Head Injury- Clinical

Manifestations, Diagnosis and

Management

• Dr Gumar Jaya Saleh SpBS

CROSS-SECTION
 HEAD INJURY -
DEFINITION
• Any injury that results
in trauma to the
SCALP, SKULL or
BRAIN.

• TRAUMATIC
BRAIN INJURY and
HEAD INJURY are
often used
 Head Injury

• Causes
– Motor vehicle accidents
– Falls
– Assaults
– Sports-related injuries
– Firearm-related injuries
 HEAD INJURY - TYPES
OPEN HEAD INJURY: CLOSED HEAD INJURY
There is penetration to the skull. There is NO penetration to the skull.
 COUP-CONTRECOUP
INJURIES

• Damage may occur

directly under the site
of impact (COUP), or
it may occur on the
side opposite the
impact
(CONTRECOUP).
 Head Injury

• Minor head trauma

– Concussion : head injury with a temporary
loss of brain function concussion can cause a
variety of physical, cognitive , and emotional
symptoms.
Cause: Sudden acceleration and deceleration
injury eg: Car accident, sports injury,
bicycle accident etc
 Head Injury

• Major head trauma

– Contusion
• The bruising of brain tissue within a focal
area that maintains the integrity of the pia
mater and arachnoid layers associated
with multiple micro-hemorrhages, small
vessel bleed into brain tissue
– Lacerations
• Involve actual tearing of the brain tissue
• Intracerebral hemorrhage is generally
associated with cerebral laceration
 HEAD INJURY -
MECHANISMS
PRIMARY INTRACRANIAL SECONDARY
INJURY INTRACRANIAL INJURY

• It is the initial neuronal • Secondary injuries are the

damage that occurs result of the
IMMEDIATELY as result neurophysiological and
of trauma. anatomic changes, which
occur from MINUTES to
DAYS after the original
trauma.
 HEAD INJURY -
MECHANISMS
PRIMARY INTRACRANIAL SECONDARY
INJURY INTRACRANIAL INJURY

• Cerebral Laceration • Edema

• Cerebral Contusion
• Impaired Metabolism
• Epidural Hematoma
• Subdural Hematoma • Altered Cerebral Blood Flow
• Subarachnoid Hematoma
• Intracerebral Hematoma • Free Radical Formation
• Diffuse Axonal Injury
• Excitotoxicity
 SCALP INJURIES
LACERATIONS SUBGALEAL HEMATOMA
 Head Injury

• Scalp lacerations
– The most minor type of head trauma
– Scalp is highly vascular  profuse
bleeding
– Major complication is infection
 SKULL INJURIES
CLOSED FRACTURES OPEN FRACTURES
• Open fractures have
potential for serious
infection.
• A closed fracture has a • Any foreign matter impaled
significant chance of in the skull should be left in
associated intracranial place for removal by the
haematoma. neurosurgeons.
• Cover it lightly with a sterile
dressing that has been
moistened with a sterile
saline.
 SKULL INJURIES
CT SCAN OT
 SKULL INJURIES
DEPRESSED FRACTURES/COMPOUND
NON-DEPRESSED LINEAL
DEPRESSED FRACTURES FRACTURES
SKULL INJURIES - BASILAR
SKULL FRACTURE
 BRAIN INJURIES
DIFFUSE FOCAL

• Contusion
• Brain Lacerations
• Concussion • Epidural haematoma
• Diffuse Axonal Injury • Subdural haematoma
• Subarachnoid haemorrhage
• Parenchymal haematoma
SKULL INJURIES - BASILAR
SKULL FRACTURE
RACCOON EYE
SKULL INJURIES - BASILAR
SKULL FRACTURE
BATTLE’S SIGN
 SKULL INJURIES - BASILAR
SKULL FRACTURE
BLEEDING FROM THE EAR CSF LEAKAGE FROM THE
CANAL EAR OR NOSE
 Head Injury

• High potential for poor outcome

• Deaths occur at three points in time after
injury:
– Immediately after the injury
– Within 2 hours after injury
– 3 weeks after injury
 BRAIN INJURIES
DIFFUSE FOCAL

• Contusion
• Brain Lacerations
• Concussion • Epidural haematoma
• Diffuse Axonal Injury • Subdural haematoma
• Subarachnoid haemorrhage
• Parenchymal haematoma
 HEAD INJURY (DIFFUSE) -
CONCUSSION
• Brain injury that does • There may be brief
not result in any confusion,
evidence of structural disorientation,
alteration. headache, dizziness,
amnesia.
• Return of
consciousness • CT scan is normal.
moments or minutes
after impact.
 Head Injury
Pathophysiology

• Diffuse axonal injury (DAI)

– Widespread axonal damage occurring
after a mild, moderate, or severe TBI
– Seen in half the cases of head injury
– Process takes approximately 12-24
hours
HEAD INJURY (DIFFUSE) -
DIFFUSE AXONAL INJURY
 Head Injury
Pathophysiology
• Diffuse axonal injury (DAI)
– Clinical signs:
•  Level of Consciousness
•  ICP
• Decerebration or decortication
• Global cerebral edema
• 90% regain consciousness from
severe DAI
BRAIN CONTUSION
SUBDURAL HEMATOMA
SCHEMATIC CT SCAN
 SUBARACHNOID
HEMATOMA
SCHEMATIC CT SCAN
HEMATOMAS
 CEREBRAL EDEMA
NORMAL CT SCAN CEREBRAL EDEMA
 SYMPTOMS
• Confusion/Irritibility • Speech/Swallowing
Difficulty
• Drowsiness
• CSF Leakage
• Dizziness
• Ear Bleeding
• Nausea & Vomiting
• Numbness/Paralysis
• Amnesia
• Coma
SYMPTOMS
SYMPTOMS
 GLASGOW COMA SCALE
MINIMUM=3/15 MAXIMUM=15/15 INTUBATION
<8/15
GLASGOW COMA SCALE
(GCS)
SEVERITY SCORE

MILD 13-15

MODERATE 9-12

SEVERE 3-8
GLASGOW COMA SCALE
(GCS)
LOSS OF
SEVERITY CONSCIOUSNESS

MILD 0-30 mins

MODERATE >30 mins to <24 hrs

SEVERE >24 hrs

 COMPLICATIONS
• Personality Changes
LONG-TERM EFFECTS
• Hypopituitarism e.g. DI • Parkinson’s

• Post-Traumatic Seizures • Alzheimer’s Dementia

• Infections e.g. Meningitis

• Vasospasm, Aneurysm

• Coma, Brain Death

 Head Injury

• Skull fractures
– Linear Skull Fracture
– Depressed Skull Fracture
– Diastatic Skull Fracture
– Basal Skull Fracture
– Compound Skull Fracture
– Compound elevated Skull Fracture
– Growing Skull Fracture
Battle’s Sign

Fig. 55-13
 Investigations

 X-ray
 CT scan: standard modality

 MRI

 Bleeding from the ear or nose in cases of suspected CSF

leak -"halo" or "ring" sign , when dabbed on a tissue
paper
 CSF leak - analyzing the glucose level and by measuring
tau-transferrin.
 Management
Pre-hospital care:
• Patients with severe head injuries should be assumed to
have a cervical spine (C-spine) injury and immobilized
with until clinical and radiographic studies can prove
otherwise
• Minimize CSF leak
– Bed flat
– Never suction orally; never insert NG tube; never use Q-Tips
in nose/ears; caution patient not to blow nose
• Place sterile gauze/cotton ball around area
Definitive Rx:
• Measures to reduce ICP
• Supportive management
• Surgery
 Head Injury

Cerebral Contusion Cerebral Laceration

 Epidural hematoma

– Results from bleeding between the dura and

the inner surface of the skull
– MC type of traumatic Intracranial bleed,
rarely occurs spontaneously
– A neurologic emergency
– Bleed is Venous or arterial origin
EPIDURAL HEMATOMA
SCHEMATIC CT SCAN
 Epidural hematoma
Source of Bleed :
Temperoparietal locus (most likely) - Middle
meningeal artery
Frontal locus - anterior ethmoidal artery
Occipital locus - transverse or sigmoid sinuses
Vertex locus - superior sagittal sinus
Clinical Features:
• LOC>>> Lucid Interval >> unconsciousness
• s/s of raised ICP
• Focal neurological deficit
• s/s of cerebral herniation
 Epidural and Subdural Hematomas

Epidural Hematoma

Subdural Hematoma

Fig. 55-15
 Subdural hematoma
– Occurs from bleeding between the dura mater and
arachnoid layer of the meningeal covering of the
brain
– Source of bleed: Bridging veins; May be caused by
an arterial hemorrhage
– Much slower to develop into a mass large enough to
produce symptoms.
Cause: Acceleration-deceleration injury, direct
trauma,
Risk factors: Elderly, dementia, alcoholics, shaken
baby syndrome, pts on anticoagulants
 Subdural hematoma

– Acute subdural hematoma(<72hrs)

• High mortality
• Associated with major direct trauma (Shearing
Forces)
Clinical Features:
Headache, fluctuating LOC, confusion, dilated
fixed pupil, deviated gaze
CT scan: hyperdense
 Subdural hematoma

– Subacute subdural hematoma

• Occurs within 4-21 days of the injury
• Failure to regain consciousness may be an
indicator
CT scan: Isodense or hypodense
– Chronic subdural hematoma(>3wks)
• Develops over weeks or months after a seemingly
minor head injury, probably from repeat minor
bleeds
CT scan : hypodense
 Epidural and Subdural Hematomas
Hematoma type Epidural Subdural

Location Between the skull and the dura Between the dura and
the arachnoid
Involved vessel Temperoparietal (most likely) - Bridging veins
Middle meningeal artery
Frontal - anterior ethmoidal artery
Occipital - transverse or sigmoid
sinuses
Vertex - superior sagittal sinus
Symptoms Lucid interval followed Gradually
by unconsciousness increasing headache and co
nfusion
CT appearance Biconvex lens- limited by suture Crescent shaped- crosses
lines suture lines

Fig. 55-15
Subarachnoid Hemorrhage
Causes:
• Rupture of Berry aneurism(MCC)
• Trauma (fracture at the base of the skull leading to
internal carotid aneurysm)
• Amyloid angiopathy
• Blood dyscrasias
• Vasculitis

Clinical Features:
• Explosive or thunderclap headache, “worst headache
of my life”,
• nausea and vomiting, decreased LOC or coma.
• Signs of meningeal irritation
Intracerebral Hemorrhage
(ICH)
Intracranial hemorrhage is hemorrhage that occurs
within the brain tissue itself; an intra-axial
hemorrhage.
Two main types:
1)Intraparencymal hemorrahge- ICH extending into
brain parenchyma; MCC- HTNsive vasculopathy
2)Intra-ventricular hemorrhage- ICH extending into
ventricles; MCC –trauma
Causes:
Hypertensive vasculopathy(70-80%)
Ruptured AVM
Trauma
Blood dyscracias
 Intracranial Hemorrhage
Extra- axial hemorrhage
• Epidural hematoma
• Subdural hematoma-
Acute
Chronic
• Subarachnoid hemorrhage
Intra-axial hemorrhage
• Intra-parenchymal
hemorrhage
• Intra-ventricular
hemorrhage
 Intracerebral Hemorrhage
(ICH)
Clinical presentation: Rapidly progressive severe headache,
building over several minutes, often accompanied by focal
neurological deficits, nausea and vomiting, decreased level of
consciousness.

S/S depend site of hemorrhage:

Basal ganglia/internal capsule - hemiparesis, dysphasia
Cerebellum - ataxia, vertigo
Pons - cranial nerve deficits, coma
Cerebral cortex - hemiparesis, hemisensory loss,
hemianopsia, dysphasia
 INTRACEREBRAL
HEMATOMA
SCHEMATIC CT SCAN
 Complications
• Neurological deficits or death
• Seizures
• Obstructive Hydrocephalus
• Spasticity
• Urinary complications
• Aspiration pneumonia
• Cushing’s ulcer
• Neuropathic pain
• Deep venous thrombosis
• Pulmonary emboli
• Cerebral herniation
 Cerbral Herniation
Brain herniation is a deadly side effect of very
high intracranial pressure that occurs when a part of
the brain is squeezed across structures within the skull.

“Brain herniation represents mechanical displacement

of normal brain relative to another anatomic region
secondary to mass effect from traumatic, neoplastic,
ischemic, or infectious etiologies. “
Cerbral Herniation
Supratentorial herniation
1. Uncal
2. Central (transtentorial)
3. Cingulate (subfalcine)
4. Transcalvarial
Infratentorial herniation
5. Upward (upward
cerebellar
or upward transtentorial)
6. Tonsillar (downward
cerebellar)
 Cingulate Herniation
The most common type, the innermost part of the frontal
lobe is scraped under part of the falx cerebri, the dura
mater at the top of the head between the
two hemispheres of the brain.
Cingulate herniation can be caused when one hemisphere
swells and pushes the cingulate gyrus by the falx
cerebri.
Cingulate herniation is frequently believed to be a
precursor to other types of herniation
 Uncal Herniation
common subtype of cerebral herniation following raised ICP
Innermost part of the temporal lobe, the uncus, can be
squeezed so much that it moves towards the tentorium and
puts pressure on the brainstem, most notably the midbrain

Clinical feature:
• Compression of I/L CN III- I/L fixed dilted pupil
• Compression of I/L PCA- C/L homonymous hemianopsia
• Compression of C/L crus cerebri- I/L hemiparesis
• Duret hemorrhage
 Diagnostic Studies
CT scan –
• A GCS score less than 15 after blunt
head trauma warrants a patient with no
intoxicating consideration of an urgent
CT scan.
 CT findings

Epidural Hematoma Subdural Hematoma

Fig. 55-15
 CT findings

Subarachnoid hemorrhage Intracerebral hematoma

Fig. 55-15
 Diagnostic Studies

• MRI – superior for demonstrating the size of

an acute subdural hematoma.
• Cerebral angiogram if hemorrhage is
confirmed (not necessary in case of classic
hypertensive hemorrhage
• Cervical spine X-ray
• EEG
• Lumbar Pucture
 Management
1) Supportive Measures:
• Endotracheal intubation for patients with decreased level of
consciousness and poor airway protection.
• Cautiously lower blood pressure to a MAP less than 130 mm
Hg, but avoid excessive hypotension.[10]
• Rapidly stabilize vital signs, and simultaneously acquire
emergent CT scan.
• Maintain euvolemia, using normotonic rather than hypotonic
fluids, to maintain brain perfusion without exacerbating brain
edema
• Avoid hyperthermia.
• Facilitate transfer to the operating room or ICU.
 Management
2) Decrease cerebral edema:
• Modest passive hyperventilation to reduce PaCO2
• Mannitol, 0.5-1.0 gm/kg slow iv push
• Furosemide 5-20 mg iv
• Elevate head 20-30 degrees, avoid any neck vein
compression
• Sedate and paralyze if necessary with morphine and
vecuronium (struggling, coughing etc will elevate
intracranial pressure)
 Management
3) Surgical Evacuation of hematoma:
• No surgical intervention if collection <10ml

Indication of surgical decompression:

• The GCS score decreases by 2 or more points between the
time of injury and hospital evaluation
• The patient presents with fixed and dilated pupils
• The intracranial pressure (ICP) exceeds 20 mm Hg

Exception :
In Subdural hematoma with GCS=15- hematoma >10mm ,or
>5mm midline shift ---- requires Surgical decompression

SAH: whn a cerebral aneurysm is identified on angiography,

clipping and coiling is done to prevent re-bleed
 Management
Sugical Decompression contd..
Types:

• Burr-hole
• Craniotomy- bone flap is temporarily removed from
the skull to access the brain
• Craniectomy – in which the skull flap is not immediately
replaced, allowing the brain to swell, thus reducing
intracranial pressure
• Cranioplasty - surgical repair of a defect or deformity of
a skull.
TREATMENT - ACUTE STAGE
(SURGERY)
DECOMPRESSIVE CRANIOTOMY
 Management
4) Medical therapy:

• Antihypertensives - reduce blood pressure to prevent exacerbation

of intracerebral hemorrhage in hypertensive encephalopathy. Eg
Nicardipine, labetolol; CCB help relieve vasospasm in SAH and
decrease further damage
• Diuretics - Mannitol, CAI
• Anticonvulsants – reduce frequency of seizures and prophylaxis of
seizures eg: Fosphenytoin
• Antipyretics- to Rx fever and pain relief eg: Acetaminophene
• Antidote-
VitK/FFP for warfarin overdose;
protamine for heparin overdose
• Antacids- prophylaxis for Cushing’s gastric ulcer eg: Famotidin
• Glucorticoids may help reduce the head and neck ache caused by
the irritative effect of the subarachnoid blood.
 Preventive Measures

Health Promotion
• Prevent car and motorcycle
accidents
• To Wear safety helmets
 Rehabilitation
Ambulatory and Home Care
• Nutrition
• Bowel and bladder management
• Spasticity
• Dysphagia
• Seizure disorders
• Family participation and education