Diagnosis and Treatment of Traumatic Brain Injury

8/18/2019 Diagnosis and Treatment of Traumatic Brain Injury

1/22

REFERAT

DIAGNOSIS AND TREATMENT OF HEAD INJURY

Disusun oleh :

Ayu Lestari

1102011057

Kepaniteraan Klinik Neurologi R!D "asar Re#o

"e$#i$#ing :

Dr% Donny &% &a$i' p

R!D "AAR RE() *AKARTA

FAK!LTA KED)KTERAN

!N+,ER+TA -AR+


2/22

DIAGNOSIS AND TREATMENT OF HEAD INJURY

INTRODUCTION

A$ong the .ast array o/ neurologi 'isease hea' inury ranks high in or'er o/

/re3ueny an' gra.ity% +n the !nite' tates trau$a is the lea'ing ause o/ 'eath in persons

younger that 45 years o/ age an' $ore than hal/ o/ these 'eaths are as a result o/ hea'

inuries% Aor'ing to the A$erian Trau$a oiety an esti$ate' 500%000 A$erians are

a'$itte' to hospitals yearly /olloing ere#ral trau$a6 o/ these 75%000 to 0%000 'ie an'

e.en larger nu$#ers $ost o/ the$ young an' otherise healthy are le/t per$anently

'isa#le'%

&ea' inury ini'ene is higher in young people shoing a peak ini'ene in young

a'ults age' 15824 ith seon'ary peaks in in/ants an' the el'erly #eteen the ages o/ 70890%

ales outnu$#er /e$ales 2 to 1 in $ost stu'ies e;ept the .ery young here the ini'ene is

the sa$e in $ales an' /e$ales% The e;ternal auses o/ #rain inury $ay .ary relati.e to the

geographi area %

The #asi pro#le$ in hea' trau$a is at one #oth si$ple an' o$ple;6 si$ple #eause

there is usually no 'i//iulty in 'eter$ining ausation an' o$ple; #eause o/ a nu$#er o/

'elaye' e//et that o$pliate the inury%

+n hea' inury one /at is pree$inent6 there $ust #e the su''en appliation o/ a

physial /ore o/ onsi'era#le $agnitu'e to the hea'% The $ehanial /ators o/ i$portane

in #rain inury are the 'i//erential $o#ility o/ the hea' on the nek an' o/ the #rain ithin

the raniu$ the tethering o/ the upper #rainste$ that allos $o.e$ent o/ the ere#ral

he$isphere aroun' that .erte; an' the striking o/ the #rain on 'ural septa an' #ony

pro$inenes% These $ehanis$ resulting in 'a$age to the struture o/ the raniu$


3/22

Definition

&ea' inury is an aute inury resulting /ro$ $ehanial energy to the hea' /ro$

e;ternal physial /ores% )perational riteria /or linial i'enti/iation inlu'e one or $ore o/

the /olloing:

on/usion or 'isorientation

loss o/ onsiousness

post8trau$ati a$nesia

other neurologial a#nor$alities suh as /oal neurologial signs sei@ure an'?or

intraranial lesion%

These $ani/estations o/ hea' inury $ust not #e 'ue to 'rugs alohol or $e'iations

ause' #y other inuries or treat$ent /or other inuries


4/22

matter. These are found in 20-40% of head injured patients studied by CT. Contusions and

lacerations occur more frequently in the frontal and temporal poles where the brain is

restricted by the frontal and temporal skull base near the sphenoid ridge. They occur beneath

the fracture sites or beneath the site of trauma (coup injuries) and/or opposite the point of injury (contra-coup injuries). Hemorrhagic contusions may be relatively minor in appearance

on initial CT scan. Over time (hours to days), the patient may develop progressive

neurological deterioration. In such instances, subsequent CT scan may reveal evolution of the

contusion into a frank intracerebral hematoma, so called delayed traumatic intracerebral

hematoma (DTIC).

Epidural hematomas occur in 5-15% of fatal injuries. They are usually caused from

bleeding from a meningeal artery - most often the middle meningeal artery. Occasionally they

result from tears in the capital or transverse sinuses with slower onset of symptoms. 85% of

epidural hematoma patients have a skull fracture. The patient may have a lucid interval

between injury and coma, but this interval may occur with all conditions listed below seventy

to eighty percent are in the temporal fossa, but they can occur at any location. If the patient is

comatose from the onset, other types of brain damage are present.

Subdural hematoma results from tearing and stretching of parasagittal bridging

veins resulting from rapid acceleration of the brain. They are more common from falls and

assaults than vehicular accidents. Arterial bleeding may account for 30% of these hematomas.

Subdural hematomas can occur in "pure" form, but many are associated with contusions and

diffuse brain injury.

Intracerebral hematoma: In closed head trauma, the causes and mechanisms are

much the same as for contusions. They are most common in the frontal and temporal poles

and they are often associated with extracerebral hematoma. Linear fractures occur in 10-50 %

of cases.


5/22

Diffuse Brain Injury

These are associated with widespread disruption of neurological function, without

obviously visible brain lesions on imaging studies. They are caused by inertial or acceleration

effects of the forces applied to the head. Rotational acceleration is thought to be the primary

mechanism causing diffuse brain injuries can be further classified as:

Mild concussion: There is temporary disturbance of neurological function without

loss of consciousness, usually with mild contusion and disorientation. The patient may not

come to medical attention and may have amnesia of five to ten minutes.

Classical cerebral concussion: There is temporary: reversible loss of consciousness

lasting less than six hours. The patient always has some retrograde amnesia and post

traumatic amnesia. Patients should be observed for subsequent development of intracranial

hematoma.

Diffuse axonal injury (DAI): This is pathologically characterized by axonal damage

or actual tissue tears and small blood vessel tears. Axons form "retraction balls' which later

appear as diffuse astrocytosis and demyelination. Diffuse axonal injury can be further

classified into mild, moderate and severe with corresponding difference, of duration of corna,

neurological findings, and degree of recovery:

Evaluation of closed head trauma

The history of an accident, nature of and circumstances of injury and condition after

an accident will aid in further evaluation of patient and subsequent management.


6/22

The initial neurological evaluation is brief to assess the level of consciousness and the

presence of focal neurological deficits. A useful and now widely used scale of measurement

is the Glasgow Coma scale. (See: Neurological Exam). This is used to triage patients and to

grade the clinical course during treatment. For instance, with patients unable to speak orfollow commands, the incidence of intracranial mass lesions requiring surgery ranges from

40%-60%.

After initial examination, a thorough examination is required. Often in major head

trauma, other organ systems can be severely injured. In these cases there is a need to treat

multiple systems simultaneously. Immobilization of the spine may be indicated since 5%-

10% of head injury patients have an associated spine or spinal cord injury. Thoracic,

abdominal and skeletal injuries must be identified and managed.

Airway maintenance is of primary importance. The oropharynx must be cleared of

debris or secretions. Intubation may be requited with cure not to extend the neck if cervical

spinal assessment has not been done.

Hypotension is hardly ever a result of intracranial bleeding unless, the medulla is

already compromised. In open head injuries, blood loss from scalp laceration can besignificant, particularly in infants and children. But, in the usual setting, other causes of shock

mast be sought. Hypotension, however, can result from spinal injury by disrupting

sympathetic tone to the peripheral vasculature.

Physical examination: It is impossible to outline an exam appropriate for all patients

because of the enormous variations in individual injuries. Some with minor head trauma are

awake and cooperative; others with multisystem, major trauma are comatose and require

examination by many physicians simultaneously. The order and priority of examination is

unique to each situation.

Inspection of cranium: Areas of scalp confusion and swelling may overlie sites of

linear or depressed fractures.


7/22

Evidence of basilar fracture.

a. Raccoon eyes: blood staining of periorbital tissue.

b. Battle's sign: ecchymosis around mastoid, air sinuses

c. Drainage of CSF from nose or ear (rhinorrhea or otorrhea, respectively).

d. Hemotympanrrm or laceration of external auditory canal.

e. Facial fracture. LeFort fracture: palpate stability of facial bones and orbital rims.

f. Palpation of mandible.

g. Orbital injury. Inspection of globe. Note presence of proptosis or edema of

conjunctiva.

h. Auscultation of neck and eye or head for bruits may reveal carotid cavernous fistula

or carotid artery injury such as a traumatic dissection or pseudoaneurysm.

Neurological examination: The initial exam serves as a baseline for future

assessment of improvement or deterioration and must be well documented.

Level of consciousness. The Glasgow Coma Scale (GCS) is used for standardized

numerical assessments useful for following the individual patient and making comparisons

with information from institutions treating head trauma. It provides a qualitative measure of

neurological injury-severity based on eye opening, verbal responsiveness, and motor

response. A mild injury is GCS of 13 to 15, moderate 8-12,

EYE OPENING GLASGOW COMA

SCALE

Spontaneous 4

To verbal command 3


8/22

To pain 2

None 1

BEST MOTOR RESPONSE

Obeys verbal commands 6

Localizes pain 5

Withdrawal 4

Flexion/abnormal

(decorticate)

3

Extension (decerebrate) 2

None 1

BEST VERBAL RESPONSE

Oriented, conversing 5

Disoriented, conversing 4

Inappropriate words 3

Incomprehensible sounds 2

None 1

Total 3-15

In patients who are communicating, a more detailed exam of orientation is appropriate

Cranial Nerve Exam. Pupil reaction to light is most important. Pupillary inequality

may signal partial or complete III N palsy as a result of an ipsilateral compression by theuncus into the tentorial notch. Rarely, it may result from contralateral herniation. In either


9/22

case, the finding is of extreme importance requiring urgent diagnosis and treatment to prevent

further effects of herniation. Rarely optic nerve compression or transaction may produce this

finding. Pupillary size reflects levels of damage to the brain stem. Damage to diencephalons

or pons causes small, but reactive pupils. Damage to the tegmentum of mid brain or thirdcranial nerves result in dilated fixed pupils. Mid position, non-reactive pupils may occur with

more diffuse mid brain injury. Drugs or drops which may after pupillary size should be

avoided in the setting of acute trauma as this will effect the ability to appropriately monitor

the patients neurological exam.

Funduscopic exam. Examine for retinal or pre-retinal hemorrhage. Papilledema is

rarely seen soon after trauma.

Corneal reflexes tests fifth cranial nerve sensation and integrity of brain stem

connections to the seventh cranial nerve.

Facial nerve. Complete paralysis usually indicates peripheral injury. Partial paralysis

may indicate a variety of central causes i.e. cortical through brain stern.

Olfactory nerve function may be lost after blunt injury. This is often due to damage

to the nerves at the cribriform plate. It is rare for the remaining lower cranial nerves to be

impaired in awake patients; but they should be tested when possible.

With deeply comatose patients oculocephalic reflexes may be appropriate to test. In

the absence of cervical spine injury, “dolls eye maneuver" can be done. The eyes deviate

from the direction of head motion and rapidly return to neutral. With a unilateral mid brain

lesion, the ipsilateral eye will not adduct, but the eyes contralateral to the lesion deviates

away from the directions of head motion. With lesions of the mid pons there is no reflex. Ice

water caloric testing may be used to assess the same reflexes, but this test consumes more


10/22

time.

Motor exam: Assesses functions of motor tracts from the brain through the spinal

cord. In the awake patient, a complete exam is possible. In comatose or uncooperative

patients responses to noxious stimuli are required to identify posturing responses as distinct

from voluntary. Decorticate posturing (flexion of elbows, wrists, and fingers and extension of

lower extremities may be seen with lesions above the mid brain. Decerebrate posturing

(extension, adduction and pronation of upper extremities and extension of lower extremities

with foot plantar flexed) is seen with lesions below the upper mid brain and above the

vestibular nuclei.

Sensory loss can be partially assessed in comatose patients when testing for motor

responses. If spinal cord injury is suspected, rectal exam should be done to assess rectal tone

and the bulbocavernosus reflex. Sensory exam in the awake patient should assess pin and

touch in the major dermatomes of the spinal cord as well as posterior column function

(vibration, and joint position).

Reflexes: Test deep tendon reflexes of four extremities and plantar reflexes. In the

absence of reflexes, spinal cord injury may be suspected. Anal wink and bulhocavernosus

reflex should be tested.

Brain Herniation may occur under the falx, through the tentorial notch either on one

or both sides, or through the foramen magnum. At the time of initial evaluation, one or all

may have occurred but in the less severely injured patient, careful and frequent assessment is

demanded for early detection.


11/22

Central herniation results from diffuse bilateral supratentorial swelling or mass

effect with downward displacement of all supratentorial structures with progressive loss of

brain function in a rostro caudal direction. Changes in mental status progress with increasing

(drowsiness to confusion to agitation to coma. Breathing “irregularities" with pauses, small

but reactive pupils, increased muscle tone, Babinski signs and posturing then occur. If

therapy is unsuccessful, continued mid-brain function is lost with eventual loss of all

brainstem function and death.

Uncal, or lateral herniation, occurs from lesions (such as hematomas) or swelling

causing the medial edge of the temporal lobe (uncus) to herniate over and through the

tentorial notch. Dilation of the ipsilateral pupil is an early sign and may occur with or without

alteration in mental status initially. Progression of herniation may produce complete third

cranial nerve palsy associated with contralateral motor paresis and loss of consciousness from

mid-brain compression. Occasionally, ipsilateral hemiparesis will occur from compression of

the opposite cerebral peduncle against the contralateral tentorial edge (Kernohan’s notch

phenomenon). If not treated successfully, progressive loss of midbrain function continues as

in central herniation.

Cerebellar tonsil herniation through the foramen magnum usually occurs from

lesions within the posterior fossa. Depression of consciousness, alteration of respiratory

rhythm, dysconjugate gaze and vertical nystagmus may signal its beginning and respiratory

arrest the end.

Clinical assessment including radiographic studies: After one has obtained the

history and accomplished the necessary physical and neurological exanimation and

resuscitation measures a decision regarding likelihood of significant intracranial injury is

made. Patients can be placed in low, moderate, and high risk groups based on physical

findings and neurological examination.


12/22

Low risk: Asymptomatic, and/or headache, dizziness, scalp hematoma,

scalp laceration, contusion or abrasion and absence of the moderate or high risk criteria.

Moderate risk: Change of consciousness, at or subsequent to injury, increasing

headache, alcohol or drug ingestion, inadequate history, age


13/22

quickly available, safe, fast and can be performed on patients with serious and multiple

injuries. It can demonstrate hematomas, subarachnoid blood, contusion, cerebral swelling,

ventricular and subarachnoid cistern compressions. Fractures of the skull can be seen well

with the use of boric windows on CT. Immediate decisions regarding surgical treatment canbe made.

MRI is rarely used at present for emergency evaluation of intracranial

trauma. It takes much longer, is cumbersome to use with resuscitation equipment, and may

be contraindicated in patients with implanted metal devices. However, its multiplanar

capacities demonstrate pathology more accurately, particularly in brain stem and posterior

fossa. Its brain use is in assessment of patients in subacute stage of injury.

Skull x-rays: Routine use of skull x-rays is controversial. They affect management in

only 0.4% to 2% of patients. A linear fracture implies that great force to skull occurred. 213

of patients hospitalized with skull-fracture have significant intracranial injury. Therefore, the

use of skull x-rays is dictated by risk assessment of injured patient (see above). In most

instances, CT provides adequate information regarding skull fractures as, well as superior

imaging of the intracranial contents, and therefore skull films are not needed.

Spine films. It the nature of injury and other risk factors are present, cervical spine

films should be made. The cranio-cervical juncture to C7 must be visualized. Specialtechniques such as a swimmer’s view may be required to visualize lower cervical spine. If

inadequate visualization is possible with plain x-rays, then spine CT may be required, but

plain x-rays are still the imaging modality of choice to screen for fractures. Similarly,

thoracic and lumbar spine films are indicated depending on history, mechanism of injury and

mental status of patient.


14/22

Management

Pre hospital: Airway maintenance of utmost importance: Thirty percent of severely

head injured patients are hypoxemic in ER. Oral or nasopharyngeal airways or intubation is

required without extension of neck if possible. Hypotension is associated with increased

morbidity and mortality. It is usually due to extracranial causes. At present isotonic saline or

Ringers lactate solution are the fluids most often used initially,

Scalp injuries: Scalp lacerations may cause significant blood toss if multiple or large.

Hemostasis is obtained by pressure or clamping of obvious arterial bleeders. Repair is doneafter thorough cleaning and inspection for foreign material, underlying fractures. Scalp

avulsion may require scalp flap or skin grafting.

Linear skull fractures: Require no treatment, but indicate high probability of

intracranial injury and therefore, a CT scan of the head should be obtained.

Depressed skull fracture: Best assessed by CT scan and skull x-rays. Elevation

required depending on depth-, and location of depression. In infants and children a depression

of a few millimeters may be left alone. Surgical repair of depression over major venous

sinuses may be best avoided because of severe blood loss if the sinus is tamponaded by

fragment removed surgically. Though there is little evidence that elevation of closed

depressed fracture affects neurological outcome, or alters the incidence of seizures, they are

usually elevated to correct cosmetic defects.

Compound skull fractures: Require elevation and debridement and closure of dura it

torn. Bone fragments can be replaced unless there is severe contamination of the wound or

the injury is old and infected.


15/22

Basilar skull fractures: Suspected on clinical grounds CSF rhinorrhea or otorrhea

occur in 5-11 %. Fracture of the ethmoid plate, orbital plate or sphenoid sinus usually cause

rhinorrhea and fracture of petrous portion of temporal bone usually causes otorrhea. Most

CSF leaks (80%) will cease within one week.

Imaging of anterior cranial fossa or temporal bone by tomography or CT with the use

of intrathecal contrast media are sometimes required to demonstrate site of CSF leak.

Controversy exists over tinning and necessity of surgical repair. Some advocate repair in all

patients since development of meningitis later is not uncommon. Others recommend-repair

only if leaks persist more than a week.

Repair is accomplished by either intracranial or extracranial approaches. Endoscopic

transnasal/trans-sinus routes of repair performed in conjunction with otolaryngologist may be

indicated in certain cases In the absence of meningitis the use of antibiotics is not indicated.

Epidural hematoma: Incidence 1 % to 2% of patients admitted for head injury.

Clinical presentation can vary from never unconscious to unconscious at all times, initially

conscious and subsequent unconscious, initially unconscious and subsequent conscious or

initially unconscious, lucid, then unconscious. Depends on severity of initial trauma. Only

one-third have classic "lucid" interval. Symptoms progress rapidly usually within 6hours.

May be delayed, however. Signs and symptoms are as described in the herniation syndrome

section, usually lateral herniation. CT scan is the best diagnostic study, but if not possible and

the patient's condition dictates immediate surgery, a burr note should be made over the

temporal area ipsilateral to the dilated pupil, or area of contusion or fracture. If found, partial

evacuation immediately decreases intracranial pressure (ICP) and is followed by craniotomy

or craniectomy to remove all clot and control bleeding site. If nothing is found, frontal and

parietal burr holes can be placed on one or both sides. In most cases, CT scan can be done

and the surgical flap tailored appropriately. Delay in diagnosis is the main cause of mortality

and morbidity. Mortality varies from 5%-43%. Mortality is less in younger patients.


16/22

Additional brain-injury (subdural hematoma, intracerebral hematoma or contusion) triples the

mortality.

Acute subdural hematoma: About one-third are "simple" subdural hematomas and

the rest are associated with cerebral contusion, intracerebral hematoma and/or diffuse axonal

injury. Patients on anticoagulation have increased risk following trauma. The spectrum of

clinical presentation is similar to extradural hematoma (see above). One third to one-half of

patients have pupillary inequality, half have hemiparesis and other findings of herniation. CT

scanning is the diagnostic.-procedure of choice disclosing the presence of clot, degree of shift

and intra-axial lesions.

If the subdural is less than 1 cm thick, it may be observed, but it must be followed by

repeat scans. Comatose patients with thin hematomas probably have parenchymal damage

and need to be aggressively monitored with imaging or ICP monitoring.

Subdural hematoma > 1 cm or with significant mass effect requires operative

treatment usually with a large craniotomy flap over the appropriate area and removal of as

much clot as possible. Associated "burst" injuries of frontal or temporal poles, may be

resected at same time. Burr holes may be used to search for clot if a CT scan was not done,

but adequate removal is rarely possible. Comatose patients treated within four hours fare

better than those treated later with 30%, vs. 90% mortality. Also, patients over 65, those

injured in motorcycle accidents, and those with ICP >45 post-operatively fare worse.

Chronic subdural hematoma. Subdural hematoma detected after the acute injury.

Three-fours are over 50 years of age. Over age 70, the incidence increases sharply to

7.4/100,000/yr. History of trauma is obtained in only 50% to 75% of patients and may be

mild. Contributing factors are alcoholism and seizures. CT and MR scans are the best


17/22

diagnostic modalities. Chronic subdural hematomas may be bilateral so no midline shift is

evident. Some are isodense on CT and the scan can easily be misinterpreted. Cerebral

angiography is very accurate, but rarely required today. Depending on their size, chronic

subdural hematomas may be managed operatively or medically.

Treatment of chronic subdural hematomas:

Operative

Burr hole. Bulk of hematoma is drained rapidly and the drain is attached to closeddrainage system-for next 24-48hrs.

Crainotomy is occasionally required for solid, organized or loculated chronic subdural

hematomas.

Subdural-peritoneal or subdural atrial shunt occasionally is required, particularly in

pediatric patients.

Medical: For asymptomatic or mildly symptomatic collections, use of low dose

steroids, rest, is successful. Serial CT scans required to assess resolution.

Cerebral contusions and hematoma. Management is often not clear cut. CT scans

are required to assess the size and extent. Some require lop monitoring and appropriate

management of ventilation and osmotic agents. Frontal and temporal pole contusions may

require removal on one or both sides. Sudden herniation may occur 1-2 weeks after injury

because of delayed enlargement, necrosis and swelling


18/22

Hematomas of posterior fossa are relatively uncommon when compared to

supratentorial space. Incidence reported from 3%-13% of all extradural hematomas and 1%

of subdural hematomas. Occipital skull fracture is found in two-thirds or more. Headache

and stiff neck are the most common symptoms. Cerebellar signs are seen in less than half and

may be confused with lesions elsewhere. Many patients may die undiagnosed. CT scan is the

best imaging study, but may require special positioning and more frequent cuts to detect

Hydrocephalus is present in one-third of patients and supratentorial lesions in about one-half.

Surgical removal is, required and with extradural hematomas the clot may extend above the

transverse sinus requiring exploration above it. Mortality is reported front 15% to 24% for

extradural hematomas and 42%-70% for subdural hematomas.

Gunshot injuries: Approximately 70% of patients die at the scene of injury. Injury

severity is dependent on size and type of missile and velocity of injury. Flaccid patients all

die. Decerebrate patients have a mortality of 95%-97%. CT scan is the best initial study for

detection of bone fragments, course of missile, hemorrhage and swelling. For viable patients,

surgery is required to remove hematoma, nonviable brain, missiles and bone fragments when

feasible, and to repair and close the dura and scalp. Depending on the severity of injury,

surgery may be done through a small craniectomy or it may require a large flap to deal withextensive bilateral brain damage. Retained bone-fragments may cause delayed abscess

formation requiring further surgery.

Medical Management of Severe Head Injuries: The basic goals are to maintain

normal blood pressure, adequate arterial oxygenation, control body temperature (hypothermia

worsens outcome) and fluid and electrolyte balance.

Management of Raised ICP: Control of elevated intracranial pressure is the most

important treatment modality for head injured patient. Approximately 40% of patients with

loss of consciousness will develop intracranial hypertension at some point during treatment

and its level is a strong predictor of outcome. Upper limits of normal in adults and older

children is 10-15 mmHg, children 3-7 mmHg and infants 1.5 6 mmHg. Cerebral blood flow

in the critical parameter for brain survival and depends on cerebral perfusion pressure (CPP)which is defined as: CPP=MAPBICP. MAP is mean arterial pressure; ICP is intracranial


19/22

pressure. Therefore, careful control of systemic blood pressure and ICP is vital in severe head

injury. One episode of hypotension (SRP=90) after injury increases mortality 50% compared

to 27% without. Hypoxia also plays a significant role. Treatment of small rises in ICP may

prevent later uncontrollable elevations of ICP. The goal of therapy is to keep ICP below 15-20 mmHg and maintain CPP above 50 mmHg.

Patient position: Elevate head 30-35° and prevent venous outflow obstruction in the

neck by maintaining a neutral plane of the head and thorax. There is no neck compression by

external object; such as a cervical collar or tape.

Anticonvulsants are usually given to prevent post traumatic seizures which may raise

ICP in obtunded or comatose patients, even if pharmacologically paralyzed.

Fluids usually are isotonic at 75-150 cc/hr in adults. In multi-injured patients, more

complicated management is required.

Antacid or H2 antagonists are given to any patient on steroids. They help prevent

stress ulcers also.

Corticosteriods: There is no clear evidence of benefit of these agents on outcome in

head injury, but they appear to provide a small benefit for patients with spinal cord injury.

Corticosteroid increase complications of infection, hyperglycemia aseptic necrosis.

Intubation is usually required if the GCS is 7 and for any evidence of respiratory

distress.

ICP monitor is usually used if GCS is < or = 8. The patient should have undergone:


20/22

full evaluation for systemic trauma, have IV access, a central venous line, arterial blood

gases; and appropriate scans or films of the head and other systemic injuries. If the CT scan

shows a surgical lesion, the patient is taken to the operating room and ICP monitors are

installed at the end of the procedure if appropriate. If the CT does not indicate surgery, anICP monitor is placed in the ICU. There are various types of monitors. An intraventricular

catheter is most accurate and allows removal of CSF which may help control ICP. It may be

difficult to insert if the lateral ventricles are small. It can become occluded and dive

erroneous information. There is slightly higher risk of causing hemorrhage at the site of

insertion. Other types are: subarachnoid screw (bolt), subdural, epidural, and

intraparenchyrnal (Camino fiberoptics). All monitoring devices have problems with

maintenance of accuracy and may become infected with prolonged use.

Measures to reduce ICP:

Hyperventilation reduces PCO2 to 25-30 mmHg, which causes vasoconstriction and

reduces intracranial blood volume. It will decrease ICP 25% to 30% in most patients. It will

lose its effect with repeated prolonged use and can worsen ischemia in area of impaired

perfusion Hyperventilation should only be used in the setting of acute herniation, but

otherwise should be avoided because of the potential to cause further injury to the brain.

Mannitol is used if ICP remains elevated above 16 mmHg for 10 minutes with patient

at rest. It is given in doses of 0.25 gm/Kg every 4-6 hours. Serum hyperosmolarity caused

by this agent is thought to reduce cerebral edema. However, the mechanism of action is

uncertain. Mannitol may also have a rheological benefit that enhances blood flow. Serum

osmolarity can also be increased by administration of hypertonic saline.

Furosemide is sometimes used with mannitol. It is less reliable when used alone. It


21/22

may exacerbate the dehydrating effects of mannitol and induce hypokalemia.

Barbituate coma is sometimes used in patients with uncontrollable elevations in ICP.

Improvements in the outcome of patients has not been clearly demonstrated. The risk of

hypertension is greater, particularly with the prior existence of cardiovascular compromise.

Its use requires extraordinarily close observation and monitoring capability

Decompressive craniectomy with the removal of a large portion of the frontotemporal

skull is sometimes done if ICP is not controlled by the measures outlined above in patients

with no demonstrated extra- or intracerebral lesion that could be removed. A wide dural

opening may be required. Recovery in 41% of patients has been reported.


22/22

CITITATION

Victor, M., Ropper, A. H., & Adams, R. D. (2001). Adams and Victor's principles of neurology . New York: Medica !"#. Di$isio%, Mcraw'Hi.

oats, . *. (200+). N- ead i%/"r "idei%es. Emergency Medicine Journal, 21(+), +02+02.

Documents

Diagnosis and Treatment of Traumatic Brain Injury