1Raised Intracranial Pressure The vertebrate cranium can be thought of as a hollow, rigid sphere of constant volume. There is one large vent;

the foramen magnum and a number of smaller foramina for cranial nerves and blood vessels. The major in-tracranial contents are the brain (including neurological elements and interstitial fluid), blood (arterial and venous) and Cerebrospinal fluid (CSF).

Content VolumePercentage of total volume

Brain (70 %)Interstitial Fluid (10 %)

1400 ml. 80 %

Blood 150 ml. 10 %

CSF 150 ml. 10 %

Total 1700 ml. 100 %

ICP

Volume

Compensated UncompensatedLoss of

Compensation

Brain Volume

Art

eria

l Vo

lum

e

Veno

us V

olum

e

CSF

Spin

al C

ord

Jag u

lar

vein

Brain Volume

Art

eria

l Vo

lum

e

Veno

us V

olum

eCS

F

Spin

al C

ord

Jag u

lar

vein

Mass

Reciprocal changes among the various components in the intracranial space occur when the volume of one of these components is changed. Because the intracranial volume is constant; when an intracranial mass expands or brain swells, compensation must occur through a reciprocal decrease in the volume of CSF (main buffer) and venous blood. Only in children whose sutures have not yet fused can the cranium itself expand to accommodate extra volume. To maintain pressure within the physiologic range the venous system collapse easily, squeezing venous blood out through the jugular veins or through the emissary and scalp veins. CSF, likewise, can be displaced through the foramen magnum into the spinal subarachnoid space. When these compensatory mechanisms have been exhausted, minute changes in volume produce precipitous increase in pressure. Brain parenchyma and arterial blood do not participate, to any significant extent, in the intracranial pressure-buffering mechanism.

2Causes of raised ICP(1) Causes related to the brain:

(a) Neurological elements (Tumors) (b) Interstitial fluid (Edema)

(2) Causes related to the Blood: (a) Arterial (Acute systemic hypertension after lose of cerebral auto-regulation) (b) Venous (Venous sinus thrombosis) (c) Both (Hematomas, increase CO2)

(3) Causes related to the CSF: As in hydrocephalus

Clinical Features(1) No symptoms and signs(2) Symptoms: A- General:

(a) Headache: is generalized in nature and often severest in the morning [because of vascular congestion due to: (1) vascular dilatation secondary to increase CO2 during sleep (2) recumbent position during sleep], and frequently relieved by vomiting (decrease ICP by hyperventilation). (b) Vomiting: which is usually without nausea. (c) Blurring of vision (due to papilledema). (d) Diplopia (due to 6th. nerve palsy).

B- Specific: Symptoms related to the cause of rise ICP.(3) Signs: A- General:

(a) Vital signs (Cushing Triad). Cushing Triad is a triad of bradycardia, hypertension and respiratory irregularities. Respiratory changes occur early, followed by bradycardia, with hypertension occur at a very late stage. (b) papilledema. (c) Squint (due to 6th. nerve palsy (usually bilateral)).

B- Specific: signs related to the cause of rise ICP.

Effect of raised ICP: Normal ICP range from 10 to 15 mm. Hg. (135 to 200 mm. H2O) Increase ICP disturbs brain function by two ways: (1) Reducing cerebral blood flow (2) Causing brain herniation

Treatment of raised ICP: The goal of the treatment is to reduce ICP in order to increase cerebral blood flow and relieve or prevent brain herniation:(1) General measures: ICP can be lowered by reducing the volume of any of the intracranial components (Brain, Blood or CSF) even if the component is normal; (A) Head elevation in (euvolemic patient) can significantly reduce ICP without altering cerebral perfusion pressure, through improvement of venous outflow from the head. (B) Hyperventilation can cause a fall in ICP by reducing intracranial blood volume through vasoconstriction by washing out CO2. It is generally initiated for acute management of increase ICP. (C) Hypertonic solutions and diuretics reduce the fluid content of normal brain. (D) Removal of CSF via ventricular cannula(2) Specific measures: directed to treat the cause of raised ICP. (3) Barbiturate Coma: Induction of coma with short-acting barbiturates is the last resort in the management of rise ICP when all other measures fail. The most commonly used drug is thiopental. It decrease ICP by inhibit cerebral metabolism and reduce cerebral blood flow.

3Blood Brain Barrier (BBB)

AstrocyteEnd feet

Astrocyte

Brain Capillary

Direct transport across endothelial cell through carrier-mediated mechanisms

Neuron

TightJunction

Endothelial Nucleus

RBC

Mitochondria

Somatic CapillaryFenestra

Pinocytotic Vesicles

RBC

Brain Barrier; Its function is to regulate the flow of biologically active substances into the brain and to protect the sensitive neural tissue from toxic materials. There are two mechanisms by which materials may be transported across the endothelial cells:(1) Lipid-soluble substances can usually penetrate all capillary endothelial cell membrane in passive manner.(2) Amino acids and sugars are transported across the capillary endothelium by specific carrier-mediated mechanisms. There are large number of mitochondria in the brain endothelial cells generate energy for active transport. When there is disruption of BBB by any cause, plasma components easily cross the barrier into the neural tissue, causing vasogenic edema.

3

In the somatic capillary, fenestrations between endothelial cells allow free flow of plasma components into the tissues. In addition, there is bulky flow of plasma components across endothelial cell via pinocytotic vesicles. In brain capillary

the endothelial cells are attached to each other by tight junctions and there are no intervening fenestrae. These tight junctions act as a barrier to the passive movement of many substances across the endothelium, and known as Blood

4

AstrocyteEnd feet

TightJunction

Endothelial NucleusRBC

MitochondriaEdematous Astrocyte

EdematousEndothelium

EdematousNeuron

Cytotoxic Edema

AstrocyteEnd feet

Vasogenic EdemaNeuron

Astrocyte

Escape of Plasmafiltrate into the intercellular space through incompetent tight junction

Cerebral Edema

Cerebral Edema is an excess accumulation of water in the intra- and /or extracellular spaces of the brain resulting in state of increase brain volume.

ClassificationsA- Extracellular Edema: Includes;

(1) Vasogenic edema: Disruption of BBB provides the underlying mechanism for development of vasogenic edema with exudation of a plasma-like fluid into the extracellular space. This fluid spreads into adjacent tissue by bulk flow and has a predilection for white matter. Nearly all focal lesions, including primary and metastatic tumors, abscesses and radionecrosis produce vasogenic edema. Vasogenic edema can also occur in the later stages of ischemia and trauma.

(2) Interstitial edema: This results from increase pressure in the ventricles and flow of water and solutes transependymally into the periventricular extracellular space.

(3) Hydrostatic edema: The increased intravascular pressure is responsible for stretching of the vessel wall which results in vasodilatation with or without widening of the tight junction and disruption of BBB as in acute uncompensated hypertension resulting in hypertensive encephalopathy.B- Intracellular Edema: Includes;

(1) Cytotoxic edema: This is due to failure of Na+/K+ ATPase pump system and intracellular accumulation of sodium. This form an osmotic gradient, along which water moves from the extracellular to the intracellular compartment causing a net intracellular accumulation of water and sodium. This occur in anoxia, ischemia and hypothermia. (2) Osmotic edema: In this type of edema, the brain is hyperosmolar with respect to plasma, allowing the brain to swell with water moving along the osmotic gradient. This can be occur in syndrome of inappropriate ADH secretion and water intoxication.

5

Imaging

Edematous brain tissue is usually hypodense on CT scan when compared to the tumor or normal surrounding brain tissue. Edema is usually hyperintense on T2 MRI scan. Newer MRI sequences such as FLAIR separates edema from normal brain water such as CSF, however, the border between tumor and edema is still best delineated by T1 MRI contrast enhanced studies which shows hypointense edema surround the hyperintense contrast-enhancing tumor.

Brain CT scan at parietal level with contrast enhancement ; shows two rounded masses homogeneously enhanced at Rt. and Lt. parietal regions surrounded by hypodense areas (vasogenic cerebral edema). The edema involved the white matter only (no involvement of gray matter as the hypodense area did not reach the surrounding skull bone (the area between skull and edema occupied by gray matter tissue)).

Treatment(1) Steroids: Although glucocorticoid (Dexamethasone) therapy

is ineffective in the treatment of cytotoxic edema and vasogenic edema related to head trauma or cerebral infarction, and it has only limited effect on interstitial edema, but it is very effective in the treatment of vasogenic edema of other causes; especially that caused by primary or metastatic neoplasm. It is thought to stabilize the cell membrane and restore the normal permeability of endothelial cells. The usual loading dose is 10 mg. intravenously followed by 4 mg. every 6 hours. When the appropriate therapeutic goal has been achieved, the dose should be slowly tapered over a period of 3 to 4 days.

(2) Osmotherapy: Hypertonic solution like Mannitol is not metabolized and it does not cross the blood brain barrier so it increase serum osmolality and thus helps to draw fluid from brain parenchyma into the vascular space. Mannitol generally is given in small boluses rather than as continuous drip. The usual dose is 0.25 g. /Kg. at 4 to 6 hours intervals. Mannitol is generally effective for 2 to 3 days, because mannitol slowly leaks out of the blood vessels, especially in areas of blood brain barrier breakdown with resulting loss of osmotic gradient. Electrolytes should be monitored closely during the use of any hypertonic agents. Hypokalemia and hypernatremia are common side effects that can complicate chronic mannitol administration. When edema is vasogenic , osmotherapy is less effective; because the edematous regions with increased capillary permeability can not maintain an osmotic gradient. Mannitol has some utility to decrease ICP in patient with local disruption of BBB because normal areas of the brain with intact BBB shrink transiently to decrease total brain mass. Osmotherapy can be used in acute management of other types of edemas.

(3) Diuretics [Loop diuretics (Furosemide)]: In contrast to osmotic agents which are effective only where the blood brain barrier is intact, furosemide decrease edema in pathological areas as well. In addition to its primary action on the kidney, it is thought to reduce CSF production as well.

(4) Acetazolamide (Carbonic anhydrase inhibitor): This drug will decrease the production of CSF and it is therefore, effective in the treatment of interstitial edema. However, it is not effective in the treatment of vasogenic or cytotoxic edemas.

6 Brain Herniation6

1

3

24

1

2

3

4

Types of Brain Herniation

FalxCerebri

1- Cingulate herniation2- Uncal herniation3- Central herniation4- Tonsillar herniation

ForamenMagnum

TentoriumCerebelli

FalxCerebri

TentoriumCerebelli

ForamenMagnum

1- Cingulate herniation2- Uncal herniation3- Central herniation4- Tonsillar herniation

Intracranial Compartments

The supporting dural septa divide the intracranial cavity into various compartments and protect the brain against excessive movement, but

limit the amount of compensatory shift and displacement that can develop in response to abnormal conditions. There are two major dural septa; the falx cerebri and the tentorium cerebelli. The term herniation refers to the abnormal shifting of brain tissue within the cranial vault. Typically the herniation occurs through a rigid opening composed of dura or bone and it is caused by focal masses. These masses could be; (1) Tumors (2) Intracranial Hematomas (3) Focal brain edemas. As a general rule; an increase in ICP without a shift of brain structures ( as in pseudo tumor cerebri or chronic hydrocephalus) is better tolerated than an increase secondary to a focal mass (as in tumor, intracranial hematoma, focal brain edema).

B- Infratentorial herniation: includes; Tonsillar herniation, which results from expansion of posterior fossa mass lesions. It may also results from lumbar puncture in patient with mass lesion in posterior fossa. The tonsil of the cerebellum herniates through the foramen magnum into the upper spinal canal, compressing the medulla which results in impair consciousness, neck stiffness and ataxic breathing.

Types of brain herniationA- Supratentorial herniations: the major supratentorial shift

can be categorized as;

(1) Cingulate herniation: a supratentorial mass lesion may displace the cingulate gyrus, which is next to the free edge of the falx cerebri and cause it

to herniate under the falx to the opposite side. The anterior cerebral artery may be compromised by tight, sharp edge of the falx cerebri. There are no clinical signs and symptoms specific to cingulate herniation.

(2) Central transtentorial herniation: this is most commonly occurs with mass lesions located far from tentorial hiatus; such as frontal, parietal

or occipital areas. There is downward displacement of the diencephalon and midbrain centrally through the tentorial incisura. The patient tends to have bilaterally small reactive pupils, exhibit chyne-stokes respirations and may show loss of vertical gaze.

(3) Uncal herniation : It is the most common herniation syndrome observed clinically. It is often caused by mass lesions of middle cranial

fossa, which cause the uncus (the most inferiomedial structure of the temporal lobe) to herniate between the brain stem (at level of midbrain) and tentorial edge into the posterior fossa. The clinical syndrome consists of progressive impairment of consciousness (compression on reticular activating system), dilated ipsilateral pupil (compression of the third nerve) and contralateral hemiparesis (direct compression of cerebral peduncle). The posterior cerebral artery may be compromised causing secondary infarction of the occipital lobe. When there is compression of the opposite cerebral peduncle against the tentorial edge (Kernohan’s notch), the (false localizing) hemiparesis is ipsilateral to the herniation.

7Impair Consciousness

ScoreResponseDeterminant4Spontaneously

Eye opening3To speech2To pain1None5Oriented (time, place, person)

Best verbalresponse

4Disoriented (confused speech) 3Inappropriate words2Incomprehensible sounds1None6Obey commands

Best motorresponse

5Localizing pain4Withdrawal to pain3Flexion to pain (decorticate)2Extension to pain (decerebrate) 1None

Glasgow ComaScale (GCS)Upper score = 15Lowest score = 3

Coma or loss of consciousness may be defined as a loss of awareness of one’s self or environment. Glasgow Coma Scale (GCS) is used to assess the level of consciousness:

Coma according to GCS is defined as inability

to obey command, to speak words and to open the eyes. Therefore; none of patients with GCS of 9 or more are found to be in coma, but 90% of those with GCS of 8 or less could be found in coma. The conscious state depends on the integrity of the reticular activating system, beginning in the medulla and extending to thalamus. The reticular nuclei seem to supply a baseline arousal level somewhat like the power control to a computer. The cerebral hemispheres may be thought of as analogous to the software and memory of a computer system. Therefore; the cause of impair consciousness can be classified into:

A- Cerebral hemispheres lesions: like diffuse cortical lesions (hypoxia, hypoglycemia ...etc)B- Brainstem lesions: includes;

1- Supratentorial mass lesion through uncal herniation (cerebral tumors)

2- Direct lesion in the brainstem itself (Hemorrhages)

Evaluation of Comatose Patient(1) Airway: Establish an adequate airway(2) Breathing: Assess respiratory pattern and ensure adequate

oxygenation and ventilation. The rate and rhythm of spontaneous respiration should be noted:

a- Cheyne-Stokes respiration: seen in patients with diffuse forebrain lesions; in whom they became hypersensitive to normal level of CO2. This results in hyperventilatory phase which blows off CO2 and results in apnea for a brief period. During apnea, CO2 accumulates to normal level; thus cycles of hyperventilation and apnea alternate.

b- Central neurogenic hyperventilation: seen in severe midbrain lesions. It is rapid, deep respiration results in high level of PO2 and low level of CO2.

c- Apneustic breathing: It is characterized by prolonged pause at full inspiration. It usually results from lesion of the Pons.

d- Ataxic breathing: It occurs in patient with medullary lesions, where the respiratory center is located. The breathing is very irregular with deep and shallow breaths occurring randomly.

(3) Circulation: assess vital signs (Cushing Triad).(4) Cervical stabilization as needed.(5) Obtain blood for basic studies and administer intravenous hypertonic glucose (in non-trauma patient).

8 (6) General examination (Chest, Abdomen ...etc)(7) Neurological examination: concentrating on GCS, pupillary size and brain stem reflexes (oculo-cephalic, oculo-vestibular, corneal reflexes…etc).

PositiveOculovestibular

Test

NegativeOculovestibular

Test

Treatment of Comatose Patient After patient evaluation, and excluding non-CNS causes of coma (like metabolic causes): (A) If herniation syndrome or signs of expanding posterior fossa lesion with brainstem compression are present, lower the intracranial pressure and obtain CT scan for diagnosis. Lumbar puncture is contraindicated. Operating room should be notified to avoid unnecessary post-CT scan delays if surgically operable lesion is detected.(B) If no evidence of herniation is detected; Brain CT scan should be obtained. If meningitis is suspected, and there is no mass lesion presence in the CT scan (especially in posterior fossa), then lumbar puncture is indicated for diagnosis. Treatment should be instituted immediately. If CT scan shows coexisting mass lesion in a patient in whom an infectious causes is strongly suspected (e.g. rupture abscess) especially in posterior fossa, CSF examination could be obtained by methods other than lumbar puncture; like ventricular tap, but antibiotic therapy should not be delayed. Epilepsy if present should be treated by anti-epileptic medications.

Oculo-vestibular reflex (Ice water Caloric test): It is usually performed with cold or ice water. The head is elevated to 30 degrees, 15 to 20 ml. of very cold water are instilled in the auditory canal with syringe. In unconscious patient with intact brainstem, conjugate tonic deviation of each eye is observed toward the side of the ear that is irrigated (Positive Oculovestibular Reflex). The test should not be performed in patient with traumatic injuries unless it is certain that there is no disruption of petrous bone (signs of middle cranial fossa fractures) is present, to avoid contamination of intracranial space from auditory canal. With damaged brainstem, the eyes are immobile despite cold Caloric stimulation (Negative Oculovestibular Reflex).

Oculo-cephalic reflex (Doll’s eye movement): It should not be performed in a patient with traumatic injury unless there is clear evidence that the cervical spine is intact. To test the oculo-cephalic reflex, the patient eyelids must be held open and his head rotated briskly from one side to the other. In patient with intact brainstem, the eyes conjugately deviated to the side opposite to the direction in which the head is turned (Positive Oculocephalic Reflex = Negative Doll’s sign). Vertical eye movements can be tested by extending or flexing the neck which also results in opposite eye movements. This reflex can not be demonstrated in conscious individual because of the intact inhibitory influences from cerebral hemispheres. With damaged brainstem in unconscious patient; the eyes have a fixed forward stare and move with the head (Positive Oculocephalic Reflex = Positive Doll’s sign).

9Head Injury

SkinsubCutaneous fascia

galea AponeurosisLoose areolar tissuePericranium

It is injury to the brain and its coverings (meninges, skull bones and scalp).

Mechanism of injury Head injury can be results primarily from two phenomena; contact forces and inertial forces. Contact phenomena appear when the head strikes or is struck by an object, which results in local compressive strains in underlying skull and brain which lead to skull fractures, coup contusion and some of intra or extra axial hematomas. Inertial forces are generated by head motions that occur during the traumatic events which may also accompany contact phenomena. These motions are described by acceleration or deceleration of the head as it is set into motion or is stopped from moving. Concussion, diffuse axonal injury without hematoma, most subdural hematomas and counter coup contusions are produced as a result of acceleration of the head.

I- Scalp injuriesIn cross section, the scalp contains five distinct layers.

The first 3 layers (Skin, subCutaneous fascia and galea Apneurosis) adhere firmly to one another and may be considered as single unit. Beneath the galea is a layer of Loose areolar tissue which is easily separated and it is the plane in which scalp flaps are raised and scalp avulsions occur. The final layer is the Pericranium (periosteal layer of the outer table of the skull), which adheres firmly to the skull, particularly at cranial sutures.

Nerve supply: Anteriorly the major cutaneous nerves are the supra-orbital and supra-trochlear nerves (branches of ophthalmic division of the 5th. cranial nerve). These accompanied the arteries of the same name and supply the scalp as far posteriorly as a line drawn across the top of the head from one ear to the other. Posterior to this line, the scalp is supplied by greater and lesser occipital nerves [branches of dorsal rami of C2 through C4 (C2 for the scalp)].

Vascular anatomy: Scalp vessels are located in the deep portion of the subcutaneous layer just above the galea.

Lymphatics: These parallel the neurovascular supply. The lower portion of the forehead (frontal and temporal ar-eas) drains through the face into submandibular nodes. The upper frontal and parietal areas drain into the superficial parotid groups of nodes. The occipital portion of the scalp drains into the retro-auricular nodes.

PosteriorAuricular

artery

Occipitalartery

Occipitalartery

External Carotidartery

Frontalartery

Superiororbitalartery

Superiororbitalartery

Blood Supply of the Scalp

Classification of scalp injuries

supply of the scalp, extensive debridement is both unnecessary and unwise, but all obviously devitalized tissue should be removed and the wound should be irrigated with normal saline wash. In the absence of an underlying skull fracture, the best technique for stopping bleeding in scalp wound is circumferential pressure of the surrounding scalp against the skull. In very large and gaping wounds, another useful technique is to place clamps (forceps) on the galea and draw it back over the dermis (skin and subcutaneous fascia), there by compressing the scalp vessels. An area of 2-3 cm. around the wound should be shaved. Scalp wounds should be closed in two layers. The first layer approximates the galea and should be closed

(1) Scalp wounds Because of the tension in the galea, wounds that include this layer tend to gape consid-erably. The tendency of the galea to retract offers a form of protection. Since the scalp blood vessels are located in the subcutaneous fascia, they do not contract. If the galea is lacerated, the contraction of this layer will cause retraction of the vessels also. Thus superficial wounds with the galea intact may bleed more profusely than deep wounds with the galea cut. All examination of scalp wounds should be per-formed using sterile technique. Many times an underlying skull fracture can be palpated in the depth of a scalp wound. Most simple wounds can be examined and closed under lo-cal anesthesia, but in case of extensive wounds or in very young children, it is necessary to use general anesthesia in the operating room. Treatment; because of the rich blood

10

Caput succedaneum

Cephalhematoma

Subgaleal hematoma

SkinAponeurosis

Pericranium

Skull

Dura

Scalp Hematomas

(2) Scalp avulsions This is usu-ally occur in the loose areolar tissue between the galea and pericranium (traumatic sepa-ration of the galea with the first two layers from the pericranium) Most scalp avulsions occur when a portion of hair is pulled at a tangential angle. Perpendicular pulling may results in avulsion of hair only.

(3) Scalp hematomas Caput succedaneum is a localized swelling of the scalp, typically located in the midline posterior parietal area over the part of the cranium that leads the way down the birth canal during delivery. The swelling is inti-mately within the superficial layers of the scalp and usually consist of tissue fluid (edema) rather than being a true hematoma. These lesions are usually not associ-ated with skull injury and require no therapy.

(a) Cephalhematoma (subperiosteal hematoma); It is the result of bleeding between the periosteum and the skull and is found al-most exclusively in the newborn. The presentation is of a localized, initially hard mass. The scalp can be moved over the mass, which itself fixed. Because the blood has collected under the pericranium and the pericranium is attached at the su-tures, the mass is limited to one cranial bone and does not cross the suture lines. The initial therapy is to leave the lesion alone. It should not be tapped because of the risk of introducing infection. The hematoma is gradually reabsorbed over sev-eral weeks. If the lesion has not been resolved by 6 weeks, plain X-ray will show whether it is calcifying. If significant lump is present and calcifying, it should be removed surgically.

(b) Subgaleal hematoma; It results from bleeding into the loose connective tissue layer between the galea and pericranium and it can be spread across half the head or even all around the scalp. It is very common after head injury in children. It should not be tapped because of high risk of infection. The treatment is to reassure the parents that the mass will resolved.

II- Skull fractures Skull fractures are classified in three ways according to:(a) Pattern; (1) Linear (2) Diastatic (3) Depressed (4) Comminuted(b) Location; (1) Skull Convexity (2) Skull Base(c) Skin integrity; (1) Opened (compound) (2) Closed

A- Skull Covexity Fractures:The clinical features includes;

(a) Clinical features of scalp injury.(b) Clinical features of underlying brain injury.

The diagnosis is usually by either Skull X-ray or Brain CT scan [but Not MRI]

with absorbable suture (like catgut). The galea is the strongest layer of the scalp and should always be repaired if possible. The second layer is the skin which should be closed with non-absorbable suture (like silk); interrupted or continuous running sutures may be used. If the resulting gap, after removing the devitalized tissue, is large to

Closed Linear Skull Fracture

Opened Depressed Skull Fracture

be closed without tension, undermining of the subgaleal space (manual separation of the galea with the first two layers from the pericranium) is useful in order to a chief wound closure without tension. Following closure, a compression dress-ing is helpful, particularly if there had been undermining of the subgaleal space. Sutures should be remain in place for 7 days in case of two layer scalp wound closure, but should be extended to 10 days in case of single layer closure (suturing of the skin layer only).

11

Brain CT scan, axial section, at parietal level; showed Rt. occipital depressed skull fracture with overlying scalp swelling. The image on the Lt. is called Bone Window; in which the brain soft tissue is sup-pressed by the CT scan computer, resulting in clearer image of skull bone. Bone window is usually used in searching for skull fractures.

Linear skull fracture: Is a single fracture line in the skull, which passes through the entire thickness of the skull. This requires no stabilization or exploration. Surgery is performed for the associated intracranial lesions (like hematomas).

Diastatic skull fracture: Is a separation of a cranial suture line. The management is the same as for linear skull frac-ture.

Depressed skull fracture: The fracture is consid-ered depressed if the outer table of one or more of the fracture edges lies below the normal anatomic level of the inner table as determined by the surrounding intact skull. The indications of surgery include;

(1) Cosmetic reasons if the fracture is closed. (2) Opened fracture which represents a neurosurgical emer-

gency because of the risk of bacterial infection of the cranial cav-

Comminuted skull frac-ture: A fracture is called comminuted when more than one linear fracture is present. If the overlying skin is closed; the management is the same as for linear skull fracture, but if it is opened; the man-agement is the same as for depressed skull fracture.

TemporalisMuscle

DuraSkull boneAponeurosis

Skin

Craniectomy

ity. The operation is performed within 24 hours. (3) There is an underlying surgically indicated intracra-

nial lesion (like hematoma). Although elevation of bone fragments occasionally

improves a focal neurological deficit originating in the cor-tex directly under depressed bone fracture (presumably by increasing local blood flow), this procedure usually produc-es no neurological changes, implying that the impact itself produced the cortical damage. The incidence of epilepsy after depressed skull fracture is apparently determined by cortical damage at the time of the impact; since it is not altered by elevation of the fragments. Thus the treatment of depressed skull fracture is based not on initiating neuro-logical recovery or preventing epilepsy; but, rather on cor-recting cosmetic deformity as well as preventing infection in open fracture.

The process of opening of the cranial cavity by remov-ing parts of the skull bones is known as Craniectomy, while the process of opening of the cranial cavity by cre-ation of reflectable bone flap is known as Craniotomy. The process of closing skull bone defect either by bone or

BoneFlap

Burrhole

4 Burr holes Lt. frontal Craniotomy

by synthetic material is known as Cran-ioplasty. Therefore; the surgery for de-pressed skull fracture as it includes remov-ing or removing and replacement of bone fragments (or synthetic material) is either Craniectomy or Craniectomy with Cranioplasty.

12 B- Skull base Fractures: These are usually linear skull fractures. The dura is easily torn which place the subarachnoid space in direct contact with the paranasal sinuses or middle ear structures, provid-ing pathway for infection through CSF leak.

Clinical signs of skull base fractures includes in; (a) anterior cranial fossa fractures: bilateral periorbital ecchymosis (Raccon eyes), anosmia (Olfactory nerve injury)

or CSF rhinorrhea. Optic nerve injury can follow fractures that involve the optic canal.(b) middle cranial fossa fractures: hemotympanum (bulging of tympanic membrane due to blood collection),

blood in external auditory canal, 7th & 8th cranial nerves palsies, ecchymosis over mastoids (Battle’s sign) or CSF otorrhea / otorrhageia (if associated with rupture tympanic membrane).

(c) posterior cranial fossa fractures: abducens nerve can be damaged in clivus fractures.The diagnosis is usually clinical. These fractures can be seen on Brain CT or Skull X-ray. Aditional suggestive radiographic findings include; pneumocephalus and air/fluid level within the air sinuses.Treatment is usually depending on the presence of CSF leak. A patient with basal skull fracture but with no CSF leak is observed for 2-3 days. If he developed CSF leak (or if he had initially CSF leak); then the observation is extend to 7 days [with or without the use of Acetazolaminde]. The patient is usually observed by placing a loose-fitting sterile gauze pad over the ear or the nose; the pad is changed every nursing shift and saved as an indicator of the amount of CSF leak. Most traumatic CSF leaks resolved spontaneously within the fist week. If the leak persists beyond 7 days, lumbar taps (punctures) are performed daily for 3 days (removing 30-50 ml. of CSF each time). If lumbar taps fail to stop the leak, then surgery is indicated. The usage of antibiotics is controversy. High does steroid is indicated in presence of facial nerve paralysis.

III- Intracranial (Brain) LesionsIn general CNS (Brain and Spinal cord) trauma is divided into;1- Primary injuries: which are the damages that result at time of accidence.2- Secondary injuries: which are defined as the damages that result within minutes, hours, or days after the events

of primary injuries, and can lead to further damage of nervous tissue, prolonging and/or contributing to permanent neu-rological dysfunction.

A- Primary Brain Injuries:These may be classified into Focal , Diffuse or Combined (Focal with Diffused) lesions;Diffuse lesions: These result from acceleration-deceleration injuries to the brain, and they are of two types; (a) Concussion It is condition characterized clinically by transient traumatic lose of consciousness for less than 6 hours

associated with some degrees of post-traumatic amnesia (amnesia for events related to the injury and afterward). The

Lt. fronto-temporal cerebral contusions

Lt. temporal acute Extradural hematoma

Lt. fronto-temporal acute Subdural hematoma

Rt. fronto-temporal acute intracerebral hematoma

inertial force causes deeper structures within the brain to deform resulting in wide spread disruption of brain function but most of the strain is insufficient to cause structural damage.

(b) Diffuse axonal injury It is condition characterized clinically by traumatic lose of consciousness from the time of injury that continues beyond 6 hours. There are microscopic damage scattered throughout the brain including focal axonal changes that lead to focal impairment of axoplasmic transport and disconnection.

The brain CT scan is usually negative in diffuse brain lesions that were not associated with focal lesions.Focal lesions: These include; contusions and intracranial hematomas. Focal lesions that occur underlying the

site of impact called coup lesion and those located far from the site of impact called Countercoup lesions. All focal brain lesions could be coup or countercoup except extradural hematoma which is only of coup type.

I - Contusions consist of heterogeneous areas of hemorrhage, brain necrosis and infarction. They appear as salt-and-pepper lesions in brain CT scan. The commonest sites for contusions are frontal and temporal poles. Contusions can over period of hours or days evolve into intra-parenchymal hematomas. The treatment is conservative unless they are complicated by surgically indicated hematoma.

II - Intracranial hematomas are classified according to anatomy of meninges into;

13(a) Extradural hematoma: is collection of blood between the inner table of the skull and the dura. It ap-pears as biconvex lesion in brain CT scan. These hematomas results from injury to; (1) meningeal vessels (like middle meningeal artery or vein) (2) Deploic veins (as in Skull fractures) (3) Dural venous sinuses. More than 50% of this hematoma arises from middle meningeal artery injury.

(b) Subdural hematoma: is collection of blood between the dura and arachnoid membrane (subdural space). It ap-pears as crescentic lesion in brain CT scan. This hematoma results from tearing of bridging veins that traverse the space between the cortical surface and venous sinuses. It is also results from injury to the surface of the brain with bleeding from cortical vessels into the subdural space.

(c) Intra-parenchymal hematoma: is collection of blood within the brain parenchyma. It appears as mass lesion in brain CT scan. This results from damage of intra-parenchymal blood vessels or as a complication of contusion.

Intracranial hematomas are considered acute if they are present within 3 days of the injury (appear hyperdense lesion in brain CT scan), subacute which become manifest 3 days to 3 weeks of the injury (appear isodense lesion in brain CT scan) and chronic which do not produce symptoms until 3 weeks from the injury (appear hypodense lesion in brain CT scan).

The indication for surgery in intracranial hematomas is largely depending on the clinical condition of the patient. The surgery either Craniectomy (with or without cranioplasty) or Craniotomy; and these are followed by evacuation of the hematoma. Chronic hematoma sometimes can be evacuated through single Burr-hole (a hole in the cranium of 1 cm. in diameter).

B- Secondary Brain Injury

Trauma initiate secondary injury processes in the brain that evolve during the early phase of hospitalization include; (a) Vascular processes:

Vascular Process

Cellular Process

Intracranial HematomaSubarachnoid HemorrhageVasospasmBlood Brain Barrier Damage

Release of free radicalsRelease of Glutamate

Vasogenic edema

Cytotoxic edema

Ischemia

Raised Intracranial Pressure

Hydrocephalus

Inflammatory Process

Hypotension HypocapniaHypoxiaAnemiaFeverSeizure

Pneumocephalus

Secondary Brain Injury

1) Blood vessels damage resulting in intracranial hema-toma, subarachnoid or intraventricular hemor-rhage.

2) Vasospasm, espe-cially if there is suba-rachnoid hemorrhage, which may result in ischemia.

3) Blood Brain Barrier damage resulting in Vasogenic edema.(b) Cellular pro-cesses: which result in production of :

1) free radicals which lead to lipid peroxidation and cell membrane destruction 2) Glutamate that lead to stimulate abnormal neuronal depolarization.

Both of these products [(a) & (b)] lead to cytotoxic edema formation through impairment of Na+/K+ pump action.

While the raised ICP is aggravated by the presence of Pneumocephalus as a result of skull base fractures (if they are associated), the resulting brain ischemia is ag-gravated by the presence of hypotension, hypocapnia, hypoxia, anemia, fever and seizure. Intracranial hypertension is also one of the aggravating factors of brain isch-emia (one of its effects).

Fracture of Skull

Cortical Contusion

Tangential Wound

(c) Inflammatory Processes: that can result in late vascular and cellular effects. These processes are manifested clinically by development of Intracranial hyper-tension and cerebral ischemia.

Gunshot (missile) wounds of the headThese are classified into:(1) Tangential wound: The bullet grazes the skull but does not pen-

etrate it. It may travel in the subgaleal space and exit through or remain in the scalp. In addition to scalp wounds, the bullet can cause varying degrees of damage to the skull (fractures), meninges (hematomas) and underlying cortex (contusions). The ef-fect on the cortex is due to sonic pressure waves of the bullet.

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Perforating Wound

Bullet and bone fragmentsContused brain

Penetrating WoundRicochet

Clinical features of brain injuriesDiffuse brain injuries usually presented with initial lose of consciousness which either recovererd within 6 hours [Con-

cussion] or last more than 6 hours [Diffuse Axonal Injury]. Focal brain injuries, on the other hand, usually presented with clinical features of raised intracranial pressure and/or brain herniation in addition to specific clinical features related to the location of the lesion itself. Diffuse and focal brain injuries are happened either alone or together giving the following clinical features;

(A) Conscious level: Patients with these lesions follow one of the following five clinical courses; (1) Conscious throughout. (2) Unconscious throughout. (3) Initially conscious and subsequently unconscious. (4) Initially unconscious and subsequently conscious. (5) Initially unconscious followed by lucid interval and then unconscious again. Lucid interval is a period of regain-

ing consciousness after unconscious period and it is proceeds the subsequent lose of consciousness. The initial transient loses of consciousness results from concussion and is followed by a return of consciousness until the growing of intracranial hematoms or development of focal cerebral edema.

(B) Clinical features of raised intracranial pressure. (C) Clinical features of brain herniation (uncal herniation is the commonest type).

(2) Penetrating wound: The skull is penetrated at one side, but the bullet does not have enough energy to penetrate the entire brain or the skull on the opposite side. Sometimes after hitting the inner table of the opposite side of the skull it will ricochet (reflected) with re-entry of the bullet into the brain tissue caus-

Management of patient with head injury The initial goal in the management of head injury is to halt any ongoing injury (scalp, skull and/or Primary brain injury)

and prevent the onset of additional injury (Secondary brain injury). Most obvious sources of additional injury related to mass effect on the brain [due to intracranial hematomas, focal brain edema or pneumocephalus (presence of intracranial air)]; which are presented clinically with features of raised ICP (with or without its effect) and/or brain ischemia. The neu-rological signs caused by brain injury usually obscure any focal findings that might be caused by secondary brain ischemia; therefore, cerebral perfusion must be monitored if brain ischemia is suspected (especially in severe head injury).

Emergency Unit: The first step is to determine whether the patient is comatose or not (Using GCS). Comatose Patient is evaluated and resuscitated as described in the Evaluation of the Comatose patient (Page 1) except of giving intravenous glucose ]. Non-Comatose patient should be evaluated for: breathing pattern, vital signs, presence of gross neurological deficit (assessment of the motor system) and stabilized him hemodynamically. Blood sample should be obtained for basic studies and blood group.

(3) Perforating wound: The bullet goes through the entire head (entrance and exit). The wound entry is generally smaller than the exit wound.

For penetrating and perforating wounds there are also varying degrees of injuries to all elements of the head. The treatment of gunshot wounds depends on the head elements that were injured (scalp, skull or brain).

ing further damage.

15GCS=15

No risk factorsGCS=15

With risk factorsGCS=3-14

With or without risk factors

Hospital admission

Brain CT scan

Abnormal CT scan

Normal CT scan

Indication for surgery Observation &Conservative

Treatment

Deteriorated

Deteriorated

Improved

Yes NoSurgery

Dischargedhome withWarning

instructions

Discharge when stableand follow up clinic

Management of Head injury

History: During first evaluation and resuscitation, history can be obtained from peoples who witness the injury, medical personnel at scene, family members, police officers or the non-comatose patient himself. History should be concentrated on:

(1) Time of injury. (2) the mechanism of injury [RTA (Road Traffic Accidence)

or direct trauma to the head](3) History of lose of consciousness. (4) presence of Post-traumatic amnesia. (5) persistant Headache.(6) persistant Vomiting. (7) Focal neurological deficit (inability to move upper or

lower limb). (8) Epilepsy. (9) Coagulation disorder or history of anticoagulant medi-

cations. (10) Age < 2 years or > 60 years. Examination: The following points should be con-

sidered during the clinical examination:(1) pulse and blood pressure; Raised ICP presented

with bradycardia and hypertension. Hypotension accom-panied by bradycardia should alert the neurosurgeon to the possibility of Neurogenic shock associated with spinal cord injury; in this case hypotension should be treated with pressors (Dopamine) rather than aggressive volume expansion after other sources of occult hemorrhage have been ruled out. Hypotension with tachycardia occur in case of Hypovolemic shock that caused by either major occult internal bleeding [intrathoracic or intraabdominal (but not intracranial)] or prolonged bleeding from missed scalp wound. It is impossible for Acute intracranial bleeding (hematomas) to cause hypovolemic shock; because before the amount of blood loss intracranially cause hypovolemic shock, would result in intracranial hematoma of enough size to cause raised ICP and brain herniation with subsequent patient death.

(2) Breathing pattern(3) Temperature; treatment of fever, because fever is potent cerebral vasodilator and can result in raised ICP. Fever also

cause increase in body’s metabolic rate which aggravate the cerebral ischemia.(4) Pupils size and reaction to light;

(a) presence of unilateral dilated pupil that does not reacting to light (or does so very slowly) in a trauma patient should be considered caused by ipsilateral uncal herniation until prove otherwise. if the third nerve function is completely lost, the eye will diviate inferiorly and laterally. Other possible causes of unilateral pupil dilatation are direct trauma to the eye, drug reaction and optic nerve injury.

(b) Bilateral dilated pupils may result from hypoxia, hypotension, bilateral third nerve dysfunction or brainstem dysfunction (as occur in late stage of uncal brain herniation).

(c) Unilateral pupil constriction is often accompanied by ptosis (Horner’s syndrome).(d) Bilateral pupillary constriction may be drug response (narcotics), represent a pontine lesion or may occur in the

central transtentorial herniation.(5) Examination of the motor system; including facial and four limbs body movements. Unilateral body weakness

should alert the possibility of contralateral uncal brain herniation or rarely ipsilateral one (Kernohan’s notch).(6) Head Examination; for clinical signs of scalp and skull injuries.Investigations:(A) Blood Examination: include;

(a) Hb. Cerebral ischemia is aggravated by presence of anemia (Hb < 10 g./dl.), due to decrease the oxygen carrying capacity of the blood resulting in tissue hypoxia.

(b) Blood sugar should be checked to rule out hyperglycemia (as one of the metabolic response to trauma) which may exacerbate the secondary ischemic brain injury by increasing blood viscosity.

(c) Blood urea.(d) Blood group.

(B) Radiology: include;(a) Brain CT scan. It is indicated if GCS less than 15 or presence of one or more of the following Risk factors:

(1) Clinical signs of skull fractures (scalp swelling and/or bruising at sit of trauma). (2) RTA (Road Traffic Accidence).(3) History of lose of consciousness.

16

Home Observation: the patients were sent home with Warning instructions to their relatives; that the pa-tients should be brought back again to the neurosurgical hospital if they developed deterioration in their consciouss level, epilepsy, severe headache, repeated vomiting or neurological deficit. Patient’s relatives education level, their transfere fa-cilities (like owning car) and patient’s home location relative to the nearest neurosurgical hospital should be considered.

Neurosurgical Ward Observation: Patients should be sent for complete blood analysis (blood group and cross match if the surgery indicated), coagulation studies, electrolytes and repeat the blood biochemistry (Blood sug-ar, blood urea) if needed.

The following chart should be done for every patient with head injury that was admitted to the neurosurgical ward for observation;

(4) presence of Post-traumatic amnesia. (5) persistant Headache.(6) persistant Vomiting. (7) Focal neurological deficit. (8) Epilepsy. (9) Coagulation disorder or history of anticoagulant medications. (10) Age < 2 years or > 60 years.

(b) X-ray screening. Usually performed for Multiply injured comatose patient (RTA) or if indicated for non-coma-tose patient, include; Cervical spine, Chest, abdomen, pelvic and limbs X-rays.

After resuscitation the patient should be re-evaluated neurologically. The GCS that has the most prognostic importance is referred as Post-resuscitation GCS, which is obtained after patient airway and hemodynamic status has been stabilized.

Head injury can be classified according to disturbed conscious level (GCS) into;(1) Mild head injury (GCS= 13-15)(2) Moderate head injury (GCS= 9-12) (3) Severe head injury (GCS= 3-8) If the brain CT scan showed lesions that require neurosurgical interferance, the patient should be prepaired for surgery

and transferred to the operation theater, otherwise the patient should be admitted for observation. Observation is usually done for:

(1) non-Surgically indicated primary brain lesions.(2) the onset of secondary brain lesions.All patients with head injuries (even with initial negative brain CT scan) should be observed for any clinical features of

the lesions that possibly developed as a result of the secondary brain injury events for at least 24 hours after the injury; therefore, the patients that require no hospitalization should be observed at home by their relatives.

The indications for Hospital admission are the same indications for Brain CT scan. The severe head injury patient should be admitted to the Intensive Care Unit (ICU), while the mild and moderate one can be admitted to the Neurosurgical ward.

A new brain CT scan is needed if there is deterioration in the above parameters which reflect the raised ICP and/or cerebral ischemia. Neu-rological deterioration is defined as an increase in the preexisting neurological deficit, the develop-ment of new focal sign, or two points decrease in GCS score. This deteriora-tion either reflect the worsening of the pre-existing primary brain injury lesions, or the development of the

Determinant TimeGCS

Vital signs

Pulse per minuteBlood pressureBreathing patternTempreture

Pupils (sizes and reaction to light) Motor system examination (for weakness)Others

(1) ICP Monitoring. Include;(a) Fluid coupled devices; like ventriculostomy catheter which is positioned with its tip in the frontal horn of

lateral ventricle and coupled by fluid filled tubing to an external pressure transducer. In addition to ICP monitoring, this device allow the treatment of elevated ICP by intermittent drainage of CSF. These devices are difficult to place into small

ICU Observation: In addition to all parameters that had been observed at neurosurgical ward, more extensive monitoring is required:

secondary brain injury lesions. These can only be diagnosed by the new brain CT scan. If the brain CT scan showed that the developing lesions require a neurosurgical interferance, the patient should be prepaired for surgery and transferred to the operation theater, otherwise the cycle of observation and conservative treatment is continued.

17

ICP Nonitoring through Ventriculostomy

compressed ventricular system and may cause ventriculitis and intracranial hemorrhage.(b) Non-fluid coupled devices; which can be inserted in the subdural space or inside the brain tissue.

They can easily inserted especially in patient with small compressed ventricles. Intracranial infection and hem-orrhage is also possible.

ICP monitoring is continued as long as the treatment of intracranial hypertension is required (3-10 days). A severe co-agulopathy is only major contraindication to ICP monitoring.

(2) Monitoring of the cerebral perfusion; by using(a) Cerebral perfusion pressure formula (calculated by

subtracting the ICP from the mean arterial blood pressure). The lower limit is 50 mmHg.

(b) Transcranial Doppler ultrasonography which use pulsed ultrasound signals that transmitted through thin areas of skull (temporal bones). It is used to measure the middle ce-rebral artery velocity.

(c) Cerebral blood flow adequacy; by measuring the jugular venous oxygen saturation [which is normal (55-70%) if the cerebral blood fow is appropriate for brain metabolic requirements] for global cerebral ischemia, and Brain tissue PO2 through special catheter for regional brain ischemia.

(3) Systemic oxygen monitoring for hypoxia by using pulse oximetry. The goal is to maintain arterial oxygen satu-ration greater than 95%.

(4) Fluid input/output chart. Foley catheter is necessary fo accurate measurement of urine output. For maitenance and replacement fluids should be glucose free if possible (like 0.9% normal saline) and blood gucose level should be checked periodically and if greater tha 200 mg/dl. a treatment with appropriate dose of insulin should strated. Also fluid such as Glucose Water should be avoided if possible because in addition to the risk of increasing blood glucose level, its water content may exacerbate the existing brain edema.

(5) Electrolytes especially Na+ and K+ should be monitored.(6) Other General measures;

(a) Thromboembolism prophylaxis; Both venous compression device and low dose heparin are effective in re-ducing the risk of thromboembolism and subsequent pulmonary embolism which is common complication after major trauma.

(b) Gastric ulcer prophylaxis; stress ulcers are common complication in critically ill patient. Intracranial injury particularly involving the diencephalone or brainstem results in increase production of Gastrin and gastric acid. Antacids and H2-receptors blockers can be used for prophylaxis.

(c) Nutritional Support; Patients with severe head injury are in hypermetabolic and catabolic state. Using Eternal Feeding (Gastric or Jejunal tube) beginning as soon as possible but certainly within 72 hours after injury.

(d) Preventing bed ulcer (bed sore); by rolling the comatose patient to the Lt., Rt. side and his back periodically. The period of staying on his sides or back should never exceed the two hours limit. Alternating pressure relief beds are also helpful.