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Brain Edema and Cerebral Edema 

Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content. Diffuse cerebral edema may develop soon after head injury. Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB. Vasogenic edema is frequently associated with focal contusions or hematomas. It eventually resolves as edema fluid is reabsorbed into the vascular space or the brain edema, cerebral edema, adema, brain swelling, herniation

Cytotoxic edema is an intracellular process that results from membrane pump failure. It is very common after head injury and is frequently associated with posttraumatic ischemia and tissue hypoxia. Normal membrane pump activity depends on adequate CBF to ensure adequate substrate and oxygen delivery to

Alteration in Consciousness

Consciousness is a state of awareness of the self and of the environment and requires intact functioning of the cerebral cortices and the reticular activating system (RAS) of the brain stem. An altered level of

Herniation

Cerebral herniation occurs when increasing cranial volume and ICP overwhelms the natural compensatory capacities of the CNS. Increased ICP may be the result of posttraumatic brain swelling, edema formation,

Uncal.

The most common clinically significant traumatic herniation syndrome is uncal herniation, a form of transtentorial herniation (Fig. 31-5) (Figure Not Available) . Uncal herniation is often associated with traumatic extraaxial hematomas in the lateral middle fossa or the temporal lobe. The classic signs and symptoms are caused by compression of the ipsilateral uncus of the temporal lobe on the U-shaped edge of

Central Transtentorial.

The central transtentorial herniation syndrome is demonstrated by rostrocaudal neurologic deterioration caused by an expanding lesion at the vertex or the frontal or occipital pole of the brain. It is less common than uncal transtentorial herniation. Clinical deterioration occurs as bilateral central pressure is exerted on

Cerebellotonsillar.

Cerebellotonsillar herniation occurs when the cerebellar tonsils herniate downward through the foramen magnum. This is usually caused by a cerebellar mass or a large central vertex mass causing the rapid

Emergency Department
Airway.

Rapid sequence induction (RSI) for intubation is an effective method for securing the airway in combative or agitated patients.

Hypotension.

If hypotension is detected at any time in the course of the emergent management of a head-injured patient, a cause should be sought other than the head injury. Hypotension is rarely caused by head injury except as a

Hyperventilation.

Hyperventilation to produce an arterial P CO2 of 25 to 30 mm Hg will temporarily reduce ICP by promoting cerebral vasoconstriction and subsequent reduction of CBF. The onset of action is within 30

Osmotic Agents.

Additional therapy for increased ICP includes the use of osmotic diuretics, such as mannitol. In the face of deepening coma, pupil inequality, or other deterioration of the neurologic examination, mannitol may be life saving. Mannitol (0.25 to 1.0 gm/kg) can effectively reduce cerebral edema by producing an osmotic

Mannitol induces an osmotic diuresis and therefore obscures the use of urinary output as a monitor of adequate fluid resuscitation in the multiple trauma patient. Blood pressure must be carefully monitored

Barbiturates.

Barbiturate therapy is occasionally used in severely head-injured patients to reduce cerebral metabolic demands of the injured brain tissue. Barbiturates also affect vascular tone, and inhibit free radical-mediated

Steroids.

Steroids have been shown to reduce vasogenic cerebral edema surrounding brain tumors but have no effect on the cytotoxic cerebral edema that develops and predominates after head injury as a result of

Cranial Decompression.

Under extreme circumstances when all other attempts at reducing ICP have failed, emergency cranial decompression must be considered. Most patients who have been unconscious since the accident, who have erratic or absent respiratory effort, with bilateral fixed and dilated pupils, no spontaneous eye

Seizure Prophylaxis.

Up to 9% of all patients who sustain blunt head trauma suffer from early posttraumatic seizures. The incidence of early posttraumatic seizures approaches 42% in patients who have sustained penetrating head trauma. Although the occurrence of seizures in the immediate posttrauma period has no predictive value for