Head Injury

Dr Prashant S Patil
Asso. Prof. & HOD
Dept. Of Gen Surgery
 Head Injury – General considerations
Cerebral blood flow ( CBF)

• Perfusion of brain with oxygenated blood is critical - O2 & glucose supply

• Normal CBF – 55ml/min/100gm of tissue
if < 20ml ischemia
If still < Death
• CBF depend on CPP ( cerebral perfusion pressure )
• CPP ( 75-105 mmHg) = MAP ( 90-110mmHg) – ICP ( 5-15 mmHg)
• Changes in TBI –
• Head injury  brain swelling, bleed & hydrocephalus  ↑ ICP -- ↓CPP & CBF  brain injury other than trauma
 Vasospasm  rupture aneurysm

• ICP & Monro-Kellie Doctrine – “ Cranium is rigid box containing nearly incompressible Brain”
Content expansion initial exclusion of fluid component ( CSF & Venous Blood)  ↓ perfusion & herniation
 Head Injury – General considerations
Herniation Syndrome

Herniation of Uncus Pupillary abnormality

of Temporal lobe over ( side of
tentorium ↑Haematoma )
↑ICT  compensatory
mechanism failure
Cerebellar tonsillar Compression of
herniation ( thro’ vasomotor Centre &
Foramen Magnum) respiratory Centre

Cushing’s triad -- ↑BP

-- ↓Pulse
-- irregular respiration
 Head Injury
Incidence –
• 3-4% of all trauma cases
• 1500/1,00,000/ yr. – 300/1,00,000 patients need hospitalisation.
• 2% of US population ( TBI patients) - long term disability
Risk factors
• Male sex
• Recreational drugs
• Youth ( 15-30 yrs. of age)
Mechanism of Injury
• RTA
• Fall
• Assault
 Head Injury- initial evaluation & management
Resuscitation in TBI is according to ATLS guidelines which involve airway & spine control

History-
Information-
• pre injury status of the patient – H/o fits, alcohol consumption, chest pain, MI
• Energy involved in the injury – speed of vehicle, height
• Post incidence consciousness status ( GCS scale)
• Hemodynamic stability
• Length & time taken for extriction
Length of Amnesia – retrograde and antegrade amnesia ( to grade severity)
Medical History – h/o drugs like anticoagulant
 Head Injury- Examination
Primary survey-
• Ensure adequate O2 & Circulation – control scalp bleed as it can be substantial
Head injury severity: clinical classification.
• Check pupil size & response to light – in mm/ ↓/-ve ( Uncal herniation can Eyes open
compress the third nerve, compromising the parasympathetic supply to the pupil,
Spontaneously 4
so that unopposed sympathetic activity produces an enlarged and sluggish pupil,
which then, if the compression continues, becomes fixed and dilated. ) To verbal command 3
To painful stimulus 2
• Check consciousness level ( GCS) [ the sum of scores on three components such as Do not open 1
eye opening, verbal and motor components ] Verbal
• Check focal deficit ( paraplegia) Normal oriented conversation 5
• Check BS levels to r/o hypoglycaemia ( as it can be dangerous) Confused 4
Inappropriate/words only 3
Sounds only 2
No sounds 1
Intubated patient T
Motor
Obeys commands 6
Localises to pain 5
Withdrawal/flexion 4
Abnormal flexion 3
Extension 2
No motor response 1
 Head Injury- Examination
Secondary Survey
Examination of Head-
• Subgaleal haematoma
• Scalp Lacerations
• Fractures – Skull Base # -- Battle Sign
-- Racoon/ Panda Eye
-- Heamotympanum/ ear bleed
-- CSF Rhinorrhoea
-- Face # -- Orbit
-- Zygoma
-- Mandible

• Check for Cr Nerve injury – 7th & 8th nerve damage  skull base #
-- Gaze paresis mid brain /
-- Dysconjugate gaze brain stem
-- Roving Eye movements dysfunction
• Ophthalmic examination --
• -- check eye movements & orbit
-- hyphaema
-- papillodema
-- retinal detachment
 Head Injury- Examination
Examination of neck & spine

• Spine  Cervical spine – injury in mod/severe TBI ( 10% cases)

LS spine/ TH spine – RTA / Fall
• Peripheral Neurological Exam– ( to r/o injury )
-- Touch/pain/reflex/sensation
• Log Roll – palpate thoracic / Lumber deformity ( test sensation on back)
• PR examination – anal tone
-- sensation in awake patient
-- anal wink ( pinprick sensation  sphincter contraction )
• Check for priapism ( in intubated patient )  cord injury
 Head Injury- Classification
Classification is based on the severity & type of injury
• Based on GCS- Mild
-- Moderate ( confusion & amnesia )
-- Severe ( coma)
• Scalp injuries – open ( lacerations / degloving injuries)
-- Closed ( beware about air under dura  dural breach
• Skull site – Vault
-- base ( ENT bleed +ve & / CSF rhinorrhoea )
• Brain tissue injury – Diffuse
-- Blunt ( direct , Coup – Countercoup )
-- penetrating ( Low / High velocity )
• Skull Type ( # ) – Linear
• -- Comminuted & depressed
• Intracranial Bleeding -- EDH
-- SDH all causes ↑ICT  ↓ perfusion ( hence maintenance of O2 & BP is imp )
-- Subarachnoid
-- Intra parenchymal
 Head Injury – Management
• MANAGEMENT OF MINOR AND MILD HEAD INJURY-
• Patients without any on going deficit & meeting the NICE criterion can be discharged but those with h/o loss of consciousness are
observed to avoid discharge during Lucid Interval.
• Discharge criteria in minor and mild head injury.
• GCS 15/15 with no focal deficits
• Normal CT brain if indicated (see below)
• Patient not under the influence of alcohol or drugs
• Patient accompanied by a responsible adult
• Verbal and written head injury advice: seek medical attention if:
-- Persistent/worsening headache despite analgesia
-- Persistent vomiting
-- Drowsiness
-- Visual disturbance
-- Limb weakness or numbness
Patients who do not meet this criteria need to be hospitalised & CT scan.
National Institute for Health and Clinical Excellence (NICE)
guidelines for computed tomography (CT) in head injury.
• GCS <13 at any point
• GCS 13 or 14 at 2 hours
• Focal neurological deficit
• Suspected open, depressed or basal skull fracture
• More than one episode of vomiting
• Any patient with a mild head injury over the age of 65 years or
• with a coagulopathy, for instance warfarin use, should be
scanned urgently
• Dangerous mechanism or injury or
antegrade amnesia >30 minutes warrants CT within 8 hours
 Head Injury – Management
• Skull fractures –
A) Closed linear fractures-- conservative management with primary closure of associated wounds if possible.
B) Skull Base fractures –
• may be complicated by CSF leak, pituitary dysfunction, arterial dissection or cranial nerve deficits, with anosmia, facial palsy or
hearing loss typical.
• Pneumococcal vaccination is valuable but prophylactic antibiotics are not required
• craniotomy or repair is not required
C) Fractures which involve the air sinuses -
• may be managed as open fractures, using broad spectrum antibiotics with or without exploration.
D) Depressed skull fractures -- involve inward displacement of a bone fragment by at
least the thickness of the skull.
• Occur when small objects hit the skull at high velocity.
• Usually compound (open) fractures, & are associated with a
high incidence of infection, neurological deficit and late-onset epilepsy.
• Significant depressed fractures need elevating, antibiotics and antiepileptic
 Head Injury – Management
• Extradural Haemorrhage
• Can occur in the context of apparently minor trauma –
-- Results from rupture of an artery, vein or venous sinus, in association with a skull fracture.
-- Typically, it is damage to the middle meningeal artery under the thin temporal bone.
-- The patient may then present in the subsequent lucid interval with headache, but without any neurological deficit.
• Isolated extradural haematoma may manifest as sudden deterioration following a lucid interval ( decompensation after some hrs.)
-- There is contralateral hemiparesis,
-- Reduced conscious level and
-- Ipsilateral pupillary dilatation ( the cardinal signs of brain compression and herniation. )
• Although this classical presentation occurs in only one third of cases, it emphasises the potential for rapid avoidable secondary brain injury
in patients with minimal primary injury.
• Lentiform lesion ( lens Shaped or Biconvex) on computed tomography-
• -- Mass effect may be evident, with compression of surrounding brain and midline
shift.
-- Areas of mixed density suggest active bleeding.
-- A skull fracture will usually be evident
• Treatment- immediate transfer to a neurosurgical unit / most accessible neurosurgical
facility, for
• immediate evacuation =>deteriorating or comatose patients
=> those with large bleeds,
for close observation with serial imaging in all cases.
 Head Injury – Subdural Haematoma

• Types – Acute subdural & chronic subdural

a) Acute Subdural haemorrhage ( rupture of cortical vessels)
• Relatively severe trauma-- associated with a high energy injury mechanism &
significant primary brain injury.
• No lucid interval as level of consciousness impaired at presentation
• Diffuse concave lesion on CT( as dura not adherent to brain)
• Require immediate transfer to a neurosurgical unit for decision on evacuation
 for pts with significant size &/ with significant midline shift
-- conservative Rx with ICP monitoring for small bleed & neurological stability
• 50 % mortality

Right-sided acute subdural haematoma (hyperdense)

The substantial midline shift reflects brain swelling as
well as bleeding: this is a high energy injury.
 Head Injury – Subdural Haematoma
b) Chronic Subdural haemorrhage -
• Occurs in the elderly, especially those on anticoagulants
minor trauma bleeding from vessel ,stretched due to atrophy tamponade clot degradation osmotic expansion  mass effect

• May take days or weeks to develop-

Presenting features like any expanding intracranial mass, include
-- pressure symptoms,
-- headache
-- drowsiness,
-- neurological deficit & /
-- seizures.
Electrolyte disturbance & infections to be r/o
• Investigation- Diffuse hypodense lesion on CT scan ( recent bleed is isodense/ hyperdense)
• Treatment-
• Evacuation may be delayed ( 7-10 d)until clotting has been improved
(in clinically stable pts)-Drainage is performed using burr holes, often under LA
Bilateral subdural haematomas:
• Emergency evacuation  rapid deterioration ( infusion of Vit K &/ transfusion of the left is mixed density, the hypodense material representing old
recombinant clotting factors needed prior to SRx) blood and the higher density indicating more recent bleeding,
probably loculated so requiring a craniotomy to evacuate.
• Craniotomy for adequate clot evacuation  Ac on Cr bleed with clot/ septae The bleed on the right is isodense, indicating intermediate age.
 Head Injury – types of brain injury
a) Sub Arachnoid Haemorrhage 
• Trauma is common cause & managed conservatively.
• No significant vasospasm ( like aneurysmal SAH )
• Apparent traumatic SAH may actually be a spontaneous SAH which then led to the fall ( CT angio will exclude it )
b) Diffuse axonal injury --
• results from high energy injury
• Patient is usually comatose
• haemorrhagic foci in the corpus callosum and dorsolateral rostral brainstem on CT may be suggestive, although the CT often appears normal.
c) Carotid dissection
• may occur after trivial trauma like coughing or nose bowing
• may be a delayed complication of skull base fracture
• Presentation
-- headache,
-- neck pain &
-- focal ischemic deficits ( due to occlusion by mural haematoma, thrombus and thromboembolism. )
• Intracranial dissection often affects the vertebral artery  SAH
• Treatment -- should prompt with urgent investigation ( Development of a delayed deficit, especially in the context of a skull base fracture
involving the carotid canal )
• Carotid dissection is generally managed with anticoagulation,
• But vertebral dissection with SAH usually requires surgical or endovascular intervention.
 Head Injury – types of brain injury
d) Non-accidental injury in children: beware delayed presentation
• Head injury in children and vulnerable adults may be due to abuse.
• Significant findings include
-- delayed presentation,
-- injuries of disparate age,
-- retinal haemorrhages,
-- bilateral chronic subdural haematomas,
-- multiple skull fractures and neurological injury without external signs of trauma
e) Cerebral contusions
• Contusions are common
• found predominantly where the brain is in contact with the irregularly ridged inside of the skull
( at the inferior frontal lobes and temporal poles)
• ‘Coup–contrecoup’ injury ( contusion of the brain on the skull at the site of impact
combined with contusion elsewhere sustained as the brain
rebounds from the initial impact )
• Contusions appear heterogenous on CT, reflecting
their composition of injured brain matter interspersed with acute blood
• Contusions rarely require surgical intervention, but may warrant
delayed evacuation to reduce mass effect.
 Head Injury – Did you know this?

• Roving eye movements- are slow, conjugate, lateral, to and fro excursions. These occur when third nerve nuclei and connections
are intact and often indicate a toxic, metabolic or alternatively bilateral hemisphere cause for coma.

• They can also be defined as slow random predominantly horizontal conjugate eye movements (though there may
be a degree of exophoria) similar to those seen in deep sleep.
Likely cause: metabolic encephalopathy (may be absent in deep coma), bilateral supranuclear lesions.

• Dysconjugate gaze is a failure of the eyes to turn together in the same direction.

• Hyphaema-- is a pooling or collection of blood inside the anterior chamber of the eye
(the space between the cornea and the iris).
The blood may cover most or all of the iris and the pupil, blocking vision
partially or completely. A hyphema is usually painful.

•
Thank You