by increased ICP. Slowly developing hydrocephalus is less likely to produce an increase in ICP, but it may produce deficits such as progressive dementia and gait changes. Computed tomographic (CT) scans are used to diagnose all types of hydrocephalus. The usual treatment is a shunting procedure, which provides an alternative route for return CSF to the circulation. When hydrocephalus develops in utero or before the cranial sutures have fused in infancy, the ventricles expand beyond the point of obstruction, the cranial sutures separate; the head expands, and there is bulging of the fontanels (Figure 1.6). Because the skull is able to expand, signs of increased ICP usually are absent, and intelligence usually is spared. Seizures are common, and in severe cases, optic nerve atrophy leads to blindness. Weakness and uncoordinated movement are
common. Surgical placement of shunt allows for diversion of excess CSF fluid, preventing extreme enlargement of the head. Before surgical shunting procedures were available; the weight and size of the enlarged head made ambulation difficult. In contrast to hydrocephalus that develops in utero or during infancy, head enlargement does not occur in adults, and increases in ICP depend on whether the condition developed rapidly or slowly. Acute-onset hydrocephalus in adults usually is marked by symptoms of increased ICP, including headache, vomiting, and papilledema, or lateral rectus palsy from pressure effects on the cranial nerves. If the obstruction is not relieved, mental deterioration eventually occurs. The pressure of CSF is not always elevated, and the syndromes of low-pressure hydrocephalus may go undetected. Treatment includes surgical shunting for noncommunicating hydrocephalus. In communicating hydrocephalus, attempts to clear the arachnoid villi of exudate may be made, and if these are unsuccessful, surgical shunting may be required. Head Injury The brain is enclosed in the protective confines of bony skull. Although the skull affords protection for the fissures of the CNS, it also provides the potential for development of ischemic and traumatic brain injuries. This is because it cannot expand to accommodate the increase in volume that occurs when there is swelling or bleeding in its confines. The bony structures themselves can cause injury to the nervous system. Fractures of the skull can compress sections of the nervous system, or they can splinter and cause penetrating wounds. The term head injury is used to describe all structural damage to the head and has become synonymous with brain injury. In the United States, head injury is the leading cause of death among persons younger than 24 years of age. The main causes of head injury are road accidents falls, and assaults, and the most common cause of fatal head injuries is road accidents involving vehicles and pedestrians. Head injuries can involves both closed injuries and open wounds. Skull fractures can be divided into three groups: simple, depressed and basilar. A simple or liner skull fracture is a break in the continuity of bone. A comminuted skull fracture refers to a splintered or multiple fracture line. When bone fragments are embedded into the brain tissue, the fracture is said to be depressed. A fracture of the bones that forms the base of the skull is called a basilar skull fracture. Radiologic examination usually is needed to confirm the presence and extent of a skull fracture. This evaluation is important because of the possible damage to the underlying tissues. The ethmoid cibriform plate, through which the olfactory fibers enter the skull, represents the most fragile portion of the neurocranium and is shattered in basal skull fractures. A frequent complication of basilar skull fracture is leakage of CSF from the nose (rhinorrhea) or ear (otorrhea); this occurs because of the proximity of the base of the skull to the nose and ear. This break in protection of the brain becomes a probably source of infection of the meninges or of brain substance. There may be lacerations to the vessels of the dura, with resultant cranial bleeding. Skull fractures can damage the cranial nerves (I, II, III, VII, VIII) as they exit the cranial vault.
Types of Brain 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, infection, or cerebral hypoxia. The direct brain injuries include diffuse axonal injury and the focal lesions of laceration, contusion, and haemorrhage. Secondary brain injuries are often diffuse or multifocal, including concussion, infection and hypotoxic brain injury. Although the skull and CSF provide protection for the brain; they also can contribute to trauma. When the mechanical forces inducing head injury cause bouncing of the brain in the closed confines of the rigid skull, a coup-contrecoup injury occurs. Because the brain floats freely in the CSF, blunt force to the head can cause the brain to accelerate in the skull and then to decelerate abruptly on hitting the inner confines of the skull. The direct contusion of the brain at the site of external force is referred to as a coup injury; whereas the opposite side of the brain receives the contrecoup injury from rebound against the inner skull surfaces (Figure 1.7). as the brain strikes the rough surface of the cranial vault, brain tissue, blood vessels, nerve tracts, and other structures are bruised and torn, resulting in contusion and hematomas.
Ischemia is considered the most common secondary brain injury. It can results from the hypoxia and hypotension that occur during the resuscitation process or from the impairment of the regulatory mechanisms by which cerebrovascular responses maintain an adequate blood flow and oxygen supply. Insults that occur immediately after injury or in the course of resuscitation efforts are important determinants of the outcome from severe brain injury. More than 25% of patients with severe head injury sustain one or more secondary insults in the time between injury and resuscitation, indicating the need for improved airway management and circulatory status. The significance of secondary injuries depends on the extent of damage caused by the primary injury.
Certain secondary injuries have been discussed, such as increased ICP, cerebral edema, and brain herniation. In mild head injury, there may be momentary loss of consciousness with demonstrable neurologic symptoms or residual damage, except for possible residual amnesia. Microscopic changes usually can be detected in the neurons and glia within hours of injury, but brain imaging is normal. Concussion is defined as momentary interruption of brain function with or without loss of consciousness. Although recovery usually takes place within 24 hours, mild symptoms, such as headache, irritability, insomnia, and poor concentration and memory, may persist for months. This is known as the postconcusssion syndrome. Because these complaints are vague and subjective, they sometimes are regarded as being of psycholohical origin. Postconcussion syndrome may need cognitive retraining or psychological support. In moderate head injury, many small haemorrhages and some swelling of brain tissue occur. These contusions are often distributed along the rough, irregular inner surface of the brain and are more likely to occur in the frontal or temporal lobes, resulting in cognitive and motor deficits. Moderate head injury is characterized by a longer period of unconsciousness and may be associated with focal manifestations such as hemiparesis, aphasia, and cranial nerve palsy. In this type of injury, the contusion often can be visualized on CT scan. Severe head injury involves more extensive damage to brain structures and a deeper level of coma than moderate head injury. In severe head injury, primary damage to the brain is instantaneous and irreversible, resulting from shearing and pressure forces that cause diffuse axonal injury, disruption of blood vessels, and tissue damage. It often is acc9ompanied by neurologic deficits such as hemiplegia. Severe head injuries often occur with injury to other parts of the body such as the extremities, chest, and abdomen. Blood may extravasate into the brain; if the contusion is severe, the blood may accumulate, as in intracranial haemorrhage. Similarly, when laceration of the brain directly under the area of injury occurs, especially if the skull is fractured, haemorrhage may be sufficiently extensive to form a hematoma. www.medicalvillage.blogspot.com for more medical notes
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