Head injury 2

Headinjury
BABI
C1
2013 E.C
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Cerebral blood flow
The brain is dependent on continuous CBF for oxygen and glucose delivery, and hence survival.
Normal cerebral blood flow (CBF) is about 55 mL/minute for every 100 g of brain tissue
Ischaemia results when this rate drops below 20 mL/min, and even lower levels will result in
infarction unless promptly corrected.
The flow rate is related to CPP(75–105 mmHg)  is the pressure gradient required to perfuse the
cerebral tissue
MAP(90–110 mmHg)- ICP(5–15 mmHg).
MAP 1/3 (Systolic BP) + 2/3 (Diastolic BP)
The normal brain, variations in vascular tone maintain a constant CBF across a range of MAP
between 50 and 150 mmHg (or higher in the setting of chronic hypertension), and a
corresponding range of CPP, the process of cerebral autoregulation.
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volume of the intracranial contents
Monro-kellie doctrine states that the total volume of the intracranial contents must remain
constant because the cranium is a rigid & non-expansible container.
Total volume=Brain tissue (80%) + CSF fluid (10%) + intravascular blood (10%) +Volume
lesion
Intra cranial volume(1400) = Volume CNS(1100) + Volume CSF(150) + Volume blood(150)
+Volume lesion
Venous blood & CSF fluid may be displaced out of the container to provide pressure buffering
(keeping the total volume constant).
So early after injury patients may have normal intracranial pressure/ ICP, but once the limit of
displacement reached ICP rapidly increases
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Herniation
The rapid increase in ICP which accompanies the exhaustion of compensation mechanisms
ultimately results in herniation of brain tissue.
The uncus of the temporal lobe may herniate over the tentorium resulting in pupil abnormali-
ties, usually occurring first on the side of any expanding haematoma.
Cerebellar tonsillar herniation through the foramen magnum compresses medullary vasomotor and
respiratory centres, classically producing Cushing’s triad
 Cushing’s triad
 Hypertension
 bradycardia
 irregular respiration
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Anatomy of the SCALP
S skin –firmly bound to the 3rd layer by perpendicular fibers.
C connective tissue
fat lobules bound in tough fibrous septa
contain blood vessels of the scalp.
vessels retract when lacerated.
 bleeding is arrested by:-
Pressing with fingers…
Placing a series of artery forceps…
Suturing in two layers…
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SCALP
A aponeurosis  fibrous sheet, found over much of the vertex.
attaches occipitalis m. to frontalis m.
L loose CT- accounts for the mobility of the scalp.
It is in this layer that :-
the surgeon mobilizes the scalp.
machinery w/c has caught the hair avulses the scalp.
native Americans “scalped their victims.
blood tracks freely in this layer  bilateral orbital edema(raccoon aye) following sever head
injury or cranial operation.
P periosteum  adheres to the suture lines of the skull.
collection of blood beneath this layer  out lines the affected bone  cephalohematoma(chidren)
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Anatomy of the meninges
Dura
endosteum + true meningeal layer
Forms falx ,tentorium ,diaphragm
Arachinoid
vascular membrane
Arachinoid granulations
Pia
highly vascular
 Dips into sulci & fissures
Carries cortical vessels
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CLASSIFICATION TBI
1. Based on GCS(clinical severity)
Minimal – GCS 15/15, no loss of conciousness
 Mild – 13-15/15 , loss of consciousness <5minutes
Moderate – 9-12/15, loss of consciousness >5 minutes, CT finding- contussion, laceration,
heamatoma , Focal neurologic deficit such as seizure,weakness, speech difficulty, memory,
cranial deficit
Severe – GCS 5-8/15(3-8)
Critical GCS <5
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 Mild 14-15
 Moderate 9-13
 Severe <8

clinical severity
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Limitations GCS
 Sedation and neuromuscular blockade
 Alcohol intoxication
 Intubation
 Eye and Oral injury
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2. Mechanism of injury
Closed/Blunt head injury :-Acceleration/Decceleration
1. Primary
I. Local
 Scalp injury
 Skull injury-simple Vs cpd
 Brain parenchymal injury e.g.,contusion
II. Diffuse
 DAI
 Concussion
2. Secondary
I. Intracranial
II. extra cranial
Penetrating head injury
High velocity e.g., Gun shot
Low velocity e.g., Stab injury
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3. Based temporal
Primary
Secondary
4. Based on pathophysiology
Diffuse
Local

Marshall scale
shown to predict the risk of ICP and outcome in adults accurately, but lacks reproducibility in
patients with multiple types of brain injury.
Category Definition
Diffuse injury I (no visible
pathology)
No visible intracranial pathology seen on CT scan
Diffuse injury II Cisterns are present with midline shift of 0-5 mm and/or lesions densities
present; no high or mixed density lesion >25 cm3 may include bone
fragments and foreign bodies
Diffuse injury III (swelling) Cisterns compressed or absent with midline shift 0-5 mm; no high or
mixed density lesion >25 cm3
Diffuse injury IV (shift) Midline shift >5 mm; no high or mixed density lesion >25 cm3
Evacuated mass lesion V Any lesion surgically evacuated
Non-evacuated mass lesion VI High or mixed density lesion >25 cm3; not surgically evacuated
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RADIOLOGICAL CLASSIFICATION

Rotterdam scale
Is a more recent CT-based classification developed to overcome the limitations of the Marshall scale
Predictor value Score
Basal cistern
Normal 0
Compressed 1
Absent 2
Midline shift
No shift or shift ≤5 mm 0
Shift >5 mm 1
Epidural mass lesion
Present 0
Absent 1
Intraventricular blood or subarachnoid hemorrhage
Absent 0
Present 1
Sum score Total + 1
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Mortality at six
months increases
with the score: 5
score 1: 0%
score 2: 7%
score 3: 16%
score 4: 26%
score 5: 53%
score 6: 61%

ANATOMIC CLASSIFICATION
1. Scalp-
(Contusion, laceration )
2. Skull-
fractures (linear, depressed, comminuated, diastatical)
3. Meninges
(subdural, epidural, subarachnoid)
4. Brain parenchyma and ventricles
(contusions, intraparenchymal hematoma, concussion, TAI, blunt cerebrovascular injury,
intraventricular hemorrhage)
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Head injury components
1. Scalp laceration
2. Bone fracture
3. Traumatic brain injury
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The term head injury is often substituted for TBI, but it is broader because
it may include injuries to the face and scalp, such as lacerations and
abrasions, which may occur without underlying brain trauma.

Scalp laceration
Significant blood loss may occur because scalp is densely vascularized
Scalp is highly resilient, and only the most severe avulsing injuries lead to permanent damage (eg avulsion
injuries usually result from entanglement of hair in machinery or in vehicular accidents in which the head is
dragged on the pavement)
Classified as
Superficial
Above to glial aponeurosis
Deep
Deep to glial aponeurosis
Major complication is infection, if it infected it directly drain into brain via emissary vein.
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Management
Apply direct pressure to control bleeding
Closely inspect the injury if laceration only
Laceration repair
Short or a single layer
o Percutaneous suture
Long or has multiple arms:
o Debridement and closure in the OR
Debridement & closure
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BONE FRACTURE/SKULL#
Skull vault #
Open Vs closed
Depressed vs non-depressed
Linear Vs comminuted
Basal skull #
Anterior skull base facture
Middle skull base fracture
Posterior skull base fracture
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Linear skull # Depressed skull # Comminuted skull #
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RF
Male
Lower socioeconomic status
alcohol and drug use and
underlying psychiatric and cognitive disorders
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CAUSE
⁂Falls(elderly)
⁂MVA
⁂Sport related injuries/Combat related trauma
⁂Violence/Assaults
⁂Penetrating missiles
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Skull vault fracture
Skull fractures generally indicate that a significant amount of force was transmitted to the head exceed
the mechanical integrity of the calvarium and should increase the suspicion for intracranial injury.
Fractures that cross meningeal arteries can cause rupture of the underlying vessels and subsequent
EDH formation.
 Based on clinical type
Closed fracture is covered by intact skin.
 Subpericranial blood clot infection may result in pott’s puffy tumor(subperiosteal abscess
associated with osteomyelitis)
Open/compound, fracture is associated with disrupted overlying skin
 fracture of the skull associated with tear of the Dura and the arachnoid resulting in CSF leakage
(either to the external environment or through the base of skull, otorrhea, rhinorrhea)
 Result in intracranial infection which could be generalized meningitis or focal infections such as
subdural empyema, brain abcess, osteomyelitis of the skull.
 If intracranial air can be seen on the x-ray, then the dura has been breached too.
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The fracture lines may be
single (linear);
multiple and radiating from a point (stellate); or
multiple, creating fragments of bone (comminuted).
Llinear fracture
 Mostly skull vault fracture is a single fracture that most often extends through the entire
thickness of the calvarium.
 They occur most often in the temporoparietal, frontal, and occipital regions.
 Majority are have minimal or no clinical significance.
But, fractures that cross the middle meningeal groove in the temporal bone or major venous
dural sinuses may disturb these vascular structures causing significant extra axial bleeding.
Separation (ie, diastasis) of skull sutures can occur following trauma and most often involves
the coronal or lambdoid sutures.
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LINEAR #
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MGT
No specific intervention is necessary if CT scan reveals no underlying brain injury.
Patients are admitted for observation if there is any suspicion or clinical evidence of brain injury
If there is evidence of ICH on non-contrast CT  observed in facilities with neurosurgery.
goal  detect any worsening of neurologic function within 24 hours of injury as a delayed
complication of ICH.
If there is no evidence on CT of ICH  observed in the emergency department (ED) for four
to six hours prior to discharge to detect delayed complications of trauma
If the patient is neurologically intact and there are no significant extracranial injuries
discharged, provided there is adequate supervision at home for the subsequent 24 hours.
Clear discharge instructions must be provided, including
oinstructions to return to the ED immediately should symptoms suggestive of intracranial
injury (eg, headache, vomiting, lethargy) develop.
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Depressed skull fractures
may result from a focal injury of significant force drives a segment of the skull below the level of
the adjacent skull.
Increased risk of infection, neurologic deficit, late onset epilepsy
The inner and outer cortices of the skull are disrupted,
fragment of bone is
pressed in toward the brain in relation to adjacent intact skull.
overlap the edge of intact bone, or
may plunge completely below the level of adjacent normal skull.
The inner cortex of the bone fragments often has multiple sharp edges that can lacerate dura,
brain, and vessels  creating a portal of entry into the CSF, thereby increasing the risk of CNS
infection.
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Either
Closed (simple)
exist when no scalp laceration is present over or adjacent to the fracture
open (compound)
exist when a scalp laceration lies over or adjacent to the fracture site.
The majority of depressed skull fractures are open
clinicians should assume that any depressed skull fracture is open until it is proven otherwise
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MGT OF DEPRESSED #
Tetanus prophylaxis
Abc ???
Anticonvulsants
Craniotomy
depressed more than 1 cm are managed with early surgery to reduce the risk of infection
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Indications for craniotomy
Depression greater than the cranial thickness(thickness of adjacent bone),
Intracranial hematoma/pneumocephalus, and
Frontal sinus involvement.
Evidence of dural penetration/parenchymal injury
It is required to
Elevate the bigger fracture & remove small fracture,
Indication
oNeurologic deficit
oLoss of consciousness
oSeizure
oCosmetic areas
Repair dural disruption, and
Obtain hemostasis
Fractures overlying dural venous sinuses require restraint.
Surgical exploration can lead to life threatening hemorrhage
from the lacerated sinus.
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 Wound infection
 Gross cosmetic deformity

Fractures of the skull base
Are common in head-injured patients, and they indicate significant impact
Copious clear drainage from the nose or ear makes the diagnosis of CSF leakage within hours or
up to several days after trauma (because of communication created between the subarachnoid
space, the paranasal sinuses, and the middle ear.) Obvious, but the drainage may be discolored
with blood or small in volume if some drains into the throat.
The halo("ring" or "target" sign) test can help differentiate.
Allow a drop of the fluid to fall on an absorbent surface such as a facial tissue.
If blood is mixed with CSF, the drop will form a double ring, with a darker center spot
containing blood components surrounded by a light halo of CSF.
does NOT differentiate among CSF, saline, saliva, and other clear fluids and has not been
formally studied in a clinical setting
If this test is indeterminate, the fluid can be sent for beta-trace proteins & beta-2 transferrin
testing  Arbohydrate-free isoform of transferrin exclusively found in the CSF
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Fracture of the temporal bone
ocan damage the facial or vestibulocochlear nerve,
resulting in vertigo, ipsilateral deafness, or facial paralysis.
oA communication may be formed between the subarachnoid space and the middle ear,
allowing CSF drainage into the pharynx via the eustachian tube or from the ear (otorrhea)
oExtravasation of blood results in ecchymosis behind the ear, known as Battle’s sign.
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HALO SIGN
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CN PALSY
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 Facial nerve palsies that
appear acutely in
association with basilar
skull fractures are due to
nerve transections.
 These injuries do NOT
respond to glucocorticoid
therapy and carry a poor
prognosis for recovery of
nerve function

Battle’s sign otorrhea
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Hemotympanum
blood behind the tympanic membrane.
It is a common finding in basilar skull fractures that
involve the petrous ridge of the temporal bone and
generally appears within hours of injury.
detected by otoscopy,
 reveals the blue to purple hue taken on by the tympanic
membrane
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Fracture of the anterior skull base
 can result in
anosmia (loss of smell from damage to the olfactory nerve),
CSF drainage from the nose (rhinorrhea), or
periorbital ecchymoses, known as raccoon eyes
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raccoon eyes
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Physical signs of skull fractures
 Anterior cranial fossa
Nasal bleeding
Orbital haematoma（Racoon eyes)
Cerebrospinal fluid rhinorrhea
Cranial nerve injuries, nerves I – VI
 Posterior cranial fossa
Bruising over the suboccipital region, which develops after a day or two (Battle’s sign)
Cranial nerve injuries – nerves IX, X and XI (rare)
Middle cranial fossa
Orbital haematoma
Bleeding from the ear
Cerebrospinal fluid otorrhoea (rare)
Cranial nerve injuries, nerves VII and VIII
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Basal skull fracture management
If asymptomatic, they require no treatment.
Skull base fractures requiring intervention include those with an associated cranial nerve deficit
or CSF leak.
The majority of CSF leaks resolve spontaneously within one week of injury and without CNS
complications
NG tube insertion is contraindicated in skull base fracture
CSF leak
 Elevation of head off the bed for several days may heal it. In addition lumbar drain can
augment this method.
 Lumbar drain allows the defect to heal by eliminating normal hydrostatic pressure.
Traumatic cranial neuropathy
Facial nerve palsy
Give steroids. If no response after 48-72hours surgical decompression of the
petrous portion of CN-VII may be considered
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Penetrating skull fracture
Occur as a result of gunshot wounds, stab wounds, and blast injuries.
They generally involve significant brain injury and intracranial hemorrhage
Tangential skull fractures warrant special mention.
Caused by an impact that occurs at an oblique angle to the skull.
High association with intracranial injuries.
E,g.  tangential gunshot wounds (GSW)
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TBI
is defined as “brain damage resulting from external forces, as a consequence of direct impact,
rapid acceleration or deceleration, a penetrating object or blast waves from an explosion.”
TBI often referred as ‘silent epidemic’. Silent insofar as society don’t take it as a health problem
until it happens and also unaware of chronicity of it’s sequelae.
TBI is ‘heterogeneous’ disease as its demographic factors, manifestations varies widely
An understanding of the sequelae after Traumatic brain injury is paramount for its management
TBI is a heterogeneous condition with spectrum of pathologies, Prevention is always better than
any intervention.
Individual pathologies has to be managed with good clinical judgment as time factor is of
paramount importance in TBI.
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Traumatic brain injury
Leading cause of death in North America for individuals between the ages of 1 and 45.
Many survivors live with significant disabilities, resulting in major socioeconomic burden as well
Rates of TBI are highest in the very young (age group zero to four years), adolescents and young
adults (15 to 24 years) & (age >65 years)
 Approximately 78 percent of TBI are treated in the emergency department only(very young ); 19
percent of patients require hospitalization(elderly ), and 3 percent are fatal
The incidence is significantly higher in men, M:F=2-2.8:1 & 3.5:1 in severe TBI.
Moderate and severe TBIs are associated with neurologic and functional impairments.
Extracranial injuries are present in about 35 percent of cases.
Multiple systemic traumatic injuries can further exacerbate brain injury because of associated
blood loss, hypoxia, and other related complications.
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PATHOPHYSIOLOGY
The pathophysiology of TBI-related brain injury is divided into two separate but related
categories:
primary brain injury and
secondary brain injury.
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PRIMARY BRAIN INJURY
Occurs at the time of trauma includes injuries such as brainstem and hemispheric contusions,
shearing of white matter tracts (diffuse axonal injury) & cortical lacerations
Primary insult results in tissue deformation that causes damage to neurons, glia, axons, and blood
vessels that manifests as primary injury
MZM – heterogeneous
direct impact
rapid acceleration/deceleration
penetrating injury and
blast waves
Result from external mechanical forces transferred to intracranial contents.
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SECONDARY BRAIN INJURY
Cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hrs or days
Primary injury followed by a more delayed phase of injury, which is mediated by intracellular and extracellular
biologic pathways and can be present for minutes, hours, days, and even weeks after the primary insult called as
secondary injury..
These mechanisms include
Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell membranes
Electrolyte imbalances(calcium overload)
Mitochondrial dysfunction
Inflammatory responses
Apoptosis
Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury
These lead in turn to neuronal cell death as well as to cerebral edema and increased intracranial pressure that can
further exacerbate the brain injury. This injury cascade shares many features of the ischemic cascade in acute stroke.
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During time lapse between primary and secondary injury many patients experience
superimposed secondary insults.
Five secondary insults consistently correlated with poor outcome: arterial hypotension, reduced
cerebral perfusion pressure (CPP), elevated ICP, hypoxemia, and pyrexia.
Preventing/treating secondary insult and hence secondary injury remains a focus of TBI
Management
Example of secondary injury
Synaptic dysfunction
axonal degeneration
neuronal death
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CAUSE(SECONDARY INSULT)
Extra cranial
hypoxia
Hypotension
Fever
Seizure
Hyperglycemia
Hyperthermia
Intracranial
Hematoma
Brain swelling(edema/hydrocephalus)
Infection
intracranial hypertension(decrease MPP), inceased ICP
thrombosis
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hypoxia(decrease substrate delivery of oxygen and glucose to injured brain
(increase metabolic demand)
exacerbate ongoing injury mechanisms

CLOSED HEAD INJURY(CHI)
1. concussion,
2. contusion, and
3. diffuse axonal injury
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Concussion
Temporary neuronal dysfunction following non penetrating head trauma(transient alteration of
consciousness following a non- penetrating blow to the head)
Mildest form of diffuse injury, commonly occurs in athletes
The head CT is normal, and deficits resolve over minutes to hours.
transient LOC <1min, amnesia(anterograde) of the event, Confusion, Headache, Dizziness,
N&V, Vacant state, Delayed verbal Expression, Inability to concentrating, Disorientation
second-impact syndrome
Occurs when the brain swells rapidly, and catastrophically, after a person suffers a second
concussion before symptoms from an earlier one have subsided because brain is much more
susceptible to injury from even minor head trauma in the first 1 to 2 weeks after concussion.
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Mechanism: transient torsion with malfunction of the reticular activating system.

Concussions grading according to Colorado grading system
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IMMEDIATE POST TRAUMATIC ANTEROGRADE AMNESIA
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Imaging:
no structural abnormalities or minimal swelling.
CT is done to r/o other serious injuries.
PET scan s/o global reduction in cerebral glucose metabolism
Management:
Reassurance, for persistent headache acetaminophen preferred over NSAIDs. Amitryptaline can
be useful for headache and anxiety
Complication: there is substantial concern that repetitive minor head trauma may initiate a
chronic neurodegenerative process called chronic traumatic encephalopathy (CTE).
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Contusion
Bruise of the brain - an area of hemorrhagic necrosis usually occurring on the crests of gyri.
Due to breakdown of small vessels and extravasation of blood into the brain. in 22 – 30 % of TBI.
Contusion also occurs as the brain slides forwards and backwards over the ridged cranial fossa floor
The contused areas appear bright on CT scan
The frontal, occipital, and temporal poles are common sites.
Edema may develop around a contusion, causing mass effect, but contusion itself rarely cause
significant mass effect. May enlarge or progress to frank hematoma, particularly during the first 24 hrs.
Coup injury
Occurs under the site of impact with an object
Countercoup injury
occur in brain tissue opposite the site of impact
Result from deceleration of the brain against the skull.
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Location: MC in sub frontal and
anterior temporal area due to
irregular contour of ACF and
MCF bones

Head immobile when stuck = coup injury, and mobile when stuck =
contrecoup injury
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.

Natural history of contusion
 Gradual resorption of damaged tissue and reactive gliosis >>>>> sunken brown cystic spaces
aka plaques jaunes.
Small contusion 2-3 weeks, larger require more time.
Blossoming of contusion: cascade : recurrent haemorrhage>>> Vasogenic edema >>>>
inflammation >>>> ischemic necrosis
IMAGING:
 MRI T1W most sensitive (98%) (methHb), CT (56%). CT used more often as small
contusion are generally clinically not significant 13
 Acute appearing as mottled areas of intermixed high and low CT density lesions within a
superficial portion of the brain.
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Diffuse Axonal Injury
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(spheroids) - swollen
proximal ends of severed axons
Visualized pathologically and on neuroimaging studies(MRI is more sensitive) as multiple small
lesions seen within white matter tracts.
In more severe cases Small hemorrhages seen in the corpus callosum and the dorsolateral
midbrain on MRI.
Typically involves the gray-white junction in the hemispheres - On CT scan: loss of grey-white
interface, slit ventricles
Patients with severe DAI typically present with profound coma without elevated ICP, and often
have poor outcome.
High (50%) mortality rate
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When the axonal injury occurs in the context of trauma, the process is designated as TAI(traumatic
axonal injury) rather than diffuse axonal injury, because the process may be focal, multifocal, or diffuse.
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.
Axon can be severely impaired in the absence of gross lacerations or hematomas.

Symptoms: Generally comatose or variable degree of unconsciousness from the
instant of injury, and subsequently have only limited recovery.
Grading:
Grade of
TAI
Description
Grade I Diffuse axonal damage in corpus callosum, white matter of
cerebral hemisphere, brain stem and cerebellum
Grade
II
Grade I plus Focal lesion (punctate hemorrhage) in corpus callosum
Grade III Grade II plus focal lesion in brain stem
Grade 2 and 3 can be seen on imaging.
The principal mechanical loading: rotational acceleration
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MGT
No definitive management
ICP management if edema present
Supportive and general nursing care
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Intracranial haematoma
Hematomas can expand rapidly and cause brain shift and subsequent
herniation
Haemorrhage within the cranium occurs in four main sites:
A. Extradural
B. Subdural
C. Subarachnoid
D. Intraparenchyma
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Extra-axial (outside the substance of the
brain) hematomas

A. Extradural Haematoma
Accumulations of blood in “potential space” between the inner table of the skull and the outer
surface of the dura mater (periosteal layer)
results from dural arterial disruption, especially of the middle meningeal artery.
Not to be associated with underlying brain damage.
EDH is common at temporal bone due to the pterion(the groove of the middle meningeal artery),
the thinnest part of the skull, that overlies the largest meningeal artery(Temporoparietal > anterior
cranial fossa > posterior fossa > parasagittal regions).
lucid in the early phases, timely surgical evacuation.
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Has classical three stage clinical presentation (seen only 20%).
1. LOC from the concussive aspect of the head trauma.
2. patient then awakens and has a “lucid interval,” while the hematoma subclinically
expands.
3. Deterioration - As a result of brain compression & herniation
 Reduced consciousness level and
 Contralateral hemiparesis
 Ipsilateral pupillary dilatation due to CN III
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 due to uncal herniation

EDH
On head CT
blood clot is bright/hyperdense
biconvex in shape(Lenticular-shaped /lentiform)
has a well-defined border that usually respects cranial suture lines(Doesn’t cross the cranial
sutures, but cross dural fold).
Evident skull fracture
Compression of the brain and midline shift which indicates mass effect
Presence of low-density areas within an EDH, or evidence of contrast extravasations into the
hematoma on a post contrast head CT are indications of hyper acute or active bleeding into the
hematoma, and may portend rapid expansion of the hematoma and could be associated with
worse prognosis
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Age less common in infants, very young children and elderly
mean age of patients with EDH is between 20 and 30 years of age
Symptoms: hemiparesis (C/L or I/L), decreased level of consciousness, and dilation of the I/L
pupil.
 Lucid interval- named by Jacobson in 1886: initial LOC >>> transient complete recovery >>>>
rapid progression of neurological deterioration present in 14%-21%9
concurrent brain injuries such as acute subdural hematoma, contusions, and lacerations in
approximately 30% of cases of EDH, unconscious from the time of injury.
Excellent prognosis if treated timely whereas intradural lesions Experience good outcomes only
in 44%10
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Venous EDH
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 10-40% of all EDH
 Occurs in children
 frequently occurs at anterior temporal pole (sphenoparietal sinus)
 Usually benign due to low pressure bleed

EDH is neurosugical emergency.= >30 mL volume, regardless of GCS score
Require open cranioctomy for evacuation of the congealed clot and hemostasis.
Prognosis after successful evacuation is better for EDH than SDH
Conservative management for patients with:
Clot volume <30 cm3
Maximum thickness <1.5 cm
GCS score >8 without focal neurological deficit
<5 mm midline shift
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EDH generally does not cross suture lines, can cross dural
fold
Swirl sign
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Subdural hemorrhage
SDH is the accumulation of blood between the arachnoid membrane and the dura.
Bilateral in 15% of cases
Associated with underlying cerebral injury, so has poor prognosis than EDH
It can be classified as; Seen on imaging as crescent-shaped extra-axial collection
overlying a cerebral convexity, b/c is limited by dural attachments
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ACUTE SDH
Results from venous bleeding, typically from tearing of a bridging vein running from the
cerebral cortex to the dural sinuses.
Consists of a thick, congealed clot
Most SDHs occur over the cerebral hemispheres, but they may also occur between the
hemispheres or layer over the tentorium
Elderly and alcoholic patients are at higher risk for acute SDH formation after head trauma due
to brain atrophy & those with previous traumatic brain injury.
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The bridging veins are subject to stretching and tearing during
acceleration/deceleration of the head, because the brain shifts
in relation to the dura, which firmly adheres to the skull

On head CT scan
Clot is bright or mixed-density
Crescent-shaped (lunate),
Doesnot cross the midline due to the presence of the falx
May have less distnict border
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ASDH
The mortality rate of traumatic ASDH varies from 30% to 90%,
Mechanism of Acute SDH
Contact load- ASDH with coexisting contusions and lacerations, with intracerebral hemorrhage,
burst lobe with the temporal or frontal lobes are most frequently involved. Usually unconscious
from the time of injury.
Inertial load - ASDH can sometimes result from rupture of bridging veins or superficial cortical
arteries. there may be little or no concomitant contusion or laceration. may experience a lucid
interval. MC mechanism in RTA
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BRIDGING VEIN
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.

MGT
Nonoperatively managed hematomas may stabilize and eventually reabsorb, or evolve into
chronic SDHs.
Antiedema measures and serial imaging
<10 mm thick and <5 mm midline shift,
 GCS >=9,
normal pupil,
ICP < 20 mmHg
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mgt
Inducation for open craniotomy for evacuation
Thickness >1 cm or
Midline shift >5 mm
OR
<10 mm thick and <5 mm midline shift, and
GCS score <9 with ≥2 point decrease(GCS drop by two or more points from the time of injury
to hospitalization), and/or
pupillary dysfunction, and/or
ICP >20 mm Hg
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Chronic Subdural Hematoma
 Is a collection of blood breakdown products that is at least 2 to 3 weeks old.
 Consists of a viscous fluid with the texture and dark brown color reminiscent of motor oil.
 Separation of dura at points of contact with bridging veins that normally connect venous sinuses
and the cortical surface.
 These veins traverse a longer, more tightly tethered course as the brain undergoes atrophy with
aging or substance abuse (high-risk Populations)
 Could occur with minor trauma; Therefore, patients may not have clear history of trauma in 50%
Cerebral atrophy Esp. in the elderly stretch bridging veins, then rupture after only minor trauma
bleed, and then tamponade (stop bleeding due to the pressure which has been produced by the bleed)
dural collagen synthesis is induced and fibroblasts spread over the inner surface of the dura to form
a thick outer membrane & thinner inner membrane, resulting in complete encapsulation of the clot 
degradation of the blood clot over days or weeks leads to osmotic expansion  producing pressure
symptoms ,especially headache and drowsiness, neurological deficit and seizures. .
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Patients may present with headache, seizure, confusion, light-headedness, cognitive impairment,
apathy, somnolence, contralateral hemiparesis, or coma.
Risk factors:
Older age
Excessive alcohol Intake (alcoholics)
Anticoagulation therapy
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Inner and outer membranes encase a core of degenerating blood that is gradually encroached
upon by the expanding membranes. Because these membranes possess numerous delicate blood
vessels, recurrent hemorrhage occurs often leading to gradual expansion of the lesion (CSDH is a
dynamic living structure).
Surgical drainage of the hematoma and removal of the membranes is necessary for definitive
treatment.
on CT
Hypodense
A true chronic SDH will be nearly as dark as CSF.
Traces of white are often seen due acute-on-chronic SDH
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acute-on-chronic SDH
Small, recurrent hemorrhages into the collection (chronic SDH) lead to expansion of the
collection enough to be symptomatic.
Source of acute hemorrhage may be the vascularized membranes formed in the matured
hematoma.
 Chronic SDH >1cm or any symptomatic SDH needs to be surgically drained via burr hole
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CSDH
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acute-on-chronic SDH Hypodense

Feature EDH SDH
Crossing suture line No Yes
Crossing dural fold Yes No
Association with fracture More than 90% Less consistent
Biomechanical load Only contact load Contact or inertial
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SAH
Hemorrhage in the subarachnoid space between the arachnoid and pia mater, later is
adherent to brain.
Occur with disruption of small pial vessels and commonly occurs in the sylvian fissures
and interpeduncular cisterns.
33-60% of all severe TBI
IVH or superficial ICH may also extend into the subarachnoid space.
Imaging: appear as hyperdense outline of cortical gyri CT/MRI t2 flair (most
sensitive)
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Complications
Communitcating HCP (arachnoid granulation block)
non communicating HCP (aqueduct block by large IVH or chronic ependymal proliferation i.E.
Ependimitis)
Post traumatic vasospasm
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IVH
IVH has been reported in 1% to 5% of closed head injury patients.
Sources of bleed:
 Primary IVH (no parenchymal bleed)
 tearing of tiny subependymal vessels
 choroid plexus on sagital impact causing negative pressure due to ventricular
dilation and hence traction on vessels
 Secondary IVH
 IV extension of hemorrhage from an intraparenchymal hematoma, or from
 retrograde reflux of SAH via the foramina of Luschka and Magendie.
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Traumatic SAH Traumatic IVH Aneurysmal SAH
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MGT of SAH & IVH
Usually they resolve on their own over weeks to months
Analgesic and other supportive measures
EVD placement if patient develops hydrocephalus
Mannitol usually has no role until massive edema and herniation signs present
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INTRAPARENCHYMAL HEMORRHAGE
Isolated hematomas within the brain parenchyma are most often associated with hypertensive
hemorrhage or AVMs.
Bleeding may occur in a contused area of brain, so Patients with contusion on the initial head CT
scan should be reimaged after 24 hours.
Mass effect from developing hematomas may present as a delayed neurologic deficit e.g.
hemiparesis.
Delayed traumatic intracerebral hemorrhage is most likely to occur within the first 24 hours.
Indication for craniotomy
Any clot volume >50cm 3
Clot volume >20cm 3 with neurologic deterioration (GCS 6–8) & associated midline shift >5
mm or basal cistern compression
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Collection of confluent, relatively homogeneous blood within the brain parenchyma exceeding 5
mm in size.
Unlike contusion
Less surrounding edema than with contusions.
Intracerebral hemorrhages are also located deeper in the brain than contusions are.
Hematoma border well defined than contusion, can evolve with time.
20-30% of all traumatic hematoma
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One-third of patients with severe TBI develop a coagulopathy, which is associated with an
increased risk of hemorrhage enlargement, poor neurologic outcomes and death.
result from
existing patient medications such as warfarin or antiplatelet agents,
through the systemic release of tissue factor and brain phospholipids into the circulation
leading to inappropriate intravascular coagulation and a consumptive coagulopathy.
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Initial Assessment
ABCDEs
Hypoxia and hypotension are known to worsen outcome in TBI (due to secondary injury),
making cardiopulmonary stabilization critical.
Patients who cannot follow commands require intubation for airway protection and ventilator
control
Motor activity, speech, and eye opening can be assessed in a few seconds and a GCS score
assigned
External signs of head injury, including bleeding from the scalp, nose, or ear, or deformation of
the skull or face.
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Medical Management
To minimize secondary injury and the systemic consequences of head injury.
Phenytoin prophylaxis
In patient with documented CHI and evidence of intracranial hemorrhage or a depressed skull
fracture.
decrease the incidence of early posttraumatic seizures.
Monitor BG
Antipyretics
Ulcer prophylaxis
Compression stockings or athrombic pumps- used when the patient cannot be mobilized rapidly for
prophylaxis of DVT
Head-injured patients have an increased prevalence of peptic ulceration and GI bleeding.
Peptic ulcers occurring in patients with head injury or high ICP are called Cushing’s ulcers
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TBI patients who are asymptomatic, who have only headache, dizziness, or scalp lacerations,
and who did not lose consciousness, have a low risk for intracranial injury and may be discharged
home without a head CT scan. Printed discharge instructions, which describe monitoring for
confusion, persistent nausea, weakness, or speech difficulty, should be provided to the caretaker
Patients with a history of altered consciousness, amnesia, progressive headache, skull or facial
fracture, vomiting, or seizure have a moderate risk for intracranial injury and should undergo a
prompt head CT. If the CT is normal, and the neurologic examination has returned to baseline
(excluding amnesia f the event), then the patient can be discharged to the care of a responsible
adult, again with printed criteria for returning to the emergency room. Otherwise the patient must
be admitted for a 24-hour observation period.
Patients with depressed consciousness, focal neurologic deficits, penetrating injury, depressed
skull fracture, or changing neurologic examination have a high risk for intracranial injury. These
patients should undergo immediate head CT and admission for observation or intervention as
needed.
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Neuroimaging scales
Skull fracture
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intraparenchymal hemorrhage
Cerebral contusion
Intraventricular hemorrhage
Focal and diffuse patterns of axonal injury with cerebral edema
Two currently used CT-based grading scales are the Marshall scale and the
Rotterdam scale:
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