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Head injury
An insult to the brain, not of degenerative or congenital nature caused by an external physical force that may produce a diminished or
altered state of consciousness, which results in an impairment of cognitive abilities or physical functioning. It can also result in the
disturbance of behavioral or emotiona
functioning.

Pathophysiology: Mechanism of Injury

* Blunt Injury: Motor vehicle collisions, Assaults, Falls,
* Penetrating Injury: Gunshot wounds, Stabbing, Explosion

Secondary Injury:
Type of injury: Secondary injury refers to the progressive damage that occurs after the initial trauma and can worsen the
neurological outcome. It is characterized by a cascade of pathological processes, including:
Primary
* Injury:
Primary injury: Irreversible cellular injury as a direct result of the injury, Prevent the even
The primary injury refers to the initial mechanical damage Ischemia and hypoxia: Head injury can lead to reduced blood flow and oxygen supply to the brain. This can occur
* by the
caused Secondary injury:
trauma, which Damage
can be classifiedto cells
into two that
main are due
not toinitially injured. Occurs hours to weeks after injury, Prevent hypoxia and ischemi
direct vessel injury, increased intracranial pressure (ICP), or systemic hypotension. Ischemia and hypoxia
types: contribute to neuronal cell death and further tissue damage.
* injury:
Focal Primary mechanical
Focal injuries injury
occur at the toimpact
site of axonsand and blood vessels results from rotational and translational accelerations
Excitotoxicity: Following injury, there is an excessive release of neurotransmitters, such as glutamate, leading to
involve
* direct damage to acceleration
Rotational the brain tissue.causes
This candiffuse
result from
shearing/stretch ofneurons.
overexcitation of axonalThis
andexcessive
vascular cell membranes,
activation increasing
can cause a cascade their permeability
of intracellular events that result in
forces such as a skull fracture or penetrating injury, leading to neuronal damage and cell death.
(“mechanoporation”
contusions (bruising) or lacerations (tearing) of the brain tissue.
Inflammatory response: Traumatic brain injury triggers an inflammatory response within the brain, involving the
Diffuse injury: Diffuse injuries occur when there is rapid release of inflammatory mediators and activation of immune cells. While inflammation plays a role in clearing
Intracellular calcium in ux triggers proteolysis, breakdown
acceleration or deceleration of the head, causing widespread
of the cytoskeleton, and interruption of axonal transpor
debris and promoting tissue repair, excessive or prolonged inflammation can contribute to further brain injury.
damage throughout the
Accumulation of brain. This can
b amyloid result in shearing
precursor protein,forces
the formation of axonal bulbs (retraction balls), secondary axotomy, and an in ammatory
that disrupt the integrity of neuronal structures, leading to Cerebral edema: Swelling of the brain tissue, known as cerebral edema, can occur as a result of injury. Edema can
response
diffuse axonal injury (DAI). DAI involves damage to the axons be caused by increased vascular permeability, disruption of the blood-brain barrier, or the accumulation of fluid
(nerve fibers) throughout the brain, disrupting communication within cells. Cerebral edema can lead to increased ICP, further compromising blood flow and oxygen delivery to the
between different brain regions. brain.

Two types of brain injury occur

* Closed brain injury
* Open brain injur

Closed head injury Open Head Injury

Resulting from falls, motor vehicle crashes, etc Results from bullet wounds, etc
Focal damage and diffuse damage to axon Largely focal damag
Effects tend to be broad (diffuse Penetration of the skul
No penetration to the skul Effects can be seriou

Most common type of focal brain injury, characterized by bruising or bleeding.typically occur as a result of blunt force trauma , such as in motor vehicle accidents, falls, or physical assaults. commonly observed in combination with

Cerebral contusion
other types of head injuries, such as skull fractures or diffuse axonal injury.

Cerebral Contusion
The pathophysiology of cerebral contusions involves a series of events:

Impact and Compression: causes the brain to collide with the bony structures of the skull, leading to contusions and occurs at the site opposite to the point of impact, known as the coup injury. Additionally, a contrecoup injury can
* Most common Focal brain Injur
occur on the opposite side of the brain due to rebounding forces within the skull.
* Sites—> Impact site/ under skull # Anteroinferior frontal Anterior Temporal Occipital Regions ->Petechial
Vascular Injury and Bleeding: impact can damage the small blood vessels within the brain, resulting in bleeding and can lead to hematoma within or around the contused area.
Petechial hemorrahges—>coalesce —> Intracerebral Hematomas later on.
Inflammatory Response: Following the injury, can contribute to the enlargement of the contusion and the progression of secondary injury.

Speci c Head Injuries C. CSF testin

* Skull Fracture
• Ring sign, glucose or CSF transferri
* Basilar Fractur
D. Should be started on prophylactic antibiotic
A. Most common-petrous portion of temporal bon
• Ceftriaxone 1-2 g
B. Dural tear
* Scalp Laceration
1. CSF otorrhe
(5) May lead to massive blood los
2. CSF rhinorrhe
(6) Small galeal lacerations may be left alon
3. Battle Sig
* Skull Fractur
4. Raccoon Sig
• Linear and simple comminuted skull fracture
5. Hemotympanu
(1) Exploration of woun
6. Vertig
(2) Prophylactic antibiotics are controversia
7. Hearing los
(3) Occipital fractures have a high incidence of other
injur
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• Traumatic Subarachnoid Hemorrhag
- Most common CT nding in moderate to severe TB
- If isolated head injury, may present with headache, photophobia and meningismu
- Early tSAH development triples mortalit
- Size of bleed and outcom
- Timing of C
- Nimodipine reduces death and disability by 55%

Epidural Hematoma Diagnosis

Occurs in 0.5% of all head injurie CT is diagnosti
Blunt trauma to temporoparietal regio Initial Ct—> Hyperdense Lentiform collection beneath skul
middle meningeal artery involved most commonly (66% Actively bleeding- Mixed densitie
Eighty percent with associated skull fractur Severe anemia- isodense/hypodens
May occur with venous sinus tear Untreated EDH imaging over days—> Hyperdense—> Isodense—>
classically associated with a lucid interva Hypodense w.r.t. brai
Classic presentation only 30% of the tim

Treatment
Subdural Hematoma
Sudden acceleration-deceleration injury with tearing of bridging vein
Common in elderly and alcoholic
Associated with DA
Classi ed as acute, subacute or chroni
Acute <2 week
Chronic >4 week

Rx- larger- urgent remova

Small with mass effect/ signi cant change in conscious/ focal
de cits-Removed
Small with signi cant brain injuries + mass effect out of proportion to
size of clot-Non operative approac

Cranial neuropathies occur in about 10% of admitted and 30% of severe injuries
Frontal injury, basal skull fracture, and pressure effects account for mos
Anosmia – frontal injur

Visual symptoms result from oculomotor dysfunction, refractive error shifts, damage to the cornea and intraocular structures, visual eld
loss caused by anterior and posterior visual pathway damage
Traumatic optic neuropathies-at the entry and exit of the optic cana

Auditory disturbance
1. Fracture of petrous temporal bone(longitudinal
2. Hemotympanu
3. Tympanic membrane perforatio
• Facial nerve palsies -longitudinal or transverse petrous temporal fracture

Concussion
• No structural injury to brai
• Level of consciousnes
1. Variable period of unconsciousness or confusio
2. Followed by return to normal consciousnes
• Retrograde short-term amnesi
- May repeat questions over and ove
• Associated symptom
- Dizziness, headache, ringing in ears, and/or nause
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Di use axonal injury

• Hallmark of severe traumatic Brain Injur
( DAI )
• Differential Movement of Adjacent regions of Brain during acceleration and Deceleration
• DAI is major cause of prolonged COMA after TBI, probably due to disruption of Ascending Reticular connections to Cortex
• Angular forces > Oblique/ Sagital Force

The shorn Axons retract and are evident histologically as RETRACTION BALLS
Located predominantly i
1. CORPUS CALLOSUM
2. PERIVENTRICULAR WHITE MATTER
Grading of DAI
3. BASAL GANGLIA • Grade I-Hemisphere DA
4. BRAIN STEM
• Grade II-Additional posterior callosa
• Grade III-Dorsolateral midbrai
MRI
• T2 weighted , FLAIR, T2* gradient echo MRI sequences early and late post-injury
• Markers of DAI
1. number and volume of lesions resulting from contusions and large deep haemorrhages (T1, T2, FLAIR, and T2*
2. Residual haemosiderin of microvascular shearing injuries(T2*
3. Degree of atroph

• Diffusion tensor imaging (DTI)-reveal evidence of loss of neuronal and glial cells (increased diffusivity) and parallel bre tracts
(reduced anisotropy
• Spectroscopy may show a reduction in N-acetyl aspartate, consistent with neuronal los

Post traumatic amnesia

• Confused and disorientate
• Lack the capacity to store and retrieve new informatio
• Duration of PTA, not of retrograde amnesia, is a useful predictor of outcome
• Treated with haloperidol and oral resperidone with benzodiazapin

Level Of Consciousness Children's Coma Scale

Levels of TBI
* Mild TB
TBI= traumatic brain injury
- Glascow Coma Scale score 13-1
* Moderate TB
- Glascow Coma Scale score 9-1
* Severe TB
- Glascow Coma Scale score 8 or les
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Head Injury-Initial Evaluation and Management
1. Prevent Secondary Brain Injury
2. Maintainance of MAP above 90mm of H
• Hypoxemi 3. Airway control with cervical spine immobilizatio
• Hypotensio
• Orotracheal Rapid Sequence Intubatio
• Anemi
• Hyperglycemi
• Evacuation of mas

Non invasive methods for ICP

Audiological tech- displacement of TM and perilymphatic pressure as a correlate of IC
Infrared light- thickness of CSF from re ected light as a correlate of IC
Arterial BP wave contours and blood ow velocity – mathematical mode
Changes In optical nerve head with optical coherent tomograph
IOP as correlate of ICP =With ICP cutoff of 20mmhg it has Speci city of 0.7 and sensitivity of 0.9

Increased ICP-Management
Hypertonic Saline: Mannitol
• Improves CPP and brain tissue O2 level • Osmotic agen
• Decreased ICP by 35% (8-10 mm HG • Effects ICP, CBF, CPP and brain metabolis
• CPP increased by 14 • Free radical scavenge
• MAP remained stabl • Reduces ICP within 30 minutes, last 6-8 hr
• Greatest bene t in those with higher ICP and lower CP • Dosage: 0.25-1 gm/kg bolu
• Repeated doses were not associated with rebound, hypovolemia or HT
• 30 mL of 23.4% over 15 minute

Hyperventilation
• Not recommended as prophylactic interventio
• Never lower than 25 mm H
• Reduces ICP by vasoconstriction, may lead to cerebral ischemi
• Used as a last resort measur
• Maintain PaCO2 at 30-35 mm H
• •Steroids not recommende

Barbiturate Coma
• Not indicated in the E
• Lowers ICP, cerebral metabolic O2 deman
Anticonvulsants
• Reduce occurrence of post-traumatic seizure
• No improvement in long-term outcom
ICP Monitoring
• Should be performed on TBI with GCS <
• Increased ICP may be managed by drainag

Cognitive and neuropsychiatric sequelae

• Personality changes, egocentricity, childishness, irritability, aggressiveness, poor judgement, tactlessness, stubbornness, lethargy,
disinterest, reduced drive and initiative, reduced sexual interes
• Low mood, depression,anxiety disorder

Epilepsy
• More common with penetrating injur
• In Blunt trauma predicted by depressed skull fracture, an intracranial clot requiring surgery, and altered awareness for more than 24
hours associated with contusion
• Concussive convulsions (occurring seconds after the impact
• Immediate epilepsy (occurring up to 12 hours after injury
• Early seizures (12 hours to one week post-injury
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1. Early posttraumatic seizures—> within min to hours of injury

• 1.No radiological intracranial injury noted in many case
• 2.Do not progress later epileps
• 3.Most do not need R
• 4.Outcome good
2. Late seizure à >24 hrs after injur
• Visible intracranial injury
• Penetrating injuries/ depressed #/ SDH/ Lower GCS scor
• Long term risk of epilespy high- nee

• Intravenous phenytoin within 24 hours of high risk injury prevents early seizures, but not late seizures, even in high risk patient
• Antiepileptics continued for atleast 1 yea

Post traumatic headache

Post-traumatic headache, by de nition, starts within 14 days of the injury, or with recovery of awareness
If it continues for more than eight weeks it is said to have become chronic
Can be tension or migraine or combination of tw
Local soft tissue injury contribut

Predictors of outcome
Acute predictors
• admission GC
• present/absent pupillary response
• Attendant hypoxic/ischaemic injur
• imaging ndings, especially depth of lesio
• biochemical marker
• Duration of coma and PTA
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