Head Trauma & Management
Dr. Utham Murali. M.S ; M.B.A.
Asso.Prof of Surgery
IMS / MSU / Malaysia.
Learning Outcomes
• List the types of Head injury
• Identify the difference between Primary & Secondary brain injury
• Explain about the Medical & Surgical mgt of mild, moderate & severe head injury
• Describe about Extradural haematoma, Sub-dural haematoma and Sub-
arachnoid haemorrhage
Definition
• Head injury is defined as traumatic
injuries involving the cranium and
intracranial structures (i.e., Scalp /
Skull or Brain).
• Traumatic Brain Injury (TBI) & Head
Injury are often used interchangeably.
• Maxillofacial injuries is not part of
head injury.
Surgical Anatomy
Epidemiology
• 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.
• The most common causes include motor vehicle accidents , falls,
assaults, sports-related injuries, and penetrating trauma.
• Head injuries occur in all age groups, with a peak incidence between
the ages of 16 and 25 years and is more common in males than
females.
Pathophysiology
•Brain is contained within the skull, a rigid and inelastic container.
Hence only small increases in volume within the intracranial
compartment can be tolerated before pressure within the
compartment rises dramatically.
•A second crucial concept in TBI pathophysiology is the concept of
cerebral perfusion pressure (CPP),which is the difference between the
mean arterial pressure (MAP) and the intracranial pressure (ICP). CPP
= MAP – ICP
Classification – According To
• Type of injury – Open / Closed (or) Blunt /
Penetrating
• Site of injury
• Pathology of injury
• Severity of injury
Open Injury Closed Injury
• Obvious external wound • No obvious external signs
Blunt Head Injury
• A moving head strikes a fixed
object or a moving object strikes
an immobile head →scalp injury,
fractures of the skull, contused
brain etc.
• 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.
Penetrating Injury
Classified into 2 types - velocity
•High velocity - Bullets
•Low velocity injury
- Knifes/Arrows/Screwdrivers etc.
Site of Injury
•Scalp injury
•Skull injury
•Brain injury
•Intracranial vascular injury
Scalp Injuries
LACERATIONS SUBGALEAL HEMATOMA
Skull Injuries – Fractures
OPEN FRACTURES CLOSED FRACTURES
SKULL INJURIES
CLOSED FRACTURES OPEN FRACTURES
• Open fractures have potential for serious
infection.
• A closed fracture has a significant chance • Any foreign matter impaled in the skull
of associated intracranial haematoma. should be left in place for removal by the
neurosurgeons.
• Cover it lightly with a sterile dressing that
has been moistened with a sterile saline.
Skull Injuries – Fractures
DEPRESSED FRACTURES LINEAR FRACTURES
Skull Injuries – Basilar Fractures
Brain Injuries
PRIMARY SECONDARY
It is the initial damage that occurs It is the result of neurophysiological and
IMMEDIATELY as result of trauma. anatomic changes, which occur from
•Cerebral concussion MINUTES to DAYS after the original trauma.
•Cerebral edema
•Cerebral contusion •Intracranial hematoma
•Cerebral laceration •Brain herniation
•Cerebral ischaemia
•Diffuse axonal injury •Infection
•Epilepsy
Primary Brain Injury
• Cerebral concussion is slight distortion causing temporary physiological changes leading to
transient loss of consciousness with complete recovery.
• Cerebral contusion is more severe degree of damage with bruising and cerebral oedema
leading to diffuse or localized changes.
• Cerebral laceration is tearing of brain surface with collection of blood in different spaces
and with displacement of dural parts.
• 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
Brain Injuries
DIFFUSE AXONAL INJURY CONTUSION
Intracranial Vascular Injury
•Epidural Haematoma
•Subdural Haematoma
•Sub – Arachnoid Haematoma
•Intracerebral Haematoma
Extradural Haematoma – EDH
•Haematoma in extradural space
•Common site – Temporal region
•Tear of MMA
•Commonly presents with “lucid
interval” / Features of ↑ ICP
•CT scan - lentiform (lens shaped
or biconvex) hyperdense lesion
•The treatment of an EDH is
immediate surgical evacuation via
craniotomy.
Subdural Haematoma – SDH
• Haematoma between dura & brain.
• Occurs as a result of tearing of cortical
veins & due to cortical laceration.
• Described as acute or chronic depending
on the age.
• ASDH usually present with an LOC
from the time of injury & is progressive.
• Clinical features of CSDH include
headache, cognitive decline, focal
neurological deficits and seizures.
• CT scan – Concavo – convex lesion
• The treatment of an SDH is surgical
evacuation via craniotomy.
Subarachnoid Haemorrhage – SAH
• Haematoma in the space between
the arachnoid space and the pia
mater [subarachnoid space]
• May be spontaneous / trauma
• Spontaneous – Intracranial
Aneurysm
• Features of ↑ ICP
• LP / CT scan / Angiogram
• Clipping / Embolisation /
Craniotomy
Intracerebral Haematoma – ICH
• Haematoma is formed within the
brain parenchyma.
• Due to areas of contusion
coalescing into a contusional
haematoma.
• CT scan - appear as hyperdense
lesions with associated mass
effect and midline shift.
Minor: GCS 15 / No LOC or amnesia
Mild: GCS 14 or 15 + LOC or amnesia
Severity Impaired alertness or memory
Moderate: 9-13 or LOC ≥ 5 min
Severe: GCS 3 - 8
Effects of Brain Injury
• Brain oedema is accumulation of fluid, both intracellular and extracellular. It is due to congestion and
dilatation of blood vessels. It may be diffuse or localized.
• Brain necrosis is of severe variety with destruction and is due to haemorrhagic infarction.
• Brain ischaemia is due to increased pressure. This in turn leads to alteration in the perfusion of brain
which itself aggravates the ischaemia and this forms a vicious cycle, causing progressive diffuse
ischaemia of brain.
• Coup injury occurs on the side of the blow to the head. Contre-coup injury occurs on the side opposite
to the blow on the head.
Coup or Contrecoup injuries
• Damage may occur directly under
the site of impact (COUP), or it
may occur on the side opposite
the impact (CONTRECOUP).
Coning
• It is due to ↑ ICP causing either:
i. Herniation of contents of supratentorial
compartment through the tentorial hiatus (or)
ii. Herniation of the contents of infratentorial
compartment through the foramen magnum.
•In supratentorial herniation, there is
compression of ipsilateral III CN & Midbrain
•In infratentorial herniation there is
obstruction of cerebral aqueduct with damage to
brain function.
Clinical Approach
• History
• Examination
History Taking
• Mechanism of injury
• Loss of consciousness or amnesia
• Level of consciousness at scene and on transfer
• Current symptoms / Evidence of seizures
• Probable hypoxia or hypotension
• Pre-existing medical conditions
• Medications (especially anticoagulants) / Allergies
ATLS – Guidelines
ABCDE – Approach
Evaluation
Resuscitation & Primary survey
Neurological Assessment
Secondary survey
Examination
Neurological Assessment Secondary survey
• Level of consciousness • Status and protection of airway.
• General assessment and other
• Glasgow coma scale injuries like fractures, abdominal
organ injuries, thoracic injuries are
• Pupillary reaction to light and size
looked for.
• Vital Signs • Presence of any scalp haematoma,
fractures of skull bone which may
• Reflexes be depressed has to be looked for.
• Any blood from nose or ear, CSF
• Limb movements—normal/mild rhinorrhoea or CSF otorrhoea has
weakness/ severe weakness/spastic
to be looked for.
flexion/extension/ no response
Glasgow Coma Scale Pupillary Response
Investigations
• Basic Tests
• X-ray skull: To look for fracture, relative position of the calcified pineal gland.
• CT scan: Plain (not contrast) to look for cerebral oedema, haematomas, midline
shift, fractures, ventricles, brainstem injury.
• Carotid arteriography / MRI scan
• Investigations for other injuries like ultrasound of abdomen.
• Monitoring of intracranial pressure
ICP – Monitoring
Criteria for Hospitalization
• Any altered level of consciousness
• Skull fracture
• Focal neurological features
• Persistent headache, vomiting, systolic hypertension, bradycardia
• No CT scan available or abnormal CT Head
• Alcohol intoxication
• Bleeding from ear or nose
• Associated injuries
Treatment – Mild Head Injury [14-15 GCS]
Discharge - Criteria NICE Guidelines – CT-scan
•Glasgow Coma Score (GCS) <
• GCS – 15 / 15 13 at any point
•GCS 13 or 14 at 2 hours
• No Focal neurological deficit
•Focal neurological deficit
• Follow-up – A & E Dept •Suspected open, depressed or
basal skull fracture
•Seizure
•Vomiting > one episode
Treatment – Moderate to Severe Injury
Prevention of Hypoxia
Aim
(SBI) Control of ↑ ICP
Maintenance of Perfusion
Others
Cervical Immobilization Resuscitation
Control of ICP - Medical
Normal ICP = 8-12 mm Hg Reverse - Trendelenberg
• Position head up 30º
• Avoid obstruction of venous drainage -
head
• Sedation +/– muscle relaxant
• Normocapnia 4.5–5.0 kPa
• Diuretics: furosemide, mannitol
• Seizure control
• Normothermia
• Sodium balance
• Barbiturates
Control of ICP – Surgical
• Early evacuation of focal haematomas:
EDH, ASDH [ Burr-hole / Craniotomy ]
• Cerebrospinal fluid drainage via
ventriculostomy
• Delayed evacuation of swelling contusions
• Decompressive craniectomy
Complications
Early Late
•Chronic subdural haematoma.
•Brainstem injury—due to
•Early post-traumatic epilepsy—they
coning. need anticonvulsants for 3 years.
•Late post-traumatic epilepsy is due
•Compression over cerebellum
to scarring and gliosis of cerebrum.
and medulla. •Post-traumatic amnesia.
•Post-traumatic hydrocephalus.
•CSF rhinorrhoea / CSF - Leak
•Post-traumatic headache.
Good Recovery – 5
Moderate Disability – 4
Outcomes
Severe Disability - 3
Persistent Vegetative State – 2
Dead – 0
Summary of TBI management
Steps Rationale
Respiratory support (intubation & ventilation) Comatose, unable to protect airways
Elevate head 30-45° Facilitate venous drainage
Straighten neck, no tape encircling the neck Facilitate venous drainage
Avoid hypotension (SBP<90mmHg) Prevent hypoxia – edema
Control hypertension Avoid transmission of pressure to ICP
Avoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatation
Control ventilation, aims PaCO2 35-40 mmHg Avoid vasoconstriction / -dilatation
Adequate sedation To reduce brain metabolism
Do CT brain Ascertain intracranial pathology rapidly
References
