No one can confidently say that he will still be living tomorrow.

~Euripides

Nearly 1.5 to 2 million persons are injured and 1 million

succumb to death every year in India.

Road traffic injuries are the leading cause (60%) of TBIs followed by falls (20%-25%) and violence (10%). Alcohol involvement is known to be present among 15%-20% of TBIs at the time of injury.

Thirty-eight per cent of injured persons had a serious injury to the head and face region.

S1 Unit

 DEFINITION & TYPES OF HEAD INJURY PATHOPHYSIOLOGY Clinical Features PRIMARY BRAIN INJURIES EXTRADURAL HAEMATOMA

and SUBDURAL HAEMATOMA ASSESSMENT OF SEVERITY OF HEAD INJURY INVESTIGATION CONSERVATIVE MANAGEMENT OF HEAD INJURY SURGICAL MANAGEMENT OF HEAD INJURY COMPLICATIONS OF HEAD INJURY

NITHA.J

Head injury
Traumatic insult to the head that may result in any

injury to the soft tissue bony structures and/or brain.

TRAUMATIC BRAIN INJURY[TBI]

Traumatic brain injury (TBI) is a nondegenerative,

noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness.

Based on the Severity

GCS: Best predictor of neurological outcome

GLASGOW COMA SCALE

EYE OPENING
SPONTANEOUS TO SPEECH TO PAIN NIL

SCORE
4 3 2 1

MOTOR RESPONSE

SCORE

OBEYS LOCALISES WITHDRAWS ABNORMAL FLEXION EXTENSION RESPONSE NIL

6 5 4 3 2 1

VERBAL RESPONSE ORIENTED CONFUSED CONVERSATION INAPPROPRITE WORDS INCOMPREHENSIBLE SOUNDS NIL

SCORE 5 4 3 2 1

Severity of TBI

Severity

GCS

Minor

15

Mild

14-15

Moderate

9-12

Severe

3-8

OPEN HEAD INJURY Implies communication b/w the intra dural contents & outside CLOSED HEAD INJURY Scalp is intact and there is no communication between the intradural contents and the atmosphere

OPEN HEAD INJURY

PATHOLOGICAL CLASSIFICATION

FOCAL Confined to specific areas Cerebral laceration Contusion Intracranial hemorrhage

DIFFUSE Distributed in a more general manner Cerebral edema Concussion Diffuse axonal injury

Based on the time of onset

Primary Brain Injury Diffuse axonal injury Cerebral concussion Cerebral contusion Cerebral laceration Traumatic subarachnoid haemorrhage
Secondary Brain Injury

Brain swelling
Intracranial Haemorrhage Infection

CLASSIFICATION OF SKULL FRACTURE

BY TYPE

OPEN

CLOSED

LINEAR

SKULL FRACTURE

PATTERN

COMMINUTED

DEPRESSED

VAULT ANATOMIC SITE BASE

COMMINUTED FRACTURE

DEPRESSED FRACTURE

SCALP LACERATION

GCS
The scale was published in 1974 by Graham Teasdale

and Bryan J. Jennett, professors of neurosurgery at the University of Glasgow. The pair went on to author the textbook Management of Head Injuries (FA Davis 1981, ISBN 0-8036-5019-1), a celebrated work in the field.

 The University of Glasgow is the fourth-oldest

university in the English-speaking world and one of Scotland's four ancient universities

Nithin Humayoon

Neuronal Injury
Chromatolysis
Wallerian Degeneration Retrograde Degeneration

Transneural degeneration
Regeneration

 Brain metabolism
CMRO2: 3.5 ml/100g/min

Cerebral Blood flow

55ml/100g/min

Cerebral Autoregulation

Cushings Reflex

ICP and brain herniation

The addition of mass lesion is compensated by displacement of CSF and venous blood out of cranial cavity.

As further expansion of mass occur quite small rise in volume result in large increase in ICP and Brain herniation can occur

MECHANISM of brain injury

Distortion of the brain
Mobility of the brain in relation to the skull and

membrane Configuration of interior of skull Deceleration and acceleration of injury Cerebral Concussion Cerebral Contusion Cerebral Laceration

Primary brain injury

Diffuse neuronal damage
Shearing lesions Contusion

Lacerations
Traumatic SAH Extent of primary injury is reflected by state of

consciousness and presence of focal neurological deficit

Secondary brain injury

Brain swelling: odema, venous congestion, hypoxia
Intra cranial hemorrhage:Extradural, subdural,

intracerebral Infection Open head injury: Generalized meningitis, subdural empyema, brain abscess Closed head injury: Infection of sub pericranial blood clot

Causes of secondary brain injury

Hypoxia:PO2 < 8kPa
Hypotension: Systolic BP<90mm Hg Raised ICP: >20mm Hg

Low cerebral perfusion pressure:<65mm Hg

Pyrexia Seizures Metabolic Disturbance

 Raised ICT

Cerebral compression Decreased Cerebral perfusion Brain ischaemia C/l hemiparesis

Pressure on motor cortex

Herniation of cingulate gyrus: Subfalcine herniation Temporal lobe herniation Compress ipsilateral IIIrd nerve Dilation of ipsilateral pupil

Central Herniation and Tonsillar herniation Compress Brain stem Increase in BP, Bradycardia, Abnormal resp.pattern

 Coup and Contrecoup injury

Causes of death in head injury

Brain hypoxia
Coning Diffuse severe irreversible neuronal injury

Metabolic changes
Aspiration in unconscious patients

 "father of modern neurosurgery"

 Harvey Williams Cushing, M.D. (April 8, 1869 -

October 7, 1939) was an American neurosurgeon and a pioneer of brain surgery. He is widely regarded as the greatest neurosurgeon of the 20th century and often called the "father of modern neurosurgery".

Cushing's triad
is the triad of widening pulse pressure (rising systolic,

declining diastolic), change in respiratory pattern (irregular respirations), and bradycardia.

It is sign of increased intracranial pressure, and it

occurs as a result of the Cushing reflex.

Philip Daniel

Clinical Features
Altered consciousness
Pupillary changes Symptoms and Signs of raised ICT

Signs of skull fracture

Signs of meningeal irritation Signs of focal neurological deficit Signs of coning

Altered consciousness
Assessed by Glasgow Coma Scale
Used to assess severity of head injury

Pupillary changes
1. Change in pupil size 2. Change in light response
Normal pupil size: 2.5-5mm
Anisocoria & asymmetrical sluggish light response- 3rd CN compression on side of mass lesion (hematoma)

 Pinpoint pupil
<1mm Pontine hemorrhage

Bilateral dilated unreactive pupil Severe midbrain compression

Symptoms and Signs of raised ICT

Normal upper limit: 15mm Hg SYMPTOMS
Impairment of consciousness Headache Vomiting Convulsions

SIGNS
Papilloedema Bradycardia Hypertension Changes in respiration B/l Babinskis sign

Fracture skull
Signs of base of skull fracture Bilateral periorbital edema (racoon eyes) Battles sign (bruising over mastoid)

Skull fracture
CSF rhinorrhoea/CSF

otorrhoea Hemotympanum

Signs of meningeal irritation

Neck stiffness
Kernigs sign Straight leg raising test

Brudzinskis sign

Focal neurological deficit

Cortical involvement
Frontal lobe-

C/l paralysis(monoplegia),Gaze palsy,Changes in mentality,personality, behaviour, bowel and bladder involvement If dominant hemisphere is involved Motor aphasia, agraphia
Parietal lobe- C/l cortical sensory loss. If dominant hemisphere

involved alexia, apraxia, jargons aphasia Temporal lobe- Hearing impairment, auditory agnosia Occipital lobe- Homonymous hemianopia, visual agnosia

Cranial nerve involvement

IIIrd N. Dilated non reacting pupil, ptosis, diplopia, divergent paralytic squint VII N. Facial Palsy IV N. Diplopia on downward gaze(SO Paralysis) VI N. Diplopia on looking outwards to paralysed side(LR Paralysis) VIII N. Loss of hearing, vertigo, nystagmus I N. Anosmia II N. Blurring of vision, field defects

Coning
Supratentorial herniation Deterioration in level of consciousness Dilatation of pupil on side of compressing mass Hemipareisis on ipsilateral side

Coning
Infratentorial herniation Further damage to brain function Loss of vital functions

 RACOON!!!

PRIMARY BRAIN INJURIES

BY POOJA P S

PRIMARY BRAIN INJURIES

Diffuse axonal injury
Cerebral concussion Cerebral contusion

Cerebral laceration
Traumatic subarachnoid haemorrhage (SAH)

DIFFUSE AXONAL INJURY

Acceleration deceleration type of forces causes

mechanical shearing at the grey white matter interface (due to differential brain movement). This causes disruption and tearing of axons myelin sheath and blood capillaries over an extensive area. Can present as mild confusion followed by recovery or coma or death

Cerebral concussion
It is a clinical diagnosis
A brief temporary physiological paralysis of function

with out organic structural damage with amnesia/transient loss of consciousness followed by complete recovery . Brady cardia, hypotension and sweating may be present.

CEREBRAL CONTUSION
Circumscribed areas of brain tissue destruction

accompanied by extravasation of blood into the affected tissues. Produced by blunt force. Most common in frontal and temporal lobe.

FEATURES OF CONTUSION
Bruising Swelling of cortical gyri Brain edema Shearing damage to nerve cells and axons. Bleeding due to tearing of small blood vessels in

the brain. Focal neurological deficit ( > 24 hrs ) may be present Recovery may/may not occur.

Cerebral laceration
A cerebral laceration is a similar to contusion except

that, the pia-arachnoid membranes are torn over the site of injury in laceration Focal deficits are the rule.

 Bleeding into the subarachnoid spacethe area

between the arachnoid membrane and the pia mater surrounding the brain (containing blood vessels) WFNS(World Federation of Neurological Surgeons) grading of SAH

Subarachnoid hemorrhage

SUBARACHNOID HAEMORRHAGE

SYMPTOMS
Thunderclap headache "like being kicked in the head", or

the "worst ever; This headache often pulsates towards the occiput Vomiting Seizures Confusion Decreased level of consciousness or coma Neck stiffness, Fever Hemi paresis Rarely back pain and radicular pain

SIGNS
Raised blood pressure (adrenaline Release due to

bleeding ) Positive kernigs sign. Fundoscopy-subhyaloid hemorrhage , vitreous hemorrhage and papilloedema Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure.

 Subdural hemorrhage is a classic finding in shaken

baby syndrome

BY PRAJI.S.PRASAD

SUBDURAL HAEMATOMA
70%-due to falls, 25% due to vehicle accidents.
Classical finding in battered baby syndrome Mostly venous and capillary haemorrhage.

Common in older age group.

Divided into 3 types based on the time of onset of symptoms. 1. Acute-immediately and rapidly after the trauma 2. Subacute-several days to 2-3 weeks after the injury due to the pressure of hematoma. 3. Chronic-weeks to months.

Acute Subdural Hematoma

Most lethal of all head injuries. High mortality rate if not rapidly treated.

Closely resembles extra dural haemorrhage .

Symptoms develop 24 to 48 hours. Longer lucid interval.

Chronic Subdural Haematoma

Affects older individuals.
Minor injury causes subclinical hematoma. Clot liquefaction over next 2-4 weeks results in clot

expansion and development of signs and symptoms of mass. Effects may resemble brain tumor or stroke.

EXTRADURAL HAEMATOMA
Neurosurgical emergency.
Exclusively due to trauma. Skull # + tearing of middle meningeal artery.

Commonest site temporal bone.

Not always arterial. Mostly seen in young adults. Lucid interval-present in typical cases.

Clinical features
Concussion
Lucid interval Confused and irritable

Drowsiness and evidence of hemiparesis.

Compression of third nerve-initial constriction

followed by dilatation of pupil on the side of haemorrhage Hemiparesis of same side of haematoma

Prathibha Raj M R

Initial assessment is by Advanced Trauma and Life

Support (ATLS) Primary survey Resuscitation Secondary survey Definitive management

GENERAL PRINCIPLES
Team work Patients are more likely to die from airway obstruction

than from any remediable intra cranial lesions Surgically remediable intra thoracic and intra abdominal lesions take precedence over any intra cranial procedures Compressing intra cranial hematomas are unlikely to be present when patient is first seen The initial GCS assessment is of crucial importance The immediate institution of the correct care of unconscious patient does lower the morbidity and mortality from major head injury

INITIAL ASSESSMENT
RECORD
Blood pressure Pulse rate

Respiratory rate
Type of breathing

NEUROLOGICAL ASSESSMENT
GCS
PUPIL Size and equality LIMBS Reflex limb movements Stroke may be due to primary cerebral damage; is very

rarely due to a compressing intra cranial hematoma Spinal injury - Paraplegia,quadriplegia

 Rule out associated skull fractures

Presence of CSF rhinorrhoea or otorrhoea Mandibular or facial fracture

HISTORY
Loss of consciousness Post traumatic amnesia Skull fracture Focal neurological signs Persistent headache Vomiting Other medical conditions like patients on

anticoagulants,hemophiliacs alcohol intoxication Cause and circumstances of injury

RESUSCITATION
Airway
Breathing Circulation

Disability
Exposure

Airway assessment
Respiratory rate
Stridor and dyspnoea Air entry

Intactness of rib cage

AIRWAY MANAGEMENT
Immediate measure in an unconscious patient
Removal of loose dentures Positioning prone or on one side with the head low

Mouth suction
Insertion of Endotracheal tube

Endotracheal Intubation:Indications
Unconscious patient
GCS<8 Oropharyngeal bleeding

Emergency tracheostomy-crushed larynx,massive posterior

pharyngeal bleeding
Indication of ventilatory support Extensive Chest injury Generalized brain swelling Status epilepticus Acute reduction in intra cranial pressure For CT scanning in unconscious patient For all surgery or extensive pulmonary soiling

Circulation Assessment
Pulse
BP

CIRCULATION
Control of bleeding and restoration of blood volume Examination of whole body to assess other injuries and bleeding into body cavities Fracture of major long bones-shock,reflex lowering of BP---correct splintage Treatment of oligaemic shock is replacement of circulating volume(iv fluids-NS,Plasma expanders, blood transfusion) Haemodynamic status stabilised and monitored with pulse,BP,Urine output and CVP

Neuroassessment
Vitals
GCS Pupils

Symptoms: Drowsiness, recurrent

vomiting,seizures,headache CSF leak

Disability
Assessment of focal neurological deficit

Exposure
Intactness of skull and spine are assessed Fracture stabilised

Management
Neuro observation
Monitor vitals Catheterisation

Antibiotics
Antiedema measures Antacids Intravenous fluids

Triage
Triage originated and was first formalized in World

War I by French doctors treating the battlefield wounded at the aid stations behind the front. Much is owed to the work of Dominique Jean Larrey during the Napoleonic Wars.

PRIYANKA P.G

 SKULL XRAY
CT CEREBRAL ANGIOGRAPHY

LUMBAR PUNCTURE

SKULL XRAY
INDICATION Laceration or contusion of scalp Obvious depression of skull Compound fracture Suspected penetrating injury

COMPUTERISED TOMOGRAPHY
INDICATION
MILD HEAD INJURY 1.

2.
3. 4. 5.

NICE CRITERIA GCS < 13 at any point GCS 13 or 14 at 2 hours Focal neurological deficit Suspected open depressed or basal skull fracture Seizure;Vomiting > 1 episode

OTHER INDICATIONS
Age > 65
Coagulopathy Dangerous mechanism of injury

Anterograde amnesia > 30 mts

MODERATE TO SEVERE
AIMs To identify intra cranial haematoma Scalp soft tissue injury Skull fracture Intracerebral contusion

CT FINDINGS
Extra dural haematoma Lentiform hyperdense lesion

b/w skull & brain

 Acute subdural haematoma hyperdense areas giving a diffuse & concave appearance
Subacute subdural haematoma isodense areas

Chronic subdural haematoma hypodense area

Cerebral contusion - heterogenous

Subarachnoid Haemorrhage

FIRST WEEK
Repeat scan at 3 days
Post op Investigation of CSF leak

Intracranial infection

FIRST MONTH
Intracranial infection
c/c subdural haematoma Hydrocephalus

 CEREBRAL ANGIOGRAPHY- subarachnoid

haemorrhage
LUMBAR PUNCTURE subarachnoid haemorrhage,

meningitis

By Priyanka R Nair

OBJECTIVES
Nursing of the patient in the period of

unconsciousness. Repeated observation of the patient to detect the development of complications at the earliest.

Measures
Position-head of the patient should be placed 30

degree up, it is the known as REVERSE TRENDELENBERG. Collar must not be too tight This is to avoid obstruction of venous drainage from the head.

Tracheostomy -indications
If the patient is ventilator dependent. To facilitate tracheobronchial toilet. To prevent respiratory infections.

Advantages: Decreases dead space by half Work of breathing is decreased Tracheobronchial toilet is facilitated Incidence of resp.infection is decreased

 Patient should be ventilated to a pCO2 of 4.5-5 kPa.

If the arterial pCO2 increases the intracranial pressure

will increase since the normal auto regulation of the brain is disturbed in head injury.

 The central venous pressure should be maintained at

3-8 cm of water to prevent hypotension, so a central line should be started.

 Intracranial pressure (ICP) and cerebral perfusion

pressure (CPP) should be constantly monitored.

CPP=Mean arterial pressure(MAP) -ICP

CPP should be maintained >65mm Hg in a severely

head injured patient. So if the ICP is 20mm Hg the MAP should be >85mm Hg. If needed ionotropes can be used to support the CPP and the blood pressure.

ICP MONITORING

A tunnelled parenchymal ICP monitor can be inserted through a twist drill burr hole

MEASURES TO DECREASE THE ICP

Sedation with/without muscle relaxants

Patient is sedated using Propofol or Midazolam. Muscle relaxants like Atracurium can be used.

 Diuretics- Frusemide and Mannitol can be used to

decrease the cerebral swelling and raised ICP. Mannitol an osmotic diuretic is used mainly in subarachnoid haemorrhage.It is contraindicated in extradural haematoma.

Seizure control Seizures will increase the brain metabolic rate and thereby increase the ICP. So prophylactic anticonvulsants can be used in the first week to decrease the incidence of seizures. Phenobarbitone 60mg Q8H or Phenytoin 100mg Q8H can be used. If the ICP cannot be controlled it can lead to status epilepticus. Here EEG burst suppression therapy with Lorazepam or Thiopentone may be used.

 Normothermia should be maintained-

Pyrexia may decrease the cerebral blood flow so this should be avoided.Active cooling may be used to decrease the metabolic rate.

 Maintaining fluid and electrolyte balance-

Severely brain injured people are susceptible to disturbances in sodium homeostasis like Diabetes insipidus and Syndrome of inappropriate antidiuretic hormone(SIADH). SIADH can lead to dilutional hyponatremia will in turn can precipitate seizures.

 IV fluids should be administered until nasogastric

feeding can be commenced .If patient is conscious, oral feeding can be started . If the patient is in pain analgesics like Fentanyl or Codeine may be used. Pantoprazole 40mg iv OD may be given to avoid gastritis

 If fever occurs due to meningitis following basal skull

fracture lumbar puncture should be done and empirical treatment for meningitis should be started.
Any other source of infection should be ruled out
Antimeningitic prophylactic regimen(CP 20lakh unit

iv Q6h, Chloromycetin 500mg Q6h iv, Metronidazole 500 mg iv Q8h):Indications-Comminuted fractures, otorrhoea, rhinorrhoea, pneumocephalus

Care of the unconscious patient

Nasogastric tube feeding.
Care of the eyes by padding. Urinary catheter for drainage of urine and to monitor

the urine output. Urinary incontinence may occur in frontal lobe lesions. Change of position of the patient to avoid bed sores.

 Limb physiotherapy to prevent deep vein thrombosis. Chest physiotherapy to prevent respiratory infections. Care of the endotracheal tube.

Indications for ICU admission

if severely injured if requiring ventilatory assistance

Repeat CT scan should be considered: If there is deterioration of the mental state of the patient. If there is a continued rise in the ICP. If there is a failure to improve over 24 hours .

Rachana Chandran

Discussed as under Scalp injuries

Skull injuries
Cerebral injuries

SCALP INJURIES Scalp haematoma Aspiration,compression bandage & antibiotic coverage

Scalp Laceration Clean-excision of devitalised tissueirrigation-suture

SKULL FRACTURES Linear fractures No specific treatment required Depressed fractures 1) Small and shallow without any focal signs-no indication for surgery 2) Compound

Compound depressed fracturesSmall-conservative management Large1. Wound enlarged 2. Saline irrigation 3. Creation of burr hole 4. Elevation of depressed bone

HAEMATOMAS Extradural haematoma

Aspiration done surgically to remove mass & decrease the intracranial pressure Neurosurgically evacuated through a burr hole or craniotomy

Acute Subdural haematoma

Small haematomas-conservative management
>10mm thickness or a midline shift in CT >5mm regardless of GCS Craniotomy done with or without bone flap removal Factors- GCS, pupillary reaction, age & presence of anticoagulants

Chronic Subdural Haematoma

Evacuation with burr hole or craniotomy

Subarachnoid Haemorrhage Indication for surgery- CT large haematoma, decreased consciousness, focal neurological deficit

Clipping & coiling done Clipping via craniotomy to locate aneurysm

Traumatic Subarachnoid haemorrhage- managed conservatively Intracerebral

haemorrhage

Surgery indicated-haematoma >3cm,presence of structural vascular lesion in a young patient

CRANIOTOMY Definition Indications- mainly for brain lesions, traumatic brain injury Done under general anaesthesia

Preceded by an CT scan

CRANIOTOMY

Surgical management of raised intracranial pressure:a) b) c) d) Early evacuation of focal haematomas Cerebrospinal fluid drainage by ventriculostomy Delayed evacuation of swelling contusions Decompressive craniectomy

BY Radhika.V

 Post Concussional Syndrome Commonest among complications Includes neuropsychological symptoms

Most Important- post traumatic headache

Most often associated with WHIPLASH INJURIES

 Post Traumatic Epilepsy

Occurs in < 5% people Intradural haematoma- 18% chances Extradural haematoma- 2% chances
Risk increased in the following states:a) Post traumatic amnesia of > 24 hours b) Cases of dural penetration c) Missile injuries

Two types- early and late (true) I. Early- occurs within a week of the injury Cause- bruising & oedema near injury II. Late- after a week Cause- scar formation in the brain Post traumatic epilepsy is mainly of JACKSONIAN type

Treatment
Phenytoin & Phenobarbitone can be used
the first week to decrease incidence of seizures

Long term beneficial effects are not proved

 Infections
Associated with delayed operation Causes Bacterial Infections- mainly MENINGITIS Treatment- Empirical treatment with Broad Spectrum Antibiotics until culture reports are obtained Rarely; osteomyelitis, brain abcesses etc

Cerebrospinal fluid fistula Common in fractures of base of skull

Difficult to detect due to increased bleeding from nose & mouth

Presents as Rhinorrhoea and/or otorrhoea Diagnosis by skull films to detect fractures

Treatment suspected/diagnosed cases are treated with

Broad spectrum antibiotics after culture of normal flora of nose,ear & mouth Meningitic cover given Normally resolves within 48 hours, if lasts >48 hours, indication for dural repair Exact site of fracture must be found to determine approach of surgery

CSF LEAK THROUGH FISTULA

 Hydrocephalus Occurs due to ventricular dilatation after injury Acute situations- burr hole/ventricular drainage Not detected until weeks or months

Evidence of hydrocephalus-

Rate of recovery slows down Giddiness, urinary and gait disturbances develop
Treatment Immediate-measures to reduce intracranial pressure Longterm- monitoring of ICP CSF shunt may be required

 Cranial Nerve Palsies Most common- 3rd & 6th nerves Treatment of appropriate cause Craniofacial injuries Injury to orbit and paranasal sinuses

Rehabilitation

Concerted efforts of medical, nursing, physiotherapy, speech & occupational therapies

Assessed by Glasgow Outcome Score(GOS)

Good Recovery
Moderate disability Severe disability Persistent vegetative state Dead

5
4 3 2 1

Other factors include: age, presence of other injuries

BELONGED TO???

PREVENTION IS BETTER THAN CURE!!! If the unpreventable happen however..

Let us Doctors do the job!!!