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07.qxd 3/10/08 9:35 AM Page 289<br />

intoxication is a very common factor, being found in from<br />

one-third to one-half of all cases (Corrigan 1995). Although<br />

multiple forms of brain injury may occur, this syndrome<br />

refers primarily to cases occurring with sudden ‘acceleration–deceleration’,<br />

as during a motor vehicle accident or a<br />

fall or blow to the head; trauma due to gunshot wounds and<br />

crush injuries are not considered here. This chapter will discuss<br />

the clinical features and treatment of the various<br />

aspects of traumatic brain injury, the etiology of these clinical<br />

features, and the differential diagnosis between traumatic<br />

brain injury and concussion.<br />

Clinical features and treatments<br />

In considering the clinical features (and their treatments)<br />

of traumatic brain injury, it is convenient to divide them<br />

into two groups, namely an acute phase and a chronic phase.<br />

The acute phase, from a neuropsychiatric point of view, is<br />

often dominated by a delirium; as the confusion clears,<br />

patients gradually enter into the chronic phase, which in<br />

turn may be characterized by numerous sequelae, including<br />

cognitive deficits that may, at times, be severe enough<br />

to constitute a dementia.<br />

ACUTE PHASE<br />

Almost all patients with significant traumatic brain injury<br />

will sustain a loss of consciousness, of variable duration,<br />

immediately after the injury. Those who do survive will<br />

typically emerge into a delirium. This delirium, in addition<br />

to such characteristic symptoms as confusion, disorientation,<br />

and decreased short-term memory, is also often<br />

marked by hallucinations, delusions, and, especially, agitation,<br />

which is seen in the majority of cases (Rao and<br />

Lyketsos 2000; van der Naalt et al. 2000).<br />

It must be borne in mind that although the delirium in<br />

such cases is generally due to the intracranial injuries directly<br />

caused by the trauma, that other factors, as discussed in<br />

Section 5.3, may also be involved as the hospitalization proceeds.<br />

Toxicity from such medications as opioids, baclofen,<br />

anticholinergics, metoclopramide, and even amantadine<br />

must be considered, along with metabolic factors, such as<br />

hyponatremia, hypoglycemia, hypomagnesemia, and systemic<br />

effects of infections, such as pneumonia. Other metabolic<br />

factors to consider relate to the frequency with which alcoholism<br />

is involved, and include Wernicke’s encephalopathy<br />

due to thiamine deficiency and delirium tremens. Consideration<br />

may also be given to the effects of global cerebral<br />

ischemia secondary to severe hypotension and, in those with<br />

fractures of long bones, to the fat embolism syndrome.<br />

Treatment of patients during the acute phase is, at least<br />

initially, generally undertaken in either a trauma unit or an<br />

ICU. Neurosurgical treatment may be required for evacuation<br />

of epidural or subdural hematomas or large contusions<br />

or intracerebral hemorrhages, and serial CT scans<br />

are obtained. In comatose patients, intracranial pressure<br />

7.5 Traumatic brain injury 289<br />

monitoring is often indicated, and treatment with intravenous<br />

sedation, mannitol, and other agents may be<br />

required to reduce pressure. Intubation is often required,<br />

and pneumonia is a frequent occurrence.<br />

Treatment of delirium, in all cases, involves simple environmental<br />

measures designed to reduce confusion. These<br />

include, whenever possible, having the patient in a quiet<br />

room, with a window. Large calendars and digital clocks<br />

should be in full view, and the nurse’s call button should be<br />

readily available. Sleep is essential and consequently the<br />

room should be darkened and very quiet at night, and all<br />

non-emergency procedures (e.g., vital signs, weights, baths,<br />

laboratory testing) should be forbidden during the sleeping<br />

hours. Restraints may occasionally be required and can be<br />

life-saving. For patients prone to get out of bed unsupervised,<br />

keeping the bedrails up may be sufficient; if not, or if<br />

these are impractical, utilizing a ‘low-boy’ bed, surrounded<br />

by mats, may help prevent injury. In some cases, roundthe-clock<br />

sitters may be required.<br />

In cases where these environmental measures are ineffective,<br />

pharmacologic treatment may be considered with either<br />

an antipsychotic or, in certain emergent cases, lorazepam.<br />

Antipsychotics are indicated for treatment of hallucinations<br />

or delusions, and are also effective for agitation. A secondgeneration<br />

agent, such as risperidone, is often used, and, in<br />

practice quetiapine and olanzapine are also utilized. Initial<br />

doses should generally be low, for example 0.5–1 mg of<br />

risperidone, 12.5–25 mg of quetiapine, and 2.5–5 mg of olanzapine.<br />

The first-generation agent haloperidol is also often<br />

used, with initial doses of 2–5 mg. Repeat doses, in approximately<br />

similar milligram amounts, may then be given every<br />

hour or so until the patient is calm, limiting side-effects<br />

occur, or a maximum dose is reached: rough guidelines for<br />

dose maxima are 5 mg for risperidone, 150 mg for quetiapine,<br />

20 mg for olanzapine, and 20 mg for haloperidol. In<br />

cases when the patient responds satisfactorily, a regular daily<br />

dose is ordered for the next day (with the total daily dose<br />

approximately equivalent to the total required initially),<br />

divided into two or three doses. Provision is also made for<br />

further as-needed doses, with the total daily dose being<br />

adjusted according to the amount needed in p.r.n. doses. The<br />

eventual maintenance dose is then continued until the<br />

patient has been stable for a significant period of time, at<br />

which point it may be gradually tapered. Lorazepam is very<br />

commonly used, and given the rapidity of its effectiveness<br />

when given intravenously, has a place in emergent situations;<br />

however, given that lorazepam may also worsen confusion, it<br />

is appropriate to substitute another agent as soon as this is<br />

practical. If lorazepam is used, one may give anywhere from<br />

0.5 to 2 mg i.v. every hour as needed until the patient is calm,<br />

limiting side-effects (such as sedation) occur, or a maximum<br />

of approximately 12 mg is reached.<br />

Once patients have been stabilized, general rehabilitation<br />

efforts may be started, including physical, speech, and<br />

occupational therapy. Eventually, most patients are transferred<br />

to a specialized rehabilitation facility, where these<br />

general efforts are continued.

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