TRIPASS XR تري باس

 

Cerebral circulation is dictated by the cerebral perfusion pressure (CPP), and ensuring adequate blood flow is

of the utmost importance in patients with TBI. The CPP is

proportional to the difference between the mean arterial

pressure (MAP and the intracranial pressure (ICP) (CPP oc

• Patients with intracranial hemorrhage can quickly deteriorate and require frequent neurologica l re-eval uations.

• Limit secondary brain injury by identifying and addressing concu rrent hypoxemia, hypotension, and increased

intracranial pressure.

MAP - ICP). The intracranial space is a fixed volume, and

the ICP is determined by the amount of brain tissue,

blood, and cerebrospinal fluid (CSF) within it. Increases in

Table 85-1. Glasgow Coma Scale (GCS).

Eye Opening

Spontaneous

To verbal command

To pain

No response

Best Motor Response

Obeys commands

Localizes to pain

Withdraws to pain

Abnormal flexion

Abnormal extension

No response

Best Verbal Response

Oriented, converses

Confused

Inappropriate

Incomprehensible

No response

4

3

2

6

5

4

3

2

5

4

3

2

363

CHAPTER 85

either of these variables will cause secondary elevations in

the ICP. The brain can autoregulate cerebral perfusion

under normal physiologic conditions, but cannot do so at

the extremes of either MAP or ICP. Therefore, processes

that significantly decrease the MAP ( eg, traumatic shock)

or increase the ICP (eg, intracranial hemorrhage) may

impair cerebral perfusion and exacerbate secondary brain

injury.

The following is a list of specific injury patterns seen in

patients with TBI:

Concussions represent a traumatic alteration in

neurologic function in the absence of abnormalities

on computed tomography (CT) imaging. Symptoms

including recurring headaches, sleep disturbances,

and difficulties with concentration that can persist for

months (postconcussive syndrome).

Skull fractures can be categorized by location

(basilar vs calvarium), pattern (linear, depressed,

or comminuted), and by whether they are open or

closed injuries.

Cerebral contusions represent punctate intraparenchymal hemorrhages with surrounding edema and occur

most commonly in the frontal, temporal, and occipital

lobes. Contusions that occur both at the direct site of

injury and the opposing side of the brain secondary

to indirect deceleration forces are known as coup and

contrecoup injuries, respectively.

Traumatic subarachnoid hemorrhage (SAH) is the

most common abnormality recognized on posttraumatic CT imaging. Traumatic SAH occurs when injury

to the small subarachnoid vessels leads to secondary

hemorrhage within the subarachnoid space.

Subdural hematoma (SDH) is most commonly

encountered in patients with significant cerebral atrophy (elderly, alcoholics). They occur when excessive

shearing forces injure the small bridging veins in the

subdural space. SDHs classically appear on CT imaging as crescent-shaped hematomas that freely cross

suture lines. As a distinct history of trauma may not

be present, always maintain a high index of suspicion

in elderly patients with nonspecific mental status

changes.

Epidural hematoma (EDH) is most commonly seen in

patients with temporoparietal skull fractures and secondary injury to the middle meningeal artery. They occur

when high-pressure arterial bleeding separates the dura

from the inner table of the skull to form a hematoma.

EDHs are classically lentiform or bean-shaped in appearance on CT imaging and do not cross the cranial suture

lines (Figure 85-1). The classic presentation is a patient

with blunt head trauma who initially appears well after

the injury (the so-called lucid interval) only to rapidly

decompensate several hours later.

Diffuse axonal injury (DAI) occurs when sudden deceleration mechanisms transmit shearing forces diffusely

Figure 85-1. CT sca n of the head showing an

epidural (patient's left) and a subdural (patient's

right) hematoma.

across the axonal fibers of the brain. CT imaging is

nonspecific, and patients tend to have poor outcomes.

Penetrating brain injury is usually catastrophic because of the immense amount of kinetic energy transmitted to very sensitive brain tissues. Mortality rates

from gunshot wounds to the head approach 90%.

In addition to the specific injury patterns listed previously, TBI can lead to drastic increases in ICP, resulting in

herniation. Transtentorial herniation of the temporal lobe

uncus is the most common form and typically presents

with altered mental status and a dilated or blown pupil

secondary to compression of the oculomotor nerve ( cranial nerve [CN] III). Transforaminal herniation of the

cerebellar tonsils through the foramen magnum can occur

with significant increases in the ICP, especially with poste ­

rior fossa hemorrhages, and is rapidly fatal due to compression and consequent dysfunction of the brainstem.

CLINICAL PRESENTATION

� History

Always attempt to identify the exact mechanism of injury,

as this may predict the severity of damage to the central

nervous system (CNS). For example, clarify the height of a

fall, the speed of a motor vehicle collision (MVC), or the

use of seatbelt restraints or airbag deployment. Emergency

medical service personal can be invaluable in this setting.

Inquire about any loss of consciousness, as this may

portend more significant injury. The antecedent use of

alcohol or illicit drugs may complicate the neurologic

assessment, and their influence should be documented.

Ask about the use of any prescription or over-the-counter

medications, as anticoagulants can induce life-threatening

bleeding despite only minor injury. Finally, look for any

signs and symptoms suggestive of increased ICP (altered

mental status, vomiting, headache), as this will require

emergent neurosurgical intervention.

..... Physical Examination

As with all trauma patients, begin with a rapid primary

survey, and aggressively address any emergent life threats.

Carefully note vital signs, as they can predict the likelihood

of secondary brain injury. Cushing reflex, defined as pro ­

gressive hypertension, bradycardia, and a decreased respiratory rate, is frequently indicative of a potentially

life-threatening increase in ICP.

A gross inspection of the scalp may reveal gaping lacerations or obvious cranial deformities. Carefully inspect

all deep lacerations for violation of the galea, as disruption of this tough layer of connective tissue mandates

careful primary closure. Palpate the skull to detect stepoff deformities indicative of underlying fracture. Examine

the eyes and the ears for any signs of injury. Battle sign

(retroauricular ecchymosis), raccoon eyes (periorbital

ecchymosis), hemotympanum, and CSF rhinorrhea or

otorrhea are all signs of an underlying basilar skull frac ­

ture (Figure 85-2). Carefully palpate the cervical spine

and always assume an occult C-spine injury until proven

otherwise.

Perform a comprehensive neurologic exam to identify

any findings suggestive of significant injury. Examine the

pupils, taking care to note size, symmetry, and reactivity.

A dilated unresponsive pupil in the setting of cranial

trauma indicates transtentorial herniation until proven

otherwise. Document an initial GCS and repeat fre ­

quently to detect any signs of decompensation. The unco ­

ordinated flexion (decorticate) or extension (decerebrate)

of one's upper extremities on painful stimulation indicates severe intracranial injury with possible brainstem

compromise.

Figure 85-2. "Raccoon eyes" suggestive of a basilar

skull fracture.

HEAD I NJURI ES

DIAGNOSTIC STUDIES

..... Laboratory

A routine trauma panel including a complete blood count,

chemistry, coagulation studies, and toxicology screening

should be ordered on all patients with significant multisystern trauma. That said, there are no laboratory studies

specific for the diagnosis or management of TBI.

..... Imaging

An emergent noninfused head CT is the study of choice for

the evaluation of patients with potential TBI. It is quick,

noninvasive, and highly sensitive for the diagnosis of both

bony and intracranial injuries. Patients who present more

than 48 hours after injury may require intravenous (IV)

contrast to delineate the presence of isodense subdural

hematomas. CT imaging does expose patients to poten ­

tially harmful ionizing radiation, and the patient's clinical

presentation should always guide the decision to image.

Indications for CT imaging in adult patients are debatable, but most agree that any of the following findings warranttesting: GCS <15, age >65 years,high-energymechanisms

(fall >3 ft) focal neurologic deficits, �2 episodes of vomiting,

evidence of depressed or basilar skull fracture, posttraumatic

seizure, persistent anterograde amnesia, persistent severe

headache, or the presence of coagulopathies. The indications

for CT imaging in pediatric patients are similarly debatable

but typically include the presence of any of the following: loss

of consciousness, abnormal mental status, vomiting, palpable

skull fracture or signs of basilar skull fracture, scalp hemato -

mas, and high-energy mechanisms.

PROCEDURES

Severe TBI patients with subdural or epidural hematomas

and evidence of impending or evolving herniation require

intracranial decompression and clot evacuation via emergent burr-hole placement performed by a neurosurgeon or

emergency physician.

MEDICAL DECISION MAKING

The primary survey and presenting GCS should guide the

work-up and management of patients with TBI. The

differential diagnosis should include all of the aforementioned conditions, including cerebral contusions, intracranial hemorrhage, and DAl. Rapidly decompensating

patients should be considered evolving herniations until

proven otherwise. Emergent CT imaging will help establish

the proper diagnosis and guide further treatment

(Figure 85-3).

TREATMENT

The management of TBI begins with the primary survey.

Patients with severe TBI (GCS :s;8) require emergent endotracheal intubation to maintain airway protection. Perform

GCS 1 5, minor mechan ism,

age < 60, no anticoagulant

use, AND no neurologic

deficit, vomiting,

intoxication, headache, or

seizure activity

DC home with

competent caregiver

CHAPTER 85