Ⅴ.

Head Trauma
660

Head Trauma
AHMED AMMAR; MARIAM ALRASHID; MUNIR NASSER; HOSAM AL JEHANI;
OSSAMA ABD AL HADI; and ABDUL RAHMAN AL ANIZI
Department of Neurosurgery, King Fahd Hospital of the University, King Faisal
University, Al Khobar, Saudi Arabia

Key words: traumatic brain injury (TBI), Glasgow coma scale (GCS), secondary
brain damage, intracranial pressure

Introduction
Head trauma and traumatic brain injury (TBI) are the most frequent cause of death
in young adults all over the world. TBI is also the leading cause of major disabilities in the
same age group. There are several causes of TBI such as road traffic accidents (RTA),
falling of heights, violence, sports, penetrating wounds, industrial and domestic accidents.
RTA ranked at the top of that list of these causes. A study in Saudi Arabia revealed that
the number of death caused by RTA was estimated to be over 4500 victim over the year
2008, and TBI was the main cause of death of nearly 75% of them. In USA, nearly 50,000
cases of death was reported each year as a result of traumatic brain injury, where 45% of
them were the result of road traffic accidents, and the rest where the result of falls
(26%), assaults (17%), sports injuries (13%), and domestic and industrial injuries.
Males are twice more likely to be injured than females, and most of the victims are under
the age of 30. The annual cost of head injury in USA was reported to be $48.3 billion
dollars. The social and family impacts of the head trauma to young victims are
overwhelming, which definitely affects the socio-economic plan of any country.

Classification of head Trauma

It is rather common that the two terms, head trauma and Traumatic brain injury
(TBI), are used indicating the same meaning. However, to be specific, head trauma may
include brain injury, skull fractures and scalp injury whilst Traumatic Brain Injury
(TBI) as it was defined by Mass AI et al1. is a direct brain damage due to an external force.
TBI and head injury is generally classified based on 3 factors which are; the level of
consciousness as indicated by Glasgow Coma Scale, the period of loss of consciousness
as an immediate result of the impact of the trauma, and post traumatic amnesia.
Therefore, TBI and head trauma may be classified as follow:
1. Severe head trauma; in cases where GCS is 8 or less, loss of consciousness more
than 24 hours and posttraumatic amnesia is for more than one day.
2. Moderate head trauma; in cases where GCS is between 9-12, loss of consciousness
less than 24 hours but more than one hour and posttraumatic amnesia is for a
period between one hour and 24 hours.
3. Mild head trauma; in cases where GCS is between 13-15, and the period of
loss of consciousness less than one hour as the period of post traumatic amnesia.
 Head Trauma 661

Pathophysiology of Head Trauma:

The pathophysiology of head trauma is a complex process, which can be divided into
primary brain injury and secondary brain injury. Primary brain injury is defined as the
direct mechanical injury to the brain right after the trauma or assault. Death results from
direct brainstem injury that causes arrest of respiratory and cardiac centers, or due to
injury of blood vessels. In some cases, massive edema and rapid increase of intracranial
pressure is the cause of death.
Secondary brain injury is a result of physiological and biological cascade of events
which causes deterioration of the clinical condition of the patient from few hours to
several days. Secondary brain damage may be due to calcium and sodium ions influx into
neurons and mitochondria. Brain edema and increase of intracranial pressure and
subsequently decrease of cerebral perfusion pressure is the cause of most fatalities and
neurological complications of head trauma.

Clinical and pathophysiological consideration

The strategy of writing this chapter is to present the different complications and
clinical presentations of head trauma. The pathophysiology is explained in brief. As the
head trauma by definition is an external assault to the head, so we choose to explain the
effect of the head trauma on the scalp followed by skull, then dura related hematomas and
we end by the effect of the trauma on the brain tissue.

History and physical examination in head trauma patients:

Since most patients who present to the ER with a head trauma are confused or
unconscious, important information has to be obtained rapidly through a focused
history and examination. This will insure a better directed management and will provide
valuable prognostic information. The following are suggestions that can be used in
patients presenting to the ER with head injury, though this should be individualized
appropriately.

History
The following important points should not be ignored;
■ Age and gender, in adults the older the patient the worse the outcome especially

those > 65 year of age. Pediatrics tend to deteriorate rapidly. Women tend to
develop more brain swelling and intracranial hypertension after a head injury,
that’s why they appear to do worse than men2 .
■ Mechanism of accident, penetrating injuries versus blunt injuries. The projectiles

that cause penetrating injuries are classified into high-velocity, such as gunshot
and low-velocity, such as knives and arrows. Injuries from high velocity objects
produce extensive tissue damage compared to low velocity objects which produce
focal damage. Penetrating injuries in general exhibit higher risk of infection
and bare a worse outcome. Blunt injuries include, MVA, assaults and falls. In
662 Head Trauma

patients who are involved in MVA, pedestrians do worse than vehicle occupants2.
In pediatrics accidental injuries has to be differentiated from physical abuse.
■ Loss of consciousness, the duration of LOC and wither it was associated with
post-traumatic amnesia is important in determining the severity of the trauma
and predicting outcome.
■ Nausea, vomiting, headache and visual disturbances might indicate increased ICP.
■ Post traumatic seizures
■ Co-morbidities, such as DM and HTN, have been associated with worse outcome.
Tight control of blood glucose proved to improve survival outcome.

The Clinical Examination:

The general examination
■ Vital signs: a combination of hypertension, bradycardia and irregular respirations
is known as the Cushing reflex. It is seen in cases of increased intracranial
pressure but it is neither sensitive nor specific. Irregular respirations might be a
sign of pons or medulla injury. Pyrexia is seen in medullary lesion.
■ Inspection and palpation of the head for skin: It is absolutely important to
look for any lacerations or cut wounds ecchymosis, subgaleal hematoma, and
fractures. Palpation for a bony step off (a discontinuation of the shape of the
skull) is an indication of a displaced fracture.
■ Signs of basilar skull fracture: CSF otorrhea, CSF rhinorrhea, hemotypanum, peri-
orbital ecchymosis (raccoon’s eyes) and ecchymosis on mastoid process (battle’s
sign)
■ Facial fractures
■ Neck rigidity: seen in patients with SAH and may be seen in cases of increased ICP
and impending herniation
■ Signs of spine trauma: Stability of cervical spine should be considered and
respected

Neurological Examination
Mental Status
■ Consciousness and alertness evaluated through the Glasgow Coma Scale (GCS).
If patient cooperative, orientation and memory has to be evaluated.

Cranial nerves
■ Optic nerve: check patient’s visual acuity through a Snellen chart, if unable to see
that, ask him to count fingers. If he fails, ask if he can detect hand motion and in
the end if he can appreciate light. If patient uncooperative: swinging flash light
from one eye to another will demonstrate optic nerve injury if present.
■ Pupils: size, reactivity and symmetry. An abnormality can be elicited in an
 Head Trauma 663

injury to the eye, the optic nerve, the oculomotor nerve, and the midbrain or the
pons. Yet, an ipsilateral fixed dilated pupil is classically associated with
transtentorial herniation. In patients with severe head injury bilateral fixed
pupils is seen in 20-30% of patients in which 70-90% will have a poor outcome
(dead or vegetative) compared to 30% with bilateral reactive pupils .
■ Fundoscope: papilloedema indicate increased intracranial pressure but might be
absent in acute cases
■ Eye movement: these movements are an important index of the functional
activity present with in the brain stem reticular formation3. Therefore, they are
an important localizing tool. If patient uncooperative and neck fracture has
been ruled out oculocepahlic and oculovestibular responses are implicated.
■ Corneal and gag reflex: indicate the integrity of the 5th, 7th, 9th and 10th cranial nerve
and the brain stem
■ Facial symmetry: if patient uncooperative a painful stimuli (supraorbital nerve
irritation) can elicit any facial asymmetry

Motor examination
■ Full motor exam is carried out in all 4 limbs
■ If patient uncooperative: apply a painful stimulus to detect any movement,
check most importantly to symmetry. Asymmetrical posturing, tone, or reflexes
may indicate underlying contralateral mass lesion.
■ Intact deep tendon reflex in the presence of a flaccid limb might indicate a
central nervous system lesion not a peripheral nerve lesion
■ Babinski reflex: indicates an upper motor neuron lesion

Sensation examination
■ Sensory examination is carried out in all 4 limbs and major dermatome
■ If patient uncooperative: check for a response upon painful stimuli

Motor and sensory examination along with anal and bulbocavernous reflex is better
implicated in cases where a spine injury is suspected.

Scalp Injury:
The scalp is composed of 5 layers; skin, subcutenous tissue, apneurosis (galea), loose
areolar tissue and skull periosteum. In head trauma a layer or more might be injured, the
majority of these injuries fortunately can be managed with simple suturing.
The scalp is highly vascular due to the rich anastomosis supply from both the external and
internal carotid arteries. Therefore significant bleeding might be associated with scalp
injury especially in the pediatric group. Compression dressing is usually applied as a
temporary measure to control the bleeding, later on when appropriate the wound is
cleaned, the edges shaved and then the scalp is closed layer by layer. The subcutenous and
galea is usually closed with Vicryl 2.0-3.0 inverted simple interrupted sutures and the skin
664 Head Trauma

is closed with Dermalon 3.0-4.0 simple interrupted sutures. In cases where significant
tissue loss is apparent, the defect is closed with galeal scoring, skin grafts or flaps.
A potential subgaleal space might predispose the accumulation of a hematoma after
a head injury. It can be palpated on examination as a fluctuating soft swelling and
might appear in the CT scan. These hematomas are managed conservatively and exhibit
spontaneous resolution. In rare cases where the heamtoma is infected, evacuation and
drainage is indicated.

Skull Fractures:
There are different types of skull fractures such as:
1. linear skull fracture
2. Diastatic fracture
3. Growing fracture
4. Ping-pong fracture
5. Skull Base fracture
6. Depressed fracture
7. Compund communited fractures
8. Crushed fracture
Skull base fracture exhibit a unique entity, it was estimated to bare 4% of all head
trauma cases. The clinical manifestations includes, bilateral preorbital ecchymosis
known as raccoon eyes (black eyes), ecchymosis of the mastoid process known as
battle’s sign, cerebrospinal fluid (CSF) rhinorrhea or otorrhea, cranial nerve palsy,
bleeding (with or without CSF leak) through the mouth or nose and or ear, and maybe
death. CT scan is the most valuable diagnostic process that usually shows the fractured
bone, CSF in air sinuses and pressure in the subdural space or different parts of
intracranial cavities. Conservative treatment in the form of excellent antibiotics and bed
rest are the usual method of treatment. In cases of optic nerve compression, surgery is
indicated to decompress the optic nerve. The risk of meningitis is high and therefore it
is a must to cover the patients with broad spectrum antibiotics for at least two weeks. In
most cases, CSF leakage seize spontaneously in few days. In the case where CSF
rhinorrhea persists, lumbar drain and bed rest is an option before considering surgery to
repair the dural defect either via bifrontal craniotomy or via nasal neuroendoscopic
technique.

Case demonstration:
An 18-year-old girl who was a victim of RTA had lost consciousness for few minutes.
She was brought to the hospital conscious with GCS of 15. There was bleeding from the
lacerated wound in the right temporal area. No neurological deficit. Brain CT scan
showed right temporal depressed skull fracture, (Figure 1). She was taken to the
operating room, where the right temporal small craniotomy was performed. The
penetrating and comminuted pieces of bones were removed and the depressed pieces of
bone were elevated. A dura tear was found. The dural tear was extended, and small
subural hematoma was removed. The small area of contused brain tissue was removed
 Head Trauma 665

as well. The lacerated scalp wound was cleaned and sutured. The patient made an
excellent recovery and was put on broad spectrum of antibiotics for 10 days, and was
given antiepileptic medication (phenytoin) for 6 months. Post operative CT-Scan was
satisfactory.

Fig. 1 Brain CT-Scan shows temprol depressed fracture

Epidural Hematoma:
Epidural hematoma (EDH) is defined as a collection of blood between the outer
periosteal layer of the dura and the inner table of the skull. EDH is almost always the
result of a blunt head trauma and constitutes 1% of head trauma admissions. It
commonly affects young adults and older children and the reason for that could be
explained by the tight adherence of the dura to the skull in the elderly population and the
flexible nature of the skull in infants. Males are more commonly affected than females.
Traumatic EDH is typically the result of a skull fracture that subsequently injures the
underlying blood vessels. When the bleeding begins; it accumulates and dissects the dura
further more limited usually by the suture lines where the periosteal layer of the dura fuses
with the periostium of the cranial vault resulting in the classical lens shape hematoma.
Because of the thinness and fragility of the temporal squamous bone compared to the rest
of the skull, 70-80% of EDHs are seen in the temporal area. The rest are seen in the
frontal, occipital and posterior fossae. The MMA is the most common source of EDHs
because of its course through the temporal squama and it predisposition to fractures.
Dural sinuses and bridging veins are occasionally the source4.
The clinical presentation is classically described as a brief period of loss of consciousness
followed by a “lucid interval” followed by a sudden neurological deterioration and
ipsilateral fixed dilated pupil. Unfortunately this presentation is seen in less than 30% of
the cases and it can also be seen in other neurosurgical emergencies such as subdural and
intracerebral hematomas. Another confounding clinical finding in EDHs is the Kernohan
phenomeneon with focal finding ipsilateral to the side of the EDH due to the rapid shift
of the central basal brain structures and compression of the contralateral cerebral
peduncle on the tentorial “Kernohan” notch. This is seen in 10-15% of cases of EDH.
666 Head Trauma

EDH is one of the neurosurgical emergencies that can be successfully treated.

Unfortunately in the mean time according to the last publication by Bullock et al. in
20065, there is insufficient data to establish standards or guidelines but recommendations
have been suggested as demonstrated in Figure 2.

Fig. 2 Epidural Hematomas management strategy

Cohen et al 6 demonstrated that patients with dilated pupil who underwent surgical evacuation
within 70 min from the injury have a good outcome compared to patients who underwent
surgery beyond that. All patients in the 2nd group unfortunately died.

In our hospital, all patients with confirmed EDH in plain CT scan are observed in the
ER for at least 6 hours, until the result of the follow up CT scans are checked, regardless
of their neurological status. The need for admission depends on the patient’s initial
presentation and the follow up CT. Initial presentations that necessitates admission
include depressed or decreasing level of conscious, and focal neurological deficit. As for
the follow up CT; if there is an increase in the size of EDH, patients are admitted
wither they are symptomatic or not. Conservative management mandates a regular
radiological and clinical follow up. This includes an hourly examination of the pupils and
level of consciousness and a follow up CT scan in 4- 6 hours from the injury or a
sooner scan done if any neurological deterioration is detected. Another CT scan is
obtained the following day.
As mentioned previously the majority of hematomas lay in the temporal area,
therefore a standard frontotemporal parietal craniotomy is usually performed for better
exposure of temporal and frontal areas and better visualization of the vessels. Within
 Head Trauma 667

limits of c-spine precautions, the head is rotated to the opposite side with a shoulder roll
under the ipsilateral shoulder to aid in rotation, the head is placed on a horse-shoe head
rest (3-point rigid fixation could be avoided to avoid extension of fractures). A question
mark skin incision is started 1 cm anterior to the tragus and curved above the pinna till
it transects the superior temporal line where it is curved superiorly and anteriorley to a
an anterior extent transecting or just lateral to the midline. The 1st burr hole is usually
positioned in the lower temporal area where a small craniectomy is carried out if
needed (depending on papillary status). Then a full frontal craniotomy is carried out and
the hematoma is then appropriately evacuated with suction, irrigation, and cup forceps.
Once the hematoma is evacuated, the dura should look relaxed and shiny. If the dura is
dusky or bluish in color, or it is becoming tense, an underlying lesion has to be ruled out
such as subdural hematoma. It is crucial to determine the source of bleeding and
coagulate it to maintain hemostasis. Dural tack up sutures are placed all around the
craniotomy and 2 are placed centrally tacked up to the bone flap, to prevent
reaccumulation of the hematoma7.
The most single important prognostic factor in EDH was found to be the level of
consciousness on presentation. That explains the variable mortality rates that start
from 0% and reach 40% depending on the cases. Immediate diagnosis and intervention
are the keys to successful management of EDH8.

Posterior fossa injury:

Because of the confined space of the posterior fossa and its proximity to the brain stem,
any lesion there exhibits a unique concern and mandates a close observation. The
majority of lesions seen in the posterior fossa after a head injury are EDHs, it constitutes
1.2-12.9% of all EDHs. A neurological deterioration or a mass effect demonstrated in the
CT scan as obliteration or distortion of the 4th ventricle, effacement of the basal cistern,
or obstructive hydrocephalus indicates a surgical intervention. The rest can be managed
conservatively with serial CT scans and close observation. This goes for subdural
hematomas and intraparenchymal lesions too24.
The following cases have been presented in our hospital and are added to demonstrate
the rationale behind the diagnosis and management of EDH.

Case demonstration:
A 20 year old man, a victim of MVA, is presented to the ER with post-resuscitation
GCS of 10/15, and equally reactive pupils. The CT scan showed bilateral extra-axial
homogenous hyper-dense biconvex shaped lesions present in the temporal fossa and
extending upward measuring around 1.5 cm in thickness with no edema, no midline
shifting as the barin looked to be compressed by the epidural hematomas from both sides,
Figure 3. Subarachnoid hemorrhage also was seen.
668 Head Trauma

Fig. 3 Brain CT-Scan shows bilateral epidural hematomas and

subarachnoid hemorrhage

The patient was rushed to the OR from the CT-Scan room and immediate surgical
evacuation of both hematomas was carried out. The dura was opened in both sides, a
subdural hematoma was discovered and evacuated. The source of bleeding was
determined; it was a branche from the middle meningeal artery and was coagulated. Dural
tack up sutures were done circumferentially and centrally. The patient made an excellent
recovery and left the hospital walking in 2 weeks time. The timing of surgery which was
less than 2 hours from the time of trauma till the skull was opened was determining factor
for such good outcome.

Subdural hematoma:
SDH is defined as a collection of blood or fluid between the inner meningeal layer of
the dura and the arachnoid matter. SDHs are generally divided into three main entities;
acute, subacute, and chronic. ASDH is a SDH presenting within 3 days, subacute
between 3rd and 2-3 weeks, and chronic after 3 weeks of a head trauma.
The incidence of ASDH was found to be 12-29% in patients admitted with severe TBI9.
Similar to EDH, the main cause of SDH is TBI, in which MVA is the primary cause in
young adults while falls are the primary cause in elderly (> 65) and infants. Males
constitute the majority of patients.
Traumatic ASDH is usually the result of a severe head trauma of complex mechanisms
that subsequently exerts a massive strain on the brain surface causing an injury to
occur in the cortical vessels, most commonly cerebral veins. Bleeding from these vessels
accumulates in the potential subdural space and the wide spread sever impact causes
associated cerebral contusions and varying degrees of surrounding edema and swelling.
Less commonly, ASDH is the result of an accelerating-decelerating type of injury,
during a head motion, the bridging veins are stretched. Because of the lack of
reinforcement in these veins, their fixation point in the dural sinuses, and the relative
potential effect of cerebral atrophy and inherent stretching associated with that; these
vessels are easily torn producing a pure SDH over an intact cortex. The latter mechanism
is associated with a less severe primary brain injury and a better prognosis. ASDHs are
commonly found more and less, in the temporal and frontal areas, respectively 4,10.
SDH can be manifested clinically with unspecific signs and symptoms including;
 Head Trauma 669

altered level of consciousness, dysphasia, hemiparesis, hemiplegia or signs of increased

intracranial pressure. It has been noticed that aSDHs are present in severe TBIs, which
is why 80% of patients present to the hospital with GCS <9 and 50% present with
pupil abnormalities9.
According to Bullock et al9 there is insufficient data provided in the literature to
establish standards or guidelines regarding the management of ASDH. Suggested
options are recommended as described below.

Surgical evacuation for SDH patients is indicated in the following presentations:

■ ASDH with a thickness > 10 mm, regardless of GCS

■ ASDH with a midline shift > 5 mm, regardless of GCS

＊
■ GCS < 8 and ICP > 20mmHg, regardless of thickness or midline shift

＊
■ GCS < 8 and asymmetric or fixed and dilated pupil

■ GCS < 8 and decrease of 2 or more points on GCS since hospital admission＊
＊
Regardless of SDH thickness or midline shift.

The main purpose of surgical intervention in this group of patients is to relieve the
increasing ICP and its sequele. Even a very thin layer of ASDH with a significant
midline shift might be a candidate for surgical intervention. This is because the variability
in the thickness of ASDH compared to the degree of the midline shift predicts the
outcome. The disability and mortality rate was found to be increased as the midline shift
exceeds the thickness of the hematoma with a great degree11. For those patients who
require surgery, early intervention is recommended as soon as possible. Our experience
and the experience of many other centers suggest that timimg of surgery is an important
factor for the outcome. We found out that patients who underwent surgery within 2
hours of injury had a favorable outcome and less mortality rate compared to those
patients who underwent surgery after 2 hours.
A standard fronto-temporal parietal trauma craniotomy is performed as described in
the previous section. Once the bone flap is removed, a wide cruciate dural incision is
carried out starting from the area of maximum clot thickness. The clot is evacuated with
copious of irrigation and suction. Thorough inspection of the subdural space and the
cerebral cortex must be preformed to rule out any source of bleeding that needs
coagulation or large (> 2cm) unsalvageable cerebral contusions that need resection. After
homeostasis is secured, the dura is sealed with a watertight closure. Depending on the
status of the brain, the bone flap is either replaced or preserved in situations where
significant brain edema is observed; so is the consideration of the insertion of invasive
intracranial pressure monitoring device7.
ASDHs do not provide the rewarding outcome after surgical intervention that is
usually seen in EDH patients. SDH are the worst traumatic injury affecting the brain. This
can be attributed to the associated parenchymal brain injury and the subsequent
secondary brain injury that is commonly present with ASDH. Mortality rates ranges from
40-60% 8. There are several factors which influence outcome, such like; age, younger
patients in general may have favorable outcome than patients older than 65 years, the
period of loss of consciousness and GCS, the signs of brain herniation and brain stem
injury.
670 Head Trauma

Case demonstration:
35 years old patient, was rushed to our hospital as a victim of RTA. On arrival to our
hospital, he was intubated and GCS was 4, the right pupil was dilated, however both
pupils were responding positively for light stimuli. The patient was rushed to CT-Scan
which showed right fronto-temprol ASDH, SAH and shifting of the midline; (Figure 4).
So, the patient was taken from the CT-Scan room to the Operating Room, where large
fronto- tempero-parietal craniectomy was performed, dura was opened, and the
hematoma was removed, A intraparenchymal ICP sensor was inserted, a large dural patch
was used to loosely close the dura . The bone was not returned back. Patient was sent to
the ICU. He was kept intubated and ventilated for 3 days. He was put on dehydration
methods. The patient made a remarkable recovery and was discharged after 3 weeks.

Fig. 4 Brain CT- Scan shows right fronto-temperol ASDH.

Chronic SDH
Chronic SDH is commonly seen in the elderly. Only 50% of patients give a history of
head injury, often a mild injury. Other risk factors include alcohol abuse, seizures,
coagulopathies, anti-coagulant therapy, any condition predisposes to falls and low
ICP12. CSDH may be presented as alteration of level of consciousness, headache,
dysphasia, hemi paresis, seizures or it can mimic neurological conditions, such as
dementia, TIA, stroke, and tumors.
CSDH usually forms after an ASDH, the blood breakdown products with in the
hematoma attracts an inflammatory response that cause the formation of two
membranes, an outer thicker vascular membrane adjacent to the dura and inner thinner
membrane adjacent to the cortex. These membranes confine the hematoma. In most of
the cases the hematomas appear like collection of fluid consisting of liquefied blood and
CSF, which appear as “motor oil”. Wither the hematoma slowly increases in size due to
recurrent bleeding from the fragile neovascular membrane, or liquefied clot attracting CSF
into the cavity by osmosis is uncertain 4,10.
CSDHs should not be missed in a CT scan; as the hematoma appears usually as
 Head Trauma 671

isodense to the brain parenchyma over the 2nd and the 3rd week; Figure 5.

Fig. 5 Brain CT-Scan shows large left fronto tempero-parietal

CSDH

Bilateral CSDH are present in more than 30% of the cases, so no midline shifting can
be appreciated. After the 3rd week CSDH appears hypodense. It is not rare to see
different areas of density inside the hematoma cavities indicating repeated attacks of
bleeding; Figure 6.

Fig. 6 Brain CT-Scan shows left fronto – tempro-parietal

CSDH. The mixture of high, low and isodense areas inside
the hematoma cavity, indicating repeated attacks of bleeding
in different events.

Surgical evacuation is indicated in most cases, yet in the mean time there is no
agreement regarding the best surgical technique. Burr hole drainage, twist drill
craniostomy, and craniotomy are all options. The choice depends on the degree of
complexity of the hematoma. We frequently choose the 2 burr holes method as our first
line of treatment in most of the cases.
Surgical management is associated with possible complications including; seizures,
intracerebral hemorrhage due to the rapid decompression, tension pneumocephalus,
subdural empyema, and reaccumalation of subdural fluid. In cases of the reaccumalation
of CSDH, craniotomy is indicated to allow removal of the outer and inner memberanes.
672 Head Trauma

Rarely cSDHs are managed conservatively; this option is left for patients with small
hematomas (< 1cm thick) and no neurological deficit. This group of patients should be
educated regarding the risk acute bleeding the use of anti-coagulant therapy and any
future falls.
Patients who undergo surgery have better out come than those who don’t. Mortality
and morbidity rates are increased in the elderly, alcoholics and in patients with
recurrences.

Traumatic subdural hygroma:

Subdural hygroma is a collection of CSF between the meningeal layer of the dura and
the arachnoid. It is thought that this may be the result of a tear in the arachnoid
memberane. These collections are commonly seen after a head injury, constituting 5-20%
of post-traumatic lesions 8. They are usually asymptomatic but they might present
clinically as an altered mental status, neurological deficit, seizures or less commonly
headaches. They appear in the CT scan as an extra-axial isodense (to the CSF) collection,
Figure 7. In most cases it resolves spontaneously. Surgical evacuation is rarely indicated
and usually achieved by a burr hole.

Fig. 7 Brain CT-Scan shows bifrontal post traumatic Subdural hygroma.

Injuries involving the brain parenchyma

Head injuries involving the brain parenchyma can be classified as focal lesions and
diffuse lesions. Focal lesions manifests as cerebral lacerations, contusions, intracerebral
hemorrhages and infarctions while diffuse lesions manifests as cerebral edema,
hemispheric swelling, concussions and diffuse axonal injury.

Focal Brain Injury

Cerebral lacerations: cerebral contusions are called lacerations when the pia and
arachnoid mater are torn.

Cerebral contusions: is a pathological term for “brain bruises”. Contusions are areas of
petechial hemorrhages and necrotic brain tissue resulting from an injury to the small
 Head Trauma 673

blood vessels typically in the gyral crest. They can be divided into coup, counter coup,
gliding, and intermediary contusions. Coup contusions are those found at the site of
impact, counter coup are found opposite the site of impact usually against a bony
prominence , gliding occur in the superior parasagittal margin of the cerebral hemisphere
which are notorious for post-traumatic epilepsy, and intermediary are found in the deep
structures of the brain. In the CT scan these lesions appear as heterogenous hyperdense
lesions with surrounding edema, sometimes assuming a wedge shape. The inferior,
anterior and lateral surfaces of the frontal and temporal lobes are commonly affected due
to the proximity of these cortical areas to the roughened edges of the inner table of the
skull along the floor of anterior cranial fossa, the sphenoid wing, and petrous edges 4,13.

Intracerebral hemorrhage: differ from contusions by the degree of blood content. In ICH
the blood component constitutes at least two third the volume of the lesion which
explains the homogenous hyperdense appearance found in the CT scan 3,4, (Figure 8).

Fig. 8 Brain CT-Scan shows bifrontal areas of cerebral contusion.

Any neurological deterioration or increase in ICP mandates a CT scan to rule out

expansion of the contusion or pericontusional edema or the progression to ICH.
Delayed traumatic intracerebral hemorrhage (DTICH) is a recognized entity of ICH
defined as the presence of an ICH in a previously normal appearing area of the brain in an
initial abnormal CT scan. This is due to the disruption of autoregulation most commonly
seen in severe TBI, failure to regulate cerebral blood flow to the damaged brain vessels
subjects these vessels to increased intravascular pressure leading to the hemorrhage 14. In
these patients mortality reaches up to 72% 15. Studies have demonstrated worse outcome
in patients who develop DTICH with in 48 hours of the initial injury 7.
Controversy has risen regarding the management of focal brain injuries, some favored
conservative management, and others advocated for surgical intervention. Recent
studies have shown that early surgical evacuation of these lesions in a subpopulation of
patients decreases mortality rates and improves functional outcome. Surgical indication
was found to be related to many factors including clinical, radiological findings and ICP.
The location of a lesion, intracranial hypertension, subarachnoid hemorrhage, cistern
effacement, lesion volume and hypoxic events were all found to be factors predicting
failure of non-operative management 15.
We share the recommendations of several authors on surgery for patients with
674 Head Trauma

traumatic parenchymal lesions which included the following:

■ Progressive neurological deterioration referable to the lesion

■ Signs of mass effect on CT scan

■ Refractory intracranial hypertension

■ GCS of 6-8 with frontal or temporal contusion > 20 ml in volume with midline

shift > 5mm and/or cistern compression on CT scan

■ Any lesion > 50 ml in volume

■ Any hematoma more than 20 ml in the posterior fossa.

Surgery is performed through a classic trauma craniotomy that has been described
earlier for the same reason it is in EDH and SDH; which offers a good exposure and access
to the commonest areas involved, temporal and frontal. The transcortical approach
should be preformed in already necrotic or non-eloquent area. Any unsalvagable
contused brain should be excised unless present in an eloquent area. Irrigation with
hydrogen peroxide is recommended to secure homeostasis. After that, Gelfoam and
Surgicel are applied in the hematoma bed followed by the routine closure.
Patients who are elected to be managed conservatively should be admitted to ICU with
an hourly neurological examination, continues ICP monitoring and serial CT scans.
The over all outcome of ICH and cerebral contusions is relatively better than SDH with
mortality rate ranging from 11-30% and functional recovery of 72.2% 2.

Diffuse Brain Injury:

Concussion: is a clinical definition. It is the post traumatic state that results in an
alteration of the level of consciousness. Classically, there is a brief period of loss of
consciousness with a variable degree of retrograde or anterograde amnesia. No specific
definition of “brief period” has been agreed on yet. It was thought that no anatomical or
physiological damages occur in concussion but new evidence proved that concussions are
basically a mild form of diffuse axonal injury. The majority of patients will improve
eventually with no neurological sequelae but unfortunately some will have persistent
neurological deficits. Concussions demonstrate a cumulative affect as seen in boxers
which eventually can result in chronic dementia and cerebral atrophy. Concussions are
thought of as mild head injury 3,4,16.

Diffuse axonal injury: is a primary brain injury resulting from an accelerating-decelerating

type of injury. The sudden deceleration produces a shearing force that disrupts axons and
small vessels. Axonal injury causes localized transport failures in the axon, leading to
swelling and often lysis of the axon with wallerian degeneration 16.
DAI is the cause behind loss of consciousness in head trauma patients due to its effect
on reticular formation. These lesions are demonstrated as hyperintense lesions in T2W
MRI .
CT scan usually fails to show any changes and might appear normal in comatosed
patients. Pathologically, DAI is classically presented as gross focal hemorrhagic lesions
in the corpus callosum and dorsolateral quadrant of the mid brain and pons with
microscopic changes showing axonal retraction ball, and degeneration of white matter
fiber tract 4.
 Head Trauma 675

Cerebral edema: cerebral edema is divided into two types, vasogenic edema and
cytotoxic edema. Cytotoxic edema is predominantly responsible for post traumatic
brain edema. It is the most important contributing factor in increasing the intracranial
pressure which subsequently decreases the cerebral perfusion leading to what is known
as secondary brain injury. However new evidence demonstrated that cytotoxic edema
cannot raise ICP to lethal levels 17. In CT scan cerebral edema can be appreciated as
hypodensity in the white and grey matter.

Case Demonstartion:
A 22-year-old medical student was thrown out of his car as he was driving at a high
speed and crashed to another car. He immediately lost consciousness and was brought
to the Emergency Room. At arrival, he was unconscious GCS was 5. Pupils were normal
in size and both were normally responding to light. No sign of clear lateralization.
Patient was intubated and ventilated. Urgent CT scan was done and showed subarachnoid
hemorrhage and brain edema. Intraventricular ICP sensor was inserted and the ICP
monitor was connected. The patient was treated by dehydration methods and was
given Manittol 20 % and Lasix. Repeated CT-Scan after 2 weeks showed marked brain
atrophy that indicated cellular and axonal damage. Brain MRI was performed 3 weeks
later, and showed multiple areas of high intense signals and brain atrophy indicating
diffuse axonal injury, (Figure 9).

Fig. 9 T2W Brain MRI shows areas of high intense signals indicating
diffuse axonal injury and generalized brain atrophy

The patient was extubated after 10 days, but remained disoriented, agitated, unattentive
and some memory loss. He suffered attacks of grandmal epilepsy, which was controlled
by phenytoin 100 mg three times a day.

Intracranial pressure:
In the 19th century Professors Monro and Kelly hypothesized that intracranial pressure
is determined by the volume of the brain, blood, and CSF. To maintain a constant
pressure, a change in the volume of one of these compartments has to be compensated
by another. Since these components are confined in a rigid container (closed skull),
compensation can be achieved to a degree. Beyond that, compensation is impossible and
therefore, ICP rises dramatically. The importance of ICP in TBI patients lies in the fact
that, an increased ICP causes a reduction in cerebral perfusion pressure (CPP) and
676 Head Trauma

cerebral blood flow (CBF) which may subsequently lead to secondary ischemic cerebral
injury 18. Therefore, high ICP in severe TBI is a significant predictor of worse outcome.
CPP is a major determinant of CBF; it is defined as the mean arterial pressure minus
the intracranial pressure. A concept known as pressure autoregulation maintains the CBF
constant in a range of CPP between 40-150mmHg. This is achieved by a dynamic
system of arterial vasoconstriction and dilatation. A pressure above 150 mmHg will
maximally vasodilate the vessels and increases the CBF and on the other hand, a
pressure below 40 mmHg will collapse the vessel wall and decreases the CBF 7. So, out of
the normal limits the auto regulation is lost and the CBF is then directly related to the
MAP and ICP. For example, a simple cough will elevate the ICP markedly consequently
reducing the CBF.
It has to be noted that CBF differs from cerebral blood volume (CBV). CBF is
defined as the physiological parameter that assures cerebral perfusion and adequate
oxygenation while CBV is defined as the total intracranial blood content, which is a major
determent of ICP. The importance of that lies in the fact that CBV can be reduced to
control ICP while maintaining an adequate degree of CBF 7. ICP normally varies with age,
body position and clinical condition. Table 1, shows the range of normal ICP in each
population.

Table 1 The range of normal ICP in each population.

ICP monitoring:
The guideline recommended by The Brain Trauma Foundation joint publication 19,
is adopted in our practice. ICP monitoring is indicated in patients with:
■ Severe head injury and an abnormal CT scan

■ Normal CT scan and ≥ 2 of the following risk factor at admission (SBP <90

mmHg, Age >40 years, and unilateral or bilateral motor posturing)

Severe head injury is defined as a post resuscitation GCS of < 9. Abnormal CT scan is
a CT scan that shows hematomas, contusions, edema and basal cistern effacement.
Mild and moderate head injuries are not an indication for ICP monitoring; it is
generally left to the discretion of the treating physician. In situations for example,
where a patient with moderate head injury presents with a contusion in the temporal lobe,
ICP monitoring can be implicated to avoid or detect any delayed sequale.
 Head Trauma 677

Management of increased ICP

The following are general measures that should be implemented in order to normalize
the ICP:
1. Head elevation at 30 degrees while the neck maintained at neutral position; it has
the beneficial effect of reducing the ICP immediately with out a change in the
CBF.

2. Tight control of blood pressure; it is crucial to avoid any drop of systolic BP <
90mmHg. A single drop in the SBP < 90mmHg was associated with doubled risk
of morbidity and mortality.

3. Adequate oxygenation; hypoxia defined as PO2 < 60 mm Hg must be avoided.

If patient’s GCS drops below 9, intubation is mandatory to insure better
oxygenation and eliminate the risk of aspiration. Normocarbia is recommended
in patients with severe head injury, defined as PaCO2 = 35-40 mmHg.

4. Avoid anemia; low hemoglobin levels affects negatively brain tissue oxygen
delivery and therefore promote secondary brain injury. Most centers recommend
transfusion of PRBC in patients with Hgb < 7. Studies defining the optimal
hemoglobin concentration in neurocritical patients are lacking, but a restrictive
transfusion policy seems to be safe and is often recommended 20.

5. Light sedation; it reduces HTN that is associated with unnecessary movement and
agitation.

6. CSF drainage; can be an effective method to decrease an increasing ICP.

Hyperosmolar therapy could be used as an adjunct to CSF drainage from the
initial phases of the trauma, more so if there is lack of CSF drainage.
7. Osmotherapy (or hyperosmolar therapy); mannitol and hypertonic saline have
been used as hyperosmoler agents to decrease post-traumatic cerebral edema and
ICP. The latest evidence provided in the literature proved mannitol at doses
0.25mg/kg – 1gm/kg to be superior and more effective not only in decreasing the
ICP but also in improving the CBF.
Decompressive craniotomy is considered in some cases; for patients with refractory
intracranial hypertension and diffuse parenchymal injury with clinical and radiographic
evidence of herniation bifrontal or unilateral frontotemproparital decompressive
craniotomy within 48h is an option. Anterior temporal or frontal lobectomy could be
undertaken if these areas are contused.

Systemic management of TBI patients:

1. Nutrition, patients should be fed to attain full caloric replacement by day 7
post-injury.

2. Anti epileptic, post-traumatic seizures are classified into early PTS and late
678 Head Trauma

PTS. Early PTS are seizures occurring within 7 days of injury while late PTS are
seizures occurring after 7 days. Routine seizure prophylaxis for more than 1 week
following a TBI is not recommended. Phenytoin and valporate were found to
reduce the incidence of early PTS but unfortunately, valporate was associated with
a higher mortality rate. The management of late PTS is similar to the management
of any new onset seizures.

3. DVT prophylaxis, there is class 3 evidence that recommends the prophylactic

application of intermittent pneumatic stockings or/and the prophylactic
administration of low molecular weighted heparin. However, an increased risk
of intracranial hematoma expansion was observed in patients who received
pharmacological therapy.

4. Stress ulceration prophylaxis should be considered.

REFERENCES
1. Maas AI, Stocchetti N, Bullock R . "Moderate and severe traumatic brain injury in
adults". Lancet Neurology 7 (8): 728–41,august 2008.
2. Moppett I. K.: Traumatic brain injury: assessment, resuscitation and early management.
British Journal of Anesthesia 99 (1): 18-31 2007.
3. Sumas M. and Narayan R.: Head injury. In Grossman R. and Loftus C.: Principles of
neurosurgery. 2nd ed. Lippincott-Raven Publishers, pp. 117-155, 1999.
4. Liau L., Bergsneider M., and Becker D.: Pathology and pathophysiology of head injury.
In Youmans J. R.: Neurological surgery: a comprehensive reference guide to the
diagnosis and management of neurosurgical problems. 4th ed. W.B. Saunders, pp.
1549-1585, 1996.
5. Bullock M., Chesnut R, Ghajar, et al: Surgical management of acute epidural hematoma.
In Guidelines for the surgical management of traumatic brain injury. Neurosurg Supp,
58(3): S2-7-15, 2006.
6. Mathur V. and Jallo J.: Summary and synopsis of the brain trauma foundation head
injury guidelines. In Loftus C.M.: Neurosurgical emergencies. 2nd ed. Thieme Medical
Publishers, Inc, pp. 172-180, 2008.
7. Dusick J., Kelly D., Vespa P., and Becker D.: Surgical management of severe closed head
injury in adults. In Schmidek H. H., and Roberts D. W.: Schmidek & Sweet Operative
Neurosurgical Techniques: indications, methods and results. 5th ed. Elsevier Inc, pp. 49-
52, 2006.
8. Timmons S.D.: Extra-axial hematoma. In Loftus C.M.: Neurosurgical emergencies.
2nd ed. Thieme Medical Publishers, Inc, pp. 54-56, 2008.
9. Bullock M R, Chesnut R, Ghajar J, et al.: Surgical mangemnet of acute subdural
hematoma. In Guidelines for the surgical management of traumatic brain injury.
Neurosurg Supp, 58(3): S2-16-24, 2006.
10. Jennett B., Galbraith S.: Complications after head injury. In An introduction to
neurosurgery. 4th edition. William Heinemann medical books limited, pp. 241, 1983.
11. Zumkeller M, Behrmann R, Heissler H et al.: Computed tomographic criteria and
survival rate for patients with acute subdural hematoma. Neurosurgery, 39:708-713, 1996.
12. Adhiyaman V, Asghar M, Ganeshram KN, et al.: Chronic subdural hematoma in the
eldery. Postgrad Med J, 78: 71-75, 2002.
13. Grossman R. and Yousem D.: Head Trauma. In Neuroradiology: the requisites. 2nd
 Head Trauma 679

edition. Elsevier Inc, pp. 254, 2003.

14. Gudeman S., Kishore P., and Miller J.: The genesis and significance of delayed traumatic
intracerebral hematoma. Neurosurgery, vol 5: 309-313, 1979.
15. Bullock M R, Chesnut R, Ghajar J, et al.: Surgical management of traumatic parenchymal
lesions. In Guidelines for the surgical management of traumatic brain injury. Neurosurg
Supp, 58(3): S2-25-38, 2006.
16. Alexander M.: Mild traumatic brain injury: pathophysiology, natural history, and
clinical management. Neurol, 45: 1253-1260, 1995.
17. Rosenblum W.: Cytotoxic edema: Monitoring its magnitude and contribution to brain
swelling. J Neuropathol Exp Neurol, vol 66 num.9, 2007
18. Smith M.: Monitoring intracranial pressure in traumatic brain injury. Anesthesia &
Analgesia, Vol. 106, No. 1, Jan 2008
19. The Brain Trauma Foundation. The American Association of Neurological Surgeons. The
Joint Section on Neurotrauma and Critical Care. Indications for intracranial pressure
monitoring. J Neurotrauma , 24:S37-44, 2007.
20. Leal-Noval et al. Optimal hemoglobin concentration in patients with subarachnoid
hemorrhage, acute ischemic stroke and traumatic brain injury. Current Opinion in
Critical Care , 14:156–162, 2008.
680

Neurotrauma, The ABC’s

SHARAD S. RAJAMANI MCh, FICS
Consultant Neurosurgeon, ColumbiaAsia Hospitals

Key words: Neurotrauma, initial assessment, care algorithms, protocols

Introduction
Trauma is the single largest killer of youth. A large number of trauma patients die from
head injury. A number of these deaths are preventable by prompt decisive action in the
first few minutes to an hour after trauma, the “Golden Hour”.

Most cranio-spinal trauma is easily manageable at a centre with facilities for emergency
care and access to a CT scan unit in close proximity with the centre.

Statistics and Demographics

Trauma is a killer, involving the youth and the middle aged, with a loss of man-hours
at work.

It has been said “if trauma was to be treated as a disease process, the amount of
resources spent on trauma research should exceed all other research put together”.

In reality, trauma has never been given its due importance. Most advancement and
research in trauma stemmed from the second world wars. During the past few years, the
world of medicine has woken up to the “pandemic” called trauma!

Most trauma are due to road accidents (RTA) and a much smaller figure from falls,
assaults and muggings. Also, the higher speed means a more severe an injury, the
amount of force generated is directly proportional to the velocity (E=mc).

It is estimated that nearly 6 million road accidents are recorded, and around 150,000
succumb to their injuries at the site (Statistics from 51 member countries of UNECE).
Road traffic injuries are the leading cause (60%) of Traumatic Brain Injury (TBI)
followed by falls (20-25%) and other violence (10%).
Driving Under the Influence is known to be the causative factor among 43-76% of
accidents at the time of injury.
Amongst road accidents, 70% of the deaths are following traumatic brain injuries.

Rehabilitation needs of brain injured persons are significantly high and increases from
year to year. This affects man-hours, and resource utilisation , which actually is a large
sum. Hence stress on prevention, pre-hospital care and rehabilitation in the rapidly
 Neurotrauma, The ABC’s 681

changing environments are being stressed upon to reduce the burden of TBI.

The think-first program stresses on the need of planning prior to travel by motor
vehicle. It also insists on stress-free driving.

Pre-Hospital Transfer
The primary and most important period of any trauma is the first one hour. This is
where a sizeable number of lives could be saved.

Unfortunately neurosurgeons are not primarily involved in this part of the care,
however, the effects of pre-hospital transfer and emergency services affect the outcome.
The extrication process is cumbersome, awkward and messy. It might involve the
placement of lines in the most awkward setting, and the extrication of individuals in the
vertical position. This could easily adversely affect the outcome, specially in those with
spinal injuries.

A team of emergency medical personnel is best designed for the purpose of extrication
and transport consisting of two medical staff, and a driver with or without the presence
of a supporting staff.

A primary survey is necessary in the pre-hospital transfer, securing of an IV access with

a wide bore needle (16G or 18G) is recommended so as to speed up the process of
resuscitation is also mandated. A fluid like Lactated Ringers Solution or 0.9% saline is
instituted and kept on flow during the transfer, the rate dependant on the blood
pressure of the victim.

The steps of evaluation can be divided into two overheads:

1. Assessment of the danger to the medical personnel: The dangers to personnel
are Traffic on the road, the leaking fuel, fuel tank explosion, live electrical wires
obstructing the evacuation etc. This task is usually assigned to the driver of the
vehicle. He also parks the ambulance in a prominent spot on the road, with the
lights flashing, where movement of traffic is possible without endangering the
evacuation team. At this point in time, it is preassigned to one of the medical staff
to evaluate for imminent danger from wires, fuel leaks, instability of the vehicle
etc.

2. Assessment of the patient: The patient is assessed using the ABCDE of the
ATLS described in the next topic, and the consciousness is assessed using the
AVPU technique. An important point to note is that whenever Primary survey
is being performed, the treatment is also initiated and maintained. Only once the
primary survey and secondary survey is complete, should one note the history
from an eye witness, and preferably bring him/her back to the hospital for
further questioning by the doctor.
682 Head Trauma

Resuscitation is performed as the primary survey or evaluation is being carried out. At

no point in time, should the ABC’s be overlooked.

While these patients are resuscitated for their vital parameters, the airway, breathing
and circulation, with an airway and bag-valve-mask ventilation, or rarely the Bag-
valve-tube ventilation. Splinting of fractured limbs is recommended to minimise further
blood loss. The EMT team is in contact with the hospital relaying data and condition of
the patient. This prepares the Emergency services to plan and receive the patients.

In realty two techniques of evacuation are performed by the Emergency team:

1. Snatch and Scoot.
2. Stay and Stabilise.

Unless all facilities are available in the ambulance including blood and emergency
procedure kits, with adequately trained individuals, most teams do not attempt the “stay
and stabilise” method. In fact most centres over the world prefer to use the first
technique. However, when the former is used extensively, some degree of stabilisation is
performed in the ambulance, vital parameter assessments, IV access, bag-valve-mask
ventilation, while the ambulance is rushing off to the hospital.

Emergency Services
Once the patient is in the emergency services area the steps followed are:
Assessment of the patient: While assessment of the patient begins in the vehicle and
where evaluation of his vital parameters and an IV line is inserted. The patient is put on
a cervical collar. If this is not available freely as in the case of most peripheral hospitals,
two-three newspapers folded over and over again to fit the neck is used, making sure that
this does not compromise the airway or the venous return from the neck.

The Adage

“ALL PATIENTS WITH TRAUMA HAVE A CERVICAL SPINE

INJURY – UNLESS PROVEN OTHERWISE”
Is borne in mind while managing all cranial trauma. The assessment of a traumatised
patient is divided into two broad categories as per the ATLS protocol. The Primary
Survey and the Secondary Survey. It would be prudent to mention the ATLS hands when
dealing with trauma - Open hands, arms flexed at the elbows, adducted at the shoulder.
 Neurotrauma, The ABC’s 683

The Primary Survey consists of

a. Airway: Airway assessment for obstruction is very important. This could be
foreign bodies, tongue falling back, broken teeth etc. For a tongue falling back,
the “Jaw-thrust manoeuvre” effective in alleviating the obstruction. While using
a finger to clear the airway, it is advisable to be extremely careful lest the
examiners finger is a casualty between the teeth of the semiconscious patients,
who have a tendency to bite on it. An alternative method is to insert the blade of
a laryngoscope, before inserting a finger. An oral airway might help, if the
tongue continues to fall back, but only if the patient tolerates it. Most
semiconscious or unconscious patients spit it out. In such situations, if there is
no bleeding from the nose a no 6 or 6.5 endotracheal tube can be inserted into the
nose, to the pharynx as a naso-pharyngeal airway. If the obstruction is below the
reach of a finger or suction device, an emergency cricothyroidotomy might be
needed. This is done by feeling the cricothyroid membrane at the lower border
of the thyroid cartilage, in the midline. The lower margin of this membrane
usually has a shallow notch, and stab made into it using a #15 blade. The airway
can be kept open by inserting an uncuffed paediatric endotracheal tube of size not
exceeding #5. This would help maintaining the airway. The tube can be inserted
as far as the carina. One word of caution – the tube can slip into one of the main
bronchi and a collapse of the other lung might occur.

b. Breathing: Following assessment of the airway, an assessment of whether the

patient is breathing or not is performed. If the patient is breathing, is it shallow,
adequate, or there is one of the neurological kinds of respiration. If the patient is
not breathing adequately, a bag-valve-mask is ideal to obtain temporary
ventilatory support, and this can be replaced by intubation, when the patient’s
saturation has improved, or the equipment is ready. During the procedure of
intubation or ventilation or checking for airway, prime importance is given to the
stability of the cervical spine.

c. This can be achieved with the help of a trained personnel watching for any
flexion during intubation. The rule is “No Movement Is Best”. But that may
always not be possible, and small degrees of movement would definitely occur,
and flexion is much worse than extension.

d. Circulation: The assessment of circulation is initially done by assessing the

volume of the pulse the rate of the pulse, and the peripheral circulation -
capillary refill rates etc. In cold weather, the limbs might be cold, with a normal
volume, and in patients with total cervical or dorsal spinal injuries, the periphery
might be warm while the patient in shock. A quick guide to assessment is when
the dorsalis pedis is felt in adults, the blood pressure is thought to be over
100mmHg, systolic. In any head trauma, a minimum mean pressure of 70mmHg
is necessary to perfuse the brain. In the event of a suspicion of a low volume state,
an IV access with a wide bore cannula – 16 or 14 gauge needle (Venflon / Insyte
684 Head Trauma

/ Jelco etc) is preferred, and if needed multiple cannulae. In general, low volume
states in the acute setting of trauma are due to fluid or blood loss either externally
or internally. This warrants fluid replacement. The fluid of choice is ringer
lactate or in extreme situations penta or hexa starch (haesteril). This technique
is usually adequate. Once the source of blood loss is identified and controlled,
blood can be transfused rapidly. In extreme situations, early blood transfusions
would become necessary. It is very tempting to insert a long line or central
venous access in the acute setting, especially at the first instance. This does not add
to the process of resuscitation as a rule, but should be considered once the
blood pressure is stabilised.
The presence of tachycardia usually indicates the impending hypotension, and
should be aggressively treated. There is hypotension seen occasionally with
spinal cord injuries and this manifests as bradycardia with hypotension.
Hypotension secondary to decompensation of the brainstem and the autonomic
nervous system is seen in the setting of deep coma, pupillary dilatation, and
respiratory signs. There is no accompanying tachycardia in these situations.

e. Disability: The assessment of disability includes the assessment of:

The sensorium: This can be divided into 4 stages or levels. These are
• Awake,
• Responds to Verbal stimulus
• Responds to Painful stimulus
• Unconscious
The AVPU is a quick assessment, to get a brief idea of the conscious level later
a more detailed assessment should be performed.

An assessment of the limbs and sites of bleeding is done and all efforts are made
to arrest any sources of bleeding.

e. Exposure: In the emergency room, exposure of the patient to look for any
injuries or lacerations, fractures, to look for active blood loss. Under controlled
circumstances a turning of the patient to evaluate the back is permissible, but with
adequate help – One person for the head and neck – preferably the doctor,
one for the shoulders, and hip, and one for the lower limbs (A minimum of three
personnel).

In Summary, the following steps have to be taken in receiving a patient

with head trauma:
a. Put the patient on a collar and spinal board,
b. Assess the airway,
c. Assess Breathing,
d. Assess Circulation and if with a staff nurse, the pulse rate and volume, blood
pressure too.
e. Assess Disability
 Neurotrauma, The ABC’s 685

f. Expose the patient and assess the injuries, fractures, and bleeding sites.

This should continue along with resuscitative measures, in the form of IV access,
securing of airway, and securing of respiratory status. At any given point of time, if there
is a lapse of the ABC, immediate attention should be paid to it, reverting back.

Following the primary survey, a secondary survey is carried out, this is done with the
patient as a whole and not system related.

Secondary survey consists of

a. General physical examination – including the vital parameters. Look for
identification marks.
b. Examination of the CNS: Examination of the GCS – score the patient what ever
be the situation.
c. Examination of the head, for lacerations, and depressed/linear fractures.
d. Examination the Head and neck pupils, facial lacerations, and facial fractures.
e. Examination for cervical spine tenderness.
f. Examination of the chest – respiratory rate, breath sounds, and their equality,
tracheal deviation, subcutaneous emphysema.
g. Examination of the abdomen – abdominal distention, fullness of the flanks,
shifting dullness, loss of liver dullness, bruising on the abdomen, external
genitalia, rectal examination.
h. Examination of the limbs for hematoma, fractures, undue mobility at joints, for
lacerations, and peripheral pulses, weakness of the limbs.
i. Log-rolling, and examination for injuries to the back and the anal tone in the
partly conscious and unconscious patient.

A history record sheet to deal with polytrauma might be useful so as not to miss out
any findings.

Following this a specific system-oriented management is considered. To simplify

the same, we have suggested an algorithm which would cover almost all situations. For
the purpose of simplification, we have used only two parameters in the assessment of
these patients and further management - the GCS and Pupils

The Glasgow coma score, which is a score first described in 1976 by Teasdale and
Jennett. They have divided the assessment of a head injured patient into three basic
categories, depending on the response of the patient, motor, verbal and eye opening. They
have been scored between 1-6 for motor, 1-5 for verbal and 1-4 for eye opening.

This scoring system has stood the test of time and the tribulations of a number of other
scoring systems as from Adelaide, the APACHE series etc.

The mainstay of the scoring system is the simplicity and consistency with which
686 Head Trauma

one can assess the patient. It has also been found that the chances of an inter-observer
variance are not more than “1” in a given time frame. The scoring system has a series of
major drawbacks; however one still continues to use this system.

The scoring system uses three parameters, Best Eye Opening Response, Best Motor
response, Best Verbal response, also called EMV.

The Glasgow Coma Score

The usual doubts while assessing the GCS are:
a. How, where and what kind of painful stimulus is used ?
The painful stimuli used are Pinch to the anterior axillary fold, supra-orbital
pressure, sternal pressure, nail-bed pressure.

b. What is an abnormal extensor response ?

The abnormal extensor response is described as flexion at the thumb, the
fingers, the wrist, extension at the elbow, pronation of the forearm, extension of
the shoulder, internal rotation of the shoulder and extension of the neck and back,
with extension at the lower limbs (also called the decorticate posturing.)

c. What is an abnormal flexor response ?

The abnormal flexor response is the same as the extensor response except for
flexion at the elbow. The hand usually does not reach cranial to the shoulder joint.

d. What is a flexor / withdrawal response ?

The flexor response is described as flexion of the upper limb, usually past the
shoulder, however, the thumb, fingers and the palm are open, and do not form
the classical flexed, closed fist posture. Also the lower limbs tend to flex instead
of extension, and painful stimulus to the limb causes the limb to withdraw. The
movement is not localizing movement, although the hand might come close to
the region of obnoxious stimulus. Withdrawal to pain is noticed in these patients.

There are some drawbacks of the Glasgow coma Score and these are
a. It does not take into account the general condition of the patient.
b. There are no parameters for pupillary size, shape or symmetry.
 Neurotrauma, The ABC’s 687

c. Involvement of other organ injuries can adversely affect the management

protocols, and are not recorded by the GCS.
d. Spinal injuries would change the GCS specially in the disoriented or unconscious
patient, where the motor response would be altered as low as M1.

There are also some situations where the GCS might be altered or the readings might
not be right.
a. Patient has hypoxia
b. The patient is hypotensive.
c. Has had a seizure
d. Is febrile
e. consumed alcohol/drugs
f. Has received a previous sedative.

Despite these drawbacks, the scoring system has stood the test of time. Therefore the
lacunae is filled by adding the information, specially the positive ones.

Along with the GCS, the pupillary size is also mentioned. The most important
finding is a dilated and non-reacting pupil, or an asymmetric non-reacting pupil. There
may be variations in the absolute size of the pupil from 1mm to 6 mm, provided they are
reacting, and equal, they should not arouse alarm. However, a 1mm pupil usually does
not react. Dilated pupils may be seen in acute panic states, post-traumatic psychological
shock or in patients with severe pain, and also if the pupils are assessed within seconds
of assessing the GCS. Around 16% of the population has some pupillary asymmetry
however it would advisable to assume that the pupillary asymmetry is secondary to
increasing intracranial pressure, and err on the side of evaluating for it.

The important point to note is that the pupil dilates first on the side of the lesion.
Hence the presence of an ipsilateral papillary dilatation with contralateral hemiparesis
would suggest a mass lesion, causing lateral trans-tentorial herniation (coning) on the side
of the pupillary dilatation.

Systemic Examination - Neurological:

A detailed systemic examination of the central nervous system is mandated. The
details of which are dealt with in another chapter.

Management in Emergency Services

After an assessment has been made, an initial stabilization of the patient has been
performed; the patient is then managed according to a protocol being used at any
medical center.

An ideal protocol-based treatment covers for most contingencies and leaves no

ambiguity in the treatment of head injured patients.
688 Head Trauma

While this is difficult to accomplish, a protocol is created to incorporate most

scenarios. These protocols help as guidelines, and as time goes by one tends to modify,
never breaching the broad outlines.

REFERENCES
1. Country Reports on Road Safety Performance, from 44 member countries; September
2006: International Transport Forum.
2. Neurotrauma; Raj K. Narayan, John T. Povlishock, James E Wilberger
3. National Institute for Health Care and Clinical Excellence - 2007 Guidelines for Head
Injury
4. Guidelines for the management of Severe Traumatic Brain Injury, Project for Brain
Trauma Foundation;3rd Edition, 2007
 689

Management of severe traumatic brain

injury (TBI)
ALEXANDER POTAPOV; L. LIKHTERMAN
Burdenko Neurosurgical Institute, Russia

Key words: traumatic brain injury (TBI), scull fracture, epidural haematoma (EDH),
subdural haematoma (SDH), cerebral contusion, difuse axonal injury
(DAI)

Introduction
State of consciousness is the most important integral factor of TBI severity. There is
a general agreement that in severe TBI patients have a hospital admission Glasgow
Coma Scale (GCS) of 8 or less. The overall incidence of severe forms of TBI is marked in
5-7% of all head-injured patients. According to clinical and morphological characteristics
TBI is classified into the following severe forms: traumatic lacerations and contusions,
intracranial haematomas and haemorrhages (epidural, subdural, intracerebral,
intraventricular, subarachnoid), diffuse axonal injuries and crush of the head. Their
biomechanics and pathogenesis is different. Severe focal damages – lacerations and
contusions, intracerebral and subdural and epidural haematomas as well as depressed
skull fractures are produced by coup-and contre coup mechanism of damage; diffuse
brain injury is produced by acceleration of the head without impact, and typical
combination of kinetic and static energy forces cause long-term head compression.
Primary management of patients with TBI and its sequelae starts with intensive care
followed by differentiated treatment. Beside direct surgery there’s been marked a wide-
spread use of methods of minimally invasive and reconstructive neurosurgery.

1. Brief summary of guidelines for the management of severe TBI

and experience of Burdenko Neurosurgical Institute
Modern neurotraumatology has gained a great experience in diagnosis and
management of different types and severity states of TBI summarized in evidence-
based International and National Guidelines (Adelson P.D. et al (2003), Bullock R. et al
(2006), Bratton S. et al (2007)). In this connection we find it reasonable to briefly
summarize the main recommendations for the management of severe TBI and its
surgical treatment based on the experience of Burdenko Institute. It is for this reason that
we’ll report on recommendations for the management of severe TBI.

1.1. First aid for head-injured patients

Priority should be given to the measures aimed at restoring (improving) and preserving
vitally important functions: respiration (restoration of respiration, avoidance of
hypoventilation disturbances – hypoxia, hyperkapnia) and blood circulation (evoidance
690 Head Trauma

of hypovolemia, hypoxia and anemia). In inadequate independent respiration a series of

special procedures providing respiratory tract permeability can be followed by intubation
and artificial ventilation to ensure normal blood oxygenation and avoid hyperkapnia.
Tracheobronchial sanation is possible after intubation procedure. Management of
hypovolemia and arterial hypoxia should be started with infusion of colloids and
crystalloids. Class I evidence showed that hypertonic NaCl (7,5%) saline, especially in
combination with dextrans, proved to be more effective compared to isotonic saline. It
was shown that 7,5% NaCl infusion resulted in quick normalization of blood circulation
value without raise of intracranial pressure (ICP). Intravenous 4-6 ml/kg dosage for up
to 5 minutes is recommended. It should be noted, however, that in patients with
penetrating injuries it may cause internal haemorrhage.
Emergence of symptoms of transtentorial herniations and neurological deterioration
not attributable to extracranial causes should suggest raise of intracranial pressure.
Such a situation requires urgent measures to be undertaken, i.e. the patient should be
artificially hyperventilated. Mannitol is recommended to control intracranial hypertension
with an adequate compensation of the blood circulation value.
To provide optimal conditions for patient transportation, especially if psychomotor
agitation or seizures are present, it is recommended to use sedatives. Short-term
administration of myorelaxants is possible in patients with insufficient sedation.

1.2. Blood Pressure and Oxygenation

At all stages of management of TBI (at trauma site, during transportation, in hospital)
blood hypotension (systolic blood pressure < 90 mm Hg) and hypoxia (apnoe, cyanosis,
PaO2 < 60 mm Hg or O2-saturation < 90%) should be urgently prevented or avoided.
Blood pressure and oxygenation should be monitored. Mean blood pressure should be
over 90 mm Hg throughout the whole intensive care period in order to preserve cerebral
perfusion pressure (CPP) at the level > 60 mm Hg. In persistent hypoxia intubation and
artificial ventilation are necessary.

1.3. Hyperosmolar Therapy

Mannitol is effective for control of raised intracranial pressure at doses 0, 25 gm/kg to
1 g/kg body weight. In patients with a subdural haematoma (especially temporal lobe
haematoma) undergoing surgical evacuation, an early preoperative single, high dose of
Mannitol (1,2-1,4 gm/kg) is recommended or in patients in deep coma or diffuse brain
swelling on CT scan. Arterial hypotension should be avoided. Mannitol is effective
before monitoring of ICP for patients with transtentorial herniations or neurological
deterioration not attributable to extracranial causes. To avoid kidney insufficiency it is
recommended to hold blood osmolarity level below 320 mosm/l. Normovolemia should
be preserved by fluid maintenance; catheterization of the urinary bladder is also
recommended. Periodical bolus administration of Mannitol can be more effective than
persistent infusion.

1.4. Infection Prophylaxis

Periprocedural antibiotics for intubation should be administered to reduce the
incidence of pneumonia.
 Management of severe traumatic brain injury (TBI) 691

Early tracheostomy should be performed to reduce mechanical ventilation days.

1.5. Deep Vein Thrombosis Prophylaxis

Compression stockings or intermittent pneumatic compression stockings are
recommended, unless lower extremity injuries prevent their use. Use should be continued
until patients are ambulatory.

1.6. Indications for Intracranial Pressure Monitoring

Intracranial pressure (ICP) should be monitored in all salvaged patients with a severe
TBI (GCS 3-8) and an abnormal CT scan. An abnormal CT scan is the one that reveals
haematomas, contusions, swelling, compressed basal cisterns.
ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two
of the following features are noted at admission: age over 40 years, unilateral or bilateral
motor posturing, or systolic blood pressure (BP) < 90 mm Hg.
ICP monitoring is not indicated in patients with mild or moderate TBI.

1.7 Intracranial Pressure Monitoring Technology

The ventricular catheter connected to an external strain gauge is the most accurate, low
cost and reliable method of monitoring intracranial pressure. It also allows to drain CSF
for treatment purposes. Subarachnoid, subdural and epidural monitors are less accurate.
Parencymal ICP monitors can not be recalibrated during monitoring.

1.8. Intracranial Pressure Thresholds

Intracranial pressure thresholds above 20 mm Hg are associated with poor outcomes.
Interpretation and treatment of ICP based on any threshold be corroborated by clinical
and brain CT findings.

1.9. Cerebral Perfusion Thresholds

Cerebral perfusion pressure above 60 mm Hg should be preserved. CPP <50 mmHg
should be avoided because it may lead to disturbance of cerebral pressure autoregulation.

1.10. Hyperventilation
Class I and II Evidence allowed us to formulate the following standards and
recommendations:
Long-term hyperventilation (PaCO2 < 25 mm Hg) within the first 5 days of injury
should be avoided in severe TBI patients without signs of intracranial hypertension.
Prophylactic hyperventilation (PaCO2 <35 mm Hg) should also be avoided as it may
cause disturbance of cerebral perfusion when extensive cerebral blood flow is low.
Short-term hyperventilation is indicated in patients with sudden neurological aggravation,
or it may be prolonged in case of preserved intracranial hypertension despite use of
sedatives, relaxants, fluid drainage and osmotic diuretics. Jugular venous saturation,
arteriovenous oxygen difference and brain tissue oxygen monitoring are indicated to
prevent brain ischemia in patients with hyperventilation of PaCO2 < 30 mm Hg.
692 Head Trauma

1.11. Brain Oxygen Monitoring and Thresholds

Jugular venous saturation and brain tissue oxygen monitoring detects cerebral
ischemia in the management of patients with severe traumatic brain injury.
Jugular venous saturation <50 % and brain tissue oxygen tension < 15 mm Hg are
thresholds associated with poor outcomes.

1.12. Anesthetics, Analgetics, and Sedatives

Prophylactic administration of high dose barbiturates is contraindicated for intracranial
pressure control in patients with diffuse injuries and associated with significant
hypotension. High dose barbiturate administration is recommended to control elevated
ICP refractory to maximum standard medical and surgical treatment. Hemodynamic
stability is essential before and during barbiturate therapy.
Analgetics and sedatives are indicated for avoiding agitation and improving respiraory
mechanics. Narcotic agents can cause hypotension.

1.13. Nutrition of Patients with Severe TBI

Feedings are usually begun within 72 hours after injury in order to gradually achieve
full nutritional support. Replace 140% of resting metabolism expenditure in non-
paralyzed patients and 100 % of resting metabolism expenditure in paralyzed patients
using enteral or parenteral formulas containing at least 15% of calories as protein by the
7th day after injury. There are two options for the method of early feeding: Jejunal and
Parenteral. The method of feeding should be a jejunal feeding tube or gastrojejunostomy.
It avoids gastric intolerance and simplifies care of patients.
The benefits of jejunal feeding are low risk of hyperglycemia, low risk of infection and
low cost.

1.14. Antiseizure Prophylaxis

Prophylaxis for Posttraumatic Seizures (PTS) (posttraumatic epilepsy) are classified
as early (occurring within 7 days of injury) or late (occurring after 7 days following
injury). Anticonvulsants (phenytoin or carbamazepine) are indicated to decrease the
incidence of early PTS in the acute stage of TBI. The following risk factors have been
identified: cortical contusion, depressed skull fracture, intracranial haematoma,
penetrating head wound, seizure within 24 h of injury.
At the same time it is generally accepted that prophylactic use of phenytoin,
carbamazepine, valproate is not recommended for preventing late posttraumatic
seizures.

1.15. Algorithm of Management of Intracranial Hypertension

Intensive therapy aimed at prevention and avoidance of intracranial hypertension
includes: raised position of the head, normalization of disturbed venous outflow,
elimination of hyperemia, elimination of motor excitation and posttraumatic seizures by
use of sedatives and/or myorelaxants, maintenance of adequate oxygenation, elimination
of hypercapnia, maintenance of cerebral perfusion pressure (CPP) above 60 mm Hg. The
simplest method to decrease intracranial pressure is to drain ventricular CSF using an
intracranial catheter. If we fail to normalize ICP repeated CT is recommended. Moderate
 Management of severe traumatic brain injury (TBI) 693

hyperventilation (PaCO2 = 30-35 mm Hg) is indicated when we cannot preserve

intracranial hypertension and CT fails to reveal pathology requiring surgical intervention.
If moderate hyperventilation turns to be ineffective bolus administration of Mannitol dose
0, 25-1,0 g/kg is recommended with osmolarity ≤ 320 mosm/l. If these procedures fail to
decrease ICP, CT or MRI should be repeated, and aggressive attempts undertaken
(barbiturate narcosis, deep hyperventilation, moderate hyperthermia under control of
jugular oxygen saturation and arteriovenous oxygen difference and as an extra measure
– decompressive skull trepanation).
It should be specially stressed that aggravation attempts to decrease intracranial
pressure are always related to high risk of complications. When using more aggressive
methods it is necessary to perform control CT scans to reveal delayed intracranial
haematomas, occlusive hydrocephalus etc and if necessary to perform an operation.
Algorithm for the acute medical management of severe traumatic brain injury in
infants, children and adolescences was published by Adelson P.D. et al. (2003).

2. Prognosis in severe TBI

2.1. Glasgow Coma Scale
Since its first development in 1974, GCS has become the most frequently used
classification of severity of TBI. It is generally accepted that risk of unfavourable
outcome increases with the overall GCS score decrease. Use of GCS requires standard
conditions for its application. GCS evaluation is performed only after vitally important
functions have been improved and no sedatives or relaxants have been used. GCS
assessment should be performed by the trained personnel.
Inobservance of these conditions results in incorrect interpretation of patient state and
thus provides unreliable GCS prognosis.

2.2. Age
Having analysed prognostic value of the Age Factor we found out that it was closely
correlated with mortality and disability caused by TBI. Despite some controversy in
literature it was demonstrated that children showed much better outcome than adults.
A considerable influence of age on outcome cannot be explained by increased incidence
of trauma-related complications or intracranial haematomas with aging. Age is a strong
and independent prognostic factor of unfavourable outcome in head-injured patients over
60 years.

2.3. Diameter of Pupils and Photoreaction

Change of pupil diameter > 1 mm is called papillary asymmetry. Change of pupil
diameter < 1mm in response to bright light is described as absence of photoreaction.
Change of pupil diameter > 4 mm is termed mydriasis. When examining patient’s
pupils one should specially consider if the following features are present: direct damage
to the orbit, pupil asymmetry in rest and in response to light, absence of photoreaction
or mydriasis. Pupils should be examined after adequate ventilation and haemodynamics
have been restored. It is the task for the experienced and qualified personnel. Bilateral
absence of photoreaction is considered an evidence-based and prognostically significant
694 Head Trauma

factor (parameter).

2.4. Hypotension
Direct monitoring of blood pressure allows more accurate and artifact-free
measurement, and is considered a method of choice. Methods which do not allow
measurement of average blood pressure are less effective.
Recommendations:
Blood pressure should be monitored at an early stage by qualified personnel. Class I
evidence shows that blood pressure (systolic blood pressure <90 mm HG), especially in
combination with hypoxia, is an indicator of unfavourable outcome (prognosis).

2.5. CT Findings
Prognostic CT findings include:
- primary CT anormalities within the first 12 hours of TBI
- compressed basal cisterns at the level of midbrain
- traumatic subarachnoid haemorrhage (SAH)
- collections of blood in basal cisterns
- spread of SAH by convex
- midline shift
CT scans should be interpreted by an experienced radiologist or other trained
personnel. We marked an evidently significant correlation existing between outcome and
traumatic abnormalities visualized on CT. In “normal” CT outcome depends mainly on
extracranial pathology. Absence of traumatic pathology on CT at admission does not
guarantee its absence on more late CT scans (Potapov S. et al. , 2009). Aggravation of
diffuse injury from Score I to IY by CT classification of Marshall et al is characterized by
growth of unfavorable outcomes. The mortality in patients with severe TBI is two
times higher when SAH is present. Patients with collections of blood in basal cisterns are
at high risk of unfavourable outcome (poor prognosis). Subarachnoid haemorrhage as
well as degree of its expressiveness should be considered an independent prognostic factor.
Patients with intracranial haematomas usually show unfavourable outcome. Mortality
in subdural haematomas is higher than in epidural haematomas. Haematoma volume
correlates with outcome. Compression or absence of basal cisterns on CT is regarded as
high risk factor of intracranial hypertension. Condition of basal cisterns determines
outcomes: mortality is two or three times higher for cases with compressed or absent
cisterns. There is a close connection between condition of basal cisterns and pupil
reaction.
Shifting of midline structures correlates with outcomes though it is related to other CT
signs as well. Midline shifting is an indicator of the raised intracranial pressure. Shifting
factor is less important than other CT characteristics as it mostly depends on localization
of intracerebral damage or presence of bilateral pathology. Besides, size of midline
shifting may considerably change, in particular after evacuation of intracranial
haematoma.
Retrospective analysis of the data bank on severe TBI performed by Burdenko
Neurosurgical Institute showed evidently worse outcomes in patients without modern
recommendations used.
 Management of severe traumatic brain injury (TBI) 695

3. Surgical or Medical (Conservative) Treatment of Focal Severe TBI

3.1. Severe Focal Brain Damage
Based on the studies performed at Burdenko Neurosurgical Institute there were
outlined special criteria for differentiated management of TBI which should allow to
maximally avoid possible drawbacks.
Indications for surgical treatment of focal traumatic contusions and intracerebral
haematomas include:
1) state of consciousness: sopor or come (GCS ≤ 10)
2) clinical signs of brainstem dislocation
3) CT and MRI signs of homogeneous contusion and laceration size (diameter) >
50 cm3 for frontal localization and > 30 cm3 for temporal localization; maximal
intracerebral haematoma size > 4 cm
4) CT and MRI evidence of lateral dislocation (midline shift > 5 mm and/or axial
brain dislocation (the enveloping cistern is roughly deformed)
According to recommendations by M. Bullock et al. (2006), surgical treatment is
indicated in patients with traumatic parenchymal brain damages, progressing neurological
deterioration, intracranial hypertension refractory to medical treatment and with signs
of mass-effect on CT.
Indications for medical (conservative) treatment of focal contusions and intracerebral
haematomas are:
1) state of consciousness: moderate or deep obnubilation (GCS > 10);
2) absence of evident clinical signs of brainstem dislocation
3) CT or MRI signs of contusion < 50 cm3 for frontal localization and < 30 cm3 –
for temporal localization; maximal intracerebral haematoma diameter < 4 cm
4) absence of CT or MRI evidence of midline shift < 5 mm and axial brain
dislocation (the enveloping cistern is saved or slightly deformed)
According to recommendations of M. Bullock et al. (2006) focal parenchymal lesions
should be treated conservatively in patients with slight neurological deficit, controlled
intracranial pressure and absent signs of mass-effect on CT.
On should remember that major part of victims with severe focal traumatic brain
damages belongs to the so-called risk group. Intensive therapy, dynamic clinical
observations with repeated CT or MRI examinations are indicated in this group of
patients.

3.2. Epidural or Subdural Haematomas

Epidural or subdural haematoma is the main surgical form of severe traumatic brain
injury.
According to the experience of Burdenko Neurosurgical Institute, urgent surgical
evacuation is indicated in the bulk of patients with acute or subacute extracerebral
haematomas if the following clinical signs are noted:
1) expressed brain compression
2) repeated neurological deterioration or aggravated extinction of consciousness after
total or erased lucid interval
3) the volume of supratentorial haematomas (by CT and MRI data) > 30 cm3 for
696 Head Trauma

temporal localization and > 40 ml for any other localization with the volume of
subtentorial haematomas > 20 cm3 or its width > 1,5 cm regardless the clinical
phase of TBI, including asymptomatic haematomas
4) Surgery is indicated in patients with extracerebral haematomas if one of the
following features is revealed by CT or MRI: lateral midline shifting > 5 mm,
marked deformation of the basal cisterns, large compression of the homolateral
ventricle, dislocation hydrocephalus regardless localization and volume of
haematoma, if caused by the latter and not by associated skull or brain damages
5) open penetrating head injury or associated skull and brain damage (compressed
fracture, intracerebral haematomas etc.) requiring surgical treatment despite the
haematoma volume
6) low-volume (< 20 ml) epidural haematoma of the posterior fossa causing
occlusive hydrocephalus revealed on clinical CT or MRI scans
According to recommendations by M.R.Bullock et al.(2006) surgical evacuation is
indicated in patients (despite Glasgow Comas Scale) with epidural haematoma volume
> 30 cm3, subdural haematoma width > 10 mm and midline shift > 5 mm demonstrated
on CT.
Surgical evacuation is indicated in comatose patients (GCS < 9) if the following
clinical signs are present:
- subdural haematoma width < 10 mm;
- midline shift < 5 mm;
- GCS drop by 2 items at the interval between the moment of trauma and in-
hospital admission;
- anisocoria or fixed pupils;
- ICP > 20 mm Hg;
Based on methods of neurovisualization there was outlined a group of patients with
traumatic extracerebral haematomas (subdural or epidural) who can benefit from
conservative treatment and show favourable outcomes: The indications for conservative
treatment are:
1) haematoma volume < 30 ml for temporal localization and < 40 ml for frontal or
other supratentorial localization on condition minor non-aggravating cerebral
and focal symptoms are present, and clinical signs of brain dislocation are
absent (and ICP is below 25 mm Hg); a 5-mm midline shift is possible on CT or
MRI scans on condition it does not cause dislocation hydrocephalus.
2) asymptomatic haematoma volume < 50 ml
3) small-size epidural or subdural haematomas with clinical decompensation or CT
- MRI changes caused by associated focal or diffuse brain damage
4) subtentorial epidural haematoma volume < 20 ml in patients with minimal
non-aggravating neurological deterioration and without signs of CSF pathways
blockade
5) subdural haematoma width < 10 mm in case of clear consciousness, minor
midline shift (up to 3-5 mm) and absence of basal cistern compression
According to recommendations developed by M. Bullock et al. (2006), patients with
epidural haematomas with diameter of < 30 cm3 , width < 15 mm and midline shift <
5 mm, with GCS score of 8 and without neurological deterioration can be treated
 Management of severe traumatic brain injury (TBI) 697

conservatively on condition regular CT control examinations are performed at a

neurosurgical clinic.
It should be specially stressed that conservative treatment of epidural and subdural
haematomas requires dynamic neurological control, repeated CT or MRI examinations.
That is why conservative treatment of epidural and subdural haematomas should be
performed only in neurosurgical clinics.

3.3 Depressed Skull Fractures

Patients with open skull fractures and depressions exceeding the bone width should
be surgically treated in order to prevent infectious complications.
Depressed fractures can be treated conservatively if there is no clinical or radiological
evidence of dura mater damage, intracranial haematoma, frontal sinus involvement,
marked cosmetic deformation, wound infection, pneumocephalus with bone
compression not exceeding its width.

3.4. Posterior Fossa Damage

Surgical treatment is indicated in patients with CT evidence of mass-effect or
neurological deterioration caused by posterior fossa damage. Mass-effect on CT scans in
these cases is presented by deformation, dislocation or obliteration of the IY ventricle,
compressed basal cisterns or their absence on CT and occlusive hydrocephalus.
Patients with posterior fossa damage should take conservative treatment with regular
CT or MRI examinations, provided there is no signs of mass-effect on CT scans or
neurological dysfunction without rough disturbances.

3.5 Diffuse Axonal Damage (DAI)

Patients in the acute stage of DAI apparent on CT or MRI should avoid any operative
intervention. Surgery is indicated only in patients with DAI accompanied by focal
damages (depressed fractures, epidural or subdural haematomas etc) or diffuse brain
swelling with a risk of brainstem compression. DAI in these conditions is often
accompanied by subdural collections of CSF above the anterior structures of large
hemispheres. By mistake they can be taken for large-size hygromas and as such surgically
removed. One should avoid surgery because of a non-aggressive character of CSF
collections and a tendency to resorp with time.
Severity and outcome of DAI depend not only on primary axonal damage but also on
secondary brain damage (oedema, swelling, metabolism disturbances) and extracranial
complications. Effective management of DAI should be aimed at preventing secondary
brain damage and extracranial pathology. Minimally invasive, endovascular or stereotactic
surgery is indicated in patients in the late stage of DAI in order to avoid surgical
complications like normotensive posttraumatic hydrocephalus, carotid-cavernous
fistulas, chronic subdural haematomas etc.
Prognosis and outcome in 6 months following DAI depend on duration and depth of
coma. According to the experience of Burdenko Neurosurgical Institute, the survived
majority of patients in coma lasting 7 days showed moderate disability and even good
recovery. In coma lasting 8 days or more the prognosis was rather poor - severe disability
or vegetative state.
698 Head Trauma

The correlation analysis showed an evidently significant dependence of outcome of

DAI on duration and depth of coma. The longer and deeper coma is, the worse
prognosis (outcome) is expected. Age factor here plays an important role. The analysis
showed a close correlation existing between duration of coma and outcomes in children
and adults; this correlation was significantly higher in children. Children in prolonged
coma develop severe disability or vegetative state with a relatively low mortality rate.
Adults usually show high morality rate and relatively moderate disability.
Long-term (1-8 years) follow-up of DAI shows good recovery predominance in
children. At the same time, this age group shows the longest duration of vegetative state.

Conclusion
Though incidence of TBI is considerably lower compared to mild head injury, it
remains the main cause of mortality, long-lasting sequelae and disability among
population and is regarded as a serious economic and social burden for the family, society
and state. That is why correct organization of neurotraumatological management for
patients with traumatic brain injuries is the primary task for Public Health Care in any
country. Beside adequate intensive therapy and urgent surgery further steps are necessary
in order to prevent secondary brain damage.

REFERENCES
1. Adelson P.D., Bratton S.L., Carney N.A. et al.// Guidelines for the acute medical
management of severe traumatic brain injury in infants, children and
adolescents//Pediatric Crit Care Med 2003; 4: S417-S491
2. Bullock R., Chestnut R., Ghair J. et al//Guidelines for the surgical management of
traumatic brain injury//Neurosurgery, 2006, 58, S2—62
3. Bratton S., Bullock M.R., Carney N. et al//Guidelines for the management of severe
traumatic brain injury. 3d Edition/J.Neurotrauma 2007, v.24, S.1
4. Potapov A., Kravchuk A., Zakharova N.//Head trauma, p. 807-919 in Book of Kornienko
V., Pronin I. “Diagnostic neuroradiology”, 2009, Springer-Verlag, Berlin - Heidelberg
 699

Neuromonitoring for Head Injury

Monitoring of intracranial pressure and
cerebral blood flow and metabolism
-basic and advanced monitoring tools-
NOBUYUKI KAWAI, M.D., KENYA KAWAKITA, M.D., TAKASHI TAMIYA, M.D.
Department of Neurological Surgery, Kagawa University Faculty of Medicine

Key words: brain tissue oxygen saturation, cerebral blood flow and metabolism,
cerebral perfusion pressure (CPP), dynamic CT, intracranial pressure
(ICP), jugular venous oxygen saturation (SjvO2), laser Doppler flowmetry
(LDF), microdialysis, monitoring, near infrared spectroscopy (NIRS),
positron emission tomography (PET), single photon emission
tomography (SPECT), stable xenon CT, traumatic brain injury (TBI),
transcranial Doppler (TCD)

Introduction
The most important monitoring in practical neurosurgery is patient observation.
Regular assessments of consciousness levels, verbal responses and motor responses
should be performed and recorded according to the Glasgow Coma Scale (GCS) in the
clinical flow chart. A witnessed deterioration in GCS or the development of new focal
signs should be regarded as a life-threatening sign and mandate immediate CT scanning.
In an unconscious, sedated patient in the intensive care unit (ICU), an assessment of
intracranial pathology made by clinical examination is limited. Standard general
monitoring for all such patients is required including oxygen saturation (SaO2), ECG,
mean arterial blood pressure (MAP) and urine output. The brain-specific monitoring
includes intracranial pressure (ICP) monitoring and cerebral blood flow (CBF) and
metabolism monitoring. The primary goal of management for a critically ill patient is the
prevention of secondary brain damage due to neuronal hypoxia and hypoperfusion. Ideal
monitoring provides a continuous, objective, and readily interpretable measure of
intracranial pathology even in an unconscious patient. As with any monitoring system,
one would like to detect potentially harmful complications and intervene before they
result in permanent morbidity and mortality. This chapter focuses on the applications
and limitation of bedside monitoring of ICP, CBF, cerebral oxygenation and metabolism
in the brain in patients with traumatic brain injury (TBI).

ICP monitoring: basic and very useful

As the cranial vault is essentially a closed, fixed bony box, its volume is constant. This
theory is described by the Monro-Kellie doctrine, proposed in the early 19th century:
700 Head Trauma

v. intracranial (constant) = v. brain + v. CSF + v. blood + v. mass lesion

As all these components are fluids, and non-compressible, once the cranial vault is
filled, the pressure raises dramatically. Raised ICP may reduce the cerebral circulation by
reducing the cerebral perfusion pressure (CPP) (defined as the difference between
mean arterial pressure and ICP). As an intracranial mass lesion or edematous brain
expands, some compensation is possible as cerebrospinal fluid (CSF) and blood move to
the spinal canal and extracranial vasculature. Once this mechanism is fully exhausted, a
rapid and steep rise in ICP is seen, even with only small changes in intracranial volume
(Fig. 1).

Fig. 1 Volume-pressure curve. Edema and hematoma associated with head injury
reduce compliance and pressure begins to rise earlier and more steeply.

Raised ICP is a common problem in patients with traumatic brain injury (TBI).
Frequent causes are intracranial mass lesions, disorders of CSF circulation, brain edema,
or more diffuse pathologic processes (e.g. hypercapnea). ICP monitoring provides
continuous data regarding the pressure within the cranial vault. ICP monitoring may be
required for patients with a GCS of 8 or less and is essential in patients in whom
neurological assessment is unattainable (such as barbiturate therapy or neuromuscular
blockade) (Fig. 2). Indications for ICP monitoring vary from unit to unit. The Brain
Trauma Foundation recommends ICP monitoring in traumatic coma patients (GCS ≤
8) with an abnormal CT scan (Diffuse Injury II-IV or high or mixed density lesions > 25
ml either). Patients admitted to the ICU with traumatic coma and a normal CT scan over
40 years with abnormal motor posturing or significant extracranial trauma associated with
systemic hypotension (BP < 90 mmHg) should be considered for ICP monitoring (Fig.
2). The gold standard for assessing ICP is an intraventricular drain inserted into one of
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 701

Fig. 2 Indications for ICP monitoring and risk of increased ICP.

Fig. 3 ICP monitoring with an intraparenchymal ICP sensor and transducer (Codman®).
702 Head Trauma

the lateral ventricles and connected to an external pressure transducer. The external
auditory meatus (equivalent to the foramen of Monro) is usually used as the reference
point. In addition to monitoring pressure, these catheters allow withdrawal of CFS to treat
raised ICP. The main limitation of this method is the risk of infection, which increases
over time and is in the range of 6-11 percent. Coagulopathy is the contraindication to ICP
monitoring due to high risk of intraparenchymal or intraventricular hemorrhage. The
catheter may be difficult to place with increased ICP, since the lateral ventricles change
shape under increased pressure and are often quite small because of the brain expanding
around them from injury and swelling. The best alternative to the ventricle catheter are
intraparenchymal probes (Fig. 3). Alternatively, subarachnoid, subdural and epidural
devices can be used. However, the accuracy of these devices, especially epidural devices,
is lower than that of intraventricular or intraparenchymal catheters. Pressure measured
in the lumbar CSF space is not reliable and may be dangerous (brain herniation) in
patients with space occupying lesions.
Normal ICP depends on age and body posture. Normal ICP in a supine position ranges
between 5 and 15 mmHg in an adult. In an infant, 1.5-6 mmHg are considered normal,
whereas in children values between 3 and 7 mmHg are considered normal. There is no
defined set point at which interventions for intracranial hypertension should be initiated,
but levels above 20 mmHg are usually treated. However, there has been no randomized
controlled trial showing an outcome benefit for patients with ICP monitoring when
compared with patients without ICP monitoring. It is probably more important to
maintain an adequate CPP. Reduced CPP and brain herniation have been considered the
principle mechanisms of secondary brain damage following severe head injury2. When
CPP is used as a target for therapy there is controversy as to which threshold to be used.
CPP should be maintained above the expected lower limit of autoregulation, which is
above the level at which CBF is expected to fall. The revised guideline of the Brain
Trauma Foundation (BTF Guideline, 2003) suggests a lower limit of 60 mmHg. Clinical
studies indicate that a CPP of at least 60 mmHg is sufficient to maintain adequate
brain tissue oxygen levels and a CPP > 60 mmHg does not provide further benefit in
patients with head injury3,4. A controlled study indicated that aggressive management of
CPP above 70 mmHg may increase the incidence of acute respiratory distress syndrome
(ARDS)1. A previous study suggests that cerebral perfusion is more sensitive to arterial
hypotension, especially hemorrhagic hypotension than to intracranial hypertension. In
a hypotensive patient, even a small increase in ICP could be harmful. Alternatively, an
elevated mean arterial pressure may protect the brain from ischemia against a raised ICP.
ICP monitoring should be continued until the patient can be assessed clinically, ICP has
stabilized (< 20 mmHg) and cerebral edema has resolved on CT scan. This occurs in the
majority of patients within 7 days of the head injury or surgery. Patients with refractory
intracranial hypertension may require monitoring for a longer period, although this may
increase the risk of infectious complication and loss of wave form. In this situation, ICP
monitors may need to be replaced or removed and patients should be assessed by serial
CT scan or clinically.
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 703

Cerebral blood flow and metabolism monitoring

The human brain consumes a huge amount of energy. The brain (2% of body mass)
receives 15-20% of the cardiac output and utilizes 20% of the total (resting) oxygen
consumption and 25% of the total glucose consumption. To maintain adequate brain
function, the energy is mostly supplied by glucose oxidation (during aerobic respiration
38 molecules of ATP are produced for every molecule of glucose). When the glucose and
oxygen supply is decreased due to reduction of the cerebral blood flow (CBF), the
brain is functionally impaired and later results in irreversible neuronal damage.
Thresholds for ischemia have been described with neurophysiological (functional)
failure occurring at 16-20 mL/100g/min and irreversible metabolic failure occurring at
8-12 mL/100g/min. Reduction in CBF does not necessarily result in ischemia because
further reduction in cerebral metabolism is common in severe TBI. The diagnosis of
cerebral ischemia requires demonstration that the CBF is insufficient for a given
metabolic demand. Therefore, it is essential to simultaneously evaluate the cerebral
blood flow and metabolism to make important management decisions in practical
neurosurgery.
Monitoring of CBF and metabolism is divided into continuous (bedside) monitoring
techniques and static (imaging) methods. Continuous monitoring techniques include the
middle cerebral artery flow velocity measured with transcranial Doppler (TCD), cortical
perfusion with laser Doppler flowmetry, oxygen delivery with jugular venous oxygen
saturation (SjvO2) catheters, near infrared spectroscopy (NIRS) and brain tissue oxygen
sensors, and metabolism with microdialysis. On the other hand, static imaging using
single photon emission tomography (SPECT) and positron emission tomography
(PET) can obtain values for CBF, oxygen utilization and glucose metabolism with high
topographical resolution, although with the disadvantage of limited accessibility and low
frequency of observation. Continuous monitoring techniques and static imaging
methods are potentially complementary. This section describes the applications and
limitation of neuromonitoring approaches to evaluate the CBF, cerebral oxygenation and
metabolism in the brain.

Bedside monitoring
(a) Transcranial Doppler: basic and useful
Transcranial Doppler (TCD) ultrasonography is a non-invasive method of assessing
the state of the intracranial circulation. TCD provides a means of measuring relative
changes in cerebral perfusion by evaluating blood flow velocity (FV) in the basal
cerebral arteries through thin regions of the skull, usually the transtemporal route
(above the zygomatic arch) (Fig. 4). The linear relationship between CBF and mean FV
is only present if the diameter of the insonated vessel and the angle of insonation
during the examination do not change. TCD can be used for measuring FVs from
several vessels of the Circle of Willis, but most published data refer to the middle
cerebral artery (MCA). MCA has a favorable orientation readily accessible to TCD and
the insonation depth is between 45-60 mm through the transtemporal route (Fig. 4).
Furthermore, the MCA delivers about 70-80% of the ipsilateral carotid artery blood flow,
and can therefore be considered to reflect global cerebral flow to the majority of the
704 Head Trauma

Fig. 4 Measurement of the middle cerebral artery (MCA) flow velocity through
transtemporal route with a 2 MHz Doppler probe.

ispilateral cerebral hemisphere. There is an inverse correlation between the severity of

head injury and the MCA FV. Low FV in the intracranial circulation after TBI is due to
low CBF and high ICP levels. However, the raw admission FV data is not a reliable
predictor of outcome for individuals except where extremely low FVs were recorded.
In practical neurosurgery, TCD is widely used to detect cerebral vasospasm after
subarachnoid hemorrhage (SAH) and determine which patients should be further
evaluated by conventional angiography. In TBI, cerebral vasospasm after severe head
injury has long been recognized and is usually associated with traumatic subarachnoid
blood (Fig. 5). The FVs recorded in such cases are usually between 100 and 150 cm/sec,
usually lower than those found after aneurysmal SAH, and the time course is shorter,
occurring within the first 2-5 days5. CBF can be occasionally impaired below the
ischemic threshold resulting in cerebral infarction. TCD is useful in monitoring the
temporal course of cerebral vasospasm and thought to be valuable in the day-to-day
evaluation of traumatic SAH patients. However, one must take into account that a
variety of factors such as technical issues, anatomical issues, intracranial and extracranial
physiological issues including ICP, mean arterial pressure, hematocrit, and arterial
CO2 content influence the flow velocities.
TCD is also useful in testing autoregulation and cerebrovascular reactivity in TBI
patients. When autoregulation is intact, FV should remain unchanged with a changing
CPP. Lowering arterial blood pressure (ABP) is not acceptable for ethical reasons in TBI
patients. Instead, increase in ABP using various vasopressors is a popular and relatively
safe way to evaluate the autoregulatory status. Impaired autoregulation is frequently
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 705

Fig. 5 Traumatic subarachnoid hemorrhage and cerebral vasospasm. CT scan showed traumatic
subarachnoid hemorrhage and delayed hematoma formation in the left sylvian fissure. The patient
exhibited right hemiparesis on day 6. 3D-CT and conventional angiography revealed vasospasm in the
middle cerebral artery.

reported in the most severe TBI patients6. Likewise, measurement of cerebrovascular

reactivity to CO2 has been widely applied in clinical practice to evaluate cerebral arterial
function. A significant correlation between the changes in MCA FV measured by TCD
and arterial CO2 levels has encouraged the use of TCD to measure CO2 cerebrovascular
reactivity. In normal individuals, a 1 kPa (7.5 mmHg) increase in CO2 causes a 22%
change in MCA FV. Impaired or absent CO2 reactivity indicates the ability of the
cerebrovascular bed to vasodilate and loss of the cerebrovascular reserve. CO2 reactivity
may provide predictive information in patients with TBI.
Elevated levels of FV can either indicate a narrowed MCA (vasospasm or stenosis), of
high CBF (hyperemia). Since they require a different therapeutic approach, their
distinction is critically important. The ratio of intracranial to extracranial velocities
(Lindegaard ratio) might be used to differentiate the two states and vasospasm is likely
when this ratio exceeds 3. Concomitant jugular venous bulb oximetry (see below) may
also provide valuable information in this setting. Decreased jugular vein oxygen
saturation (below 55%) is helpful to consider vasospasm, on the other hand values above
85% are suggestive of hyperemia.
(b) Laser Doppler flowmetry: basic but uncommon
Laser Doppler flowmetry allows real-time measurements of microcirculation (red
blood cell flux) with excellent dynamic resolution without quantification of CBF. The
laser beam reflects off moving red blood cells and undergoes Doppler shift. The degree
of Doppler shift is proportional to the velocity of the cell. This light randomly reflects back
706 Head Trauma

Fig. 6 Principles of measuring of jugular venous oxygen saturation showing normal SjO2 in the
presence of normal blood pressure (blood flow), and reduced cerebral SjO2 with a reduction in
blood pressure (blood flow).

out of the tissue and onto a photodetector, which then calculates the average velocity of
cells within the tissue. The sample volume is quite small (1-2 mm3) and only relative
changes can be assessed. Clinical application of LDF is limited as this method is invasive
(exposing the brain surface).
(c) Jugular venous oxygen saturation: basic and useful
Jugular venous oxygen saturation (SjvO2) measures the oxygen saturation of the
venous efflux from the brain as an indicator of the amount of oxygen extracted by the
brain (Fig. 6). SjvO2 is measured with a catheter that is placed by retrograde cannulation
of the internal jugular vein until the tip is at or near the jugular bulb, usually at the first
to second cervical vertebrae. A SjvO2 catheter contains two optical fibers. Light is
directed into the blood by one of the fibers, reflected back to the second fiber, and
transmitted to a photosensor. The photosensor measures the absorption of the reflected
light at the various wavelengths with SjvO2 displayed as a percentage of oxygenated
hemoglobin to total hemoglobin.
By monitoring the SjvO2 in conjunction with arterial blood gases, the arterio-venous
difference in oxygen content can be established as a more specific means of assessing the
relationship between blood flow and metabolism. Cerebral oxygen consumption
(CMRO2) is described by the following equation (CaO2 = arterial oxygen content,
CjvO2 = oxygen content of jugular venous blood):
CMRO2 = CBF × [CaO2 - CjvO2]
The difference in oxygen content between arterial and jugular venous blood is
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 707

expressed by the term of AVDO2. By rearranging the above equation it is expressed that:
AVDO2 = CMRO2 / CBF
In practice, the AjvDO2 can be calculated from the following equation:
AVDO2 = 1.34 × Hb [SaO2 – SjvO2] + 0.003 [PaO2-PjvO2]
One gram of hemoglobin can carry 1.34 mL of oxygen and therefore fully saturated
hemoglobin contains about 20 mL of oxygen per 100 mL of blood. In contrast, the
dissolved oxygen content of this blood is 0.3 mL oxygen per 100 mL of blood. As
dissolved oxygen is negligible and can be ignored and hemoglobin is constant, the
AVDO2 can be determined by the difference in SaO2 and SjvO2. The normal range of
AVDO2 is 4-9 mL O2 per 100 mL of blood (values <4 indicate hyperemia, >9 indicate
ischemia).
Normal values of SjvO2 range from 60 to 80% and are relatively constant due to the
coupling between CBF and CMRO2. Uncoupling following injury is associated with
energy perturbations. A decrease in the SjvO2 represents an increase in cerebral oxygen
extraction. This may result from systemic hypoxia, low CBF secondary to hypotension
or vasospasm or increased ICP with a subsequent decrease in CPP (Fig. 6). Factors that
increase cerebral oxygen demand such as seizures or fever may also play a role (Fig. 7).

Fig. 7 Causes of low SjvO2 and high SjvO2. SjvO2 represents a balance between
oxygen supply and consumption in the brain and normal SjvO2 is 60-80%.

The interpretation of increased SjvO2 is potentially more difficult. One possibility is that
the patient has abnormally high blood flow (hyperemia) to the brain secondary to the loss
of autoregulation. A more common situation is where the brain tissue is not viable for
oxygen extraction from the blood (massive infarction) or where ICP is so high that blood
708 Head Trauma

is largely shunted past the capillary beds leading to arterial blood in the jugular vein.
Several studies have investigated the association between SjvO2 and clinical outcome.
Both abnormally high and low SjvO2 levels have been associated with poor clinical
outcome in TBI patients. In a study of continuous SjvO2 monitoring in TBI patients, one
or more episode of jugular desaturation (< 50%) is strongly associated with poor
neurological outcome7. SjvO2 monitoring is also useful in monitoring of therapeutic
interventions, for example, in setting the safe degree of hyperventilation used following
head injury to reduce ICP. It is now common practice to set the degree of
hyperventilation whilst maintaining the SjvO2 within the normal range, but further
randomized, prospective studies are necessary to determine the optimal use of SjvO2-
directed therapy to improve outcome.
There are several limitations to SjvO2 monitoring in routine clinical use. Firstly, by
monitoring global hemispheric oxygen venous saturation, focal areas of ischemia may not
be detected, and a relatively large volume of tissue must be affected before the SjvO2 level
drops significantly. Furthermore, posttraumatic alterations in CBF are often
heterogeneous. Regional CBF may be simultaneously increased in some areas of the brain
and decreased in others. Secondly, only one jugular vein is monitored. Although blood
in the jugular bulb is derived from both cerebral hemispheres (approximately 70%
ipsilateral and 30% contralateral), it is generally accepted that most patients have a
dominant side of venous drainage, usually the right. Thirdly, SjvO2 requires frequent
recalibration and a high percentage of readings are erroneous because of catheter
movement, displacement, or clot formation.

Fig. 8 Principles of near infrared spectroscopy. This tool detects a relative change
of regional tissue oxygenation via photon scattering.
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 709

(d) Near infrared spectroscopy (NIRS): basic but unclear role

Near infrared spectroscopy (NIRS) is a non-invasive method of measuring regional
cerebral oxygen saturation (rSO2) using a scalp oximeter similar to pulse oximetry
(Fig. 9). The technique of NIRS is based on the principle of light attenuation by the
chromophores* oxyhemoglobin (HbO2), deoxyhemoglobin (Hb) and cytochrome
oxidase. Changes in the detected light levels can therefore represent changes in the
concentrations of these chromophores. Clinical use of NIRS in the brain has been well
established in neonates where transillumination is possible. The accuracy and reliability
of NIRS has been questioned because the sample volume cannot be clearly defined
and the extracranial tissue layers may contaminate the readings. Sensitivity and
quantification are other limitations of NIRS monitoring in the brain. Several companies
have devised algorithms that seek to provide an absolute measure of cerebral oxygen
saturation, but the accuracy of these methods remains a concern. In spite of several
limitations, the technique has demonstrated some potential in multimodal bedside
monitoring of TBI patients8. NIRS has future promise as a bedside tool for cerebral blood
flow measurements and as a cerebral imaging modality for mapping structure and
function. Much further work is needed before we can identify a clear role for this
technique in the setting of head injury.
*Chromophore: groups of atoms in an organic compound that absorb light at certain
wavelengths. A particular chromophore gives the compound its distinctive color by
causing it to absorb light selectively.
(e) Brain tissue oxygen sensors: advanced
Measurements of SjvO2 provide an index of global oxygen metabolism and may
miss the focal area of ischemia. The development of sophisticated probes (<1mm
diameter), which can be placed directly into the brain parenchyma, has enabled the
measurement of focal brain tissue oxygen tension (ptiO2), carbon dioxide tension
(ptiCO2), hydrogen ion concentration (pH) and temperature. Currently, two types of
PtiO2 sensors are available for human intracerebral monitoring: the Licox (Integra
Neuroscience, Plainsboro, NJ) and the Neurotend (Codman, Raynam, MA) devices.
These sensors are placed adjacent to the ICP monitoring catheter in the brain tissue via
a modified skull bolt. The Licox sensor consists of a miniature electrode for the
measurement of brain oxygen. The sampling area of the Licox probe is about 14 mm2.
The Neurotend system is a multiparameter sensor measuring ptiCO2, pH, and
temperature in addition to ptiO2. The sampling area of the Neurotend probe is about 14
mm2. Catheters are precalibrated and can be inserted directly into the brain tissue,
which can be normal brain tissue or penumbra close to a lesion. Although termed
tissue gas sensors, the characteristics of the measurements have not been fully determined.
It is currently thought that the tissue gas tensions using these sensors equate to end-
capillary partial pressures.
In practice, the tissue gas oxygen can be used as an indicator of the balance between
oxygen delivery and metabolism. Studies have shown that ptiO2 values in patients with
normal ICP and CPP are between 25 and 30 mmHg in TBI patients. A low PtiO2 is caused
by a number of pathophysiological conditions presenting tissue hypoxia, including
intracranial hypertension, systemic hypotension, hypocapnea, and vasoconstriction
due to excess hyperventilation. The critical threshold for ischemic damage and a poor
710 Head Trauma

outcome has been proposed at ptiO2 values of 10-15 mmHg in TBI patients9. In contused
brain, ptiO2 is always below 10 mmHg. Therefore, in order to detect avoidable hypoxia
and ischemia, it is recommended that the probe is placed in non-lesioned brain. It is
important to understand the heterogeneous nature of the brain when interpreting
oxymetry data especially in TBI patients. Furthermore, depending on the probe’s
relationship to the arterial microvessels, a gradient within the tissue can exist with
oxygen levels decreasing from artery to venous circulation. The probes appear reliable and
safe for up to 7 days, and are feasible and sensitive for the detection of systemic
pathophysiological events over this time.
(f) Microdialysis: advanced
The principle of microdialysis (MD) is based on the passive transfer of water-soluble
substances from the extracellular fluid across a semi-permeable dialysis membrane
(polycarbonate membrane) into a carrier liquid, called the perfusate (normal saline or
Ringer’s solution) (Fig. 9). Diffusion drives the passage of molecules across the membrane
along their concentration gradient. Molecules at high concentration in the brain
extracellular fluid (ECF) pass into the perfusate with minimum passage of water and, as
the perfusate flows and is removed at a constant rate, the concentration gradient is
maintained. The transition of the application of MD from animal studies to clinical bed
side monitoring has required the development of specific clinical MD products
(CMA/microdialysis, Stockholm, Sweden) (Fig. 9). This method has been investigated
as a monitor of cerebral metabolism in patients with severe TBI and subarachnoid
hemorrhage10. MD measures biochemical changes in the brain ECF that are known to be

Fig. 9 Measurement of brain metabolism with an intracerebral microdialysis catheter.

Neurochemical substances cross a dialysis membrane from the extracellular space into the
dialysate.
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 711

early markers of tissue damage and ischemia and therefore has the potessntial to
monitor the process of secondary injury in these patients.
Intracerebral MD probes (CMA70, CMA/microdialysis) can be inserted at the time of
craniotomy or in the intensive care unit. In TBI patients with diffuse injury one catheter
may be placed in the right frontal region. In patients with focal mass lesions one
catheter should be placed in the penumbra that is the pericontusional tissue. A second
catheter may be placed in normal tissue. They require fixation to prevent dislodgement
which can be achieved by tunneling the catheter under the scalp and securing it with
sutures. The samples are continuously collected into microvials that are analyzed at the
bedside by a microdialysis analyzer (CMA600 analyzer, CMA/microdialysis) (Fig. 9). This
instrument enables the measurement of glucose, lactate, pyruvate, glutamate and
glycerol using kinetic enzymatic reaction. In TBI patients a high lactate/pyruvate ratio has
been found to be correlated with the severity of clinical symptoms and fatal outcome after
severe trauma. Glucose, glycerol and glutamate have been shown to be useful markers of
disturbance of energy metabolism. Overall, MD may be useful in severe cases of TBI in
which monitoring of ICP and CPP is required. Further studies are required to determine
whether MD can be applied to monitor and direct treatment for individual patients.

Static imaging
(a) Stable xenon CT: basic and useful
The main advantage of stable xenon computed tomography (Xe/CT) is that it
noninvasively provides rapid access to quantitative regional CBF information coupled to
CT anatomy. The technology can be incorporated into all existing CT technology at
relatively little expense. This technique utilizes inhaled nonradioactive xenon (inspired
concentration of 28-32%) and concurrent acquisition of CT images. These data allow
calculation of CBF using application of the Fick principle*. Changes in radiographic
contrast on tomographic brain images provide a means of calculating wash-in of Xe on
a pixel-by-pixel basis. With the advent of portable CT machines, Xe/CT may have
expanding roles as neuroimaging tools in the neurological intensive care unit.
Studies can be repeated within a short period of time allowing assessment of clinical
intervention, such as hyperventilation or CPP augmentation. Such data have been used
to demonstrate early hypoperfusion consistent with ischemia after TBI, raised ICP
secondary to hyperperfusion and abnormal CO2 reactivity and autoregulation. Despite
these advantages, quantitative CBF studies can be difficult to perform in patients with
pulmonary injury or disease since the technique is based on the assumption that the end-
tidal Xe concentration is identical to the arterial concentration. Xe is an anesthetic
agent and may cause sedation and respiratory depression. The direct vasodilatory effect
of Xe may also be responsible for increasing cerebral vascular caliber and result in
artificial increase in CBF.
*The amount of a substance taken up by the circulation per unit of time equals the
arterial level of the substance minus the venous level multiplied by the blood flow.
(b) Dynamic CT: basic
The development of multi-detector computed tomography (CT) and the availability
of image reconstruction software have enabled this technique to be used in the clinical
setting. CT perfusion involves sequential acquisition of axial data during a bolus
712 Head Trauma

administration of iodinated contrast medium. Since the change in CT enhancement is

proportional to the concentration of contrast, perfusion is calculated from the time course
of contrast enhancement profiles for each pixel in relation to the profile of arterial
contrast enhancement (the arterial input function). In practice, the selection of an
‘arterial’ pixel represents a significant problem in implementing this technique, since the
identification of an ‘arterial’ pixel with no partial volume effects from brain parenchyma
can be difficult. On the basis of the central volume theorem, CT perfusion is able to
provide parametric images of cerebral blood volume (CBV), mean transit time (MTT),
and CBF. Perhaps the greatest advantage of this technique is the measurement of CBV,
since of the physiological variables affecting ICP, CBV has the greatest potential to be
modulated by medical interventions. It is a widely accessible, rapid, and accurate
technique that can provide a means for directing therapy and predicting outcome after
TBI. However, the number and location of selected brain slices is limited due to
radiation exposure, and repeat imaging after a therapeutic intervention is limited by the
volume of contrast medium that can be safely administered.
(c) Single photon emission computed tomography (SPECT): advanced
SPECT uses conventional γ-emitting tracers with multiple detectors to generate
tomographic images. Technetium-99m-hexamethylpropylamine-oxime (99mTc-HMPAO)
and 123I-iodoamphetamine (123I-IMP) have been commonly employed to investigate CBF
in the brain (Fig. 10). The technique is simple and three dimensional, but the produced
images are of relatively low resolution and generally non-quantitative (Fig. 11).

Fig. 10 Diffuse hypoperfusion in a patient with diffuse traumatic brain injury. MRI FLAIR images
showed multiple high intensity spots in the frontal white matter and corpus callosum. SPECT with 99mTc-
ECD exhibited diffuse brain hypoperfusion in the bilateral hemispheres.
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 713

Fig. 11 Principles of SPECT and PET.

(d) Positron emission tomography (PET): advanced

PET measures the accumulation of positron-emitting radioisotopes in the brain.
The tracers can be administrated via the intravenous or inhalational route, and for
imaging the brain, 15-oxygen (15O) is employed to measure CBF, CBV, oxygen metabolic
(CMRO2), and oxygen extraction fraction (OEF), whereas 18-fluorodeoxyglucose
(18FDG) is used to measure cerebral glucose metabolism (Fig. 12). The emitted positrons
are annihilated in a collision with an electron resulting in the release of energy in the form
of two photons (γ rays) released at an angle of 180˚ to each other. This annihilation
energy can be detected by coincidence detectors, and the region of each reaction can be
localized in the brain by computer algorithms (Fig. 11). Although PET is clearly capable
of defining cerebral physiology and pathophysiology, the necessity to transport sometimes
unstable patients, and the cumbersome technology makes PET of limited utility as a
practical neuromonitoring tool.
PET has been successfully used to investigate changes in physiology after TBI. The
findings of these PET studies demonstrate that early reductions in cerebral perfusion can
result in cerebral ischemia that is associated with poor outcome, despite optimal
management of ICP and CPP. However, other studies have failed to show conclusive
evidence of cerebral ischemia in TBI patients. Indeed, TBI patients commonly
demonstrate global hypometabolism and metabolic crisis, which fails to recover in
patients who have a poor outcome11. PET studies can be repeated and used to assess
changes in physiology with commonly used therapeutic interventions, such as
hyperventilation and CPP augmentation. Such studies have demonstrated that moderate
reductions in PaCO2 can result in increase in the volume of brain tissue with CBF
values below the well recognized ischemic threshold (<20 mL/100g/min). The
714 Head Trauma

Fig. 12 Cerebral glucose metabolism in a patient with brain contusion and subsequent intracerebral
hematoma in the right frontal lobe. FDG-PET revealed severe glucose hypometabolism not only in the
right hemisphere but also the left hemisphere. The patient survived with a state of persistent
consciousness disturbance.

development of these ischemic areas is not reflected by reductions in jugular oxygen

saturations below the commonly accepted threshold for ischemia (<55%)12. It is clear that
the effect of common therapeutic interventions should be measured and only continued
where benefit is demonstrated. FDG-PET has also been used to quantify recovery from
TBI. While FDG uptake in the acute phase correlates poorly with clinical state, sequential
changes in FDG uptake in the brain parallel functional recovery.

Conclusion
Monitoring of brain after acute injury is central to the practice of neurocritical care for
patients with TBI. The most widely available monitoring is bedside clinical neurological
monitoring. Standard neuromonitoring techniques such as ICP and CPP measurement
are considered to be particularly important to prevent secondary brain injury. However,
such measurements may be insufficient in detecting subtle manifestations of brain
injury. The more recently developed neuromonitoring techniques including CBF
monitoring techniques, jugular venous oxygen saturation (SjvO2) and brain tissue
oxygen tension (ptiO2) monitoring, and cerebral microdialysis (MD), may provide
more detailed information regarding cerebral blood flow and metabolic function.
Moreover, new developments in imaging technology, both hardware and software,
have improved our understanding of the pathophysiology in TBI patients. Even as
 Neuromonitoring for Head Injury Monitoring of intracranial pressure and cerebral blood flow and metabolism -basic and advanced monitoring tools- 715

many of these tools are now becoming integrated into regular neurocritical care,
research is ongoing to determine the validity, reliability, and utility of these techniques
in the clinical management of TBI patients and in predicting and potentially improving
the clinical outcome.

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3. Juul N, Morris GF, Marshall SB, et al. (2000) Intracranial hypertension and cerebral
perfusion pressure: influence on neurological deterioration and outcome in severe
head injury. J Neurosurg 92, 1-6.
4. Untergerg AW, Kiening KL, Hartl R, et al. Multimodal monitoring in patients with head
injury: evaluation of the effects of treatment on cerebral oxygenation. J Trauma 42, S32-
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5. Martin NA, Doberstein C, Zane C, et al. (1992) Posttraumatic cerebral arterial spasm:
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injured patients. J Neurotrauma 12, 779-81.
8. Al-Rawi PG. (2005) Near infrared spectroscopy in brain injury: today’s perspective. Acta
Neurochir (Suppl) 95, 453-7.
9. Valadka AB, Gopinath SP, Contant CF, et al. (1998) Relationship of brain tissue pO2 to
outcome after severe head injury. Crit Care Med 26, 1576-81.
10. Bellander B-M, Cantais E, Enblad P, et al. (2004) Consensus meeting on microdialysis
in neurointensive care. Intensive Care Med 30, 2166-69.
11. Vespa P, Bergsneider M, hattori N, et al. (2005) Metabolic crisis without brain ischemia
is common after traumatic brain injury: a combined microdialysis and positron emission
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716

Depressed Skull Fracture

ÁPIO CLÁUDIO MARTINS ANTUNES, M.D., Ph.D1
ANDRÉ CERUTTI FRANCISCATTO, M.D.2
RAFAEL MODKOVSKI, M.D.2
THIAGO TORRES DE ÁVILA, M.D.2
1
Professor of Neurosurgery,
Porto Alegre School of Medicine, Rio Grande do Sul Federal University.
Head of Neurosurgical Unit, Hospital de Clinicas de Porto Alegre.
2
Resident of Neurosurgery, Hospital de Clinicas de Porto Alegre.

Key words: skull fracture, depressed, head injury, cerebral contusion, EDH, SDH,
traumatic SAH, Ping Pong fracture, Green Stick fracture

Depressed skull fracture is one of the most common conditions needing emergency
operation in neurosurgical practice (20). This fracture is considered clinically significant
if the outer table of a free piece of the fractured fragments lies below the inner table of the
skull. A depressed fracture may be closed or open (compound) if there is a skin
laceration over the fracture (4). Open fractures may be clean or dirty. An open depressed
fracture represents an emergency due to potential insemination of bacteria into the cranial
cavity (24).
Fractures with depressed fragments are more serious due to high risk of injury to the
underlying dural sinuses and brain. Intracranial lesions like cerebral contusions and
lacerations, diffuse axonal injury, concussions and brain edema may develop following
head injuries and may be localized to the epidural, subdural, subarachnoid, and
intracerebral regions (4, 10, 23).
Depressed fractures of the cranial vault in children under 1 year of age are different
from those that occur in older children and adults. This difference is due to the relative
plasticity of the infantile skull, which is not completely ossified. The skull bones of the
newborn and nursing infants, in general, possess great malleability. For this reason, the
depressed fractures occurring at this age are called “Ping Pong” or “Green Stick”
fractures. These terms describe nothing more than the conversion of the normal convex
surface of the cranium to a concave one secondary to trauma. It is possible for these
fractures to lacerate the underlying brain (16).

EPIDEMIOLOGY
Depressed cranial fractures may complicate up to 6% of head injuries in some series,
and account for significant morbidity and mortality. Compound fractures account for
up to 90% of these injuries (4, 22).
Seventy five percent of depressed fractures occur in the frontal or parietal regions, 10%
temporal, 5% occipital, and 10% other (2, 11, 12), and most of them are closed fractures
(75-90%) (22).
Congenital depressions of the skull have an incidence of 1/10,000 births (16).
 Depressed Skull Fracture 717

ETIOLOGY
In adults, skull fractures typically occur from motor vehicle accidents, falls or violence
(12, 20, 23). The cause of depressed skull fractures includes various perinatal factors for
the newborn and, postnatally, mainly head injury (16).

CLINICAL PRESENTATION
Approximately 25% of patients with depressed skull fracture never lose consciousness,
and another 25% report amnesia for less than an hour (14). The presentation may
vary depending on other associated intracranial injuries such as epidural hematoma, dural
tears, and seizures. The majority of significantly depressed fractures are discovered by
examination.
A diagnosis of skull fracture should be considered even in infants with minor
mechanisms of head injury who look well. However, infants with depressed skull
fracture rarely present without local signs of head injury on physical examination (8).

IMAGING STUDIES
Plain X-ray, computed tomography (CT), and magnetic resonance (MRI) are the most
common techniques in patients who have been submitted to a head injury (3).
Radiographs: If a skull fracture is diagnosed on radiography (Figure 1), the risk of an
intracranial haemorrhage is elevated (about 4.9 times higher than before testing) but one
cannot rule out an intracranial haemorrhage in patients for whom a skull X-ray does not
show a skull fracture. Hence, other than a fracture at the vertex that might be missed by
CT scan and picked up by a plain film, skull x-ray is of no benefit when a CT scan is
obtained (3).
CT scan: CT scan is the standard modality for aiding in the diagnosis of skull fractures
(Figure 2). Thinly sliced bone windows of up to 1-1.5 mm thick, with sagittal
reconstruction, are useful in assessing injuries. Helical CT scan is helpful in occipital
condylar fractures, but 3-dimensional reconstruction usually is not necessary. Twenty-
five percent of cases with fatal injuries do not demonstrate a skull fracture, although the
incidence of intracranial hematomas in patients who have skull fractures is much
higher than in those who do not (15). Skull fractures do not usually correspond with the
severity of brain injury (15, 19, 23, 25, 26). The indications for CT examination are severe
impairment of consciousness, focal neurological signs, and penetrating head injury.
Clinically, this is a high-risk group. A moderate-risk group are the ones injured with
minor disturbances of consciousness, progressive headaches, fracture of the skull base,
and those with multiple injuries. The low-risk group are patients with mild or moderate
posttraumatic headaches without loss of consciousness (3).
MRI: The availability of MR imaging data obtained in comatose patients after head
injury is scarce, because MR imaging is somewhat cumbersome to perform in patients
requiring ventilation and because, in the first hours after injury, its relevance is clearly
inferior to CT.MRI or magnetic resonance angiography is of ancillary value for suspected
ligamentous and vascular injuries (3).
718 Head Trauma

Fig. 1 Radiograph showing large left

frontal fracture.

Fig. 2 CT scan obtained with bone window

setting reveals right temporal depressed skull
fracture.
 Depressed Skull Fracture 719

MEDICAL THERAPY
Patients with open (compound) depressed cranial fractures may be treated
nonoperatively if there is no clinical or radiographic evidence of dural penetration,
significant intracranial hematoma, depression greater than 1 cm, frontal sinus
involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross
wound contamination. Nonoperative management of closed (simple) depressed cranial
fractures is a treatment option. Closed, linear cranial fractures are considered
nonoperative lesions unless associated with surgical intracranial masses (4). Simple
depressed fractures in neurologically intact infants are treated expectantly: these
depressed fractures heal well and smooth out with time, without elevation (24).
In patients with relatively clean compound injuries that are closed within 12 hours, 48
hours of antibiotic coverage is probably adequate. In patients with gross contamination,
dural laceration, or delayed closure, coverage for at least 5 to 7 days is recommended in
addition to tetanus toxoid (24). Sulfisoxazole or Cephazolin are commons
recommendation.

INDICATIONS FOR SURGICAL THERAPY

Most surgeons prefer to elevate depressed skull fractures if the depressed segment is
more than 5 mm to 1 cm below the inner table of adjacent bone. Indications for
immediate elevation are gross contamination, dural tear with pneumocephalus, and an
underlying hematoma (17, 19, 24). At times, craniectomy is performed if the underlying
brain is damaged and swollen. In these instances, cranioplasty is required at a later date
(24). In children with closed depressed fractures when CT suggests a dural tear, elevation
of the fracture and dural repair is indicated to prevent the development of a growing
fracture (24).

INTRAOPERATIVE DETAILS
Procedure is typically made under general anesthesia. To maintain intracranial
pressure, mannitol (1 g/kg) may be given in bolus at the beginning, and the PaCO2
should be kept at 30-35 mm Hg during the surgery. The scalp incision should be
cosmetically acceptable. A bicoronal incision is preferred for forehead depressions. For
closed depressed fractures behind the hairline, broad-based horseshoe-shaped (inverted
“U”) scalp flap can be used. Badly lacerated or devitalized scalp overlying the fracture
must be trimmed back to clean bleeding margins. Occasionally, an area of avulsed or
devitalized scalp is so extensive as to preclude direct closure of the wound. When this
occurs, a rotational scalp flap or rarely a free flap is required (24).
Bony fragments are elevated, and the dura is inspected for any tears. If a dural tear is
found, it should be repaired. Any foreign debris must be removed. Then, the wound is
copiously irrigated with sterile saline. Special attention is given to hemostasis to prevent
postoperative epidural collection. Bony fragments are soaked in antibiotic/isotonic
sodium chloride solution and are reassembled. Larger pieces may be wired together or
better fixed with miniplaques.
720 Head Trauma

There was no difference in infection rate between surgical cohorts who had bone
fragments replaced versus removed—results supported by a series of 225 patients with
depressed cranial fracture reported by Braakman (2), and a treatment strategy reported
as early as Macewan in 1888 (13).
Alternatively, titanium mesh also may be used to cover the defect in closed fractures.
Methyl metacrylate can be used instead of the bone pieces, but this should be avoided in
children. Indeed, absorbable bone plates and screws are recommended for use in
children (24).

DEPRESSED SKULL FRACTURES OF THE PING-PONG TYPE

The treatment of these fractures is surgical according to different authors, although
some of these fractures that happen in childbirth can elevate themselves spontaneously
(16). In cases with intact dura, a small, 1-cm scalp incision over the nearest suture
and elevation with a periosteal elevator passed just past the center of the depression result
in rapid resolution. Care must be taken to avoid levering on normal bone at the site of
entrance into the skull to prevent another depressed fracture (24).
There is some experience and recomendations that pressure above the angle of the
depression may elevate it. One has to perform the manipulation with the fingers seeking
the most prominent spot and applying pressure : in some cases, this reduces the fracture.
This technique is somewhat difficult and may produce additional trauma to the malleable
skull and soft tissues in the newborn. A breast milk extractor have been used for the
procedure in newborns with a depression larger than 2 cm in diameter (16).

DEPRESSED FRACTURES INVOLVING THE FRONTAL SINUS

Because of the location of the frontal sinus and its proximity to numerous intracranial
structures, inadequate treatment may lead to life-threatening intracranial infectious
complications. Meningitis, encephalitis, and brain abscess are the most common
intracranial complications. Other complications include persistent cerebrospinal leakage,
mucopyoceles, frontal osteomyelitis, meningoencephalocele, and nonunion of the
frontal bone. Orbital involvement may result in ophthalmoplegia, orbital abscess,
diplopia, enophthalmos, proptosis, preseptal cellulitis, and partial or complete loss of
vision. The most important tenet of frontal sinus fracture management remains the same:
create a safe sinus. This is accomplished by following four basic principles: reestablish the
frontal bony contour to its premorbid state, restore normal sinus mucosa with a patent
drainage system if possible, eradicate the sinus cavity if the normal mucosa or drainage
system cannot be reestablished, and create a permanent barrier between the intracranial
and extracranial systems to prevent overwhelming infectious complications (19).
Complex fractures affecting the orbit or intracranial contents require cranialization
or possibly obliteration (1, 22).

VENOUS SINUS TEARS

Depressed skull fractures overlying the major venous sinus in the absence of a CSF
 Depressed Skull Fracture 721

fistula or an associated hematoma, are often managed nonoperatively because of the high
associated risks of major sinus bleeding or sinus occlusion and venous infarction. Local
wound debridement and closure are often sufficient in these cases. In the presence of
clinical and radiographic evidence of sinus occlusion, however, surgical therapy may be
necessary with sinus repair or ligation depending on sinus damage, location, and
presence of trombosis (6). Because of the variability of sinus anatomy and the inability
of CT to adequately delineate the extent of a venous sinus injury, angiography or CT
angiography is recommended when surgery is being considered (24).

FOLLOW-UP
Adults with simple linear fractures of the vault, without any loss of consciousness at
the time of initial presentation and with no other complications, do not require long-term
follow-up. On the other hand, infants with similar fractures with dural tears need to be
monitored more closely because of the possibility of the skull fracture expansion (24).
Patients with contaminated open depressed skull fractures treated surgically should be
monitored with repeat CT scans a few times over the next 2-3 months to check for abscess
formation. Follow-up also is dictated by the complications associated with skull fractures,
for example, seizures, infections, and removal of bone pieces at the time of initial
debridement.

PROGNOSIS
Compound fractures are associated with an infection rate of 1.9 to 10.6% (13, 18, 22,
23), an average neurological morbidity of approximately 11% (4), an incidence of late
epilepsy of up to 15% (1, 14), and a mortality rate of 1.4 to 19% (1, 2, 18, 22).
Elevation of depressed fragments does not significantly improve neurological deficits.
Studies of both adults and children with compound or simple fractures support this
concept (22).
Prevalence of early post-traumatic epilepsy is 12.3% and there is no significant
association between dural tear and prevalence of post-traumatic epilepsy. Mortality rate
was 1.4%, but paediatric populations have a better outcome (21).

IN A NUTSHELL
A depressed skull fracture is considered clinically significant if the outer table of a free
piece of the fractured fragments lies below the inner table of the skull.
Depressed fractures in children under 1 year of age are called “Ping Pong” fractures and
represent a conversion of the normal convex surface of the cranium to a concave one.
CT scan is the standard modality for aiding in the diagnosis of skull fractures.
Elevation and debridement is recommended as the surgical method of choice.
Primary bone fragment replacement is a surgical option in the absence of wound
infection at the time of surgery. All management strategies for compound depressed
fractures should include antibiotics.
722 Head Trauma

MULTIPLE CHOICE QUESTIONS

1- About depressed skull fractures, it is incorrect:
a) Aesthetical considerations are important for decision if to operate or not.
b) Depressed fracture frequently causes intracranial lesions like diffuse axonal
injury.
c) An open depressed fracture represents a potential to insemination of bacteria into
the cranial cavity.
d) Because of relative plasticity of the infantile skull, fractures of the cranial vault in
children under 1 year of age are different from those that occur in older children
and adults.

2- Indication for Computed Tomography is:

a) impairment of consciousness
b) focal neurological signs
c) penetrating head injury.
d) depressed skull fracture discovered by physical examination
e) all the above

3- Patients with open (compound) depressed cranial fractures may be treated

nonoperatively when
a) There is clinical evidence of wound contamination or infection
b) Some fractured fragments penetrated the duramater
c) Frontal sinus are involved
d) There is no gross cosmetic deformity

4- About the surgical treatment of depressed skull fractures, it is correct :

a) A broad-based horseshoe-shaped scalp incision is preferred for forehead
depressions
b) There is difference in infection rate between surgical cohorts who had bone
fragments replaced versus removed
c) Methyl metacrylate can be used instead of the bone pieces, but this should be
avoided in children.
d) Elevation of depressed fragments significantly improves neurological deficits.

REFERENCES
1. Al-Haddad SA, Kirollos R. A 5-year study of the outcome of surgically treated depressed
skull fractures. Ann R Coll Surg Engl. 2002 May;84(3):196-200.
2. Braakman, R.: Depressed skull fracture: Data, treatment, and follow-up in 225
consecutive cases. J Neurol Neurosurg Psychiatry, 1972, 35:395–402.
3. Besenski N. Traumatic injuries: imaging of head injuries. Eur Radiol 2002, 12:1237–1252.
4. Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, et al; Surgical
Management of Depressed Cranial Fractures. Neurosurgery, 2006 Mar; 58 (3 supl); S56-
60; discussion Si-iv.
5. Colak A, Berker M, Ozcan OE: Occipital depression fractures in childhood. A report of
 Depressed Skull Fracture 723

14 cases. Childs Nerv Syst 1991, 7:103–105.

6. Gossman DG, Archer SM, Arosarena O. Management of frontal sinus fractures: a
review of 96 cases. Laryngoscope. 2006 Aug;116(8):1357-62.
8. Greenes DS, Schutzman SA: Infants with isolated skull fracture: what are their clinical
characteristics, and do they require hospitalization? Ann Emerg Med 1997, 30: 253-9.
9. Heary RF, Hunt CD, Krieger AJ, Schulder M, Vaid C: Nonsurgical treatment of
compound depressed skull fractures. J Trauma 1993, 35:441–447.
10. Hung CC, Chiu WT, Lee LS, Lin LS, Shih CJ: Risk factors predicting surgically significant
intracranial hematomas in patients with head injuries. J Formos Med Assoc 1996,
95:294–297.
11. Jamieson KG,Yelland J D N : Depressed skull fractures in Australia. J Neurosurg ,
1972, 37:150–155.
12. Jennet B . Epidemiology of head injury. J Neurol Neurosurg Psychiatry 1996;60:362–9.
13. Jennett B, Miller J: Infection after depressed fracture of skull. Implications for
management of nonmissile injuries. J Neurosurg 1972, 36:333–339.
14. Jennett B, Miller, J D, Braakman, R.: Epilepsy after nonmissile depressed skull fracture.
J Neurosurg , 41:208–216, 1974.
15. Macpherson BCM, Macpherson P, Jennett B . CT incidence of intracranial contusion and
hematoma in relation to the presence, site and type of skull fracture. Clin Radiol 1990,
42:321–326.
16. Mastrapa TL, Fernandez LA, Alvarez MD, Storrs BB, Flores-Urueta A. Depressed skull
fracture in Ping Pong: elevation with Medeva extractor. Childs Nerv Syst. 2007
Jul;23(7):787-90.
17. McRae M, Momeni R, Narayan D. Frontal sinus fractures: a review of trends, diagnosis,
treatment, and outcomes at a level 1 trauma center in Connecticut. Conn Med 2008
Mar;72(3):133-8.
18. Mendelow AD, Campbell D, Tsementzis SA, Cowie RA, Harris P, Durie TB,et al ;
Prophylactic antimicrobial management of compound depressed skull fracture. J R Coll
Surg Edinb 1983 ,28:80–83.
19. Metzinger SE, Guerra AB, Garcia RE. Frontal sinus fractures: management guidelines.
Facial Plast Surg. 2005 Aug;21(3):199-206.
20. Özer FD, Yurt A, Sucu H, Tektas SE, Depressed Fractures Over Cranial Venous Sinus.
J Emerg Medicine, 2005, 29 ( 2 ) , 137–139.
21. Wylen EL, Willis BK, Nanda A: Infection rate with replacement of bone fragment in
compound depressed skull fractures. Surg Neurol 1999, 51:452–457.
22. Van den Heever CM, van der Merwe, DJ : Management of depressed skull fractures:
Selective conservative management of nonmissile injuries. J Neurosurg, 1989, 71:186–190.
23. Vender J, Bierbrauer K: Delayed intracranial hypertension and cerebellar tonsillar
necrosis associated with a depressed occipital skull fracture compressing the superior
sagittal sinus J Neurosurg (5 Suppl Pediatrics) 2005, 103:458–461.
23. Yavuz MS, Asirdizer M, Cetin G, Günay Balci Y, Altinkok M. The correlation between
skull fractures and intracranial lesions due to traffic accidents. Am J Forensic Med
Pathol. 2003 Dec;24(4):339-45.
24. Zauner, A.; Prabhu, S.S.; Bullock, M.R.R. Surgical Management of Traumatic Brain
Injury in Youmans J R, Winn HR: Neurological Surgery, 5th Ed. Philadelphia:Saunders,
2004, Chap . 328, pp 5145-5180.
25. Zee CS, Go JL. CT of head trauma. Neuroimaging Clin N Am 1998 Aug;8(3):525-39.
26. Zimmerman RA, Bilaniuk LT, Gennarelli T, Bruce D, Dolinskas C, Uzzell B. Cranial
computed tomography in diagnosis and management of acute head trauma. AJR Am J
Roentgenol 1978 Jul;131(1):27-34.
724

Extended Decompression and

Neuroprotection for Traumatic Brain
Injury (TBI)
TOMOYA MIYAGI, M,D Ph. D, MINORU SHIGEMORI, M,D Ph. D
Department of Neurosurgery, Kurume University School of medicine

Key words: TBI, ICP, ICU Management, Decompression

Introduction
The most important factors in determining the outcomes of a patients with traumatic
brain injury (TBI) is the degree of severity and types of primary brain damage, and the
secondary damage to the brain such as low-oxygen and low-blood pressure et al.1) For
severe TBI patients prompt and appropriate decompression to reduce intracranial
pressure (ICP) and ICU management are commonly required2).
The second edition of “Guidelines for the Management of Severe Head Injury” 3) was
published by Japan Society of Neurotraumatology (JSNT) in 2006. These guidelines
include a wide range of topics in the management for severe TBI, from prehospital care,
primary cares, ICU management and surgical treatment. The essence of extended
decompression and neuroprotection for TBI is also focused in this JNST Guidelines.

Initial Treatment
Following determination of the degree of urgency, the initial intracranial diagnosis and
resuscitation must be quickly performed after admission of the patient. So that the
development of secondary brain damage due to extracranial factors may be prevented.
The breathing and circulation should be stabilized, and then the states of the brain
damage should be evaluated (Table 1,2).
Evaluation of the brain damage.
1) Consciousness level by the Glasgow Coma Scale (GCS)4) (Table 3).
2) Pupillary findings.
3) Motor palsy.
A score of 8 or less on the GCS is generally defined as severe, 9-13 as moderate, and 14-
15 as mild. If GCS score of 8 or less, the total GCS score deteriorates more than 2
points, development pupillary inequality, hemiplegia or actual Cushing phenomenan are
observed, there is the risk of cerebral herniation. If breathing and circulation are stabile,
a head CT scan, as well as a rapid infusion of mannitol (0.25-1.0g/kg), and emergency
surgery should be considered.
 Extended Decompression and Neuroprotection for Traumatic Brain Injury (TBI) 725

Table 1 Primary survey and Resuscitation (ABCDEs approach)

(JSNT Guideline) 3)

Table 2 Management target value of respiration and circulation in the Primary survey.
(JSNT Guideline) 3)

Table 3 Glasgow Coma Scale (GCS) 4)

726 Head Trauma

ICU Management
After initial treatment, evaluation of severity, appropriate therapeutic strategy and strict
ICU management should be considered. The outcomes of patients will be predicted by
using the TCDB CT classification (Table 4, Fig. 1)5). Treatment strategy of ICU
management is shown in Table 5. The control of ICP and preservation of cerebral
perfusion pressure (CPP) are most important in severe TBI with intracranial
hypertension.

Table 4 Traumatic Coma Data Bata (TCDB) CT classification 4)

Fig. 1 CT classfication of Traumatic Coma Data Bank.

 Extended Decompression and Neuroprotection for Traumatic Brain Injury (TBI) 727

1. Treatment threshold of ICP.

(1) GCS score 3-8
(2) Systemic BP less than 90mmHg.
(3) Midline shift and loss of cisterns on CT.
(4) The use of hypothermia or barbiturate therapy.
2. ICP contral
(1) Head elevation: 15-30°.
(2) Use of Mannitol: 0.25-1.0g/kg body weight, bolus injection.
(3) Hyperventilation: PaCO2 : 30-35mmHg.
(4) CSF drainage.
(5) Anesthetics, Analgesics, and sedatives: Propofol or midazolam are mainly used,
and continuous administration of fentanyl and vecuronium if necessary.
In patients with refractory intracranial hypertension following above managements,
barbiturate, hypothermia, decompressive craniotomy, and/or internal decompression
may be used.
3. The use of Barbiturate:
(1) Thiopental, bolus injection: 2-10mg/kg. Maintained at: 1-6mg/kg/hr.
(2) Pentobarbital, bolus injection: 2-5mg/kg. Maintained at: 0.5-3mg/kg/hr.
Good control of ICP may be achieved, and the burst suppression on the EEG is
considered to be an indicator of an effective blood concentration. But the benefit of
barbiturate in neuroprotection is still controversial.
4. The use of Hypothermia: The reduction of body temperature to 33-35°C for 24-72
hours by use of the whole body cooling with a water blanket under sedation is
commonly used.
The effect of ICP reduction and brain protection may be better than other
treatments. But there is risks of complication such as infection, arrhythmia,
hypokalemia, and reduced platelets. The benefit of hypothermia in the improvement
of outcomes is still controversial. The further study is needed concerning therapeutic
time window, appropriate target temperature, duration, method of rewarming and/or
effective subgroups of patients, et al 6).
5. Decompressive craniotomy and internal decompression: This is usually performed
when ICP is greater than 30mmHg, even after any medical treatment. In some cases,
internal decompression is added to external decompression on one or both sides (Fig.
2,3). ICP may be well controlled, but the final benefit of external and internal
decompression to improve the outcome is also still controversial (Fig. 4).
The following indication criteria is propoced from the U.S. and Europe7,8).
(1) Age <50, excluding GCS of 3 with fixed bilateral pupil.
(2) Cerebral swelling observed by CT.
(3) Surgery can be performed before extensive brain ischemic.
728 Head Trauma

Fig. 2 Illustration of operative methods.

Fig. 3 Case of bilateral decompressive craniectomy.

6 years boy with GCS 5 on admission, he was treated by mild hypothermia but ICP was uncotrolled .
A) Prepoerative CT sacns showed diffuse brain swelling. B) Intraopevative findings.
C) Post operation CT scans. D) CT scans the 7th operative days.
This patient resulted in favorable outcome.
 Extended Decompression and Neuroprotection for Traumatic Brain Injury (TBI) 729

Fig. 4 Case of rt fronrtal internal decompression.

70 years women with GCS 8 on admission, he was treated by Rt frontal internal decompression.
A) Prepoerative CT sacns showed diffuse brain swelling. B) Intraopevative findings.
C) Post operation CT scans. D) CT scans the 7th operative days.
This patient resulted in favorable outcome.

Table 5 Treatment target of Intensive Care Unit

730 Head Trauma

Conclusion
As to the management of ICP, there are many guidelines and recommendations,
however unfortunately there is no definite high-level evidence based on well designed
randomized controll study.
The pathophylogical event in the acute stage of severe TBI is quite variable , an
appropriate individual based approach in ICU management is necessary under
experienced medicals teams.

REFERENCES
1. Takashi Tokutomi: Pathophysiology and Critical Care Management of Traumatic
Brain Injury. Jpn J Neurosurg 14: 425-431, 2005
2. Teasdale GM, et al: Craniocerebral Trauma: Protection and Retrieval of the Neuronal
Population after Injury. Neurosurgery 43: 723-738, 1998
3. JSNT Guideline 2nd. Neurotraumatology, 29: 1-115, 2006
4. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale.
Lancet 2: 81-84, 1974
5. Marshall LF, et al:A new classification of head injury based on computerized tomography.
J Neurosurg, 75:S14~20,1991.
6. Minoru Shigemori, Tomoya Miyagi: Controversy in mild hypothermia for traumatic
brain injury. Shinkei kenkyu no Shinpo 50: 315-326, 2006
7. Guerra WK: Surgical decompression for traumatic brain swelling: Indication and
results. J Neursurg 90: 187-196, 1999
8. Munch E, et al: Management of severe traumatic brain injury by decompressive
craniectomy. Neurosurgery 47: 315-323, 2000
 731

Therapeutic Hypothermia for Traumatic

Brain Injury
TAKASHI TOKUTOMI, M.D.
Department of Neurosurgery, Kurume University School of Medicine, Kurume,
Japan. 67 Asahi-machi, Kurume-shi, 830-0011 Japan

Key words: traumatic brain injury, hypothermia, treatment

PATHOPHYSIOLOGY
Brain damage following traumatic injury is a result of direct and secondary
mechanisms. Mechanical forces result in shearing and compression of neuronal and
vascular tissue at the time of impact (direct or primary brain injury). A series of
pathological events may then ensue, leading to further brain damage (secondary brain
injury). These secondary mechanisms involve the initiation of acute haemostatic and
inflammatory responses, including thrombin and plasmin formation and intrathecal
release of proinflammtory cytokines, resulting in a breakdown of the blood-brain
barrier, edema formation, swelling, and hemorrhage. It has been noted that even small
decreases in brain temperature can reduce the secondary brain injury by multifactorial
chemical and physical mechanisms. The possible mechanisms proposed for neuronal
protection by hypothermia are indicated in Table 1. The reduction of oxygen and
glucose consumption caused by a reduction in the rates of enzymatic reactions with
hypothermia may attenuate the cerebral metabolism and blood-flow uncoupling after TBI
and may protect the injured brain from suffering ischemia. Early brain ischemia after TBI
is considered to involve the development of secondary brain injury. Amelioration of the
blood-brain barrier break-down by means of hypothermia may be associated with an
improvement in posttraumatic brain edema formation.

Table 1 Possible mechanism of neuroprotection by hypothermia

• Reduction in cerebral metabolic rate

• Inhibition of inflammatory response
• Protection of blood-brain barrier permeability
• Attenuation of extracellular glutamate
• Reduction of nitric oxide production
• Attenuation of lipid peroxidation
• Reduction of free radical production
• Recovery of post-ischemic protein synthesis
• Prevention of protein kinase C down-regulation
• Increase of anti-apoptotic protein Bsl 2
732 Head Trauma

CLINICAL USE
Mortality and morbidity rates for patients with severe traumatic brain injury (TBI)
continue to be high, despite the highly developed monitoring systems and treatment
options that are available. Several preliminary clinical studies have shown that patients
treated with mild hypothermia after TBI have an improved neurological outcome.
Contrary to our expectations, however, a large multicenter randomized clinical trial has
failed to show a benefit of hypothermia therapy1. Many factors such as treatment
window, inter-center differences in fluid and blood pressure management, patient
selection, and systemic complications may have influenced this negative study. Although
many experimental studies have indicated that hypothermia has neuroprotective effects
in TBI models, the results of such studies are not always extensible to humans. Possible
adverse effects of hypothermia on systemic conditions such as increasing the risk of
subsequent infection, coagulopathy, electrolyte disorders, and cardiac arrhythmia must
be considered. The inhibitory effect of hypothermia on inflammatory response, which
may be combined with the impairment of immune function, most likely contributes to
the increase in the risk of subsequent infection, especially pneumonia, during and after
rewarming. Although coagulation disorder during hypothermia has been noted, the risk
of coagulopathy after TBI may not be enhanced by hypothermia of 32-33 oC or higher.
Serum potassium levels decline with hypothermia. The probable mechanism of this
decline in potassium is a combination of intracellular shift and increased urinary
excretion through hypothermia-induced polyuria. Hypokalemia during hypothermia and
rebound hyperkalemia during rewarming may cause severe ventricular arrhythmia.
An oversupply of potassium during cooling may raise the risk of rebound hyperkalemia
induced by the redistribution of potassium with rewarming. The occurrence of these side
effects increases with decreasing target temperature. Temperatures below 32 oC must be
avoided because ventricular arrhythmia may occur. The target temperature usually
needs to be maintained for more than 48 hours to derive for the therapy to yield a
benefit2. Since the deleterious effects of hyperthermia have been shown in TBI patients,
even very mild hypothermia near normothermia may have a beneficial effect.
Temperature control in the acute phase is thus one of the most important therapies for
the management of severe TBI.
Different depths of hypothermia may have varying protective effects on the
development of secondary brain injury however, the clearest benefit from the induced
hypothermia in clinical use at the moment appears to be the reduction of intracranial
hypertension. This effect is probably due to a reduction of cerebral blood volume, the
inhibition of post-traumatic inflammatory response, or amelioration of the blood-
brain barrier dysfunction with hypothermia. To reduce intracranial hypertension, very
mild hypothermia seems to be sufficient3. Aggressive treatment of elevated intracranial
pressure (ICP) has been shown to reduce mortality. If we can control the side effects of
hypothermia by using an optimal reduction in temperature, therapeutic hypothermia may
be a more promising therapy. Further studies must be performed to determine the
optimal target temperature, duration of cooling, and re-warming strategies.
 Therapeutic Hypothermia for Traumatic Brain Injury 733

COOLING TECHNIQUES
Patients were intubated and placed on volume-controlled ventilation under sedation
with midazolam or propofol and paralysis with vecuronium. A paralytic agent is usually
necessary to prevent shivering as the cooling occurs. PaO2 was maintained at at least 100
mmHg and PaCO2 was maintained at 35-40 mmHg. Nutritional support was started
within 48 hours and maintained by the administration of adequate parenteral or enteral
solutions by at least 7 days after injury. Hypothermia was induced by surface cooling with
the use of water-circulating blankets (Fig.1). Brain temperatures are usually higher
than rectal or bladder temperatures by about 0.2-0.8 oC, and the differences are greatest
when the rectal or bladder temperatures are elevated. Patients are slowly rewarmed after
48-72 hours of hypothermia if ICP is controlled. If ICP remains higher or re-increases
during rewarming, we continue the mild hypothermia for as long as another 48 hours.

Fig. 1 Therapeutic mild hypothermia

REFERENCES
1. Clifton GL, et al. Lack of effect of induction of hypothermia after acute brain injury. N
Engl J Med. 344:556-563, 2001
2. Brain Trauma Foundation. Prophylactic hypothermia. Guidelines for the management
of severe traumatic brain injury. J Neurotrauma 24: S21-S25, 2007
3. Tokutomi T, et al. Effect of 35°C hypothermia on intracranial pressure and clinical
outcome in patients with severe traumatic brain injury. J Trauma (in press)
734

Traumatic Brain Injury in Children

ALEXANDRU V CIUREA, MD, PhD1, STEFAN M IENCEAN, MD, PhD2,
AURELIA MIHAELA SANDU, MD3
1
Professor of Neurosurgery, University of Medicine and Pharmacy, Bucharest,
Romania
2
Neurosurgery, Emergency Hospital “Prof Dr Nicolae Oblu” Iasi, Romania
3 th
4 Department of Neurosurgery, Clinical Hospital „Bagdasar-Arseni”, Bucharest,
Romania

Key words: traumatic brain injuries (TBI) in children, pediatric coma scale ( PCS ),
trauma infant neurological score (TINS)

Traumatic brain injuries (TBI) in children are head injuries resulting from a traumatic
etiology (external physical force, rapid accele-ration or deceleration of the head). TBI is
the leading cause of disability and death in children and most common causes of head
injury are: falls, sport accidents, child abuse, assaults and motor vehicle accidents.
According to age distribution of head injury, two risk groups are identified: 0-4 years old
and 15-19 years old and boys are affected by head traumas twice the rate of girls.
Immediate posttraumatic response could be different in children than in adults
because of these age-related particularities, but consequences are similar.

Physical exam of a child with TBI must be quick, safe and consists
of several steps:
1. assessment of airway, breathing and circulation (ABC exam)
2. checking for signs of cervical spine cord injury - rare in young children
3. evaluation of level of consciousness, pupils’ size, and their reaction to light
4. assessment of local traumatic injuries
5. neurological exam, calculating trauma scores, according to trauma scales used into
respective neurosurgical department
6. general physical exam and in politraumas calculating MISS (Modified Injury
Severity Scale)
7. establishment of useful paraclinical tests.
Neurologic exam of the child must be individualized according to the age and level of
consciousness. The level of consciousness of children with cranial traumas is described
by pediatric scales, according to age ; the most important neurotrauma pediatric scale is
Pediatric Coma Scale ( PCS ) ( Simpson & Reilly, 1982 ), a paediatric version of the
Glasgow Coma Scale :
 Traumatic Brain Injury in Children 735

Normal scores are:

a. 0 - 6 months = 9 ; best verbal response is crying, normal verbal score = 2, and best
motor response is usually flexion with a normal motor score expected of 3.
b. 6 - 12 months = 11; normal verbal score expected is 3, an infant will usually locate
pain, and so normal motor score expected is 4.
c. 1 - 2 years = 12 ; normal verbal score expected is 4, and the infant will locate pain
but not obeys commands, so normal motor score expected is 4.
d. 2 - 5 years = 13 ; normal verbal score expected of 4, and the infant will usually
obeys commands, so normal motor score expected is 5, and
e. > 5 years = 14 ; normal verbal score expected is 5.
PCS is extremely useful for all pediatric TBI, in perfectly connection with the age, and
over 5 years we can use Glasgow Coma Scale (GCS).
Trauma Infant Neurological Score (TINS) is used for evaluation of TBI severity in
infants and children under 3 years old, combines clinical and history elements:
mechanism of trauma, orotraheal intubation on arrival, neurological exam, presence of
subgaleal hematoma.

Max/Min 0 1 2
Mech of trauma 1/2 -- Fall<1m or mild blow Fall > 1m or penetrating inj.
Intubated on arrival 0/1 No Yes --
Alertness 0/2 Fully alert but arousable Decreased Unconscious
Motor Deficit 0/2 None Lateralizing signs No movement
Pupils 0/2 Reactive bilaterally Anisocoria or non reactive pupil Dilated and non reactive
Scalp injury 0/1 None Subgaleal hematoma

Total scores range from 1-10 points ; TINS > 2 indicates the need for a CT scan.

Grading of traumatic brain injury

Grading the severity of TBI in children should be done, as in adults, according to GCS
score in: minor head injury (HI) (GCS score = 13-15), moderate HI (GCS score = 9-12)
and severe HI (GCS score = 3-8). Each category has specific diagnosis, evaluation,
management, different treatment strategies, complication and particular outcome.

Head Injury Severity Scale (HISS) introduces two new criteria:

a. Minimal TBI: GCS score = 15 points, no loss of consciousness (LOC), no post-
traumatic amnesia (PTA)
736 Head Trauma

b. Mild TBI: GCS score = 14 points, brief LOC under 5 minutes, PTA
c. Moderate TBI: GCS score = 9-13 points, LOC over 5 minutes, focal neurological
deficit
d. Severe TBI: GCS score = 5-8 points
e. Critical TBI: GCS score = 3-4 points
More accurate grading of TBI must also take into consideration other important
criteria: mechanism of injury (e.g. the fall off a swing is a more aggressive mecha-nism
of trauma than fall from the same level etc.), LOC, PTA, vomiting and post-traumatic
seizures.

Minor head injury

Almost 90% of pediatric HIs are minor. The child is alert, with a normal neurologic
performance, and presenting inconstant vomiting. GCS score = 13-15. Local exam
may show: epicranial hematoma, skin abrasions or lacerations.
Grading in minor HI
1. Grade 0 minor HI – no LOC, impact site localized pain, bruises, scalp abrasions,
epicranial hematoma; CT-scan is not necessary, the patient is discharged home
with instructions.
2. Grade 0 with risk minor HI - no LOC, but the patients belong to the following
categories: extreme age, history of neurosurgery, ventriculoperithoneal shunt,
seizures, anticoagulant therapy, drugs or alcohol abuse (very rare in children); CT-
scan is performed, and the patients is admitted for at least 24 hours.
3. Grade 1 minor HI – LOC, PTA, persistent headache, vomiting, large scalp
wounds; CT-scan must be performed within the first 6 hours after trauma, and
the patient requires hospitalization even if the CT-scan is normal.
4. Grade 2 minor HI – GCS=13-14 points, LOC maximum 30 minutes, no focal
deficits; the patient requires CT-scan and hospitalization. Skull X-ray positive for
a skull fracture, requires head CT-scan, native and bone window, and admission
for observation of the child. CT-scan can show a small size focal lesion, located
within a noneloquent area, lacking of neurological signs. In this case, HI is not
considered minor anymore and the classification of HI, according to the severity
should be done only after craniocerebral diagnostic imagery scan.
The child is discharged home but only after informed consent of parents. They must
contact immediately a neurosurgeon in case of persistent or increased headache,
vomiting, changes within level of consciousness, drowsiness, seizures.
CT-scan is mandatory in children with neurosurgical interventions and shunted
patients; also in all road accidents, passenger or pedestrian, and in child abuse. In these
two situations CT-scan will be extended to cervical spine.

Mild head injury

According to HISS, a child with mild head injury (MHI) is has GCS of 14 points, brief
LOC under 5 minutes and PTA. MHI is of great importance in children, because of
possibility of multiple posttraumatic neurobehaviour sequelles. Children presenting with
 Traumatic Brain Injury in Children 737

MHI may subsequently deteriorate and die from intracranial causes, situation known as
“talk and die” syndrome.

Moderate head injury

In moderate HI there is a history of trauma with LOC, changes in mental status,
repeated vomiting, and focal neurological deficit. The child may present, even during
examination, LOC or seizures. Local exam may show scalp lesions: epicranial hematoma
or, more frequently, skin abrasions or lacerations. GCS score ranges between 9 to 12
points. Immediate CT-scan and admission into a pediatric neurosurgical department are
mandatory. Therapy is individualized according to age, type of injury, PCS, TINS and
GCS scores, CT-scan and evolution.
Children with favorable outcome, with normal neurological exam, and normal CT-
scan, can be discharged after few days hospitalization, and can be observed at home.

Severe head injury

The child with a severe HI is unconscious, and has a GCS score between 3 and 8 points
(comatose patient). Clinical exam of a posttraumatic unconsciousness child consists of
assessment of vital signs, neurological exam, pupils’ size and their reaction to light,
brainstem reflexes, checking for cervical spinal cord injuries etc., and obtaining history
of trauma. A CT-scan, native and bone window, is performed immediately, and
according to the neuroimaging result the child is admitted into the pediatric intensive care
unit (PICU) or is taken directly into the operating room, where specific treatment is
initiated. It is better to extend CT-scan to cervical spine and in road traffic accidents to
thoracic and abdominal area. Patients with severe HI must be admitted in PICU with
special facilities for infants, toddlers and children.

Paraclinical Explorations
Paraclinical examination in newborns and infants can be done by transfontanelle
ultrasonography, but in general this is unsatisfactory. Gold standard examination in TBI
is native CT-scan. In selected cases MRI can be performed. CT-scan exam can be
repeated according to initial findings, lesion transforming risk and clinical outcome. Also
cervical spine investigation should be made.
Special indication for CT-scan in children with TBI:
- Newborn and infants under 3 months
- Suspected child abuse or shaken baby syndrome
- Scalp lesion: bruise, swelling, wound over 5 cm in diameter, in children < 1 y.o.
- TINS score over 2, in children under 2 years old
- GCS score under 15, persisting 2 hours after trauma
- Focal neurological deficits, LOC, abnormal mental status, drowsiness
- Antero- or retrograde PTA, lasting more than 5 minutes
- Persisting vomiting (in general, more than 3 times)
- Posttraumatic seizures, in children with no history of epilepsy
738 Head Trauma

- Open skull fracture, depressed skull fracture, anterior tense fontanelle

- Signs for a skull base fracture: hemotympanum, “raccoon’s eyes”, Battle’s sign
- CSF leakage: rhinoliquoreea, oroliquoreea, otoliquoreea
- Potential dangerous traumatic mechanism: high-speed road traffic accident, fall
from height of greater than 3 m, etc.
- Coagulopathies, anticoagulant therapies
- History of neurosurgical operation or ventriculoperithoneal shunt.

Specific posttraumatic pathology in children

According to age, TBI has several characteristics for: newborn and infant, age less than
6 months, infant and toddler, age ranging from 6 months to 2 years, preschool child, aged
from 2 to 5 years, school child, age between 6 to 12 years and teenager, over 13 years.

1. Caput succedaneum is encountered during the neonatal period, and it is a consequence

of a prolonged labor or instrumented delivery. Caput succedaneum is a scalp swelling
extending across the midline and over suture lines. It is usually of no clinical importance,
and spontaneously resolves within couple of days after birth.

2. Cephalhematoma (CPH) is a newborn specific posttraumatic lesion. It is a

subperiosteal hemorrhagic collection, unilateral and most commonly over the parietal
bone. It is limited to one bone by the attachment of the periosteum to the sutures. An
underlying linear skull fractures may also be present. CPH appears within hours of
delivery as a soft, fluctuant swelling on the side of the head. CPH are usually small and
require no treatment.CPH spontaneously withdraw within the first three months,
without any surgical treatment or tap. In cases with persistent collection, infection or later
in calcified lesion, CPH requires surgical treatment.

3. Subaponeurotic (Subgaleal) hematoma is a collection of blood developing between

the periosteum and galea aponeurotica. It is less common and it can be caused by a
forceps delivery or vacuum extraction. It can contain a large amount of blood and
crosses suture lines. Subgaleal hemorrhage is a potentially life-threatening complication
of delivery, which can lead to hypovolemic shock in newborns. Differential diagnosis
between epicranial collections is of great importance. Subaponeurotic hemorrhage
requires immediate treatment consisting blood transfusion (in order to maintain
normovolemia) and evacuation by thick needle.

4. Posttraumatic subarachnoid hemorrhage (SAH) in newborn is a consequence of

prolonged labor or forceps delivery. A minimal subarachnoid hemorrhage has not
clinical signs and treatment is symptomatic. Internal hydrocephalus occurs in a few weeks
time if the quantity of blood is higher. Posttraumatic SAH is an important predictive
factor of obstructive internal hydrocephalus.

5. Diffuse brain swelling (DBS) in newborns is due to birth asphyxia and secondary
reperfusion. DBS is mixed, by vasogenic and cytotoxic edema. The diagnosis is established
 Traumatic Brain Injury in Children 739

by CT-scan and the treatment is specific, according to the clinical status. Posttraumatic
DBS can accompany any cerebral lesion in children and it requires ICP monitoring. After
failure of conservative therapy, bilateral decompressive craniectomy may be needed as
the last resort treatment strategy.

5. Skull fractures in newborns are extremely rare, following a difficult labor. Linear skull
fractures are usually of no clinical significance and require no specific treatment. Also
diastatic fractures do not require surgery
Depressed skull fractures are closed (simple fracture) or open (compound fracture).
Closed depressed skull fractures require surgical therapy according to the depth of
deformity. A particularly type of newborn fracture is “ping-pong” fracture. It is usually
encountered in parietal bone, and requires surgery: the depressed bone is elevated by
means of a periosteal elevator.
Surgery for depressed fracture, closed or compound, situated over the superior
sagittal sinus (SSS), is made after performing a CT-scan with coronal and sagittal
reconstruction. Surgery for fractures over the SSS, could need repairing of the SSS.
Compound fracture, containing bony fragments depressed or not with dural laceration
represent an emergency for surgery.
Growing skull fracture (GSF) is found in children under three years old, located in the
parietal region. There is a bone diastasis with leptomeningeal herniation and elevated ICP
after a linear skull fracture with periosteum tear and dural laceration. History of trauma,
clinical aspects and CT-scan establish the diagnostic. Surgery : craniectomy and
duraplasty.
Skull base fracture are suspected in the presence of characteristic signs, such as
periobitar or postauricular ecchymosis (Battle’s sign), epistaxis, otorhagia etc., and are
diagnosed by CT-scan. They require surgical treatment in the presence of a CFS fistula,
with rhinoliquorea or otoliquorea, in cases of failure of conservative therapy.

6. Brain concussion is a transient LOC or disorientation, as a result of a closed head

trauma. After regaining consciousness the child has a normal clinical exam and a
normal CT-scan. Concussion is a diffuse posttraumatic lesion, due to a transient and
completely reversible disturbance in neuronal function. The treatment is symptomatic
and observation of the child.

7. Brain contusion is a focal posttraumatic lesion, secondary to traumatic forces which

induce vascular injuries and cause intraparenchimatous hemorrhagic foci. The lesion has
a progressive character, evolving either to limiting the hemorrhagic lesion and resolution,
or to growing in size or number. Clinical findings depend on the location and clinical
pattern may be minor, moderate or severe TBI, with or without focal neurological
deficits. The diagnostic and follow up is performed by CT-scan. Treatment is pathogenic
and symptomatic.

8. Brain lacerationis is a focal posttraumatic lesion with a complete disruption of

brain parenchyma, hemorrhage and tissue necrosis, and tearing of pia mater.
Brain laceration can be:
740 Head Trauma

- Direct brain laceration, without craniocerebral wound, located at the impact

site, beneath the skull fracture, and with craniocerebral wound, when all
anatomical layers till the brain parenchyma are torn.
- Indirect brain laceration, through a “contre coupe” mechanism.
Clinical findings depend on location and size of the lesion and associated injuries
(hematoma). The diagnostic is made by CT-scan. The treatment depends on the type and
size of lesion and the development of intracranial hypertension syndrome development.
Direct brain laceration with craniocerebral wound always requires surgical treatment.
Brain lacerations without craniocerebral wound are treated conservatively or surgically
(rare in children), according to the clinical aspects.

9. Child abuse / Shaken baby syndrome is a posttraumatic syndrome presenting multiple

injuries resulting from bad treatment or beating of the child. Almost all cases are found
in children under 3 years old, with a maximum of incidence under 1 year. Clinical
findings include vomiting, pallor, irritability, overcrying, drowsiness, multiple bruises,
respiratory disturbances etc. Although there are no patognomonic findings for child
abuse, there are some characteristic factors which raise the index of suspicion: retinal
hemorrhages, subdural hematoma, intraparenchymal hemorrhage, other cerebral
hemorrhages, cerebral edema, and bone fractures (long bones, ribs). The mechanism of
trauma is shaking injury, with or without impact (shaken impact syndrome), and
direct pure impact injury.
CT-scan is mandatory at admission and the child requires PICU observation. The
treatment depends on the multiple lesions and outcome is, generally, poor, because of the
multiple trauma complexes in a growing infant.

10. Craniocerebral wounds in children/Penetrating head injury are rare in children; all
anatomic structures, scalp, skull, dura mater, leptomeningeal layer and brain parenchyma
are involved. According to the nature of traumatic agent, two categories of craniocerebral
wounds are distinguished: gunshots craniocerebral wounds and craniocerebral wounds
produced by different agents other than gunshots. Local exam shows traumatic mark and
neurological exam evaluates the level of conscious-ness, focal neurological syndrome, and

Fig. 1 Diastatic skull fracture and Fig. 2 Right craniocerebral wound

leptomeningeal herniation (open skull fracture and direct brain laceration)
 Traumatic Brain Injury in Children 741

meningeal syndrome. Classicall skull X-ray and CT-scan, showing extend of the lesion
and the presence of associated injury, complete the diagnosis. Urgent surgical treatment
is mandatory, and its purpose is to remove the bone fragments, and cerebral detritus,
reconstruction of anatomical layers, and antibiotherapy.

11. Epidural hematoma in children (EDH) is a posttraumatic endocranial blood

collection between the inner table of the skull and dura mater, and results from tearing
of dural blood vessels.
Epidural hematoma may be:
- Convexital supratentorial or cerebellar. The source of bleeding is usually arterial,
meningeal middle artery, fracture, diastatic fracture (diploic veins).
- Suprasinusal (over the superior sagittal or transverse sinus). The source of
bleeding is usually venous.
Usually EDH is unilateral and located most frequently into the temporo-parietal
area, followed by frontal and occipital regions, and less common vertex and posterior
fossa. Pediatric acute EDHs are quite rare, with a frequency of occurrence around 3% of
all head injury. In newborns EDH is extremely rare, and can occur in prolonged labor.
The frequency rises with age, according to the increased severity of HI in older children.
Diagnostic must be quick and urgent surgery is needed.
Clinical feature of EDH include: immediate posttraumatic or delayed LOC, focal
neurological deficits, intracranial hypertension and progressive worsening in cerebral
herniation. The clinical features of EDH in newborns and infants are vague consisting of
hypothonia, seizures, and tense fontanelle. The clinical signs depend on the source of
bleeding, which assert the rapidity of progression (supraacute, acute, subacute
hematoma), location of EDH and presence of associated lesions.
According to the level of consciousness, and presence of comatose status, clinical
features may be:
- brief posttraumatic LOC, followed by lucid interval for several hours, and then
progressive alteration of level of consciousness
- persistent posttraumatic coma
- posttraumatic coma, followed by regaining of consciousness
- posttraumatic conservation of consciousness without coma
- posttraumatic conservation of consciousness with delayed coma
A special situation is the occurrence of an EDH in a hydrocephalic shunted child,
which represent an emergency. CT-scan must be performed without delay. Posterior fossa
EDH blocks cistern magna, leads to brainstem compression and acute obstructive
hydrocephalus with acute intracranial hypertension. Posterior fossa EDH occurs less
frequently than supratentorial hematomas but it is the most common traumatic space-
occupying lesion of the posterior fossa in children.
Diagnosis, localization and size of EDH is made by CT-scan. EDH may appear as an
extraaxial lenticular-shaped mass situated between the brain and the skull; a normal CT-
scan performed immediately after trauma, does not exclude the possibility of further
development of an EDH. A child harboring a skull fracture, presenting vomiting, must
be observed clinically and CT-scan for development of an EDH.
Surgical indications are established by clinical status and CT-scan:
742 Head Trauma

- Coma with anisocoria and CT-scan showing EDH, require urgent surgery
- Coma and worsening of neurological state in case of EDH’s volume > 25 ml
- EDH’s volume > 30 ml, even in the absence of clinical signs
- EDH’s volume > 25 ml, in posterior fossa or temporal region location
- Midline shift > 4 mm, with worsening of neurological status
- Increasing in volume of EDH
Surgery consists of evacuation of the hematoma through craniotomy. It is important
to perform an initial blood replacement to the shocked child; this should be carried out
in 20-30 minutes, before starting operatory procedures. For posterior fossa EDH there
is no special surgical technique: suboccipital craniectomy, evacuation of the hematoma,
hemostasis, dura mater suspension and wound closure.
Conservative treatment is attempted in an alert child, without focal neurological
deficits, in which CT-scan showed an EDH having a volume < 25 ml, a thickness < 10
mm and midline shift < 4 mm, under attentive clinical observation and repeating of the
CT-scan in a neurosurgical center, where surgery can be performed if needed.

12. Posttraumatic subdural hematoma (SDH) in children occurs with an overall

frequency of 5%, less common before 3 years old. In infants and toddlers post-traumatic
SHD occurs in shaken baby syndrome, and following head injury caused by accidental
falling. In children aged between 5 to 6 years acute posttraumatic SDH is generally
produced by falls, motor vehicle accidents. In older children common causes are motor
vehicle accidents, falls, playing accidents, etc.
Subdural hematomas are acute in the first two days, subacute within the next days until
3-4 weeks, and chronic after 4-6 weeks. Chronic posttraumatic SDH in children is
considered to be a consequence of conservative treatment or misdiagnose of an acute
posttraumatic SDH. According to the location and volume of the hematoma, clinical signs
are alteration of LOC, focal neurological signs, and intracranial hypertension, in various
grades of intensity.
In acute posttraumatic SHD, clinical signs occur immediately and consist of coma,
motor deficits and anisocoria, which requires urgent surgery. In infants and toddlers
clinical findings associated with acute posttraumatic SDH may include apathia, vomiting,
seizures, tense of anterior fontanelle and coma.
A child with a subacute posttraumatic SDH may experiences a variable period of
LOC, followed by clinical improvement and then clinical worsening, motor deficit,
anisocoria and coma; sometimes loss of consciousness can be absent. Deterioration can
be rapid in children, with repeated generalized or jacksonian seizures, hemiplegia,
decorticated or decerabrate rigidity, anisocoria and coma.
Chronic posttraumatic SDH in children is a consequence of a misdiagnosed
posttraumatic SDH. Chronic posttraumatic SDH can have other etiology in toddler:
perinatal SAH, prolonged, difficult labor, following meningitis, and coagulophaties.
Clinical features are unspecific: more common seizures are found, irritability, delayed
psychological and motor development. In infants and toddlers tension of the anterior
fontanelle and abnormal increase of the head circumference. Motor deficits and cranial
nerves palsy may occur, and during the deterioration phase, lethargy and alteration of
level of consciousness. Extremely rare the child is asymptomatic.
 Traumatic Brain Injury in Children 743

CT-scan is mandatory for diagnostic and therapeutical management. Acute

posttraumatic SHD appears on the noncontrast head CT-scan as a crescent-shaped
hyperdense area between the inner table of the skull and the surface of the cerebral
hemisphere; in subacute posttraumatic SDH and in the chronic phase posttraumatic SDH
is iso-, hypodense to brain tissue. Sometimes, the thickness of the SDH is not directly
proportionate to the compressive effect on brain parenchyma. Sometimes small
posttraumatic SDH can have important mass effect or large subdural collection can have
reduced clinical signs.
Treatment of posttraumatic SDH depends on the time of diagnostic, clinical findings,
location, child’s age, and it can be conservative or surgical.
Conservative treatment in acute posttraumatic SDH is indicated only when the child
is alert, without focal neurological signs, without any signs of intracranial hypertension
and CT-scan showing a subdural collection less than 3 mm thick, without midline
shift or midline shift smaller than 3-4 mm. The child must be attentively clinical
observed and CT-scan must be repeated. In cases when CT-scan does not show surgical
indications, but the general clinical condition is severe, with a GCS score < 9, but
without focal neurological or other intracranial hypertension signs, monitoring of the ICP
will indicate the optimal therapy.
Acute posttraumatic SDH with focal signs or increased ICP requires urgent surgery.
Surgical treatment consists of hematoma evacuation, hemostasis, and treatment of
associated lesions. Also in subacute and chronic posttraumatic SDH treatment is always
surgical. Many neurosurgical techniques were proposed: drainage of hematoma through
burr holes, drainage of the fluid into a closed external system, evacuation of the
hematoma and excision of the membranes by wide craniotomy.

Fig. 3 Epidural hematoma on left Fig. 4 Posterior fossa epidural

brain hemisphere (mixed lesions: hematoma (on left cerebeller
skull fracture, epidural hematoma, hemisphere )
pneumoencephalus)
744 Head Trauma

Selective references
1. Balmer B, Boltshauser E, Altermatt S, Gobet R Conservative management of significant
epidural haematomas in children. Childs Nerv Syst , 2006, 22, 363-367.
2. Blumenthal I. Shaken baby syndrome Postgrad Med J, 2002, 78, 732-735.
3. Ciurea AV, Kapsalaki EZ, Coman T et al Supratentorial epidural hematoma of traumatic
etiology in infants. Childs Nerv Syst ,2007, 23, 335-341.
4. Drapkin AJ. Growing skull fracture: a posttraumatic neosuture Childs Nerv Syst,2006,22,
394-397.
5. Figaji AA, Fieggen AG, Peter JC Early decompresive craniotomy in children with severe
traumatic brain injury. Childs Nerv Syst , 2003, 19, 666-673.
6. Kamerling SN, Lutz N et al Mild traumatic brain injury in children: practice guidelines
for emergency department and hospitalized patients. Ped Emerg Care ,2003, 19, 431-440.
7. Kan P, Amini A, Hansen K et al. Outcomes after decompressive craniectomy for severe
tramatic brain injury in children. J Neurosurg (5 Suppl Pediatrics) ,2006, 105, 337-342.
8. Raimondi AJ: Trauma, in Raimondi AJ (ed): Pediatric neurosurgery. Springler-Verlag,
1998,pp 343-377.
9. Simpson D, Reilly P. Paediatric Coma Scale. Lancet, 1982, 2, 450.
10. Stein SC, Spettell C The head injury severity scale (HISS): a practical classification of
closed-head injury. Brain Inj ,1995, 9, 437-444.
11. Suskauer SJ, Huisman TA. Neuroimaging in pediatric traumatic brain injury: current and
future predictors of functional outcome. Dev Disabil Res Rev. 2009;15(2):117-23.
12. Villarejo FJ: Cranioencephalic trauma , Atlas of pediatric neurosurgical techniques.Karger,
1985, pp 85-104.
 745

New trends in the pathophysiology,

diagnosis and treatment of
diffuse axonal injury:
A proposal of simple guidelines
VISOCCHI MASSIMILIANO, MD
Institute of Neurosurgry, Catholic University Medical School, Rome, Italy

Key words: Diffuse axonal injury, Transcranial Doppler Sonography, Brain Swelling,
Cerebral Hyperaemia, Hyperflow Syndrome, Bilateral Decompressive
Craniectomy

SUPPORTED BY

THE ITALIAN SOCIETY OF NEUROSONOLOGY AND CEREBRAL

HAEMODYNAMICS (SINSEC – Italian Chapter of the European Society of
Neurosonology and Cerebral Haemodynamics – ESNCH).

THE CEREBRAL HAEMODYNAMICS GROUP OF THE ITALIAN SOCIETY OF

NEUROSURGERY (SINCH).

DEFINITION
Diffuse cerebral lesions are classified as mild and classic concussion and diffuse
axonal injury (DAI).
The pathologic pattern of DAI was first described by Strich and then by Adams as
"diffuse axonal swelling secondary to tearing-torsion of encephalic nervous fibres".
DAI is always a neuropathological diagnosis. Although it is true that radiological
findings of DAI were described by Gentry et al., these particular radiological signs are only
the hallmarks of the most severe forms of DAI. Associated to this basic pattern,
haemorrhagic - necrotic lesions of the brainstem, most frequently of dorsolateral
quadrants of rostral pons, of corpus callosum and adjacent structures (fornix, gyrus
cinguli, septum pellucidum, nucleus caudatus and thalamus dorsalis) were described as
well. According to Gennarelli’s CT criteria the patient’s primary DAI damage can be
classified as grade 1 : no macroscopic lesions; grade 2 : focal lesions in the corpus
callosum and white matter; grade 3 : focal lesions in the dorsolateral quadrants of the
rostral brainstem and same lesions of grade two (Fig 1). Thus diffuse microscopic
haemorrhagic lesions of the midline and subcortical grey matter deals with the
pathological definition of DAI. Moreover neuropathological studies show that DAI of
variable severity is present in any patient that is immediately in a coma after impact where
746 Head Trauma

A B

Fig. 1 A) CT scan study. Brain stem contusion consistent

with Gennarelli’s grade III DAI.
B) Centrum Semiovalis and corpus callosum
contusion in Gennarelli’s grade II DAI

A B

Fig. 2 A) Severe brain swelling at the admission which did

not allow cerebrospinal fluid shunt.
B) at discharge after hyperflow correction and
restoration of normal ventricular size.

Fig. 3 Intracranial hypertension "masks" hyperflow velocitometric pattern.

The TCD recording is of a patient who recovered foilowing freat ment.
Phase 1: At admission.
Phase 2. Hyperflow pattern
Phase 3. Hyperflow syndrome complicated by intracranial hypertension
(hypoflow pattern)
Phase 4. Unmasking effect of decompressive craniectomy (hyperflow pattern)
 Diffuse axonal injury: A challenge to gennarelli theory? 747

TAB 1 Diffuse encephalic lesions are common in severe head trauma patients; they
may be present in moderate trauma patients and are rare among mild head trauma
patients. Intra cranial lesions are classified based on CT scan findings

TAB 1

Diffuse encephalic lesions classification based on CT scan findings*

• Type I diffuse lesions (12.5%): no pathological findings on CT scan.

• Type II diffuse lesions (42%): basal cisterns are present; midline shift < 5 mm
and/or hyper dense focal lesions with a volume smaller than 25 cm3 (including
bone fragments or foreign bodies).

• Type III diffuse lesions (37%): Diffuse brain swelling with cisternal
compression, midline shift < 5 mm, with no hyper dense focal lesions > 25 cm3

• Type IV diffuse lesions (7.8%): Hemispheric brain swelling with midline shift
> 5 mm, with no focal lesions bigger than 25 cm3.

• Type V and type VI lesions of Marshall CT scan classification are those with
focal lesions: lesions treated surgically are type V; non surgical lesions bigger
than 25 cm3 are classified as type VI.

(*Marshall LF, Marshall SB, Klauber MR. (1991)A new clasification of head injury
based on computerized tomography. J Neurosurg; 75:S14-S20)

acceleration/deceleration played a role. Delayed or secondary axotomy is a different

concept to “secondary axonal injuries” and refers to delayed lesions in patients with
functional DAI that evolve to structural DAI. The prognosis is complex and the
pathophysiology of this disease is the subject of much concern. In fact all patients
become rapidly comatose and the clinical picture is often unfair. Although some
Authors in the past over estimated the severity of the disease concluding that half of them
die and the remaining ones are in persistent vegetative state or show severe neurological
deficits. The exact knowledge of the pathohysiological mechanisms underlying DAI, brain
swelling, hyperflow syndromes and intracranial hypertension is mandatory in facing such
intriguing disease.

PATHOPHISIOLOGY
DAI
Diffuse lesions are due to kinetic forces that cause encephalic rotation inside the
skull. That leads to distension or rupture of axons or even vascular structures in
different encephalic regions. Understanding these mechanisms is essential to the clinic
and intensive management of head trauma. Brain and skull have different responses to
the same forces applied during a head trauma due to different densities. These differences
in movement may lead to cerebral vein rupture and also to impact of brain against rigid
748 Head Trauma

skull structures. Peripheral encephalic regions have higher amplitude of movement

than central regions because of the stability given by brainstem. This difference stretches
out axons and vessels and may lead to temporary dysfunction or even complete rupture.
The complex DAI pattern deals with primary and seconday lesions.
Primary lesions occur at the time of trauma. High kinetic energy causes cerebral
movement and this is the primary factor in diffuse lesions. A direct impact of skull against
an external structure is not necessary when acceleration and deceleration forces are
involved.
Secondary lesions are due to complications after trauma as hypoglycemia, hypoxia
(respiratory and/or anemic), high CO2 levels, and hydro electrolytic disturbances which,
virtually, can lead encephalic cells to death. In this complex pattern neurotoxic substances,
hydrocephaly, intra cranial hemodynamic alterations and other metabolic and infectious
systemic disturbances can further complicate the global patient’s trend- Finally there are
also cellular death mechanisms, neuronal, endothelial and glial mechanisms, due to
biochemical and ionic disturbances related to both primary and secondary lesions.

BRAIN SWELLING and HYPEREMIA

In 1973 Bruce stated that , diffuse cerebral swelling after a closed head injury can be
due mainly to cerebral hyperaemia and subsequent increase in cerebral blood volume
(CBV) and not to brain oedema. Although it is true that the influence of Bruce’s paper
about hyperemia in children was very important in the seventies, this concept has been
challenged many times since then. Many Authors have shown that intracellular oedema
and not an increase in CBV is the main cause of brain swelling. Actually CBV is
frequently reduced and not increased in these patients and cerebral metabolic rate
with or without cerebrovascular reactivity can be impaired as well. Otherwise the acute
cerebrovascular congestion or hyperaemia, when present, is significantly related to
intracranial hypertension and unfavourable outcome. Several methods have been
introduced to measure this hyperaemic state, such as measuring Hunsfield Units on CT,
lateral ventricular or cisterns sizes or studying CBF. The CT appearance of diffuse
swelling may develop more readily in children because of the lack of cerebrospinal
fluid available for displacement and may have a relatively benign course unless there is
a severe primary injury or a secondary hypotensive insult. Transcranial Doppler
sonography (TCD) has provided a rapid and non-invasive assessment of cerebral
haemodynamics especially blood velocity and pulsatility in the basal cerebral arteries.
There is a proportional relationship between blood velocity and regional CBF when C02,
cerebral perfusion pressure (CPP) and brain metabolism are stable. The use of mean flow
velocity values to discriminate normal from abnormal flow is recommended, since it is
less dependent on systemic cardiac factors, compared to other velocities. It therefore
serves as a continuous index of cerebral blood flow in the measured vessels. An increase
of mean flow velocity in TCD recording is strongly related to the development of
diffuse cerebral swelling. Several studies of serial recordings of TCD velocities following
head injury have been reported and increased velocities in the basal arteries have been
recognised; increased velocity can be due to increased cerebral blood flow (CBF) as well
as narrowing of the intracranial arteries. Therefore, a simultaneous index of CBF is needed
 Diffuse axonal injury: A challenge to gennarelli theory? 749

to differentiate the two conditions. The Lindegaard index may be used for this purpose.
The Middle Cerebral Artery (MCA) mean flow velocity and the Internal Carotid Artery
(ICA) mean flow velocity ratio (Lindegaard index) were evaluated in all patients.
According to the literature, the Lindegaard index is the most reliable indicator of
vasospasm and vasoparalysis. A Lindegaard index below 3 is the most used cutoff point
of vasoparalysis; measurements above this ratio are considered as resulting from
vasospasm and secondary hypoflow. The cerebral extraction of oxygen (CE02), ie the
difference between the saturation of the arterial 02 (SaO2) and the one of the jugular 02
(SjO2), is of outstanding importance in order to identify an hyperflow syndrome. The
combination of the Lindegaard Index < 3, the absence of dicrotic waves, the presence of
bilateral TCD pattern and the Jugular O2 saturation >75% is consistent with cerebral
hyperflow. Hyperaemia, when associated to severe head injury, can be found along
with high intracranial pressure (ICP) as a consequence of an increase of intracranial
volume; about 40% of brain swelling deteriorate to coma, develop neurological signs or
complicate with an increase in ICP more likely in adults than in children. Such finding
may lead to secondary haemorrhages especially after ICP decreasing maneuvers.
Impairment of cerebral autoregulation has been demonstrated in brain injured patients.
In case of hyperflow due to loss of autoregulation, commonly seen in the so called
brain swelling, the treatment of choice consists in a decreasing of the vascular bed as well
as the blood volume; hyperventilation and barbiturates accomplish the "etiological
therapy" of such a syndrome. Otherwise one must be aware that osmotic therapy may
increase CBF in vasoparalysis by decreasing blood viscosity .

DAI and ICP

In 1982 Gennarelli and his group have shown that similar clinical and structural
changes can be produced experimentally in subhuman primates using non-impact
controlled angular acceleration of the head "in the absence of any increase in ICP or
hypoxaemia. The increase of ICP, mortality and DAI are strongly related to childhood.

DAI and HYPEREMIA

TCD assesses conditions of increased or decreased cerebral blood flow velocity
parallel or similar to modifications of CBF. A secondary vascular involvement in severe
brain injury is claimed as responsible for the appearance of vascular hyperemia and diffuse
brain swelling complicated by an increase in ICP in 75% of the cases. The prevalently
median localization of the haemorrhagic lesions represents the radiological evidence of
a centroencephalic convergence of shock waves. The hypothalamic and brainstem
reticular substance is located in the midline and it is the major site of regulation of
cerebral circulation. Consequently DAI macroscopic lesions close to these structures could
be involved in TCD hyperflow patterns. According to Monro-Kellie doctrine on the
constancy of intracranial blood volume, an increase of intracranial blood volume (i.e.
vasomotor paralysis) produces an increase in ICP up to the progressive CBF reduction,
resulting in the so-called "brain tamponade".
750 Head Trauma

SUGGESTED GUIDELINES
ICP monitoring and haemodynamic assessment are of paramount importance in the
management of DAI.
ICP monitoring and ventricular drainage, when possible, should be adopted in the next
future for all the DAI patients, since DAI can be complicated by intracranial hypertension,
as demonstrated in all the patients undergone ventriculostomy in our study.
In order to avoid fatal mistakes CEO2 evaluation and TCD monitoring provide a
reliable assessment of the time course of CBF changes in brain swelling, being able to
identify the right time for the etiologic therapy which can be administered by using
barbiturates and hyperventilation in hyperflow phases and osmotics up to extreme
and heroic decompressive surgery in hypoflow phases of the same syndrome.
In conclusion a speculative viewpoint on how the field will evolve in 5 years time deals
with the worldwide diffusion of the use of TCD bedside in brain injury patients and
particularly in DAI.

REFERENCES
1. Visocchi M, Meglio M, Procaccini E, Cioni B, Carducci P (1995) [Cerebral vasospasm
and intracranial hypertension: transcranial Doppler ultrasonographic findings] Rays
20:467-72.
2. Visocchi M, Chiaretti A, Cabezas D, Meglio M (2002) Hypoflow and hyperflow in
diffuse axonal injury. Prognostic and therapeutic implications of transcranial Doppler
sonography evaluation. J Neurosurg Sci 46:10-7
3. Visocchi M, Chiaretti A, Genovese O, Di Rocco F: Haemodynamic patterns in children
with posttraumatic diffuse brain swelling. A preliminary study in 6 cases with
neuroradiological features consistent with diffuse axonal injury . Acta Neuroch (2007)
149: 347–356.