HEAD INJURIES

Dr Phillipo L. Chalya M.D. ;M.Med [Surg]

Surgeon specialist Dept of Surgery

BMC

OUTLINE

Definition Surgical Anatomy Epidemiology Etiology Mechanism of injury Classifications Pathophysiology Clinical presentation Workup Management Complications

DEFINITION

Head injury is defined as traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures

Head injury can also be defined as any alteration in mental or physical functioning related to a blow to the head

Maxillofacial injuries is not part of head injury

SURGICAL ANATOMY

Structures to be considered in head injuries Scalp Skull Meninges Brain CSF

Scalp Skin

Thick, hair bearing with many sebaceous glands

Connective tissue Fibro-fatty Many blood vessels

Aponeurosis [epicranial] Tough structure joining

occipitalis muscle posteriorly and frontalis anteriorly

Loose areola tissue Occupies the

subaponeurotic space Pericranium

Periosteum covering the outer surface of the skull

Skull 22 bones in total Consists of:-

8 cranial bones [cranium] 14 facial bones

Cranium is that part of the skull that encloses the brain

The cranium is made up of the vault [the upper part] and the base of the skull [lower part]

The inner aspect of the base of the skull consists of 3 cranial fossae:- Anterior cranial fossa Middle cranial fossa Posterior cranial fossa

Meninges

3 layers Dura mater Arachnoid mater Pia mater

Dura mater

Conventionally 2 layers: Endosteal layer (periosteum) Meningeal layer (true dura)

Septa: made up of dural folds Divides the cranial cavity into 3

compartments 2 upper compartments [supratentorial

compartments] 1 lower compartment [infratentorial

compartment] Major dural folds include:-

Falx cerebri Tentorium cerebelli

Falx cerebri Sickle-shaped Upper part is fixed and

the lower part is free Lies vertically in the

longitudinal fissure between the 2 cerebral hemispheres

Divides the supratentorial compartment into 2 parts

The 2 supratentorial compartments are occupied by the two cerebral hemispheres

Tentorium cerebelli

Crescent shaped Lies horizontally between the occipital lobe

of the cerebrum and the cerebellum Posteriorly is fixed Anteriorly is free with an opening [tentorial

notch] for passage of the midbrain Has a protective function it prevents shuddering movements of the

brain within the cranial cavity and the folds prevent damage to nervous tissue during sudden rotational movements

Arachnoid Mater

Internal to the dura mater Is an avascular membrane Lies between the pia mater internally

and the dura mater externally It is separated from the pia mater by the

subarachnoid cavity or space, which is filled with cerebrospinal fluid.

Called arachnoid because the cobweblike trabeculae crossing the subarachnoid spase to become continuous with the pia mater

Pia Mater

Vascular membrane Closely invests the brain Descends into gyri Extends over cranial nerves as they

come out the brain – fuses with the epineurium

Forms Tela Choroidea of 3rd & 4th ventricles

Fuses with ependyma to form Choroid Plexus in Lateral, 3rd & 4th ventricles --> CSF

Brain

Divided into three major areas Cerebrum Brain stem Cerebellum

Cerebrum

The cerebrum is composed of 2 cerebral hemispheres

The hemispheres are connected by the corpus callosum

Consists of 4 lobes Parietal lobe Frontal lobe Occipital lobe Temporal lobe

Brain stem

Three major divisions Midbrain Pons Medulla

10 of the 12 pairs of cranial nerves arise from the brainstem (ipsilateral signs)

Cortical pathways pass through the brainstem and decussate (cross) in the medulla (contralateral signs)

Cerebellum

This is the largest part of the hind brain

EPIDEMIOLOGY

Incidence

Morbidity/mortality

Age

Sex

Race

Head injury continues to be an enormous public health problem, even with modern medicine in the 21st century

It is one of the most common cause of admissions to the A&E department worldwide

Incidence

Morbidity /mortality

Head injury are the major cause of morbidity and mortality among trauma admissions

Age

Head injuries occur in all age groups, with a peak incidence between the ages of 16 and 25 years and a second peak in the elderly who have a high incidence of chronic subdural haematomas

Head injuries are a leading cause of trauma related deaths in patients young than 45 years

sex

Males are more affected than females The male to female ratio is 2:1 [M:F=

2:1] worldwide

AETIOLOGY

Road traffic accidents Fall injuries Assault injuries Sport injuries Penetrating injuries e.g. bullets,

knives, screwdrivers, arrows, nails etc

MECHANISM OF INJURY

Blunt head injury Penetrating head injury

Blunt head injury

Direct trauma to the head Occurs in 2 ways: a moving head strikes a

fixed object or a moving object strikes an immobile head →scalp injury, fractures of the skull, contused brain etc

Deceleration head injuries These are injuries resulting from rapid

deceleration of the head causing the brain to move within the cranial cavity and to come into contact with bony protuberances within the skull brain contusions, lacerations etc

Penetrating head injury

The severity of penetrating injury is directly proportional to the K.E. of the moving object

K.E. = 1/2mv2, where m= mass, v= velocity Classified into 2 types according to the

velocity which is the main determinant in the equation High velocity injury

Bullets Low velocity injury

Knifes, arrows, screwdrivers etc

CLASSIFICATION

According to mechanism of injury

According to the integrity of the dura mater

According to the site of injury

According to the pathology

According to severity

According to mechanism of injury

Blunt head injury [Non-missile injuries]

Penetrating head injury [Missile injuries]

Blunt head injury

Occurs as a result of blunt force trauma or non-missile injury to the head injury to the scalp, skull and other intracranial structures

Can also occur as a result of rapid deceleration and acceleration causing the brain to move within the cranial cavity and come into contact with bony prominences within the skull contusion, laceration and shearing strains within the brain substances

Penetrating head injury

A penetrating head injury occurs when a sharp object pierces the skull and breaches the dura mater

According to the integrity of the dura mater

Open head injury

Closed head injury

Open head injury

Is one in which there is a wound which extends through the scalp, the skull and the dura mater, that is to say the brain is exposed

In open head injury the dura mater is not intact

There is grave danger of infection

Closed head injury

In the closed type of head injury the brain is not exposed to outside world, that is any or all , of the scalp, skull bone and dura mater are intact

In closed head injury the dura mater is intact and the risk of infection is low

Today we are talking of “ BRAIN INJURIES INSIDE THE CLOSED BOX”

According to the site of injury

Scalp injury

Skull injury

Meningeal injury

Brain injury

Intracranial vascular injury

Cranial nerves injury

Scalp injury

Scalp lacerations

Scalp cut wounds

Scalp hematoma Subcutaneous Subaponerotic Subpericranial

Skull injury

Fracture of the vault [vault skull fracture]

Fracture of the base of the skull [basilar fracture]

Fracture of the vault

According to whether the fracture is exposed to the outside world Simple [closed] fracture: The fracture is

not exposed the outside Compound [open] fracture : The fracture

is exposed to the outside According to the type of fracture

Liner fracture Depressed fracture Comminuted fracture

Fracture of the base of the skull

Fracture of the anterior cranial fossa

Fracture of the middle cranial fossa

Fracture of the posterior cranial fossa

Fracture of the anterior cranial fossa

The patient will present with:- Nasal bleeding (epistaxis), traumatic CSF

rhinorrhoea or escape of brain mater through the nose

Periorbital ecchymosis (racoon eyes), subconjuctival h’ge extending beyond the conjuctival reflections intraorbital h’ge

Anosmia if both olfactory nerves are damaged

Injuries to 3rd, 4th, 1st division of 5th and 6th at the sphenoidal fissure

3rd palsy produces dilated a pupil in a conscious patient

Fracture of the middle cranial fossa

This presents with:- Bleeding from the ears

[hemotympanum] or mouth CSF otorrhoea CSF Rhinorrhoea via the eustachian

tube Oscular disruption 7th and 8th cranial nerve palsies facial

palsy and deafness respectively

Fracture of the posterior cranial fossa

Extravasation of blood may be seen in the suboccipal region producing a swelling at the back

Post auricular [posterior to the mastoid process] ecchymosis [Battle’s sign]

Injury to the 9th, 10th and 11st at the jugular foramen

Meningeal injury

This occurs commonly as a result of fracture of the skull

The type of fracture of the skull which causes laceration of the dura mater is the depressed compound fracture

Brain injury

Primary brain injury That is damage which occurs at the

time of injury Secondary brain injury

That is damage which occurs as a consequence of primary brain damage

Primary brain injury

Cerebral concussion Cerebral contusion Cerebral laceration Diffuse axonal injury

Cerebral concussion

Temporary physiological loss of function without any organic structural damage

The patient becomes unconscious for a short period , followed by complete and perfect recovery

Develops immediately after injury It may be accompanied by autonomic

abnormalities e.g. bradycardia, hypotension & sweating

Prolonged LOC means something easy than pure concussion

Cerebral contusion

Bruising of the brain Characterized by rupture of white

fibres of the brain causing peticheal h,ge in the cerebral parenchyma

Usually produces neurological deficits that persist for > 24 hrs

Contusions may resolve together with the accompanying deficits or the may persist

Blood-brain barrier defects and cerebral edema are common and these lesions enlarge or coalesce with time

Cerebral laceration

In this condition the brain surface is torn with effusion of blood into CSFSAH [subarachnoid h’ge]

This occurs when there is a significant force to the skull laceration of the brain as a result of rapid movement and shearing of brain tissue

The pia mater and arachnoid may be torn ICH [intra-cerebral h’ge]

Focal neurological deficits are common Clinically presents as cerebral contusion

Diffuse axonal injury

This type of brain damage occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons, especially at the grey/white matter interfaces

Secondary brain injury

Intracranial hematoma Cerebral edema Brain herniation Cerebral ischaemia Infection Epilepsy

Intracranial vascular injuries

Epidural / extradural hematoma

Subdural haematoma

Subarachnoid haematoma

Intracerebral hematoma

Epidural / extradural hematoma

This is haematoma between the inner table of the skull and the dura mater

Occurs as a result of injury to the middle meningeal artery

If untreated midline shift, brain herniation, midbrain compression

Commonly presents with “lucid interval”

Subdural haematoma Haematoma between the

dura and the arachnoid mater

More common Occurs as result of tearing

of bridging veins crossing the subdural space from the cortex to the dura

Can also occur as a result of cortical laceration or bleeding from the dural venous sinuses

Described as acute or chronic depending on the age

Subarachnoid haematoma

Haematoma in the space between the arachnoid space and the pia mater [subarachnoid space]

Occurs when a vessel ruptures into the subarachnoid layer or in case of cerebral lacerations

There is extravasations of blood under pressure into the CSF space, ventricles or into the brain itself

The patient presents with severe headache of sudden onset, nausea and vomiting

Intracerebral hematoma

This is haematoma formed within the brain parenchyma

They are due to areas of contusion coalescing into a contusional haematoma

They appear as hyperdense lesions on the CT scan with associated mass effect and midline shift

Cranial nerve injuries Head injury may be associated with the injuries to

deferent cranial nerves The 3rd cranial nerve is the most important as it is

involved even by cerebral compression besides direct injury

The different cranial nerves are injured in fracture of different parts of the base of the skull

According to the pathology

Focal head injury Diffuse head injury

Focal head injury

In this type, the injury is localized to only part of the head

Focal injuries include scalp injury, skull fracture, and surface contusions and are generally be caused by direct impact

Diffuse head injury

Diffuse injuries include diffuse axonal injury, hypoxic-ischemic damage, meningitis, and vascular injury

They are usually caused by acceleration-deceleration forces

According to severity

Classified according to Glasgow Coma Score [GCS]

Classified into:- Mild head injury [GCS of 13-15] Moderate head injury [GCS of 9-12] Severe head injury [ GCS of 3-8 ]

PATHOPHYSIOLOGY

Requires understanding of the following crucial concepts:- The concept of Monro-Kellie doctrine The concept of Cerebral Perfusion

Pressure [CPP] The concept of increased ICP

Monro-Kellie doctrine The skull is a rigid structure (once the

sutures have fused) 3 components within that have a balance

80% brain 10% blood 10% CSF

If any one of these components increases [or if there is a SOL] another component must decrease to maintain the balance (ICP)

If this does not happen then there will be an increase in ICP

This observations were first reported by Monro [1783] and confirmed by Kellie 40 years later becoming known as the Monro-Kellie docrine

Cerebral Perfusion Pressure [CPP]

CPP is defined as the difference between the mean arterial pressure (MAP) and the ICP [ i.e. CPP = MAP – ICP]

CPP is the net pressure required to deliver blood to the brain

Cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg

This is due to autoregulation by the arterioles As ICP increases, in order to maintain a

constant CPP there has to be a compensatory rise in the MAP

A hypertensive response is therefore elicited which classically is associated with bradycardia

This is termed as the Cushing reflex after the eminent American neurosurgeon

Increased ICP

May result from primary or secondary brain injury

Normal ICP in adult is 0-15 mmHg, in children is 0-10 mmHg

This causes:- Cerebral herniation Cerebral edema Cerebral ischaemia

Brain herniation

Several types of herniation exist, as follows: Transtentorial herniation Subfalcine herniation Central herniation Cerebellar herniation

Upward cerebellar herniation Tonsillar herniation

Transtentorial herniation

Occurs when the medial aspect of the temporal lobe (uncus) migrates across the free edge of the tentorium

This causes pressure on the third cranial nerve, interrupting parasympathetic input to the eye and resulting in a dilated pupil

This unilateral dilated pupil is the classic sign of transtentorial herniation and usually (80%) occurs ipsilateral to the side of the transtentorial herniation

In addition to pressure on the third cranial nerve, transtentorial herniation compresses the brainstem

Subfalcine herniation

Occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx

This may compromise the blood flow through the anterior cerebral artery complexes, which are located on the medial side of each frontal lobe

Subfalcine herniation does not cause the same brainstem effects as those caused by transtentorial herniation

Central herniation

Central herniation occurs when a diffuse increase in ICP occurs

Each of the cerebral hemispheres is displaced through the tentorium, resulting in significant pressure on the upper brainstem

Cerebellar herniation

2 types:- Upward cerebellar herniation Downward cerebellar herniation

[tonsillar]

Upward cerebellar herniation

Occurs when either a large mass or increased pressure in the posterior fossa is present and the cerebellum is displaced in an upward direction through the tentorial opening

This also causes significant upper brainstem compression

Tonsillar herniation

Occurs when increased pressure develops in the posterior fossa

In this form of herniation, the cerebellar tonsils are displaced in a downward direction through the foramen magnum, causing compression on the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum

Cerebral edema Vasogenic cerebral edema Cytotoxic cerebral edema Interstitial cerebral edema

Vasogenic cerebral edema

Refers to the influx of fluid and solutes into the brain tissue through an incompetent or damaged blood-brain-barrier (BBB)

This is the most common type of brain edema and results from increased permeability of the capillary endothelial cells

Breakdown of the BBB allows movement of proteins from the intravascular space through the capillary wall into the extracellular space influx of fluid and solutes

Cytotoxic cerebral edema

In this type of edema the BBB remains intact

This edema is due to the derangement in cellular metabolism resulting in inadequate functioning of the sodium and potassium pump in the glial cell membrane

As a result there is cellular retention of sodium and water swelling of the glia, neurons and endothelial cells

Cytotoxic edema affects predominantly the grey mater

Interstitial cerebral edema

This is seen in hydrocephalus when the outflow of CSF is obstructed and intraventricular pressure increases

The result is movement of sodium and water across the ventricular wall into the paraventricular space

Cerebral ischaemia

ICP results in CPP and therefore CBF [CPP= MAP-ICP] cerebral ischaemia

This is common after severe head injury and is caused by a combination of either hypoxia and impaired cerebral perfusion

The brain is unable to autoregulate its blood supply with a decrease in blood pressure

CLINICAL PRESANTATION

History Physical Examination

History [cont’d]

Taken from an eye witness if the patient is unconscious or from the patient

Include;- Mechanism and full details of injury For example:

Fall: Height, surface, posture of fall, point of contact

Motor vehicle collision: Speed, place in car, restraint, point of impact

etc

History [cont’d]

Time of accident Level of consciousness /

unconscious? Time of onset of unconsciousness Duration of unconsciousness Lucid interval

Amnesia [loss of memory]– Retrograde Traumatic Amnesia Post-traumatic amnesia

History [cont’d] Current symptoms

Headache, vomiting, bleeding from ENT, LOC, fits, other associated injuries

Pre-morbid illness Diabetes mellitus Renal diseases Hypertension Previous history of fits

History of medications and Allergies Habit of taking alcohol or opium

Physical Examination

Head Scalp lacerations or haematoma Fractures: depressed, base of skull

(“raccoon eyes”, “Battles sign” CSF leak, blood in the ear canal or

behind the tympanic membrane, bleeding from nose or mouth etc

Face Fractures intra-oral injuries

Physical Examination [cont’d]

Neck Neck rigidity Immobilization is required until stability

is assured Trunk

Evidence of chest injuries Evidence of abdominal injuries

MSS [limbs, pelvis and spines] Closed or open wounds, fractures

Neurological Level of consciousness (GCS), pupilary

size and reaction to light Focal signs, brainstem reflexes, motor function

WORKUP

Laboratory investigations Imaging investigations Other investigations

Laboratory investigations

Haemogram Serum sugar Serum electrolytes RFT Grouping & cross-matching Coagulation profile

Imaging investigations

Skull x-rays

CT Scan brain/skull

MRI [Magnetic Resonance Imaging]

Cervical x-rays

Skull x-rays

2 views AP-views Lateral views

Can revealed Fracture of the skull Other bony abnormalities

If CT scan is easily available Skull x-ray can be avoided as with CT scan all the relevant information obtained in skull x-ray can be obtained with bone windows of CT scan

CT Scan brain/skull

Investigation of choice Can reveal

Bony injury Haematomas Evidence of cerebral edema Mass effect [midline shift]

It is necessary for operative planning

CT Scan brain/skull [cont’d]

Indications Moderate to severe head injury Deteriorating levels of consciousness Depressed fractures Focal neurological deficits Evidence of basilar fracture Penetrating head trauma Persistent severe headache and

vomiting Seizures

Magnetic Resonance Imaging [MRI]

Has no role in acute management of patients with head injury

Can be used in case of diffuse axonal injury and in follow-up prognostication

Able to detect small lesions in vital areas of brain not seen by CT scan

Preserved for later detail evaluation after acute problem has been addressed

Cervical spine x-ray

2 views AP view Lateral view

Done to exclude associated cervical spine injuries

CERVICAL SPINAL COLLAR should be kept on until a fracture or dislocation of the cervical spine has been ruled out

Other investigations

Carotid angiography Electro-encephalography Echo-encephalography

Carotid angiography Plays an important role to demonstrate the

site of the lesion Not performed in acute conditions Can indicate:-

Subdural haematoma Displacement of the cortical vessels away from

the inner table of the skull Epidural haematoma

Displacement of middle cerebral artery inward Displacement of anterior cerebral artery across

the midline Intracerebral haematoma

Displacement of the middle cerebral artery upwards

Electro-encephalography

This investigation will show areas of suppressed activity of the cortex due to injury or pressure by h’ge

Echo-encephalography

This will indicate the presence of haematoma by indicating a shift of the midline structure

It is not of much help in subdural haematoma as half of the cases are bilateral with no midline shift

MANAGEMENT

Criteria for admission The management of head injury

follow Advanced Trauma Life Support [ATLS] guideline

6 phases Primary survey phase Resuscitation phase Secondary survey phase Tertiary survey phase Supportive care phase Definitive care phase

Criteria for admission Moderate to severe head injury No CT scan available or abnormal CT Head All penetrating head injuries History of loss of consciousness Deteriorating Level of Consciousness Moderate to severe Headache Significant Alcohol or drug intoxication Skull Fracture Cerebrospinal Fluid leakage (Otorrhea or

Rhinorrhea) Significant associated injuries No reliable companion at home or

displaced home Amnesia

Primary survey phase

Aimed at identifying the immediately life threatening conditions

Elements of primary survey phase:- Airway with cervical spine control Breathing and ventilation Circulation with control of hemorrhage Dysfunction of the CNS Exposure in a controlled environment

Resuscitation phase

Done simultaneously with primary survey phase

Needs multidisciplinary approach Aimed at treating the immediately life

threatening conditions Establish a patent airway and

immobilization of cervical spine Ensure breathing and adequate

ventilatory support Restore circulatory volume and h’ge

control Brief neurological evaluation Fully expose [undress] the patient

Airway with cervical spine control

A clear patent and functional airway should be established

This can be achieved by:- Use of airways Proper position of the patient Endotracheal intubation Ambubags Tracheostomy

Breathing and ventilation

Make sure the patient is breathing properly

Achieved by:- use of oxygen masks Mechanical ventilators

Circulation with control of hemorrhage

Patients with head trauma may be associated with massive blood loss leading to hemorrhagic shock

A functional i.v. fluid should be established to restore blood volume and prevent irreversible shock

During the shock state use crystalloid fluid Glucose containing solutions should be

avoided; euvolaemia should be maintained BT should be given in case of hemorrhagic

shock

Dysfunction of the CNS

Brief neurological evaluation should be done

This involves brief assessment of the following:- Level of consciousness using GCS Pupilary size and reaction to light Motor function Sensory function Reflexes

Exposure in a controlled environment

The patient should be fully exposed to be able to exclude missed injuries

Secondary survey phase

This include:- History Physical examination Investigations

as above

Tertiary survey phase

A routine head-to-toe examination of a patient should take place within 24 hours of the injury to document any missed injuries and re-evaluate existing injuries and their treatment

Supportive care phase Position:

In a recovery position Elevate the head by 15-30o [take care of

cervical fracture] 2 hourly turning to avoid pressure sores

Urethral catheterization to empty the bladder in order to:- Avoid renal complications Enable good record of his output to be kept To ensure the bed is dry

NGT should be inserted in all patients with severe head injury except patient with nasal bleeding and rhinorrhoea To empty the stomach and for feeding

Supportive care phase [cont’d]

Monitor: Levels of consciousness Pupillary size and reaction to light Vital signs Input-output chart Motor and sensory functions

Nutrition support Patients who started on nutrition

earlier have better out come than when it is started later

Supportive care phase [cont’d

Hyperthermia Temperature of 32-34oC is

maintained for at least 48 hours and is to be started within 8 hours of traumatic brain injury

Has been shown to decrease the rate of cerebral metabolism, decreasing cerebral blood flow and intracranial pressure

Use of this technique is limited, as it increases risk of infection, cardiac arrhythmia, and coagulopathy

Supportive care phase [cont’d Hyperventilation

Controlled hyperventilation PaCO2

Supportive care phase [cont’d

Correction of contributory factors - Correction of factors increasing ICP e.g. Hypercarbia Hypoxia Hyperthermia Acidosis Hypotension Hypovolaemia

Definitive care phase

Medical treatment Surgical management

Medical treatment

Osmotherapy Corticosteroids Anticonvulsants Barbiturates Antibiotics Analgesics

Osmotherapy

Intended to draw water out of the brain by an osmotic gradient and to decrease blood viscosity

These changes decrease ICP and increase CBF

Include Mannitol Diuretics [loop] –e.g. Frusemide

Mannitol

Potent osmotic agent ICP by 2 mechanisms:-

Drawing water from the brain by osmotic gradient cerebral edema

viscosity of blood CPP and CBF Used when the BBB is intact otherwise if the

BBB is disrupted as in cerebral contusion, Mannitol can leach out into the brain and potentiate the mass effect

It becomes ineffective when brain osmolarity becomes iso-osmolar with that of the serumso it is of short-term use

Dose: 1 g/kg 4-6 hourly

Diuretics [loop]

E.g. Frusemide Potent osmotic agent Reduces ICP by reducing cerebral

edema and CSF production It may act synergistically with

mannitol

Corticosteroids

Commonly used corticosteroids e.g. Dexamethasone

ICP primarily in vasogenic edema Less effective in cytotoxic edema

Anticonvulsants

Includes:- Diazepam Phenobarbitone Phenytoin E.g.

These agents may help treat or prevent early seizures in head injury

Barbiturates

E.g. thiopentone ICP by reducing cerebral metabolism Has been shown to decrease the rate

of cerebral metabolism, decreasing cerebral blood flow and intracranial pressure

Help to ICP that is refractory to other conventional measures

Antibiotics

Prophylactic antibiotics is important in preventing meningitis and other intracranial infections

Analgesics

Avoid stronger sedatives especially morphine because they interfere with the assessment of consciousness and depress respiration

Moderate restless is useful, because it is good physiotherapy for his lung and prevent pressure sores

Surgical management

Aim Indications Type of surgery performed Site for burr holes Types of scalp incisions for

craniotomies

Aim of surgical treatment

To relieve cerebral compression To reduce ICP To elevate depressed skull pressure Treatment of open or penetrating

head injuries

Indications Deterioration in patient’s levels of

consciousness Development of focal neurological

deficits e.g. hemiplegia Pupilary unilateral dilation A rise BP associated with

bradycardia Depressed skull fracture Open head injuries

Types of surgery performed

Decompressive craniotomy Elevation of depressed fracture Surgical toilet

Site for burr holes

Parietal burr hole Temporal burr hole Frontal burr hole

Types of scalp incisions

Question mark flap Bicoronal flap Linear incision Square-sided flap

Complications

Focal neurological deficits CSF fistula Pneumocephalus Intracranial infections Posttraumatic Hydrocephalus Posttraumatic seizures Intracranial vascular injuries Posttraumatic epilepsy Carotico-cavernous sinus fistula Brain death