Head Injury

What is Head Injury• Literally refers to trauma to the head. This may or may not include injury

to the brain. However, the terms traumatic brain injury and head injury are often used interchangeably in the medical literature.

• Brain injuries are common cause for morbidity and mortality in trauma patients.

• Patient can came presenting with from minimal cognitive dysfunction to a vegetative state.

• Primary injury occurs at time of trauma• Secondary injury occurs due to hypoperfusion (hypotension, increased

ICP), hypoxia, hyperglycemia, or anemia.• Common causes: traffic accidents, home and occupational accidents, falls,

and assaults.

Type of Head Injuries

Scalp injury Scalp hematomas

Scalp laceration

Scalp avulsion

Skull fracture Linear fracture

Depressed fracture

Craniocerebral injury

Cerebral concussion

Diffuse axonal injury (DIA)

Contusion and laceration of the brain

Intracranial hematomas

APPROACH PATIENT WITH HEAD INJURY

Hamidah

• The initial approach to the patient is the rapid assessment of airway, breathing and circulation, and appropriate intervention if indicated.

• Simultaneously, all patients with blunt trauma require cervical spine immobilization until injury is excluded. This is typically accomplished by applying a hard collar or placing sandbags on both sides of the head with the patient's forehead taped across the bags to the backboard.

• Breathing– Tension pneumothorax , open pneumothorax , flail

chest with underlying pulmonary contusion• Circulation

– Hemorrhagic shock Massive hemothorax Massive hemoperitoneum, Mechanically unstable pelvis fracture, Extremity losses, Cardiogenic shock, Cardiac tamponade, Neurogenic shock, Cervical spine

• Danger and disability• Environment

Assessment of injury

• Primary survey– The first step in patient management is

performing the primary survey, the goal of which is to identify and treat conditions that constitute an immediate threat to life. The ATLS (Advanced Trauma Life Support) course refers to the primary survey as assessment of the "ABCs" (Airway with cervical spine protection, Breathing, and Circulation)

1. Airway and cervical spine• Always assume that patient has cervical spine injury• Place in hard collar and keep on until cervical spine has been

'cleared'• If patient can talk then he is able to maintain own airway• If airway compromised initially attempt a chin lift and clear

airway of foreign bodies• If gag reflex present insert nasopharyngeal airway• If no gag reflex patient will need endotracheal intubation• In the comatose patient, the tongue may fall backward and

obstruct the hypopharynx; this may be relieved by either a chin lift or jaw thrust.

• If unable to intubate will require a cricothyroidotomy• Give 100% oxygen through a Hudson mask

2. Breathing and ventilation• Check position of trachea, respiratory rate and air entry,

adequate oxygenation and ventilation must be assured• Tension pneumothorax, open pneumothorax, and flail

chest with underlying pulmonary contusion diagnoses should be made during the initial physical examination

• Tension pneumothorax is implied by respiratory distress and hypotension in combination with any of– tracheal deviation away from the affected side, lack of or

decreased breath sounds on the affected side, and subcutaneous emphysema on the affected side.

– Patients may have distended neck veins due to impedance of the superior vena cava, but the neck veins may be flat due to systemic hypovolemia

• open pneumothorax or "sucking chest wound" occurs with full-thickness loss of the chest wall, permitting free communication between the pleural space and the atmosphere.– This compromises ventilation due to equilibration of

atmospheric and pleural pressures, which prevents lung inflation and alveolar ventilation, and results in hypoxia and hypercarbia.

– Complete occlusion of the chest wall defect without a tube thoracostomy may convert an open pneumothorax to a tension pneumothorax

• Flail chest three or more contiguous ribs are fractured in at least two locations. Paradoxical movement of this free-floating segment of chest wall may be evident in patients with spontaneous ventilation, due to the negative intrapleural pressure of inspiration.

3. Circulation and haemorrhage control• Assess pulse, capillary return and state of neck veins

– Carotid pulse: systolic blood pressure at least 60mmHg– Femoral pulse: systolic blood pressure at least 70mmHg– Radial pulse: systolic blood pressure at least 80mmHg

• At this point in the patient's evaluation, any episode of hypotension (defined as a SBP <90 mmHg) is assumed to be caused by hemorrhage until proven otherwise.

• Identify exsanguinating haemorrhage and apply direct pressure• Place two large calibre intravenous cannulas for IV fluids• Take venous blood for FBC, U+Es (urea and electrolites), and Cross match• Take sample for arterial blood gasses• Give intravenous fluids • Crystalloid or colloid in adequate volume• Attach patient to ECG monitor• Insert urinary catheter• External control of hemorrhage should be achieved promptly while circulating

volume is restored. Manual compression of open wounds with ongoing bleeding should be done with a single gauze and a gloved hand.

4. DISABILITY• Glasgow Coma Scale (GCS) score should be

determined for all injured patients. Assess level of consciousness using AVPU method– A = alert– V = responding to voice– P = responding to pain– U = unresponsive

• Assess pupil size, equality and responsiveness

5. EXPOSURE• Fully undress patients• Avoid hypothermia

6. FLUID RESUSCITATION• Classic signs and symptoms of shock are tachycardia,

hypotension, tachypnea, mental status changes, diaphoresis, and pallor

• The goal of fluid resuscitation is to re-establish tissue perfusion. Fluid resuscitation begins with a 2 L (adult) or 20 mL/kg (child) IV bolus of isotonic crystalloid, typically Ringer's lactate.

• Hypovolumic shock – Up to 15% blood volume loss (750ml)– 15-30% blood volume loss (750 - 1500ml)– 30-40% blood volume loss (1500 - 2000ml)– Loss greater than 40% (>2000ml)

• Radiology– With trauma and head injury, the most immediate

plain radiograph is • Skull• Cervical spine – to exclude cervical injury• Chest – to identify lung contusion or mediastinal injury,

bony injury, simple pneumthorax or heamatorax, diaphragmatic injury and correct placement of chest drain and CVP line

• Pelvis – diagnose of pelvic fracture

• Secondary Survey– Once the immediate threats to life have been

addressed, a thorough history is obtained and the patient is examined in a systematic fashion.

– The patient and surrogates should be queried to obtain an AMPLE history (Allergies, Medications, Past illnesses or Pregnancy, Last meal, and Events related to the injury).

• Face, head and neck– Digital examination of the cranium, facial skeleton, cervical

vertebrae and associated soft tissue to exclude fracture• Central nervous system

– Check the pupil, GCS score.• Chest

– Detail chest examination with thoracic spine • Abdomen and pelvis

– Exclude any abdominal injury and pelvic fracture– Do “spring test” for ribs n pelvis

• Extremities– Presence of pain, pallor, pulselessnes, coldness and poor

capillary refill diagnose of acute ischemic

GCS IN ADULT AND PEDIATRIC PATIENT

Glasgow coma scaleÞA scale for measuring level of consciousness, especially after a head injury, in which scoring is determined by three factors: amount of eye opening, verbal responsiveness, and motor responsiveness

GCS in Adult

•Minimal head injury - (GCS 15, no loss of consciousness or amnesia)•Mild head injury - (GCS 13-15, amnesia or short loss of consciousness or impaired alertness/memory)•Moderate head injury - (GCS 9-12, loss of consciousness longer than 5 minutes or focal neurological deficit)•Severe head injury - (GCS 5-8, coma)•Critical head injury - (GCS 3-4, deep coma).

GCS in paediatrics

Verbal response

Motor response

Eye response

CLOSE HEAD INJURY AND PENETRATING INJURY

• Classification type of head injury are – Close head injury / blunt trauma

• The dura still intact • Associated with multiple wide distribution injuries

– Penetrating head injury• Dura is breached • Damage is localize to the path of bullet or knife

Brain injury Primary brain injury

• results from the immediate mechanical forces that cause brain damage

• Result of – Direct contact, such as a blow to the

head– Direct contact due to the brain striking

against the internal surface of the skull– Inertial forces originating from rapid

acceleration/deceleration such as that experienced in a motor vehicle collision. Notably, contact forces can also induce acceleration of the brain commonly leading to a combination of focal and diffuse injuries.

Secondary brain injury

• delayed pathophysiological consequences of TBI

• Includes – Cerebral oedema– Increased intracranial

pressure (ICP)– Haemorrhage– Seizures– Ischaemia due to

vasospasm, vascular/brain compression

– Infection.

CLINICAL SIGN AND SYMPTOMS OF HIGH ICP

Zaizul

Signs and Symptoms of Increase ICPSymptoms Signs

Headache. Back Pain. Papilledema. Ringing In The Ears or Hearing Loss Nausea And Vomiting Vision Problems, Such As Blurry

Vision Or Double Vision Painful Eye Movements Neck Pain Feeling Tired And Wanting To Sleep Unsteadiness While Standing Or

Walking, Known As Ataxia Altered Level Of Consciousness, Weakness, local or generalized.

•Pupillary Dilatation, Abducens (Crn VI) Palsies, •Cushing's Triad (Increased Systolic Blood Pressure, A Widened Pulse Pressure, Bradycardia, And An Abnormal Respiratory Pattern)•In Children, A Slow Heart Rate Is Especially Suggestive Of High ICP.•Irregular Respirations (Interference Of The Respiratory Drive)•Hyperventilation (Brain Stem Or Tegmentum Is Damaged)

NEUROLOGICAL EXAMINATIONRusha

Neurological examination

Symptoms of neurological disorders;1. Headache, back, neck or facial pain

(when asking about pain, include SOCRATES; site, onset, character, radiation, assoc symptoms, time (progression), exacerbating and relieving factors, and severity)

2. Fits and faints3. Dizziness or vertigo4. Disturbances of vision, hearing or smell5. Disturbances of gait6. Loss of disturbed sensation, or weakness in limb(s)7. Disturbances of sphincter control (bladder, bowels)8. Involuntary movements or tremor9. Speech and swallowing disturbances10. Altered cognition

History Taking

Past Medical History

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- Ask about head or spinal injuries- History of epilepsy or convulsions- Any previous operations- Treatment (anti-convulsants, contraceptive pills,

antihypertensive agents, steroids, anticoagulants, antiplatelet agents

- Risk factors that may predispose development of cerebrovascular disease (Hypertension, DM, Hyperlipidemia, smoking, MI)

- Previous dx of peripheral vascular disease or of coronary artery disease (↑ risk of CV disease)

Social History

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- Smoking history- Occupation and exposure to toxins (e.g. heavy metals)- Alcoholism

o Blackoutso Nutrition related conditions; e.g. peripheral neuropathy due to

thiamine deficiencyo Withdrawal syndrome; e.g. tremor, hallucinationo Cerebellar dysgenerationo Alcoholic dementiao Alcoholic myopathyo Autonomic neuropathy

Family HistoryAny history of neurological or mental disease should be documented

Physical examination

Head• Scalp- inspect & palpate for laceration, swelling, bony

depression and distortion• Orbits- palpate the margins of the orbits for

depression/irregularities• Eyes- size, reflex, movement & visual acuity - Panda eyes subconjuctival hemorrhage - Diplopia fracture of floor of orbit

Panda eye

Signs of intracranial hemorrhage• Face – palpate cheek bone for a ‘step’ & asymmetry, loss of sensation facture of cheek bone due to damage of infra-orbital nerve• Jaw & temperomandibular joint – malocclusion & open bite deformityfractured jaw & numbness of lower lip• Mouth, teeth & gums - record no of missing/damaged teeth x-ray exclude possibility inhaled & lodged to the lung• Nose – palpate and detect any bloody/fluid dischargeanterior cranial fossa fracture• Ear – blood/fluid discharge bruising behind ears (Battle’s sign)post cranial fossa fracture• Neck – palpate for bruising, deformity & any subcutaneous surgical emphysema - Pain & local tendernesscervical fracture - Penetrating descending wound of the root of the neckdamage to supra-

aortic blood vessels (carotid, vertebral, subclavian arteries), trachea, pharynx & esophagus - Severe compound clavicular injuries injuries to subclavian/axillary vessels, brachial plexus and apex of the lung

• Chest – inspect for flail chest multiple contiguous rib fractures resulting in free-floating ribs with paradoxical motion on respiration)

- Rib fracturesinjuries to great vessles, lung, spleen & liver - Sternal fracturecardiac injuries - Increase width of mediastinum aortic dissection - Check for hemothorax, pnuemothorax and cardiac temponade• Abdomen - intra-abdominal hemorrhage - Increase abdominal distension, tenderness & guarding are

significant signs -Skin bruising, penetrating wounds & assoc. rib fracture possibility

organ damag - Blood from urethra/frank hematuria kidney, bladder/urethral damage

- Rectal & vaginal examination high-riding & boggy prostate/ vaginal injuries

- Pelvic fractures assoc with severe shock

• Upper & lower limbs – palpate all major bones to detect any bony deformity & swelling

• Circulation – palpate radial & pedal pulses asymmetrical pulses indicate vascular injury

- Persisting pallor in one limb severe ischemia - Compartment syndrome(pain, tenderness & swelling over ant.

shin/calf muscle) ischemia, obliterate the pulses, muscle and nerve death

• Nerves – examine both upper and lower limbs of peripheral nerves

-Test power, tone, strength, coordination, sensation, and reflexes• Back (thoraco-lumbar spine) – paralysis/muscle weakness spinal cord injury

SKULL FRACTUREIlyas

Skull Fracture

• Break in the bone in the skull, caused by head injury

• Fragments– Lacerate or bruise brain– Damage blood vessels– Intracranial hematomas– Epidural hematomas

• Dissection of cerebral arteries

Classifications

• Simple linear fracture is by far the most common type of fracture, especially in children younger than 5 years.

• Temporal bone fractures represent 15-48% of all skull fractures.

• Basilar skull fractures represent 19-21% of all skull fractures.

• Depressed fractures are frontoparietal (75%), temporal (10%), occipital (5%), and other (10%).

• Most of the depressed fractures are open fractures (75-90%).

Linear fracture• Most common – 69%• Low-energy blunt trauma, widely distributed force• Little significance unless runs thru vascular channel, venous

sinus groove or a suture:– Vascular channel Epidural hematoma– Venous sinus groove Venous sinus thrombosis– Suture Sutural diastasis

• Growing fracture brain swelling• Most patients are asymptomatic and present without LOC.

Swelling occurs at the site of impact, and the skin may or may not be breached.

Fracture Suture

Width >3mm <2mm

Widest at centre and narrows at end

Same width throughout

On X-ray

Appear darker Lighter

Site Usually over temporoparietal area

Specific anatomical sites

Pattern Usually straight line Not in straight line

Turns Angular Curvaceous

Basilar fracture• Linear fracture at the base of the skull • Associated with dural tear• Require > force, thus rare – 4%• Characteristic

– Blood in sinuses– CSF leak – nose/ear– CSF rhinorrhea– Raccoon eyes– Battle’s sign – clotting behind ear– Cranial nerve palsy– Hemotympanum– Ocular nerve entrapment: 1-10%

• Likely to get meningitis• HANS device usage in high risks

Temporal fracture

• Temporal bone fracture.• 75% of all skull base fractures. • 3 subtypes of temporal fractures are

longitudinal, transverse, and mixed.

Transverse Longitudinal

• Longitudinal fracture – Occurs in the temporoparietal region and involves the squamous

portion of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani.

– These fractures may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells, respectively.

– Longitudinal fracture is the most common of the 3 subtypes (70-90%).• Transverse fractures

– Begin at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa (5-30%).

• Mixed fractures – Have elements of both longitudinal and transverse fractures.

• Petrous temporal bone fracture – Battle sign.

• CSF otorrhea and bruising over the mastoids • Anterior cranial fossa fractures

– Raccoon eyes • CSF rhinorrhea and bruising around the eyes

• Longitudinal temporal bone fractures – Conductive deafness

• Ossicular chain disruption and of • Greater than 30 dB that lasts longer than 6-7 weeks.

– Temporary deafness • Resolves in less than 3 weeks is due to • Hemotympanum and mucosal edema in the middle ear fossa. • Facial palsy, nystagmus, and facial numbness are secondary to

involvement of the VII, VI, and V cranial nerves, respectively. • Transverse temporal bone fractures

– Involve the VIII cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss.

Occipital condylar fracture • High-energy blunt trauma with axial compression, lateral

bending, or rotational injury to the alar ligament. • 3 types based on the morphology and mechanism of injury

with alternative classification into displaced and stable, ie, with and without ligamentous injury.– Type I - secondary to axial compression resulting in comminution of

the occipital condyle. This is a stable injury.– Type II – results from a direct blow, and, despite being a more

extensive basioccipital fracture, type II fracture is classified as stable because of the preserved alar ligament and tectorial membrane.

– Type III – an avulsion injury as a result of forced rotation and lateral bending. This is potentially an unstable fracture.

• Very rare and serious injury. • Most of the patients with occipital condylar

fracture, especially with type III, are in a coma and have other associated cervical spinal injuries.

• These patients may also present with other lower cranial nerve injuries and hemiplegia or quadriplegia

Clivus fractures

• High-energy impact sustained in motor vehicle accidents.

• Longitudinal, transverse, and oblique types have been described in the literature.

• A longitudinal fracture carries the worst prognosis, especially when it involves the vertebrobasilar system.

• Cranial nerves VI and VII deficits are usually coined with this fracture type.

Nerve involvement of basilar fracture

• Vernet syndrome or jugular foramen syndrome – Involvement of the IX, X, and XI cranial nerves with the

fracture. – Difficulty in phonation and aspiration and ipsilateral motor

paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.

• Collet-Sicard syndrome– glossolaryngoscapulopharyngeal hemiplegia– occipital condylar fracture with IX, X, XI, and XII cranial

nerve involvement.

Depressed skull fracture

• High-energy direct blow small surface area with a blunt object such as a baseball bat

• Comminution of fragments starts from the point of maximum impact and spreads centrifugally

• Most are over the frontoparietal region because the bone is thin and the specific location is prone to an assailant's attack.

• Very serious - 11% of severe head injury• Comminuted fractures, bone displaced inward• High risk of increasing ICP• Crush delicate tissue• Complex – torn dura matter• May require surgery to lift

the bone

• Approximately 25% of patients with depressed skull fracture do not report LOC, and another 25% lose consciousness for less than an hour. The presentation may vary depending on other associated intracranial injuries, such as epidural hematoma, dural tears, and seizures.

INDICATION FOR CT SCANZaizul

CT vs MRICT MRI•Sufficient to detect clinically important bleed and able to guide management.

•Sensitive to subtle lesion

•Superior in detecting skull fracture. •Able to image bone, soft tissue and blood vessels all at the same time.•May Demonstrate findings of DAI (diffuse axonal injury) such as microhaemorrhages.

More on CTSensitive Less Sensitive

•Detecting Pathology That Distorts The Normal Anatomy Of The Brain •Haemorrhages, •Neoplasms, •Abscesses.

•Brain Infarction, •Arteriovenous Malformations, •Aneurysms,•Less Sensitive Still For Detecting White Matter Disease And Leptomeningeal Disease.

Advantages Disadvantages

•Differentiating an ischaemic infarct from a cerebral bleed.•Identifying space occupying lesions (such as tumours and abscesses)•Detecting hydrocephalus.

•Small lesions (<1 cm) or brainstem lesions may be missed•Early infarction (<6-8 hours) may not be seen.

Indications for CT.

• History.– Construct a Focused history. – Witnesses of the trauma or individuals who know

the patient may be helpful in ascertaining the details of the traumatic event and other valuable patient information.

– Past medical and surgical history, drug/alcohol use and allergies are important.

• PE– GCS and Pupillary reflexes, – Full neurological examination.– Evidence of basilar skull fracture: blood in the middle

ear cavity (haemotympanum), raccoon eyes (periorbital ecchymosis), post-auricular ecchymosis, CSF leakage (rhinorrhoea or otorrhoea).

– Associated spinal injury: spinal tenderness, paraesthesias, incontinence, extremity weakness, priapism.

– Carotid dissection: carotid bruits– Abnormal eye findings: papilledoema, retinal

haemorrhage.

• Investigations.– Arterial blood gas.– FBC including platelets.– Serum electrolytes and urea.– Serum glucose.– Coagulation status: PT, INR, activated PTT.– Blood alcohol level and toxicity screening if

indicated.– Urine analysis: specific gravity, osmolality (to detect

endocrine complications such as diabetes insipidus or Syndrome of Inappropriate Antidiuretic Hormone).

Rules of Standard Guidance.

• The Canadian CT Head Rule.• The New Orleans Criteria.

* Both guidelines contain 7 criteria to guide the use of CT in patients with mild injury and have been validated.* Patients under 16 years of age were not included in the initial Canadian CT rule derivation or validation.

The Canadian CT Head Rule.

• CT is required for patients with minor head injuries (minor head injury is defined as witnessed LOC, definite amnesia or witnessed disorientation in patients with a GCS score of 13 to 15) with any one of the following.

High Risk (for neurologicaol intervention) Medium Risk (for brain injury for CT scan)

• GCS less than 15 at 2 hours after injury

• Suspected open or depressed skull fracture

• Any sign of basal skull fracture (haemotympanum, raccoon eyes [periorbital ecchymosis], CSF otorrhoea/rhinorrhoea, Battle sign [ecchymosis of the mastoids])

• 2 or more episodes of vomiting

•Aged 65 years or above

• Amnesia more than 30 minutes before impact (retrograde amnesia)Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height more than 3 feet or 5 stairs).

New Orleans Criteria.

• CT is required for patients with minor head trauma (minor head injury was defined as LOC in patients with normal findings on a brief neurological examination and a GCS score of 15, as determined by a physician upon arrival at the emergency department) with any one of the following:

High Risk (for neurolsurgical intervention) •The derivation set for

the criteria also contained a history of coagulopathy as a clinical parameter, although this was not included in the final validation. •Where possible this history should be obtained and considered with respect to CT scanning.

•Headache•Vomiting•Aged more than 60 years•Drug or alcohol intoxication•Persistent anterograde amnesia (deficits in short-term memory)

•Evidence of traumatic soft-tissue or bone injury above clavicles

•Seizure (suspected or witnessed)

Interpretation of CT.

• Basic Interptetation– Most of the picture are non-specific.– CT picture are depending on the density of the

structure.

• Principle – Pre-Contrast Study.

• Hypo- Density– Comparison with CSF and Brain Tissue

» Higher than CSH and lower than Brain Tissue (Protein, Blood , Debris)

» Tumor, Abcess,Resolving Hematoma, Evolution Infarct.

– Lower that CSF» Fat or cholesterol ; Congenital Tumor ; dermoir ,

epidermoid, lipoma.» Air ; Head injury, pneumocephaly.» Myxoid (mucus like)

• Hyper- Density– Comparison with Cranium Bone– Iso or higher than bone

» Ossification, calcification, metallic iatrogenic, blood pooling.

– Less than bonebut higher that brain tissues» Haemorrhage, compected cellurity.

• Iso- Density– As brain Parenchyma.

» Iso-density to CSF (Water like congtent)» Chronic haematoma, chronic infarct, porencephaly,

congenital cycts , encephalomalacia change.

• Hetero- Density.– Difference density as compared to the contralateral

part.

• Post Contrast CT.– Gyral, ribbon, cortical.– Solid.– Rim or Ring.– Mural Nodular.– Linear and Dot.– Heterogeneous.– No Enhancement.

Changes in adjacent tissue

• Edema pattern in CT– Vasogenic Edema

• Tumors, infection, late infarct aling white matters, fingerlike.

– Interstitial edema, • periventricular white matter, ependymitis granularis

– Cytotoxic edema• Ischemia or infarct, gray matter

• Bone• Ventricles, Sulci and cistern

Classification of Cerebral EdemaType Location Site Blood-

Brain Barrier

Probable Mechanism

Vasogenic Extracellular White Disrupted Increased vascular permeability

Cytotoxic Intracellular White or gray

Intact Cellular failure

Ischemic Intra- and extracellular

White and gray

Disrupted Anoxia

Hydro-static

Extracellular White and gray

Disrupted Increased blood pressure

Hydro-cephalic

Extracellular White Intact Impaired CSF outflow or absorption

Osmotic Intra- and extracellular

White and gray

Intact hangindent1em Relative plasma hypo-osmolality

ExamplesCT scan of a 16-year-old patient with a typical diffuse head injury. The patient's GCS at admission to hospital was 4. There is a small amount of blood in the trigone and occipital horn of the right lateral ventricle (lower arrow). There is a small punctate hemorrhage in the left internal capsule (upper arrow).

CT scan of a 50-year-old man injured in a fall. There is a large mixed-density lesion in the left temporal lobe (lower arrow) and a similar, smaller lesion in the left orbitofrontal cortex (upper arrow). The appearance is typical of cerebral contusions.

CT scan of a large acute epidural hematoma (arrows). Epidural (or extradural) hematomas have a convex medial border, which produces the lens shape that distinguishes epidural from subdural hematomas.

CT scan of a large acute subdural hematoma (horizontal arrows). The hematoma spreads over the entire convexity of the hemisphere, so that the medial border of the hematoma is concave. Note also the large amount of midline shift. The occipital horn of the left lateral ventricle is acutely enlarged as a result of trapping of CSF by ventricular distortion and obstruction of CSF flow (vertical arrow).

CT scan of a confluent traumatic intracerebral hematoma in the left frontal lobe of a patient struck by a motor vehicle (lower arrow). There is overlying scalp swelling and contusion at the site of the blow to the head (upper arrow).

An unenhanced CT of the brain in a patient with the complications of hypertensive encephalopathy. The arrows are pointing to the end-arterial border zones with changes consistent with ischemic and hemorrhagic changes.

A schematic diagram demonstrating the concept of evolving pressure differentials with regional brain swelling from large supratentorial hemispheric infarction. Note that the clinical worsening in its early states correlates with brain tissue displacement.

INTRACRANIAL HAEMORRHAGE Rusha

Intracranial Hemorrhage1. Extradural (epidural) Hematoma2. Subdural Hematoma3. Subarachnoid Hematoma4. Intracerebral Hemorrhage

1. Extradural Hematoma (epidural) Very common in children, adolescents and young adult Blood between skull & dura d/t rupture of meningeal artery Usually a/w skull fracture in temporal region Symptoms within 24 hours of trauma: Loss of conciousness Lucid interval with severe headache & drowsiness Fixed & dilated pupil on the side of injury hemiparesis on the opposite side “Lucid interval”followed by acutely progressive evidence of increased ICP

compression of brain stem coma death Morphology: Smooth inner contour (dura), biconvex. Need urgent diagnosis through CT scan Mx: immediate surgery to remove clot

# Lucid interval=> a period of consciousness after the injury before the patient became unconscious

Extradural hematoma. Such a location for hemorrhage is virtually always the result of trauma that causes a tear in the middle meningeal artery.

CT scan of extradural hematoma

2. Subdural Hematoma Blood between dura & arachnoid d/t rupture of bridging veins More common (30%) than extradural (10%) Underlying primary brain injury and 50% mortality Manifest within 48 hrs. Lateral aspect of cerebral hemispheres, 10% bilateral. Volume of the haematoma increases ICP increase herniation

(Coning=> herniation of cerebellar into foramen magnum compressing medulla cessation of respiration & death

S/S: Headache & confusion. Rarely focal signs. Types: Acute due to major brain injury s/s: deeply unconscious & develop neurological localizing signs- Chronic old, alcoholics & anticoagulants patient s/s: fluctuating levels of consciousness, pupil changes

Morphology:- Clot along brain surface contour without extension into the depth of sulci. (crescent)- Hematoma surrounded by fibrous membrane (organising),

attached to dura only. Rebleeding – greatest risk in 1st few months. Mx: Craniotomy

Subdural hematoma

3. Subarachnoid haematoma

Most cases of traumatic SAH are a/w parenchymal haematoma

In subarachnoid space Due to ruptured of berry aneurysm blood flows into the

subarachnoid space increase in ICP + destructive and toxic effects of blood on brain parenchyma and cerebral vessels

S/S: meningeal irritation, headache, neck stiffness, Kernig’s sign +ve (inability to completely extend the leg when sitting or lying with the thigh flexed upon the abdomen)

#Berry aneurysm a small saccular aneurysm of a cerebral artery, usually at the junction of vessels in the circle of Willis, having a narrow opening into the artery

Kernig’s sign

Subarachnoid hematoma

4. Intracerebral Hematoma• Common after a severe head injury. • Caused by a cerebral contusion fluid accumulation

in the damaged brain (cerebral edema)deaths. • S/S: severe headache, nausea, seizures, and coma or

death• Mx: surgery is usually avoided because it usually does

not restore brain function.

HYDROCEPHALUS Zaizul

Hydrocephalus.

• Definition– Disturbances in CSF circulation or absorption which results in

the continuous increase in the ICP which leads to hydrocephalus.

• Classification– Obstructive - ; CSF circulation is blocked within the

ventricular system, and there is enlargement in the ventricles proximal to the obstruction.

– Communicating ; CSF absorption is blocked at the level of the arachnoid granulations.

– Rarely, hydrocephalus may be due to the overproduction of CSF, as is the case in certain choroid plexus tumors.

Pathophysiology MenifestationsIncrease pressure in expandable compartment

•Neonates and infants whose anterior fontanelle is still open, •Symptoms includes tense or bulging fontanelle, apneic and bradycardic episodes, engorgement of the scalp veins, upward gaze palsy, gaps between the cranial sutures, rapid increases in head circumference, irritability, poor head control, and poor oral intake.

Increase pressure in rigid compartment

•Children with closed fontanelle•Symptoms includes lethargy or excessive sleepiness, papilledema, headache, nausea, vomiting, gait disturbance, increased fussiness, or upgaze or lateral gaze palsy

Treatments Modalities.• Ventriculoperitoneal shunting,

– creating a shunt between the cerebral ventricles and the peritoneal cavity.

• Ventriculoatrial shunt, – Right Atrium Shunt

• Ventriculopleural shunt– Pleural Cavity Shunt

• Endoscopic third ventriculostomy –– Children with obstructive type.– Involves fenestration of the floor of the third ventricle,

thereby creating an alternative CSF pathway.• Shunt Failure OR Delayed treatment may leads to irreversible

neurologic injury, including herniation, blindness, or death.

DIFFUSE AXONAL INJURY

• hx rapid acceleration/deceleration of the head, or direct impact to head;

• DAI may be responsible for mild forms of cognitive impairment seen acutely with concussions;

• severe DAI: generally no lucid interval, presents with immediate and persistent LOC

• Diffuse axonal injury is caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration.

• Axons may be completely disrupted and then retract, forming axon balls.

• Small hemorrhages can be seen in more severe cases, especially on MRI.

• Hemorrhage is classically seen in the corpus callosum and the dorsolateral midbrain.

Management

• Rapid intervention with particular attention to ABCs to minimize secondary brain injury.

• Treat elevated ICP only if symptomatic– Sedate patient and elevate head of bed 300

– Brief hyperventilation may be performed acutely to cause cerebral vasoconstriction

– Mannitol for osmotic diuretics and free radical scavenging– Surgical decompression of deteriorating patients via

trephinaton or ventriculostomy

• Intracranial bleeds require seizure prophylaxis e.g. phenytoin and may require surgical drainage

• Check coagulation studies (PT/aPTT/INR) immediately and correct any coagulopathy to minimize intracranial bleed

• Depress skull fractures and penetrating trauma may require surgical repair