Increased Intracranial Pressure and Head Trauma

Increased Intracranial Pressure

A limited volume of extra tissue, blood, CSF, or edema fluid can be added to

the intracranial contents without raising the intracranial pressure (ICP). Clinical

deterioration or death may follow increases in ICP that shift intracranial contents,

distort vital brainstem centers, or compromise cerebral perfusion. Cerebral

perfusion pressure (CPP), defined as the mean systemic bp minus the ICP, is

the driving force for circulation across capillary beds of the brain.

CLINICAL MANIFESTATIONS Symptoms of high ICP include headache

(especially a constant ache that is worse upon awakening), nausea, emesis,

drowsiness, diplopia, and blurred vision. Papilledema and sixthnerve palsies

are common. If not controlled, then cerebral hypoperfusion, pupillary dilation,

coma, decerebrate posturing, abnormal respirations, systemic hypertension, and

bradycardia may result.

A posterior fossa mass, which may initially cause ataxia, stiff neck, and

nausea, is especially dangerous because it can compress vital brainstem structures

and cause obstructive hydrocephalus. Masses that cause raised ICP also

distort midbrain and diencephalic anatomy, leading to stupor and coma. Brain

tissue is pushed away from the mass against fixed intracranial structures and

into spaces not normally occupied. Herniation syndromes include (1) medial

cortex displaced under the midline falx : anterior or posterior cerebral artery

occlusion and stroke; (2) uncus displaced through the tentorium, compressing

the third cranial nerve and pushing the cerebral peduncle against the tentorium

:ipsilateral pupillary dilation, contralateral hemiparesis, and posterior cerebral

artery occlusion; (3) cerebellar tonsils displaced into the foramen magnum,

causing medullary compression : cardiorespiratory collapse; and (4) downward

displacement of the diencephalon through the tentorium.

TREATMENT

Elevated ICP may occur in a wide range of disorders including head trauma,

intracerebral hemorrhage, subarachnoid hemorrhage (SAH) with hydrocephalus,

and fulminant hepatic failure. A number of different interventions may

lower ICP, and ideally the selection of treatment will be based on the underlying

mechanism responsible for the elevated ICP (Table 20-1). For example,

in hydrocephalus from SAH, the principal cause of elevated ICP is impaired

CSF drainage; in this setting, ventricular drainage of CSF is likely to be

sufficient. In head trauma and stroke, cytotoxic edema may be most responsible,

and the use of osmotic diuretics such as mannitol becomes an appropriate

early step. As noted above, elevated ICP may cause tissue ischemia.

This can lead to reflex cerebral vasodilatation that further worsens ischemia; paradoxically, administration of vasopressor agents to increase mean arterial

pressure may actually lower ICP by increasing perfusion. ICP monitoring can

guide medical and surgical decisions in pts withcerebral edema. Hypertension

should be treated carefully, if at all. Free H2O should be restricted, and fever

treated aggressively. Hyperventilation is best used for short periods of time

until a more definitive treatment can be instituted. After stabilization and

initiation of the above therapies, a CT scan (or MRI, if feasible) is performed

to delineate the cause of the elevated ICP. Emergency surgical intervention

is sometimes necessary to decompress the intracranial contents. Hydrocephalus,

cerebellar stroke with edema, surgically accessible cerebral hemorrhage

or tumor, and subdural or epidural hemorrhage often require lifesaving

neurosurgery.

Table 20-1

Stepwise Approach to Treatment of Elevated Intracranial Pressurea

Insert ICP monitor—ventriculostomy versus parenchymal device

General goals: maintain ICP _ 20 mmHg and CPP _ 70 mmHg

For ICP _ 20–25 mmHg for _5 min:

1. Drain CSF via ventriculostomy (if in place)

2. Elevate head of the bed

3. Osmotherapy—mannitol 25–100 g q4h as needed (maintain serum

osmolality _320 mosmol)

4. Glucocorticoids—dexamethasone 4 mg q6h for vasogenic edema from

tumor, abscess (avoid glucocorticoids in head trauma, ischemic and

hemorrhagic stroke)

5. Sedation (e.g., morphine, propofol, or midazolam); add neuromuscular

paralysis if necessary (patient will require endotracheal intubation and

mechanical ventilation at this point, if not before)

6. Hyperventilation—to PaCO 30–35 mmHg 2

7. Pressor therapy—phenylephrine, dopamine, or norepinephrine to maintain

adequate MAP to ensure CPP _ 70 mmHg (maintain euvolemia to minimize

deleterious systemic effects of pressors)

8. Consider second-tier therapies for refractory elevated ICP

a. High-dose barbiturate therapy (“pentobarb coma”)

b. Aggressive hyperventilation to PaCO _ 30 mmHg 2

c. Hemicraniectomy

Head Trauma

Head trauma can cause immediate loss of consciousness. If transient and unaccompanied

by other serious brain pathology, it is called concussion. Prolonged

alterations in consciousness may be due to parenchymal, subdural, or

epidural hematoma or to diffuse shearing of axons in the white matter. Skull

fracture should be suspected in pts with CSF rhinorrhea, hemotympanum, and

periorbital or mastoid ecchymoses. Spinal cord trauma can cause transient loss

of function or a permanent loss of motor, sensory, and autonomic function below

the damaged spinal level.

Minor Concussive Injury The pt with minor head injury who is alert and

attentive after a short period of unconsciousness (_1 min) may have headache,

a brief amnestic period, difficulty withconcentration, a single episode of emesis, or mild vertigo; vasovagal syncope may also occur. After several hours of observation, pts with this category of injury can be accompanied home and observed by family or friends. Most pts do not have a skull fracture on x-ray or

hemorrhage on CT. Constant headache is common in the days following trauma;

persistent severe headache and repeated vomiting are usually benign if the neurologic exam remains normal, but in suchsituations radiologic studies should

be obtained and hospitalization is justified.

Injury of Intermediate Severity Pts who are not comatose but who have

persistent confusion, behavioral changes, subnormal alertness, extreme dizziness,

or focal neurologic signs such as hemiparesis should be admitted to the

hospital and soon thereafter have a CT scan. Usually a contusion or subdural

hematoma is found. CT scan may be normal in comatose pts with axonal shearing

lesions in cerebral white matter. Pts with intermediate head injury require

medical observation to detect increasing drowsiness, respiratory dysfunction,

and pupillary enlargement, as well as to ensure fluid restriction (unless there is

diabetes insipidus). Abnormalities of attention, intellect, spontaneity, and memory

tend to return to normal weeks or months after the injury.

Severe Injury Patients who are comatose from onset require immediate

neurologic attention and often resuscitation. After intubation, withcare taken

to avoid deforming the cervical spine, the depth of coma, pupillary size and

reactivity, limb movements, and Babinski responses are assessed. As soon as

vital functions permit and cervical spine x-rays and a CT scan have been obtained,

the pt should be transported to a critical care unit. The finding of an

epidural or subdural hematoma or large intracerebral hemorrhage requires

prompt decompressive surgery in otherwise salvageable pts. Subsequent treatment

is probably best guided by direct measurement of ICP. All potentially

exacerbating factors should be eliminated. Hypoxia, hyperthermia, hypercarbia,

awkward head positions, and high mean airway pressures from mechanical ventilation all increase cerebral blood volume and ICP. Persistently raised ICP after

institution of this therapy generally indicates a poor outcome.